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Is Homo sapiens the only species capable of prioritization?
Just what the title states--given an absurdly large number of assignments to perform in a limited time-frame we usually attempt to do the most important ones first. Is this ability to define and execute by priority a universal feature in all sentients, or is it a socially learnt behaviour of us Homo sapiens?

I think this is a tough question - how could you tell? Many animals are seemingly capable of 'planning' their lives (for instance mating and rearing offspring at the right time, keeping them fed, safe from predators, etc, might seem to have taken some planning) but that is not to say they do any such thing. I would have thought it's all instinct, but I look forward to any answers!

of course not - prioritization is necessary to survival.  I think this is not apparent because most living things don't worry about so many things as we do.  But social relationships vs mating relationships or the act of mating vs food vs avoiding danger have very clear priorities with most living things.

Both useful comments .. I also goofed in my question a little - the concept of time itself is probably not very well understood by other species. I wonder whether I should make that into a question, and ask too.

Animal behavior is not my field but I think the answer is "no, animal feeding / foraging shows optimization of the cost / benefits of finding and capturing different foods / prey", an ecological 'paradigm' as explained here https://notes.utk.edu/bio/greenberg.nsf/d9441c1523c0c69785257015006e1937/1c127b67e45523e4852575de006d4233?OpenDocument

There is a very simple experiment you can do that will demonstrate that animals prioritize. Give a dog two bones. Preferably one which is more tasty than the other. Say one has more meat on it. The dog cannot eat both at once and you will observe it choosing one over the other. This is a clear example of prioritization.
Again with a dog, try observing one greeting two people it is fond of. If you and a friend stand a few meters apart when the dog comes up to you, the animal will choose to greet one of the humans first. Prioritization.
Any animal, or plant, fungus, bacterium or archaeon for that matter, that is ever presented with a choice between two actions during its lifetime, will have to be able to prioritize in order to chose between them. Clearly they can as our world is not strewn with, for example, panicked, confused looking squirrels trying desperately to chose which tree to climb.

Good point! Sir Dumpty, when offered a second bone whilst he is already eating one, will invariably opt to snap up the new one first; perhaps knowing the one he eats at present will remain untouched by the rest of his 'human family'... I could be wrong about understanding what goes through his mind though

@Everyone, please tell me you also have a cat called Dame Humpty!

Afraid not (+: Sir Dumpty is all by his lonesome.
p.s. Did you realize you're on the 666 score?

@Everyone, shame, poor Sir Dumpty, and yes, I only just realized my rep and its all thanks to your upvote :)

All species of the genus Homo were able to plan stone tool manufacture in a way that suggests the ability to prioritize and follow steps to an envisioned end form.

Good point! too bad the other members of our genus are extinct.


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Is there any reason the common housefly continues to return to an area?
This might come off as a really silly question. But I'm wondering (especially in the case of food) if there is any reason a fly would continue to try and sit on top of a piece of food even after swatting it away. I assume (it could be misconception) that it is instinctive that animals and insects would leave an area if it is harmful / dangerous to their existence after having close encounters more than once. Is this not the same for the fly?
I have this question mainly because I recall waving a fly away several times while eating lunch, and I couldn't understand why the fly wouldn't just find another place where there is food or somewhere safer.

I don't think it's a silly question, but it is a common error to anthropomorphise animals.
Insects respond to cues which they have evolved to respond to, and this is how they 'make decisions'. They do not have free will or any more complex decision-making process like common sense. This is evident is lots of insect behaviour: flying repeatedly at a closed window; landing on brightly coloured clothes instead of flowers; and returning to a food source when they are in real danger of being swatted!
When a fly senses the food (often by olfactory receptors), they are 'programmed' to fly towards it in response to some chemical they sense depending on the species and food. They may not have adapted a response to swatting, or perhaps the food cue overrides others. In nature swatting is not so much of a threat to a fly. Some animals may brush them away, but since they are not really doing any harm in feeding from another animal's food, they are mostly ignored.
CO2 traps are used to entice and kill mosquitoes. The mosquitoes are attracted to CO2 (as it is dispelled from the animals from which they blood feed), they will only evolve to avoid the traps if there is another cue which they could eventually associate with a negative effect.
Another thing to remember when thinking about insect behaviour is that their life strategy is very different to ours. Insects are more r-selected than humans, meaning that each individual life has not had so much energy put into it as a more K-selected animal (such as humans), and to compensate for this, many more young are produced. This often results in more risks being taken by individuals since there will still be a viable population even after many deaths.
Chapter 4 of 'The Insects' by Gullan & Cranston gives a good introduction to the sensory responses of insect behaviour. There are other books on the subject, 'Introduction to insect behaviour' by Atkins looks like a good starting point, but I have not read it yet.

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Why does ampicillin in solution turn yellow?
I have a universal tube with 10 mg mL-1 ampicillin. When I got it, it was supposed to be sterile. It was opened for approximately 20 minutes for an experiment and has since been standing around sealed for a good month now.
Within the last couple weeks, it has gradually turned yellow. Right now the colour is faint, with a green-ish tint.
Why would it turn yellow? I know NADH is yellow, so that was my first guess. But I couldn't exaplain why ampicillin would cause NADH to accumulate, so I discarded that.
Side info: Ampicillin acts on bacterial cell walls, maybe that might help.

I assume you know that, but ampicillin solution should be stored at -20°C in aliquots, it's not the most stable molecule.

Ah, I never thought it could just be an unstable molecule. I'm going to read up a bit more about the ampicillin itself then; I thought it had something to do with contamination.

Just take a look at the structure, does that four-membered ring look strained to you? ;-)

Oh wow I didn't even know that was possible. So could the colour come from the Phe-like member when it breaks off?

Why is NADH the first thing to come to mind? Time for some physical chemistry.
Beta-lactams has a shorter ring structure which give it a different absorbance (around 322 nm apparently (source needed)) which gives it a blueish hue. Typically Penicillin and Ampicillin start off as an off-white. As hinted by @Mad Scientist, the beta-lactam rings are unstable and will undergo acid-catalyzed hydrolysis which breaks the 4-membered ring.
The Penicillin core also near a ketone which can attack the ketone in the lactam (I'm pretty sure this qualifies as enol chemistry but it has been awhile). The cyclization will form a 5-membered oxazole ring. Based on my experience, unsaturated 5-membered rings will absorb at a higher wavelength tending to result in a yellowish color (570-590 nM) so I am going to suggest that is the source of your color.

Ampicillin degradation

Cheers, very informative. NADH was just because that's the only yellow compound our classes have dealt with until now.

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Why does hair turn grey or white, and why does it happen later for some?
The question is pretty simple: what is happening molecularly when hair turns grey or white? I would imagine that it is due to the lack of a particular compound. I'm also interested in why some people's onset of grey hair happens much later than others.

Each individuals hair colour is determined by the particular pigment they produce (called melanin - the same stuff in your skin that makes you tan).
As the body ages this pigment (produced by the melanonocytes - cells that reside in the hair follicle) is produced less and less, until the hair is no longer coloured, and appears grey.
This is unique to each individual because it is a genetic (and therefore highly heritable) trait. Because it is in no way linked to mortality there is no selection pressure against greying hair.
The reason that the pigment is not longer produced is the gradual depletion of the stem-cell pool with age. This is common to many tissues, hair follicles being just one. As the 'pool' of stem cells is depleted, the melanocytes are no longer replaced as frequently, and thus less pigment is produced as we age.

Are there ideas as to why the pigment production declines with age?

@RoryM - added reference to interesting review on the subject.

Thanks for the answer and the edit  (which is what I was most curious about).

Stress has finally been definitively shown to be a cause of graying hair.

As such, delay or acceleration of onset could be due to stress.

Work by Zhang et al. (2020) (postdoc in Ya-Chieh Hsu's lab at Harvard) showed that acute stress leads to hair greying through the fast depletion of melanocyte stem cells in mice.
Of note from their abstract:

hair greying results from activation of the sympathetic nerves that innervate the melanocyte stem-cell niche. Under conditions of stress, the activation of these sympathetic nerves leads to burst release of the neurotransmitter noradrenaline (also known as norepinephrine). This causes quiescent melanocyte stem cells to proliferate rapidly, and is followed by their differentiation, migration and permanent depletion from the niche. Transient suppression of the proliferation of melanocyte stem cells prevents stress-induced hair greying. Our study demonstrates that neuronal activity that is induced by acute stress can drive a rapid and permanent loss of somatic stem cells, and illustrates an example in which the maintenance of somatic stem cells is directly influenced by the overall physiological state of the organism.

You can read a more complete summary of this work here.

The reason for this is that catalase, the enzyme responsible for catalyzing the breakdown of hydrogen peroxide on the surface of the skin, diminishes as we age.The "greying" is the the effects of bleaching of the hair fiber as result of the increased peroxide levels at the skin's surface.

Not exacly can you add any references for your claims ?

To reinforce the comment made by @L.Diago, I would suggest as a new user you consult the help on answering questions. The key thing about Stack Exchange sites is that answers are voted on in an objective manner. I do not know the answer to the question, but neither I nor the poster can judge if your answer is correct unless you provide evidence (references, preferably linked) in support. This is science. Nobody (or at least, not me) is going to accept it on your word, even if you are a Nobel Prize winner.

helpful link o you can properly flesh out this answer. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3973559/

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T7 promoter leakiness
Can a gene be expressed under the T7 promoter in an E. coli strain (e.g. DH5 alpha), which does not have the T7 polymerase gene encoded in its genome? In other words, is T7 promoter leaky?
To be more specific, how is it possible that a regular E. coli strain, which does not encode for the T7 polymerase, can grow on kan selective media if it was transformed with a plasmid that has the kanR gene under T7 promoter?

I know I'm digging this up, mostly b/c I'm running into some T7 issues, but if you are referring to a specific experience, are you sure plasmid has the kan resistance under T7 promotion, not just the insert?

Apparently not, leakiness can be controlled by tightly regulating the T7 polymerase with a tight promoter (in this case lacUV5).

Isn't it possible that a regular E. coli strain that does not have T7 polymerase, has other polymerases that can recognize the T7 promoter?

The reference points to BL21.  I took a look at the MG1655 genome to see how many copies of the alpha I or II subunit, which with sigma subunits, defines the sequence specific binding affinity of the native polymerase.  That should reveal any variations in the RNA polymerase binding. There is only a single copy of RNA polymerase alpha (which along wg of RNA Polymerase).  Its hard to say that something like this is impossible.  Its true that DH5alpha isn't a B or K12 derivative I think, so its always possible, but there is not rnap component mentioned in the strain description.

@GerganaVandova I've been thinking about this, and it seems to me that phage gene transfers might be relatively rare in bacteria because their genomes have so much genetic flux.  a new polymerase would not affect any of the native genes - it would require quite a few mutations for a second polymerase to take hold in the genome given how trim bacteria tend to make themselves.


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Is it possible to sequence only the 16S rRNA component? If so, how?
There have recently been several papers on using 16S rRNA as a way of identifying species (here, and here). I'm wondering if it's possible to sequence either just that subunit of the ribosome or just the sequence of DNA that it comes from (probably not, I know). That way you can use only the sequence you need to compare against other 16S rRNA sequences to test for novel species.
If so, what is the process involved?

Maybe I am just over-reading your question, but why would you think sequencing 16S would be more complicated that sequencing any other gene?

Well I think that the simple answer is yes and in fact it is commonly done.

@nico & bobthejoe well I'm unfamiliar with the process of sequencing genes, so I don't have any idea of how it's done. Could you explain the process? I'll edit the question.

you should probably just read about colony PCR.  that is the simplest method...

Basically, all 16S genes are highly conserved, i.e., they share much identical bases. This means one can bind the 16S gene piece (after DNA was cut) to a specific other piece of DNA, even if you don't know exactly the 16S gene bases. Everything else is discarded then. Now finally, using PCR the rest is amplified and sequenced. Sequencing 16S only is much less work, so that's how they did it years ago. Today, whole microbiomes are sequenced by professional labs.

Is it possible to look at the actual rRNA molecule and get the sequence of rRNA rather than sequencing the DNA the encodes for it?

I don't know but I think it would make a good question. 8)


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variation in expression accounted for a SNP -- what's a usual percent?
I am reading a GWAS paper that found a SNP associated to predisposition to colon cancer and was assessed for gene expression of the nearby gene. They found that the genotype accounted for 55% of the variation in the nearby gene expression. 55% sounds like a lot to me, what is the usual percent accounted for a significant SNP in a study like this?

 Dunlop MG, Dobbins SE, Farrington SM, Jones AM, Palles C, Whiffin N, Tenesa A, Spain S, Broderick P, Ooi L-Y, et al.. 2012. Common variation near CDKN1A, POLD3 and SHROOM2 influences colorectal cancer risk. Nature genetics 44: 770–776.

eQTLs (expression quantitative trait loci) are variants that affect the expression of one or more genes.
There have been several 'genome-wide' studies of SNPs that directly affect expression. The actual effect sizes are hard to pin down in most of them, but in the supplementary data for this paper is a list of the SNPs with the largest effects and coefficients of determination.
There are several common SNPs (cis-acting) that account for >50% of the variation in that genes expression in this (European) population cohort. That being said, that vast majority of variants account for much less variation in the expression, but this is to be expected.
I therefore can fully suppose that a disease-linked SNP could affect the expression of a gene to that degree, particularly if it is an oncogene or tumour suppressor.
Reference:

 Wood AR, Hernandez DG, Nalls MA, Yaghootkar H, Gibbs JR, Harries LW, Chong S, Moore M, Weedon MN, Guralnik JM, et al.. 2011. Allelic heterogeneity and more detailed analyses of known loci explain additional phenotypic variation and reveal complex patterns of association. Human molecular genetics 20: 4082–92.


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Why is the Kakapo more attracted to humans than its own kind?
The Kakapo can be seen in this video by BBC. It is said that the species is strongly sexually attracted to humans. Why could this be the case?

The male kakapo (Strigops habroptila) in that video is called Sirocco. Kakapo were (and still are) very close to extinction, so in the 1980s the Kakapo Recovery Programme was launched. As part of this programme, rangers monitor all known kakapo in the wild, visiting their nests and generally ensuring they are in good health. When Sirocco was a young chick, a ranger discovered him in his mothers nest with severe breathing problems. He was brought back to the Kakapo care hut and raised by humans. As a result of this, he imprinted on his carers (see his website!).
Imprinting is common in birds, and takes several different forms. The most well-known form is filial imprinting, where young birds (and some other animals) develop a strong fixated image of who their mother is. They then learn their behaviour almost exclusively from the animal they fixated on. This is well studied in geese, for example by Konrad Lorenz.
However, Sirocco was demonstrating sexual imprinting. This is where young animals (including humans, see e.g. Bereczkei et al., 2004) learn which characteristics are sexually desirable by fixing an image of their parent(s). In Sirocco's case, he imprinted on a human and subsequently saw humans as his species, and therefore potential mates.
The exact purpose of sexual imprinting has been widely discussed (e.g. see Immelmann, 1972). Lorenz suggested that it allowed animals to recognise their own species. However, some imprintable birds will show a preference toward individuals resembling the one they imprinted on, but when introduced to their own species will still recognise them as potential sexual partners. It may therefore be the case that imprinting allows a juvenile firstly to supplement a genetic predisposition toward its own species, but secondly to recognise closely related and less related individuals. Bateson (1978) suggested that this would enable a sexual strategy of choosing mates which are sufficiently unrelated so as not to cause inbreeding depression, but sufficiently related so as not to cause outbreeding depression, and he found an example which bore out the predicted behaviour in Japanese quails.
Sirocco seems not to have the genetic ability to recognise his own species, and according to his website does not associate with other birds.

 Bateson P. 1978. Sexual imprinting and optimal outbreeding. Nature 273, 659 - 660.
 Bereczkei T, Gyuris P, Weisfeld GE. 2004. Sexual imprinting in human mate choice. Proceedings of the Royal Society of London, Series B: Biological Sciences 271: 1129–1134.
 Immelmann K. 1972. Sexual and Other Long-Term Aspects of Imprinting in Birds and Other Species. In Advances in the Study of Behavior, Vol. Volume 4 of, pp. 147–174, Academic Press

@Richard_Smith Great answer.


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Is there any recent evidence for the aquatic ape theory of human evolution?
The aquatic ape theory suggests that many features that distinguish humans from their nearest evolutionary relatives emerged because the ancestors of humans underwent a period when they were adapting to an aquatic or semiaquatic way of life, but returned to terrestrial life before having become fully adapted to the aquatic environment.  Is there any new evidence of this?

interesting - I have not heard this theory. Did you have links/references to this from your own reading?

There is a book called "Aquatic Ape Hypothesis" by Elaine Morgan which is definitely worth a read.

I'm very interested in this too. David Attenborough once did a radio programme about the aquatic ape hypothesis, and you can listen to it free online.

In short: No. http://johnhawks.net/weblog/topics/pseudoscience/aquatic_ape_theory.html

See also: http://www.aquaticape.org/whyanthro.html

The johnhawks.net article is not a good piece, being poorly written and poorly reasoned. On the other hand the http://www.aquaticape.org site is very well argued, but has no references.

maybe we can close this question at this point? can one of you someone write up what the above to get this off the books?

The Aquatic Ape theory has never gained wide acceptance. This is because it has never had strong evidential support.
The features supposedly supporting the hypothesis only do so under an extremely superficial analysis (e.g. the argument for bipedalism), frequently actually occur in other non-aquatic mammals (e.g. hairlessness in naked mole rats and rhinos, a descended larynx in red deer), show no sign of having arisen at similar times in the human evolutionary record (e.g. encephalisation evolved far later than bipedalism and bipedalism vastly predates hairlessness) and lack fossil evidence of having evolved near aquatic environments.

yes - An idea is often not a hypothesis, and hypotheses often have no supporting evidence.

Article in the Guardian by an Editor of Nature on this: http://www.guardian.co.uk/science/occams-corner/2013/may/07/aquatic-apes-creationism-evolution  I wouldn't say this theory is creationism, but it does not have the weight of any evidence behind it, which is necessary for evolutionary theories.


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What is the appropriate method to send a strain?
We are planning to send an ecoli strain to another lab. What is the appropriate way to do so. No MTA is required but the options seem to be using filter paper or sending a glycerol stock on dry ice.

Is the lab in the same country? I am asking because international (and more so intercontinental) shipping on dry ice can be a major pain.

Good for you (I can tell you, sending samples on dry ice from Europe to Australia did quickly turn into a bureaucracy nightmare! :D)

I believe Addgene send strains as bacterial stabs.
This is the protocol from Qiagen.

E. coli strains can also be stored for up to 1 year as stabs in soft
  agar. Stab cultures are used to transport or send bacterial strains to
  other labs. Prepare stab cultures as follows:

Prepare and autoclave LB agar (standard LB medium containing 0.7% agar) as described in the last issue of QIAGEN News (1).
Cool the LB agar to below 50°C (when you can hold it comfortably) and add the appropriate antibiotic(s). While the agar is still liquid,
  add 1 ml agar to a 2-ml screw-cap vial under sterile conditions, then
  leave to solidify.

Vials of agar can be prepared in batches and stored at room
  temperature until required.

Using a sterile straight wire, pick a single colony from a freshly streaked plate and stab it deep down into the soft agar several times
  (Figure 1).

￼￼￼￼￼￼￼￼￼4. Incubate the vial at 37°C for 8–12 h leaving the cap
  slightly loose.

Seal the vial tightly and store in the dark, preferably at 4°C.

When recovering a stored strain, it is advisable to check the
  antibiotic markers by streaking the strain onto a selective plate.

I believe if the shipping is <24hrs you could send a stab in ice.
Hope that helps
Ben

I think the best way is to use lyophilization. The American Type Culture Collection send the strains that way.


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What are treatable foetal conditions during pregnancy?
What are different foetal conditions during pregnancy that could be treated with appropriate prenatal genetic testing?
I only know that pregnant women are encouraged to take certain supplements to make sure certain conditions won't develop in the foetus, and which are apparently also the case for deficiencies in human growth hormone, but I imagine there must be other specific cases that are treatable for specific conditions diagnosed to only a small number of cases?

this question seems like it would require a full book to respond to it.  there must be scores or even hundreds of such conditions.  Could you maybe be more specific and focused - break the question up?  dietary conditions?  genetic tests?

Your question probably expresses a subtle confusion about the prenatal diagnostics and genetic testing.
So, genetic testing is one of the diagnostic methods in prenatal diagnostics (among with the other methods, see the list) which is used to diagnose genetic disorders of the foetus, whereas the disorders that are diagnosed on this stage are mostly genetic anomalies with dramatic impact on the feotus development, for example chromosome aberrations (like Down or Turner Syndromes). Should these conditions be diagnosed, the woman is given a choice to interrupt the pregnancy prematurely.
Less dramatic conditions (like sickle-cell disease) can be diagnosed at this time too, but are not treated before the birth.
The genetic disorders that are amenable to the dietary or medical treatment (like phenylketonuria or congenital hypothyroidism) are usually diagnosed in the newborn screening tests (newborn heel prickle test), because these screening is more precise and less dangerous compared to the pre-born diagnostics.

So are there any prenatal diagnostics that can be treated during pregnancy?


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How do I deal with sticky and viscous samples from cell lysates?
To check a protein expression I pelleted a small amount of E. coli before and after induction and lysed them by redissolving them in SDS-PAGE loading buffer and heating them to 95 °C for 1 minute.
This lead to a solution with some very sticky and viscous parts in it, that make pipetting the sample into the gel wells extremely annoying. As far as I heard, this is probably genomic DNA, and my usual way to deal with this is to centrifuge the samples and only pipet a small part out from the top. This does seem to help sometimes, but not always.
How can I avoid the formation of that sticky and viscious stuff or how can I avoid pipetting that stuff into my wells?

Just to say I have the same problem! So I look forward to the answer.

Yes, it is the genomic DNA that is causing you trouble. Although a brief 1000g spin should bring it all down, the pellet is never tight and you almost always are going to pull up some gunk with the clear supernatant. A better solution is to include a quick sonication step (5-10s) before the 1000g spin. That way, the DNA is sheared and it should pellet better. It has worked for me most times. Also, remember to use a reasonable volume of SDS buffer when you lyse the cells. Too little buffer and its always going to be hard. For comparison, I use about 200ul per 1ml culture pellet and this volume works well for both pre- and post-induced cells.

In addition to gkadam's suggestion, for my protein gels, I heat my samples at 95C for 10 minutes. I would also look into different lysing conditions. Rather than using SDS loading buffer, look into more vigorous lysing steps either with a kit like bug-buster or using a homogenizer. When pelleting your lysate, I've traditionally done a 10,000g spin for 10 minutes.
Maybe I just work with really soluble proteins...

Definitely your suggestions will make things much better. I think Mad Scientist was looking for a quick and dirty way to do it when doing small scale checks for protein expression from a new construct.


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Why do ants live so long?
I was surprised to learn that worker ants in some species live many years. I would have expected a lifespan of a few weeks or months (which is apparently the case for many species).
What factors might account for the length (and/or variation) in ants' lifespans?   (ie, is there some evolutionary preference? Some fundamental limit on the reproductive capacity of the queen?) Is there any relationship between these lifespans and different structures of ant communities?

Can you name the species in which the ants live long?

There will always be a tradeoff in terms of resource allocation between reproduction and self maintenance. Since worker ants forego reproduction to perform other roles (gathering resources, caring for young etc.) within the colony, it makes sense that this would favour a longer lifespan. This idea works for most animals (i.e. higher reproduction = lower lifespan across species in general) and is well documented (Partridge et al. 1987, Gems & Riddle 1996 (PDF link), Westendorp & Kirkwood 1998 - to name a few). However the relationship is reversed in eusocial animals: the queens of ants, some bees and naked mole rats (which are all eusocial) tend to be longer lived than their sterile workers (Hartmann & Heinze 2003). Aging patterns within ants and other eusocial organisms are a very popular research topic at the moment, but the mechanisms causing differences between social castes are not fully understood.
Eusociality is strongly associated with increased lifespan, indeed many studies on the evolution of aging have focussed on eusocial animals which have appeared to overcome aging effects to an extent (Keller & Genoud, 1999, Buffenstein 2005). The naked mole rat is one of very few species of eusocial mammals and the relationship between its lifespan and body mass is very dissimilar to that of other rodents (ignore the bat points):

Image from Buffenstein & Pinto (2009).
If a queen has a longer reproductive lifespan then over the course of its life it will create a higher number of offspring. This will cause their increased longevity genes to be more prevalent in the gene pool over time - as long as they are able to reach the limit of their reproductive lifespan and are not killed by externalities (accident or attack) in the meantime. Therefore this trait (longer reproductive lifespan) will be selected for as long as the queen is protected.
Within eusocial colonies, there is often a protective environment (Buffenstein & Jarvis 2002): there is usually a physical structure (nest or burrow); symbiotic bacteria and/or fungi creating a more hygienic microflora; and queens are also protected by other castes. This gives queens a lower incidence of death due to accident or attack which (from the reasoning in the previous paragraph) supports the selection of a longer reproductive life. This is likely to lead to longer lived workers since they share the same genes.
However queens do tend to live much longer than their workers (O'Donnell & Jeanne 1995). This is probably due to their reproductive role. All the ants in the colony are investing in reproduction (whether by physically giving birth to young or by providing it with food and protection) therefore the normal relationship (reproduction and lifespan tradeoff) mentioned at the start is not relevant, but since the queen is the only individual reproducing, it will be the only one for whom lengthened lifespan is beneficial evolutionarily.
A mean lifespan of 20 years has been observed in Formica exsecta, and a maximum lifespan of 28.5 years observed in Lasius niger. Pogonomyrmex owyheei has an observed maximum of 30 years, and mean of 17 years. These (and many more) figures were obtained from a review by Keller (1998).
Other references on this subject include (Svensson & Sheldon 1998), (Keller & Genoud 1997) (PDF link), (Calabi & Porter 1989), and (Amdam & Omholt 2002).
References

Amdam, G.V. & Omholt, S.W. (2002) The Regulatory Anatomy of Honeybee Lifespan. Journal of Theoretical Biology, 216, 209–228.

Buffenstein, R. (2005) The naked mole-rat: a new long-living model for human aging research. The Journals of Gerontology Series A: Biological Sciences and Medical Sciences, 60, 1369–1377.

Buffenstein, R. & Jarvis, J.U.M. (2002) The Naked Mole Rat--A New Record for the Oldest Living Rodent. Sci. Aging Knowl. Environ., 2002, pe7.

Buffenstein, R. & Pinto, M. (2009) Endocrine function in naturally long-living small mammals. Molecular and cellular endocrinology, 299, 101–111.

Calabi, P. & Porter, S.D. (1989) Worker longevity in the fire ant Solenopsis invicta: Ergonomic considerations of correlations between temperature, size and metabolic rates. Journal of Insect Physiology, 35, 643–649.

Hartmann, A. & Heinze, J. (2003) Lay eggs, live longer: division of labor and life span in a clonal ant species. Evolution, 57, 2424–2429.

Keller, L. (1998) Queen lifespan and colony characteristics in ants and termites. Insectes Sociaux, 45, 235–246.

Keller, L. & Genoud, M. (1997) Extraordinary lifespans in ants: a test of evolutionary theories of ageing. Nature, 389, 958–960.

Keller, L. & Genoud, M. (1999) Evolutionary Theories of Aging. Gerontology, 45, 336–338.

O’Donnell, S. & Jeanne, R.L. (1995) Implications of senescence patterns for the evolution of age polyethism in eusocial insects. Behavioral Ecology, 6, 269–273.

Svensson, E. & Sheldon, B.C. (1998) The social context of life evolution history. Oikos, 83, 466–477.

I know I'm late to this, but longer worker lifespan could be beneficial because colony size is a function of birth rate and death rate. Longer lifespans means a slower death rate and colony size can increase without forcing the queen to produce more workers than normal. If workers died quickly, the queen would have to lay a lot more eggs to increase colony size.


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Extreme examples of protein translation/use coupling/decoupling?
What are known extreme examples of protein translation/effect coupling/decoupling? For example, examples of proteins that are immediately used at the time the have been translated and vice versa, cases of proteins that are translated but then only used much later in time in/outside the cell?

Is this similar? http://biology.stackexchange.com/q/2240/389

@bobthejoe, it is not similar. The OP is asking about cases where a protein is functional just after translation or, conversely, long after it.

Proteins that are membrane localized or secreted would take time to become active or even become poised for activity. Membrane receptors may remain inactive until triggered by the appropriate ligand. Nonetheless proteins won't remain (inactive or active) for a very long time as constant turnover happens in the cell.
One example, similar to what MarchHo mentioned in their answer (pre-proteins) is that of fibrinogen. Fibrinogen gets converted to fibrin when there is an injury and haemostasis reaction cascade is initiated. Fibrinogen has a biological half life (in its latency) of ~100 hours [ref].

A specific example would be great.

@MarchHo There are several. This is essentially a principle based answer. More the number of steps to final destination, more will be the latent period.

Chymotrypsinogen is a proteolytic protein that is translated and stored in the pancreas in an inactive form. They are only activated when they are secreted from the pancreas.
Other zymogens such as apoptotic caspases have similar lengths of time between translation and use.

One example that may interest you Rory M are the so-called toxin - antitoxin pairs in bacteria. Interestingly enough, many bacterial species need a way to protect themselves from their own toxins. Thus, for a particular toxin, a corresponding antitoxin is synthesized (most often both are proteins, but the antitoxin may be RNA as well, three types of toxin - antitoxin systems are known; check out http://en.wikipedia.org/wiki/Toxin-antitoxin_system). The antitoxin remains bound to the toxin until the latter is secreted into its designated location. If the antitoxin decouples prematurely, cellular death may occur. I'm not too sure how long the two are "stored" within the cell; I imagine this could vary greatly between species.


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How did the first self replicating organism come into existence?
When people try to explain evolution, they tell me that evolution is a cumulative result of mutations & natural section of the more superior individuals of a particular species. I think I'm fairly convinced with this explanation.
But when I think about it, all of them assume that there was an organism, however simple, that was capable of self replication & occasionally mutate. How did such an organism come into existence? Can anyone explain this?
An answer I found on Reddit didn’t really convince me.

If you want a good start, I would suggest looking at the RNA World hypothesis.

Can we please leave out the entropy canard? It’s totally irrelevant. Earth isn’t a closed system. Period. Furthermore, this would be completely off topic on a biology site.

I remember reading this entire article a few years ago, it was pretty revealing. http://en.wikipedia.org/wiki/Abiogenesis

Entropy is not irrelevent for this question (how could it be in organic chemistry??). Earth is not a closed system,but in these considerations you have to consider the scale of the experiment.

However, I agree that entropy can be an enormous distraction.

If you actually run the calculations, the second law of thermodynamics does show you something related to evolution: the entire evolution of the current biosphere could not have happened in much less than a month (http://physics.gmu.edu/~roerter/EvolutionEntropy.htm).  As long as you take longer than a month (say 4 billion years), there's no problem at all.

@NoahSnyder Thanks for the article. This is why I love StackExchange :)

Evolution or (as Darwin called it) "descent with modification" is a theory which explains the origin of the species NOT the origin of life.  How the first life arose is completely irrelevant to the theory of evolution.  What evolution does explain is how and why we have such variety of life on earth all descending from the same organism.
What you're asking about is not a theory of "evolution" but rather a theory of "abiogenesis."  Although there are many interesting hypothesis for how abiogenesis happened (e.g. the RNA world, the "metabolism first" theory, etc.), the fact is we simply do not know yet how life first arose.  What we do know is that life first arose between 3.5 and 3.9 billion years ago.  That's a really long time ago compared to lots of other important events in natural history (even the Cambrian explosion where modern animal phyla evolved was only half a billion years ago), and so it shouldn't be surprising that it's a hard problem.

Yes, you are right. I am asking about a theory of "abiogenesis". But I do think that its related to Darwin's theory because it assumes that an organism with the required qualities existed. Isn't Darwin's theory based on an unproven assumption? Can you clarify?

We know that organisms with the required properties existed 3.4 billion years ago, by looking at fossils of bacteria.  There's no unproven assumption there.  Evolution describes the most recent 3.5-4 billion years of natural history.  To go beyond that you need another theory.  That's fine, that's how science works.  You wouldn't say that gravity relies on unproved assumptions because it doesn't explain electricity or radioactive decay; it's not supposed to, it's supposed to explain gravity.

Agreed. I have nothing against Darwin's theory. All I wanted was a convincing theory of abiogenesis.

@GreenNoob The theory of evolution (only creationists call it Darwin's theory, just FYI) deals with changes in populations.  It says that given a starting population, changes will occur because X,Y, and Z in a way that you seem reasonably convinced by.  That starting population is an objective fact; we can see it in the fossil record.  Further, the theory of evolution says nothing at all about where that population came from.  It could be abiogenesis, aliens, or a deity; it really doesn't matter.  Abiogenesis uses many of the same ideas as evolution, but it's a completely separate theory.

It doesn't really matter here how scientists subdivide and name topics. There is only one nature. The question is about reality, not about organization of scientific fields.

We don't know how self-replicating molecules first arose (and probably never will know exactly) but the Earth is large and had 500 million years (i.e. the prebiotic Earth timescale) or so to experiment in organic chemistry. The land-sea interface (such as tidal pools) are a good candidate site since these are areas where high concentrations of organic goodies can be found.
In this context, one focus that researchers have been looking at is self-replicating molecules.
For example, one lab in Cambridge,UK has come up with tC19Z.
tC19Z is the name of a RNA enzyme that acts like a self-replicating molecule. It can copy chunks of RNA almost 50% as long as itself. It can also make copies of other RNA enzymes. This molecule is not "alive" itself, but clearly demonstrates how greater complexity can arise.

We don't know how self-replicating molecules first arose (and probably never will know exactly) Ouch, that hurt. You mean the whole of Darwin's theory rests on an assumption that is unprovable?

No, I just mean that how are we really ever going to know what the exact sequence of events was? I suppose it depends whether you are a contingency or convergence type!

Although we don't know exactly, we do have lots of examples of ways it might have happened. Not knowing exactly which one it was is not a problem, the important thing is we can demonstrate that it could easily happen that way.

@GreenNoob: Darwins Theory of Evolution doesn't deal with this aspect of life at all, and it rests upon two very provable assumptions: Life exists; and life changes.

@WillihamTotland Can you elaborate?

@RichardSmith We can demonstrate that it could easily happen that way Can you give some examples?

@GreenNoob: See my answer.

They teach us in Physics that the entropy of an isolated system is always increasing or at least constant. Then how can an organism be born under these conditions?

The sun sends energy to the Earth, allowing for a decrease in entropy on Earth at the expense of the sun's entropy.

But when I think about it, all of them assume that there was an organism, however simple, that was capable of self replication & occasionally mutate. How did such an organism come into existence? Can anyone explain this?

That organism you're talking about is just a molecule that copies itself. Exactly how it has come about is not clear to me but it's not hard to imagine the possibility. A vast planet with molecules flying all over being bathed in ultraviolet light and if any molecule anywhere acquires the characteristic of copying itself, it will start growing exponentially and quickly spread all over the world.

If any molecule anywhere acquires the characteristic of copying itself, it will start growing exponentially and quickly spread all over the world Don't you think that's a big 'if' for a scientific theory?

Upvote for the "Sun sends energy to the Earth" part. Really cleared things up :)

No I think its a small if because its the only plausible explanation for the emergence of life I have ever encountered.

@GreenNoob It's not at all a big if - there are lots of molecules which demonstrate that property, some are biological like DNA or RNA, and some, like crystals, are mineral.

@RichardSmith Can you give examples other than DNA or RNA? I don't think that such complex molecules originally existed in the primitive earth's atmosphere.

@GreenNoob crystals are the simplest example, including ice and kaolinite. There are also lots of ways in which complex organic molecules could have arisen under conditions found on the early earth. See the wikipedia page for a round-up of them, or read Robert Hazen's book Genesis.

This is an extremely interesting and extremely fundamental question, indeed, and thus far, biologists have failed at coming up with a satisfying answer.
We know that all the parts are there, we just don't know how they were arranged, or which ones go where.
The question is, in essence, composed of three sub-questions:

How did the fundamental building blocks of life come about?
How did the first self-replicating molecules come about?
How did cell membranes come about?

The answer generally takes the form of "On primordial Earth, a small selection of the billions of organic compounds generated when UV-light hits a mess of carbon dioxide, nitrogen and water where captured in a tide pool where concentration and foam led to random chance producing self-replicating molecules in proto-cells."
This answer, while almost certainly true, is also incredibly dissatisfying, because all it tells us is what deductive logic has already taught us, almost intuitively.
Incidentally, the fact that all of this happens with a million to one odds isn't a problem: The Earth is big, and the time frame for this happening is along the lines of hundreds of millions of years: Anything that might happen once per year by a million to one shot would likely happen hundreds of times in that timeframe.
In any case, when it comes to evolution, or Darwin's Theory of Evolution, or any other theory of evolution, this is all irrelevant.
Evolution is something that happens in any sufficiently complex (open) system, assuming it has the capacity to change at all.
It is most easily observed in living organisms, because they are at the right scale, and incredibly diverse, but it happens on all scales of the universe.
In fact, the easiest way to explain how life first originated, is just to keep counting backwards when you reach the Last Common Ancestor (of All Life on Earth), and propose models for how this proto-bacterium could be even simpler, until you're left with CO₂, N₂ and H₂O, and other simple molecules.
At that end of the spectrum it is well-understood that e.g. H₂O "evolves" from H₂ and O₂, because H₂O has a quality that makes it more "fit" than either of its components, chemical stability.
Furthermore, H2 "evolves" from free hydrogen by a similar mechanism, and free hydrogen "evolves" from protons and electrons, because it has the property of being electrically neutral, which is also a desirable property.
Of course, at the level of protons and electrons, things get a little muddy, and evolution kind of breaks down as a method for explaining how things come about.
Edit: For reference: Current Models of Abiogenesis on Wikipedia.

Your odds are a little off.  A million to one isn't even close.  More like a billion, trillion, trillion, trillion, trillion to one it happened in the time period described.  It is the mathematical definition of impossible.

While many point to RNA, or a variant of it, as being the first molecule of "life" very few people know where it came from. Some suggest that it came from outer space because it's uncertain how the material for sugar-phosphate backbones could have developed on earth and that the perhaps these materials found their way here via meteorites. There are several hypotheses as to how an early earth environment may have promoted the properties of these molecules, but it's difficult to ascertain what exactly happened.
Somewhere within that abiogenesis wikipedia article is the mention of the role of deep-sea vents. The deep-sea vents and the currents that surround them basically facilitated a PCR reaction. Some of the early emerging DNA, maybe with some RNA and free nucleotides floating around, could have leveraged such an environment for replication and by sheer number (and some chance) entered into symbiotic relationship with other molecules to form the first cellular structures.

If you are interested in this question, I highly recommend you look at the work of Jack Szostak -  Nobel Prize winner at Harvard who is currently doing some of the best work in this area. His work is grounded in good experiments that point to how abiogenesis could
 have happened.

I think that it started like this:
First stage:
Chemicals like Na, Cl, O₂, O₃, CO₂, CO, HCN,  and H₂SO₄ react to form small molecules.
Second Stage:
Next those small molecules react to form macromolecules.
Third Stage:
DNA, being the most stable was first to replicate. A membrane eventually enveloped this and formed the nucleus
Fourth Stage:
Via Endosymbiosis it envelops mitochondria in an outer membrane
Fifth Stage:
Cell starts forming membrane and protein for all of its organelles. It is now a eukaryotic cell.
This is the DNA world Hypothesis.
Because DNA can be single, double, triple, or quadruple stranded in organisms(That would be ssDNA, dsDNA, tsDNA, and qsDNA respectively) it can do much more than just code for proteins or rRNA or tRNA.
In the single stranded state it can act like an enzyme forming deoxyribozymes.
In the triple and quadruple stranded states it can act inhibitory without needing another protein or methyl group.


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Is it possible to repopulate lactase in the stomach?

Possible Duplicate:
Can an adult without genetic lactase persistence still develop a tolerance for dairy foods?

In my younger years, I don't seem to have a problem drinking milk.
Nowadays, when I drink milk, I keep farting away.
After searching around the Internet, this site claimed that it is due to lactose intolerance. They have a product that claims to be able to repopulate the enzymes in the body so that it can digest milk. Is this product based on sound principles?
Can someone (other than the Dairy Care company itself) refute or support its claims?
Thanks!

Although the other question is not specific to this product, the answer does answer your question.

I think the other question answers this and is a better written question.

How does "repopulating the lactase enzyme" and "tolerating milk" mean the same thing?

If you read the answers you will see they describe essentially the technology which is in the product you asked about. The supplemented lactobacteria produce the lactase enzyme, and the tech fundamentally is sound. Whilst the question isn't worded the same, the answer you're looking for is there. Anyone answering this question would basically be repeating all the info in those answers.


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Sequencing from PCR
As far as I understand it, PCR can be used to make many copies of one gene. My question is, is it possible to sequence DNA after PCR and is it easier than sequencing it via other methods. If it is possible, how would you do it?

All sequencing methods, be it classical Sanger sequencing or next-generation sequencing (or even third generation) need a certain amount of DNA to work with.
You either need to extract DNA from a large-ish tissue sample or you need to amplify DNA content from a smaller sample. The first approach is often impractical, or downright impossible (when you want to work with single cells or very small organisms).
So PCR is used routinely to amplify DNA before sequencing. The sequencing itself isn’t influenced by this – you use whatever technique is appropriate. However, the PCR may introduce biases into the data because not all DNA fragments amplify equally efficiently. This needs to be taken care of in the downstream analysis of the sequence data if quantitative information is required (as in RNA-seq or ChIP-seq).
Coming back to your question, PCR isn’t a sequencing method in itself. It just helps getting the necessary amount of raw material in order for sequencing to work. Furthermore, most sequencing methods actually include PCR steps as well, since they rely on the generation of of overlapping DNA fragments to be stitched together.

We do it all the time. You can use one of your end/flanking primers and use that as a primer for sequencing. Companies will typically have a setup where they can take a "premixed" sample.
Since we tend to use sequetech, here are their details: http://www.sequetech.com/requirements.php?premixed=1
For a second opinion look at Elimbio's: http://www.elimbio.com/Sample_Preparation.htm

Could you expand your answer with more of the "how"?

Yes, I'm actually more interested in how they sequence the DNA.

It should work exactly the same way as sequencing a plasmid. Traditional sanger sequencing read by capillary electrophoresis.


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How would one describe the R-factor in crystallography?
Yes, there is the wikipedia definition, but how would one explain this concept to a non structural biologist?

And what is the background of the person you would like to explain the R-factor concept to?

Crystallography requires the collection of many measurements (could be a few thousand to even millions depending on the size of the molecule and complexity of the crystal (technically speaking, the size of the crystal's unit cell is a major determining factor for the size of the data set).  I'm not going to assume this is a small molecule crystal like a salt or a large molecule like a protein.  its not necessary here.
I'll call this a set of intensity measurements, even though what is actually used is the square root of the intensities measured, called the structure factor.
The only way we really know that the molecular structure model is correct is that it generates as accurately as possible the intensities that were experimentally measured.
R, which I believe stands for residual, is a fractional difference between the measured intensities and what any proposed molecular model gives.
The residual is calculated as the absolute value of F(model)-F(measured).  This means that 0.0 is a perfect match while 1.0 is a perfectly awful fit that shows the model is perfectly awful.
In practice 0.60 is usually as bad as random model will give you (there's a statistical argument as to why it doesn't go higher).  Also the measurements are usually not perfect - they contain errors in measurements or artifacts from imperfect crystals or the detector, so an R value of < 0.20 (20%) is typically what you see in a reasonable paper.  I think its commonly less than 0.15 for most structures now in fact.


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Is it possible to lose synapses over time?
I mean, what if a person is for a long time submitted to conditions in which his mental capacities are not explored, are the synapses undone? I've heard that drugs may cause such an effect, but what if the person is not submitted to drugs or any severe accident, may the forgetfulness be related to the simple lack of usage of a certain knowledge?
Is the lack of brain usage the main cause for Alzheimer's?

Regarding your question about losing synapses; yes, synapses are regularly lost in a process called Synaptic Pruning. From the Wikipedia article:

A decrease in synapses is seen after adolescence reflecting synaptic pruning, and approximately 50% of neurons during development do not survive until adulthood. Pruning is influenced by environmental factors and is widely thought to represent learning.

Synaptic pruning is most significant during development due to "excessive" Neurogenesis that creates a large number of neurons, many of which will later be pruned. It's not excessive in a bad way, it's simply the case that more neurons are generated than necessary and thus pruning is needed to keep the connections efficient. There's no "measure twice, cut once", instead pruning is used to refine connections.
Synaptic Pruning really doesn't have anything to do with forgetting; Forgetting is natural and simply happens because connections (via Recall/Rehersal) are not made strongly enough to fully encode memories into Long Term Memory.
Note that Synaptic Pruning is not the cause for Alzheimer's or other age related degenerative disorders. From Wikipedia again:

Synaptic pruning is classified separately from the regressive events seen during older ages. While developmental pruning is experience dependent, the deteriorating connections that are synonymous with old age are not. The stereotyped pruning can be related to the chiseling and molding of stone into a statue. Once the statue is complete, the weather will begin to erode the statue and this represents the experience independent deletion of connections.

Synaptic Pruning is a normal process of development and occurs in all individuals. Alzheimer's is a very visible disorder due to media focus, but not part of normal developmental/aging effects.
Instead I suggest you read more specifically about Alzheimer's disease, there's quite a bit of information on it.

+1 for a correct explanation of the fact that not only it does happen, but it is a physiological process!

This answer was very useful and instructive for me! I appreciate you so much by that!


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What is the mIU unit as used in hCG hormone levels?
My girlfriend is in her very early pregnancy, and has provided several blood samples by now where the doctors measure her hCG levels.
The hCG hormone level is measure in a unit called mIU/ml which I figure is milli-something per milliliter blood. But what is that something? What is the IU?

IU stands for "International Units" and it is an arbitrarily chosen unit of measure used mostly to quantify hormones, vitamins or various substances found in the blood.
The idea is well explained by the Wikipedia article on international units)

Many biological agents exist in different forms or preparations (e.g. vitamin A in the form of retinol or beta-carotene). The goal of the IU is to be able to compare these, so that different forms or preparations with the same biological effect will contain the same number of IUs. To do so, the WHO Expert Committee on Biological Standardization provides a reference preparation of the agent, arbitrarily sets the number of IUs contained in that preparation, and specifies a biological procedure to compare other preparations of the same agent to the reference preparation. Since the number of IUs contained in a new substance is arbitrarily set, there is no equivalence between IU measurements of different biological agents. For instance, one IU of vitamin E cannot be equated with one IU of vitamin A in any way, including mass or efficacy.

For hCG, in the 55th report for of the WHO Expert Commitee on Biological Standardization, you could find:

The Expert Committee on Biological Standardization, after consideration of this issue (11), concluded that the choice of unit should be made on a case-by-case basis and reflect, and be based on, the biological and medical as well as the physicochemical information available.
  Many biologicals exist in both active and inactive states, and the clinically relevant form of the analyte may depend on the diagnostic aim. For example, the active state of the placental hormone chorionic gonadotrophin (hCG) is the relevant molecule to measure in the diagnosis of pregnancy, whereas the biologically inactive free beta subunit (hCG-beta) is measured to diagnose choriocarcinoma. Generally, a measurement of biological activity is expressed in IU, whereas measurement of the amount of a protein or of a specific protein structure is expressed in SI. In this case there would be a compelling reason to relate the measurement of hCG to a unit of biological activity, and the measurement of hCG-beta to an SI unit of quantity. Accordingly WHO has established a reference preparation for hCG (currently the fourth International Standard, with an assigned content of 650 IU/ampoule) (7) and a reference preparation for hCG-beta (currently the first WHO Reference Reagent for immunoassay of hCG beta subunit, with an assigned content of 0.88nmol/ampoule) (18). The former preparation was assigned a value based on bioassay, whereas the latter preparation had been extensively characterized by physicochemical and
  immunological methods and calibrated in nanomol by amino acid analysis. Applying these considerations of the properties of biological analytes, and their measurement in the clinical situation allowed the WHO biological reference standard for hepatitis B surface antigen, assigned a value in arbitrary IU rather than in SI units, to be adopted by the medical devices sector of the European Commission as the standard required for the fulfilment of the so-called Common Technical Specifications (CTS) for in vitro diagnostic devices. The Common Technical Specification document supporting the European (IVD) Medical Devices Directive 98/79 EC is a legally binding document within the 25 countries of the European Union.
  Where it is appropriate for a WHO biological reference standard to be calibrated in SI units, the principles outlined in ISO 17511 (8) should be followed. This will necessitate the existence and use of an appropriate single reference method and an assignment of uncertainty, derived from calibration data. Such a reference method should not be a biological assay because the factors that affect the results of such assays are not fully understood. Where they are used, SI units assigned to biological reference standards should be derived from, and traceable to, physicochemical procedures.

Note that IU are not the same as enzyme units (U) which is a measure of enzymatic activity


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Paralogous genes in genome-wide association studies?
Has anybody tested if paralogous genes are over-represented among the genes identified by genome-wide association studies (GWAS)?
For example, if a GWAS study finds 200 genes associated to the disease/trait, and a number X of those can be classified as belonging to Y different gene families, is there a test to see if X and Y are bigger than expected, given the total number of genes and gene paralogies in a genome? Here I am talking long established copies within a species, not CNVs in different individuals of the same species.
I am thinking there is an interesting question behind this: if a gene has duplicated during the evolution of a genome, and the different gene copies have taken specialized, yet related, roles, an unbiased analysis like GWAS should be able to find cases where different paralogous copies associate to different subdiseases/subtraits within the same global disease/trait.

Hello. Could you help by clarifying your question? Do you want to know whether paralogous genes/regions are over-represented in GWAS hits? It is an interesting hypothesis - have you any ideas/references why this may be the case? It's always best to give as full and clear a question as possible. Thanks

That is an interesting question (thanks for the expansion). If the paralogous genes were still functionally related there is likely to be redundancy between them, so a SNP in one of the copies may not manifest at all. A SNP that affects a sub-trait specific to one of the copies would need to have a massive effect (or the study would require a phenomonal sample size) to find it (unless it was a targeted study only on paralogous genes known to be disease related?). I don't know fo any studies, but will be interested in others answers!

Is a Fisher's exact test (a chi-squared test with more relaxed assumptions) something you've considered?

I actually don't understand what the hypothesis is. First, there are tons of confounding factors to control for -- for instance, regulatory gene families may be more likely to expand than structural gene families, so you'd need to account for that (and a lot more). Your final question regarding subfunctionalization seems to have nothing to do with the original question of over-representation.

Aren't paralogs supposed to have divergent function? I would expect them to be under-represented.

You could test it also by counting paralogs in the hits only, then pick eg. 200 random genes (depending on how many hits your GWAS caught) and count in those.

I think it depends on just how related the paralogs are.  If they diverged a long time ago, then we can assume the SNPs that show up in your hypothetical GWAS are indeed independently associated with the disease.  However, it's not strictly possible for the same SNP to occur in another gene, it's sort of by definition a different SNP.  As GWAS methods generate correlations, not causations, if those same-but-different SNPs are associated with the disease, that's the end of the story.  Deeper inspection is required to learn more.

This is one paper where they separated out-paralogs from orthologs and did conservation of protein-protein interaction studies across species.The methods which they used could be helpful in doing similar studies.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3447968/

There is no literature report saying such a thing. However, I did a cursory check for GWAS study on neuroblastoma.

Selected SNPs with p-value>0.05
Converted p-values to a score —  -log10(p-value)
Mapped the SNPs to genes while calculating cumulative score for a gene

I just sorted the genes based on their names, assuming that many paralogs have similar names. I know it is not the right way to go about it. However, I found many similar named groups in the list.
Now the next step is find actual paralogs and to score the cumulative score for a paralog-group. This is a little task:

Get sequences of the genes
Run a BLAST search to find paralogs
Assign genes to groups and find scores

I can share the file with genes and scores. I would, however, continue only if someone is actually interested in pursuing this — this could be a research paper.
PS: If you want the file just comment your email id. Some IT admin idiot has blocked rapidshare/4shared etc


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How deep in the soil can a seed be placed and still develop into a plant/tree?
The selected answer to How does a plant grow before photosynthesis is possible? indicates that a sprout grows beneath the soil using the food stored within the seed.
Does this limited ready food place a restriction upon the depth to which a seed may be placed and still develop into a plant? What depth will be best applicable for a given plant/tree seed? Is there a mathematical relationship known?

TL;DR 1) yes, 2) depends on species, soil, climate, 3) yes

@David: Could you flesh out the mathematic relationship please? Is the math relationship universal, or species/phylum/order specific?

there is no single mathematical relationship, but I have tried to provide a general answer please let @richard or I know if you have further questions

The general mathematical relationship requires an allometric equation. There are not as many for seedlings as there are for mature trees (but see the answer by @Richard-smith for a specific example). But lets start with a basic assumption that the emerging seedling will be a very tall cone (tall = high h to r ratio).
The volume of a cone is:

$V = \frac{1}{3} \pi r^2h$

Then we need to know the density of the seedling to figure out how much carbon a seedling of height h would require. Lets say that the density is 1.5 g/cc (excluding water).
Then, assume that the biomass is 1/2 carbon (a fairly reasonable assumption).
To figure out how tall a seed could grow given carbon reserves, it would be necessary to determine the amount of carbon in storage in the seed. Say there were 5 grams. There will be a carbon cost of reallocating this to growth, say 50%. So, for a seed that has 5g of carbon, its total volume might be calculated as:
 (5g * 50% growth respiration)/(50% C content of biomass) * 1.5 g/cc = 7.5 cc

assuming that the seedling will have a radius of 0.2 cm, the height could be calculated as:

$h = \frac{V}{(3 \pi * 0.2^2)}
    = \frac{V}{0.38}$
          = 20 cm (for V = 7.5)

Note: this is just a very quick "back of the envelope" calculation with many assumptions. C is 50% of plant biomass is pretty close (the actually number is closer to 48%). The growth respiration cost is a very rough estimate, and will vary with nitrogen content of the tissue, soil temperature, and etc.. The plant will likely need carbon left to build a leaf, and another resource may be limiting.

Excellent derivation from principles, nice answer

@RichardSmith Thanks for looking it over. I just wanted to make sure I didn't miss anything obvious.

To answer your specific questions...
Does nutrient availability limit emergence depth?
Yes, the size of the nutrient store in the seed does impose a theoretical limit on the maximum depth at which seed germination and emergence can take place.
What is the best depth for a given species?
The specific depth which gives best germination for any given species is very unlikely to be the maximum depth at which seeds of that species can germinate. This is because other factors also impose limits on germination depth.
Probably the most important other factor is light - most seeds require the perception of red light in order to trigger germination. For most species then, you are unlikely to find seeds germinating and successfully emerging from depths greater than the penetrance of light.
Another important factor in some latitudes is temperature - many seeds (from 26 families) use dormancy as a way of preventing germination in the wrong seasonal conditions. In species where temperature serves as a cue to alleviate dormancy, there will be a maximum depth at which a given seed can detect the temperature fluctuations at the surface. Beyond a certain depth, surface temperature changes will not perceptibly affect local temperature.
If you ever need to find out the best depth of germination for a given species, many can be found on google, or failing that it is trivial to perform a simple experiment.
Is there a mathematical relationship?
There is a general mathematical relationship, an allometric relationship (i.e. relating size to another trait), between seed size and maximum depth of emergence, described by Bond et al. (1999):

where:
dmax = maximum depth of emergencew = seed weightc = a constant which varies with phylogeny and environmental conditions.
Many species however will not submit to this equation. For example some large-seeded species (incl. coconut, coco-de-mer, avocado), have large seeds because they may need to enable long-distance growth along the ground in order to locate optimum growth conditions. Seeds of these species will therefore not conform to the depth-size relationship above.
Reference

 Bond WJ, Honig M, Maze KE. 1999. Seed size and seedling emergence: an allometric relationship and some ecological implications. Oecologia 120: 132–136.

nice answer. I'd appreciate your opinion of mine.

Generally a rule of thumb in gardening is to plant the seed 1-2 times as deep as the seed is big. a pea can go 2 cm, a poppy can go 2mm.
The starch of the seed is converted into sugars, which causes osmotic absorption of water by the new plant cells, and they have about 100-200kpa of upwards turgic pressure maximum, that's equivalent to more than 50 meters of lithospheric pressure.
So it depends on the size of the seed, the main inhibitor is the energy needed to create the hydrostatic pressure in the stem to maintain pressure and cell growth for the given distance.
In dry clay soil which is like concrete, chances are that the plant will not be able to go up, but in sandy soil you can expect some seeds to pierce many meters of sand, unless there is zero light.


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Primer Dimer / Hairpin Algorithms
What are the algorithms / methods in use for the calculation of primer dimers and hairpins?
As an example, IDT's OligoAnalyzer tool will generate these analysis given particular sequences.
The homo-dimer analysis seems to me to just be a sliding scan of two sequences across each other. I assume this doesn't take into account possible hairpin issues? or are such structures less likely compared to the myriad of other more common problems.  In addition, how are the ΔG values calculated given a particular dimerization pattern?

It is important visualize more faces to design primer or oligo and PCR experiments:
- calculate thermodynamic parameters of DNA Hybridization (Oligo/Template)

compute hairpin-loop, dimer, bases penality and melting temperature about primer or pair primer
calculate statistics about melting temperature with the change in composition and mix PCR concentration

with google you could find more tools but you must choose a tool of a sequencing team.
almost all tools use mfold algorithm, it's simple and effective:
M. Zuker, D. H. Mathews & D. H. Turner. Algorithms and Thermodynamics for RNA Secondary Structure Prediction: A Practical Guide In A Biochemistry and Biotechnology, 11-43, J. Barciszewski and B. F. C. Clark, eds. , NATO ASI Series, Kluwer Academic Publishers, Dordrecht, NL, 1999.
I worked in a sequencing team and there was a programmer. he developed a fantastic tools. he is a little english, but he could support you: http://promix.cribi.unipd.it/cgi-bin/promix/melting/melting_main.exe


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Autosomal Recessive Trait when skipping one generation
I learned recently that given a pedigree it is possible to tell whether a disease is autosomal recessive by observing if the trait skips a generation. If the disease does skip a generation, then the disease is autosomal recessive. But the converse is false. That is a disease that is autosomal recessive does not necessarily mean the disease skips a generation.
Does someone know of a proof of this fact?

Is this not just down to chance? A recessive trait may not skip a generation if the right mix of alleles are still passed to the progeny, but a dominant trait would always (by definition) be present in the offspring. I imagine there's a much better answer/way of saying this!

What you are saying is very similar to the statement that:

Absence of evidence is not evidence of absence

Suppose you have an autosomic gene A, which has a mutant allele a, causing an illness (or any other phenotype, for that matters). The particular nature of a makes its associated phenotype recessive.
You have three possibilities:
AA -> no illness
Aa (or aA) -> carrier, with no illness
aa -> ill

Now, let's take an aa individual (ill) and cross it with a sane AA individual:
aa x AA

All of the individuals of the first generation (F1) will be carriers (Aa) because the father will always give a and the mother always A.
Now if we breed them together
aA x aA

both parents have 1/2 probability of giving a and 1/2 of giving A. We will then have a proportion of:
1/4 aa
1/2 Aa (1/4 A from mother and a from father, 1/4 vice-versa)
1/4 AA

But this is just down to statistics. You have only 1/4 chances of seeing the trait reappearing, so you are much less likely to see it if they have 1 offspring then if they have 20.
Moreover, you have Aa offsprings in the progeny... this means that these could pass the mutant allele to the third or fourth generation.
Another important thing is that all we said is true if the first cross is
aa * AA

If it was
aa * aa

or
aa * Aa

The trait will (surely in the first case, and with 1/2 chance in the second) appear directly in the first generation.

Also, note that even with 20 offspring you are not guaranteed to see an aa in the F2.

A proof that autosomal recessive not necessarily skips a generation would be parents who both have the genotype and where one forth of the offspring would show the full phenotype.


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How does this illusion work?
I found this image on Google+

If you shake your head you can see a portrait of a person. Can anyone explain how the image is constructed in the brain?

Does anyone know who made the first version of this illusion and when? also could someone give me a simple explanation of how it works, i'm not too good at all these complicated words!

If you zoom in on the image, you can see that it is not just composed of black vertical lines, but also has pixels with different gray tones in the white areas. When you move your head sideways, you perceive the gray tones more.
If you were to remove the black lines, you could see the face clearly. Initially I thought that by blurring the gray shapes when your head moved, they became more visible as they seemed larger. On reflection though I think that actually what's happening is that the high contrast between the black lines and the mostly white background causes your perception to adjust so it doesn't easily see the mid tones. This is because we have a low dynamic range in our vision (relative to absolute brightness, but compared to camera CCDs we have a high dynamic range) - we have to adjust the light sensitivity to compensate for the overall brightness of the image. This is called brightness adaptation. There's a good free textbook for further reading about this at Utah U's Webvision.
When you move your head, the black and white lines blur together which makes the overall brightness appear to be the average brightness of the black and white. So against that background your light sensitivity increases and the areas where the pixel tone is different from the average - the gray pixels of the face - start to stand out.
By reducing the brightness you can see the faint image in the background much more clearly...

Nice answer. Thanks a lot. Just one thing, you said the high contrast between the black lines and the mostly white background causes your perception to adjust so it doesn't easily see the mid tones Does this phenomenon have a specific name? Can you provide references?

Added terminology and a reference. Sorry I couldn't find any good review papers - it's not my field at all. Perhaps a human biologist can contribute better references.

As additional info: The blurring of the black and white areas is not primarily caused by the movement. The eyes can only focus a very small area of the field of view. The rest is perceived in low detail. This can be visualized easily. When you move your head and keep the focus on the image, the  portrait appears with low intensity. But when you focus an area next to the picture, you can see the portrait without moving your head at all.

Actually you can also see the portrait simply when looking from a distance (especially if you have myopia), without moving your head.


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Will fruit/seed of a bonsai yield another bonsai plant/tree?
With practice one can create a bonsai; no complicated modification of the DNA in a high-end lab required. The bonsai will even beget bonsai fruit.
What I am curious about is - if such bonsai fruit is planted again, will it give rise to a normal, or a bonsai tree?

No, seed from a bonsai tree will not automatically produce another bonsai tree. Bonsai are dwarfed due to restriction of root growth in their small containers - unless the offspring are also grown in environmentally dwarfing conditions, they will tend to grow normally.

Could you toss in any reference material on the subject please?

Sorry, this question will not be answered in the scientific literature. If you have any questions about specific details perhaps I can furnish answers with references for those details.

However, non-scientific sources will confirm my answer, for example the wiki page: "Bonsai does not require genetically dwarfed trees, but rather depends on growing small trees from regular stock and seeds."

Well ... according to another question on this forum I understand a sapling relies upon the food contained within the seed for it's initial growth. I assume then - for bonsai fruit to grow to average size then (a) it must exhibit a growth spurt and improved quality of tissues+chemical processes or (b) each bonsai fruit would have at most a single seed of the normal size or (c) the bonsai fruit/seed would in turn give rise to a similarly stunted plant. What am I missing?

Small seeds do not necessarily lead to stunted plants, but they will contain less resources for germination. Provided the seeds have enough resources to complete germination, which is quite likely if you are cultivating them deliberately, they will grow to similar final sizes regardless of the seed size. They might have different rates of growth during their early development.

Feel free to ask a new question if you feel there's a part of the picture you're missing. I'll try to tie it all together a bit more coherently in an answer to such a question.

@Everyone: In any case, I'd assume that a bonsai tree, if allowed to bear fruit, would produce normal-sized fruit and seeds, just very few of them. At least that's what seems to happen with naturally stunted trees growing e.g. in cracks in rock.

@IlmariKaronen yes thats right - although often when people choose a strain for Bonsai they pick one with small fruit so they don't look out of proportion. In that case the children would continue to bear small fruit, assuming the species was one that grows true from seed.


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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.

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.

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.

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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Are there any side-effects from a mosquitoes extinction?
Suppose that we have the ability to make mosquitoes extinct, what would be the likely effects (on disease and ecosystems for example) of such extinction? Essentially, what roles in nature do mosquitoes perform?

There was actually just such an article in Nature recently.
"They don't occupy an unassailable niche in the environment," says entomologist Joe Conlon, of the American Mosquito Control Association in Jacksonville, Florida. "If we eradicated them tomorrow, the ecosystems where they are active will hiccup and then get on with life. Something better or worse would take over."

Sometimes I wonder what the editors of Nature are thinking when they publish those "pearls"...

The "or worse" is all the answer you need, I guess.

Eliminate Culicidae (mosquitoes) because some of the species transmit virus is a very bad idea. I have used the family name to make you realize there is more than 3500 species of mosquitoes and only a few are responsible for the transmission of disease or virus.
First, the male mosquitoes are important pollinators of multiple flowers (here is an example of some http://www.mosquitoreviews.com/mosquitoes-niche-pollinate.html ).
Secondly, mosquitoes are important food source for multiple predator such has bats, birds, frogs and fish. If you think it's negligible, just come down to Quebec in august and try to go naked in the wood you will see thousand of happy female mosquitoes on your skin in a minute.
Indeed, eliminating species because the have some consequence on humans is seeing the world as a simple thing. Ecosystem are complex and removing a group of animal will have consequences on the rest of the member of the ecosystem including us. Control of the population is a much better idea. Per example, in Montreal, the SOPFIM threat the sewer with larvicide (Methoprene) to control the mosquitoes population in the city. They also threat swamp close to the city. But the most efficient way to reduce mosquitoes population is by removing stagnant water (tires, plastic bag...). And cause of those effort,there are very few case of VNO in Montreal. So before causing to the extreme, educate the people about the biology of the mosquitoes and control the population.
Cheers


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Why do we sweat after drinking water and running?
Why do we sweat after running?
Also we sweat sometime after drinking lots of water. Why it is so?
Can someone please enlighten me in this regard?

Exercise, such as running, increases muscle activity.  This increases the energy demand of these tissues, which increases the rate of cellular respiration.  Respiration releases heat as a by-product, therefore the body is hotter during and after exercise.
Sweating is a homoeostatic mechanism to keep core body temperature constant. It is a response to lower the body temperature. When the body becomes too hot, sweat is released onto the surface of the skin.  The water from the sweat then takes some of the excess heat energy from the body and uses it to evaporate.  Because water has a relatively large specific heat capacity a lot of heat can be carried away by this method.

But I sweat even after I lots of drinking water.... what could be the reason here?

@gpuguy Do you mean you sweat after exercise even if you drink water? Or do you mean that at rest, in a cool room when one wouldn't usually sweat, you drink a lot of water and then begin to sweat?

i meant: "that at rest, in a cool room when one wouldn't usually sweat, you drink a lot of water and then begin to sweat?" (especially some time after having dinner/lunch)

If the meal you eat is hot, you will get some heat and if your body will consider it as excessive heat, it will try to get rid of some by making you sweat.
Drinking water and sweating after a meal may be coincidentally related and probably caused by hot meal rather than water. A side note: When you are dehydrated, you sweat less and when well hydrated you can sweat "normally," but drinking water by itself does not stimulate sweating.
Some people with "reactive hypoglycemia" can sweat and get anxious after meals. In this case, after a meal, food passes through the stomach rapidly to the small intestine, where glucose from the food is quickly absorbed and raises blood glucose level considerably. This triggers excessive insulin release that allows quick uptake of glucose by the cells resulting in drop of blood glucose under the normal level (hypoglycemia). This triggers the release of adrenaline, which breaks down some glycogen from the liver to produce glucose. Adrenaline also triggers sweating.
Certain underlying neurological conditions (not necessary diseases), such as increased tonus of the vagal nerve (that supplies the gut) can make you sweet more in certain circumstances.
A meal can be a "stress" (psychological or physical) which can trigger the release of adrenaline, which makes you sweat (just like in anxiety from any cause).

Sources:
Diaphoresis (excessive sweating) Ehealthstar.com
Reactive hypoglycemia Mayo Clinic


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Total amount of CO₂ / Oxygen in Bloodstream in Humans
How much carbon dioxide and oxygen from/for respiration are in the bloodstream at any one time? (mass per litre of blood or similar)
And would there be much more aside from the blood in tissue, e.g. muscle, brain, etc.
So far the figures I have are as follows (please double check for me, I dont have a clue)
O₂ molecules per red blood cell: 1 billion. Red blood cells per micro litre of blood in males: 4.7 to 6.1 million. Molecules per mole: 6 x 10^23. Therefore moles of O2 per litre of blood: approx 0.01 (correct?) This seems quite low, since an inhalation is typically 0.5L and about a quarter of the oxygen is absorbed (oxygen by volume, 5% of the air) (1 thousandth of a mole of oxygen absorbed per inhalation?)
Thanks

This is little bit uncommon to use physical units for blood oxygen. Normally one just cares for the oxygen bound to haemoglobin, and doesn't consider the diluted oxygen. And trying to use your numbers I come to 0.8232 mole, that seems to be incorrect too...

Your calculation for O2 is along the right direction, but missing a factor I think.
Each red blood cell holds millions of molecules of hemoglobin, each hemoglobin molecule, when saturated (at the lung), holds four O2 molecules.  So this is off by a factor of millions at least.  Wikipedia estimates that hemoglobin makes up about 35% of the total weight of blood.  We can use this figure and an average of 4.5 l of blood for a human being ( numbers vary, but it will be within 30%).
4.5l blood * 1.060 g/ml density of blood * 1000 ml/l water * 35% = 1667 g hemoglobin
4 molecules O2/molecule hemoglobin * 1667 g hemoglobin / (64000 g/mol molecular weight of hemoglobin)  = 0.104 moles O2
so I get:
0.104 moles O2 * 30 g/mol for O2 = 3.12 g O2 in the blood at a time.
In the muscle and tissues it gradually depletes so that all four molecules will usually end up somewhere in your tissue.  So this is all assuming that counting all the hemoglobin bound O2 will approximate the count of O2 in the body.
We know this is a crude estimate as myoglobin in mammal muscle will store O2 for use later, and the average hemoglobin is not in the lungs and will have given up some of its O2.  It also doesn't count the O2 which diffuses into the blood and is carried by the water.  This is about 0.035 g / l, which is why we need hemoglobin - total blood saturation would carry about 1.15 g of O2.  Hemoglobin multiplies the oxygen carrying capacity of blood by 100 fold.
CO2 is much more soluble in water (blood/tissue) than O2 is- about 1g/l.  There is I think only 2 CO2 binding sites for hemoglobin, which means it carries out only half the CO2 oxygen that it carries  in.  Hemoglobin is is only considered to account for 10% of the total CO2 carrying capacity of humans.  So calculating CO2 respiration by hemoglobin is not a good way to estimate blood CO2.

To get the answers you're looking for, you need a couple of figures to start with:
(1) The amount of O2 dissolved in blood plasma: about 0.3 ml O2 per 100 ml plasma;
(2) The amount of O2 bound to hemoglobin in blood: about 20 ml O2 per 100 ml blood. - Ref: https://www.ncbi.nlm.nih.gov/books/NBK54103/ (which also sources the figures used elsewhere here)
Blood makes up about 7% w/v of the human body, so a 70 Kg (154 lb) person will have about 4.9 litres of blood. 5 litres of blood would hold around 1 litre of O2 bound to the hemoglobin. However, around half of the blood will be venous, not arterial, and that only has about 75% O2 saturation, so the actual amount in arterial plus venous blood will be about 1/8 less than that calculation. Obviously, the figure will vary significantly with body weight.
At normal pressure, the arterial hemoglobin is effectively saturated with O2. However, if the ambient pressure increases, then the amount of O2 dissolved in the plasma will increase proportionately (Henry's Law). Similarly, breathing a gas with a greater O2 fraction will increase the amount of dissolved O2 in a linear fashion. Nevertheless, O2's low solubility means that the dissolved O2 is only about 1/60 of that bound to hemoglobin, so unless that is severely compromised (e.g. CO poisoning), increasing the pressure or fraction of O2 has little effect on the supply to the body.
As for the O2 stored in the body, each myoglobin molecule only binds 1 molecule of O2, compared with 4 molecules of O2 per molecule of hemoglobin, so it will contribute a much smaller amount to the total. Of course, that will vary again with body weight but also with the amount of muscle and other type of tissue making up the body.


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How does a jumping spider manage to "jump" on the ceiling?
I just witnessed a small jumping spider jump on some kind of louse or bed bug on the ceiling. How does it do that without falling? I have yet to find a high-speed-camera video of a jumping spider jumping on a ceiling.
My hypothesis is that the spider would spit silk and anchor it on the ceiling, then jump, and allow itself to be swung by the silk onto the prey. But I don't have a high speed camera to prove that.
EDIT:
I now have some evidence that supports my hypothesis: I just saw a jumping spider attempt to jump on a prey and failing to land properly. It didn't fall directly to the floor. Instead, it dangled from its own silk, at about 2 cm from the ceiling, then climbed right back up the thread of silk, onto the ceiling.

Whilst I've seen no evidence either, your hypothesis that the spider uses its silk seems highly likely; small spiders are known to 'balloon', using their silk to float through the air  http://en.wikipedia.org/wiki/Ballooning_(spider). Using their silk to 'pounce' on prey seems very plausible.

good work using observation btw... that's how all science starts...

You are right - most jumping spiders have draglines they secure to the surface before they jump.  They can't defy gravity, but they can recover from a miss if they do this.

Disturb a jumping spider on a wall, and watch it seemingly defy gravity: it will jump horizontally out into the air, then return to the wall.  This seems fantastic until you spot the major ampullate dragline.  It essentially becomes the bob at the end of a pendulum string.

the book goes on to explain that the dragline is used as an airbrake and a spring to help the spider control the jump, which might make it seem to do unnatural things when jumping from a ceiling.  You might want to get a video of this if you can.
Some of the references in another book here, point to other uses of draglines - the spiders can tell each other's species by them, attract a mate.


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How does a plant cutting develop roots?
Please correct me if my understanding is incorrect; I understand branch/stem, and root are composed of different types of cells. Yet in some plants (e.g. rose, bougainvillea) a cutting from the stem is capable of developing and taking root.
How does this transformation from stem to root come about?
As an aside - I believe such root-generation happens only in plant cuttings, and not in a tree branch. Why? Is it a matter of the volume of nutrition required?

Plants grow only from regions at the tips of the roots and shoots called meristems.
Within the meristem areas there are stem cells ("blank" unspecialised cells).  Unlike animal stem cells, plant stem cells are totipotent - meaning that they can differentiate into any type of cell.  Therefore when the cutting is taken from the end of the shoot, the stem cells can differentiate into root cells or shoot cells depending on their conditions.
Because the meristems (therefore the unspecialised stem cells) are only located at the tips of shoots, you cant grow a cutting from the middle of a branch.

There are lateral meristems all along a plant - they are where branches grow from. Every node on a plant is, or was once, a meristem. That's why you cut just below a node to take a cutting. You could also create a meristem pretty much anywhere by applying auxin. That's why people use rooting/cutting powder, which is NAA, a synthetic auxin.

But, a remarkable thing is that a root meristem can be induced anywhere n a stem by applying/inducing excess auxin whereas, a shoot meristem can only be induced at a node.