CharonY

Both rely on the amplification and as such the sensitivity is comparable. The factor determining sensitivity would be more down to the actual protocol (i.e. primers used, number of cycles, detection method etc.) rather than the realtime vs. nested PCR per se. In other words, it depends a lot on the actual performance of the lab, and I am not sure whether they are well standardized (if at all). However, nested PCRs tend to be a bit more specific than realtime assays. The best thing to do is to to have the bloodwork redone if the titer is near the detection limit. Also consult some doctors and find a good one.

This is not the question as far as I understood (and is also somewhat inaccurate). The highest number of genes known so far have been recorded in a protist, if I recall correctly, which has more than double the amount of genes than humans. There are certain limitations to genome size, but it is not known where the limit is. For small organisms genome size is a limiting factor for growth speed. In environments where it is crucial to proliferate quickly there tends to be a selection for smaller genomes. On the other hand, more metabolic pathways allow utilization of resources not accessible to others. Good examples are parasites that have access to a lot of resources from their host and therefore often have reduced genomes. One question is of course what functions are really needed. If, for instance, an organisms accumulates a lot genes (for whatever events in their history) but only really utilizes, say, half of it, it means that for the other half there is no real selective pressure to maintain their function. Over time these genes are more likely to accumulate mutations, for instance than the other regions. This can lead to the eventual loss of that particular locus (I refer to it as such as it is not a functional gene anymore). However it may still contribute to e.g. the regulation of the whole genome, just by virtue of being there (i.e. as a spacer between active genes, allowing the DNA to bend in a certain way, etc.). A consequence of that is while the gene size is reduced over time (as the genes eventually lose their functionality) the genome size does not by much, unless there is a strong selective force to maintain small genomes (which is more prevalent in single celled organisms). This is only a very simplified explanation, though.

Actually, it is more likely that there was no selective pressure to maintain them.

Well, I agree that it is a nice expansion of school knowledge, though it is hardly on the forefront of biological sciences. An interesting part of that paper is actually the notion that diffusion plays smaller role than attributed to in many models in which metabolite movements within cells are simulated purely based on diffusion models. Nonetheless the author is too generalizing when he repeatedly stated the truism that the system is too complex to be approximated by simple algorithms But that may be a different question altogether. Physics is very strongly axiom driven and biological entities are hence not very amendable to physical methodologies. However there are strategies that biologists could learn from (and vice versa, obviously)

Maybe you want to start and remark on what you find most interesting in that article?

Question: if it is not an in vivo test, why not overexpress them, purify them individually and then mix them in defined ratios? The assay would be much better defined that way.

I merged the topics, as both posts essentially ask the same.

More to the point, what is supposed to be "our" DNA. Gene sequences that are exclusively found in humans as compared to whom? Those are very little (if any). As we share common ancestries we share all the basic sequences with our relatives. The only genes that could be specific are those that arose after the last speciation event. But that was not that long ago and should account for a very little.

This can be quite tricky, depending on the mode of interaction between the proteins you are thinking of. If it is only the isolated protein functions (i.e. no effect on the physiology of the cell) it may be relatively easy (though this would be essentially not different from an in vitro assay). However, if it is supposed to relate to cell activities. it can get complicated. One major issue is their control, i.e. the stochiometric expression of both proteins. Using ordinary overexpression vectors is likely to give odd results. Also if the effects you are expecting are in the extracellular space there is also the issue of the secretion kinetics that may be different from the proteins (even if using identical signal peptides). Finally there is also the question whether the proteins you are looking at are native in E. coli or whether there may be even more interference. If the proteins in question are known to interact in a specific way and/or e.g. organized in an operon and if they orginated from an organism close to E. coli (including similar regualatory sequences, the simple approach may work. Otherwise I expect issues on several levels. However, it really depends on what you really want to see in the end.

And surely you have references that demonstrate that the info was actively suppressed instead of the fact that most initial associations studies are unreliable and normally do not lead to a policy change? Which NHANES study are you referring to? These are a series of studies with different methodologies. Note that it is a survey study that alone does not necessarily result in the assessment of all risk factors. Nonetheless in NHANES III and NHANES 1999-2002 already found a close association between obesity and diabetes in different populations. However subsequent studies using the data sets elaborate on that, including National Task Force on the Prevention and Treatment of Obesity (2000), Overweight, obesity, and health risk, Arch Intern Med 160, 898-904 Colditz, GA et al, (1990) Weight as a risk factor for clinical diabetes in women AM J Epedemiol. 132, 501-513 Colditz, GA, et al, (1995) Weight gain as a risk factor for clinical diabetes mellitus in women Ann Intern Med, 122, 481-486 Malnick SD, Knobler H. The medical complications of obesity. QJM. 2006;99(9):565-579 One surprising find from the NHANES data was the identification of a population that was both overweight and fit, though further sampling indicated that they in the US that particular groups is very small (i.e. if overweight one is more likely to belong to a risk group for hypertension, etc. rather than being in the fit group). Nonetheless there is mounting evidence for a link between obesity and diabetes. As usual it is not a direct mechanistical one, though several have been proposed. Of course not every child will have the same risk, due to physiological differences, however stating that there is no evidence for it is ignoring a huge body of evidence.

Yes, though even if it fulfills a certain function, it does not become a science. I am not familiar with all the details, though many yoga tradition have a semi-mythical aspect to it, that do not have a physical correlation. Of course, some are just a semi-empirical description of e.g. organs, whose function were not known. However, the insistence on relying on mystical tradition rather than trying it to put it on a physical basis disqualifies much of it as science.

Create and characterize 10 bacterial mutants in 4 weeks. Disciplines include -Xtreme primer designing -cut n ligate -Massive electroporation - 100m plating And for the advanced: mutation stacking The gold discipline is: WTF does this mutation do?

To get back to the topic, I am pretty confident that an elder god will enter this world through my skull. Roughly around June 2013. Maybe April, depending on the weather.

Many (most) cells have no polarities, chromosomes can be circular, symmetrical body plans are the result the evolution of certain developmental mechanisms, nomenclature is often arbitrary, bla bla etc.

joshuam168, as you surmised correctly there is no mechanistic data. As I mentioned above, there were some epi-studies. However, the results were conflicting at best. Heck there was even a reports with a correlation between religiosity and dementia. In fact, a metastudy surmised that much of it can be explained by selection bias in the different studies. See e.g.: Cigarette Smoking and Dementia: Potential Selection Bias in the Elderly Hernán, Miguel A.a; Alonso, Alvarob; Logroscino, Giancarloa EPIDEMIOLOGY Volume: 19 Issue: 3 Pages: 448-450 Published: MAY 2008 In contrast, for smoking a number of toxicity pathways have been detected that add to the evidence of e.g. adverse birth outcome, cardiac diseases caused by smoking.

Well, what would be the ethical dilemma? I do not like them is probably a tiny bit weak. Form an anthropocentric viewpoint one could argue that they are among the major (indirect) killers of the animal world. On the other hand one could put up a number of arguments including: - ecological impact (as already mentioned) - reduction of biodiversity Though personally I am not sufficiently familiar with the ecological role of mosquitos in the respective habitats.

No idea what it was supposed to be about, and do not recognize the name either. Given the fact that there is no information in the post that makes any sense and given the lack of any sources I would assume that it is nonsense.

For a filtering flask it ain't that easy, but I had problems with small stoppers in test tubes. I used a piece of folded cloth to guide the stopper to the opening of the inverted tube. Then pulled it out by tugging at that cloth.

At which point does the hitting with a club and dragging into the cave come in? I always forget.

I need more info regarding type of fusion construct, how you overexpressed and how you purified it. I.e. do you mean that in the SDS page you only have the purified protein but you got two bands? Or is that the raw lysate.

A question I have is whether you want to have a single strain secreting both proteins? Second is what question you want to answer. Do you want to purify the proteins or assess the function of the proteins in vivo. The latter is a bit more tricky.

Also connected to this point, the main human gene pool originated in Africa. As such, what is considered to be white is just a subpopulation. Following that train of thought a grouping according to skin color simply does not make sense. It would be akin to making groups like dachshund vs dog. Note that it is possible to trace specific subpopulation by using allelic markers specific to them (works best in well in isolated, somewhat inbred groups). However, as Ophiolite said, if we take a non-biased approach (as e.g. the whole genome) these distinctions vanish.

Normally it does not refer to estimates but to ratios.

Shoot, I must have been confusing it with something else. Especially considering that betas are more harmful. I thus retract my above statement.

Actually technetium emits beta particles (electrons).