CharonY

It is important to understand that there are at least two different variables. One the total elements within a population. This constitutes the complete genetic variability, i.e. all variations of all genes, for example. The second is their respective occurrence (frequency) within a population. Mutation, for instance, may add a new variant of a gene into the pool, thus enhancing the overall variance of the gene pool, when it appears. However the overall composition of the pool will hardly change as at the time of the mutation only one individual carries it. With no natural selection acting on it, the likelihood is very high that the mutation vanishes within a few generations. If it there is high selective pressure to keep this novel allele, it can spread, thus increasing its frequency. The overall gene pool composition (i.e. frequency of each allele) will then significantly alter over time.

You have to be careful to differentiate between mechanisms that increase variability in the gene pool and those that change the composition. Roughly speaking natural selection and drift belong to the latter, mutations and recombinations to the former.

Standard rant: Craig Venter did not create a new species. Just re-inserted the same information back into an existing cell. The only novel bit was that the DNA was synthesized in vitro. The sequence was the original ones minus some deletions.

Lamarck and Darwin were not on opposite ends. Darwin was not sure which was the true mode of inheritance, his main contribution is the introduction of natural selection. He did not specify precisely the mode of inheritance. In fact, he did state that Lamarckian inheritance could also have played a role in that system. An apt comparison would be Mendel vs Lamarck. And who the heck thinks Lamarck is a villain of any sort? Hyperbole much?

Overall, the likelihood is exceedingly low. First, it is usually only transmitted zoonotically and almost always only by direct contact with saliva. Inhalation as infection source is exceedingly rare. Second, it is not endemic in human populations, highly limiting its potential to spread to significant parts of the population.

Considering that we are having a lot of troubles of validating biomarkers for about anything, trying to associate weak linkages of certain sub-populations with something as complex as e.g. intelligence is a rather ungrateful endeavor. Also, the basketball coach would determine suitability according to actual size, not due to genetic markers. Even if genetic markers are known, the size prediction is going to be less accurate than, say,actually measuring the size. In cases of pygmies there is definitely a strong genetic component and clearly identifying these could be a good predictor of size. Nonetheless, it also depends on how homogenous the population is, which usually correlates somewhat with degree of isolation. Note that genetic disposition does not necessarily equal the phenotype. Also note that phenotypes are not easily linked to a certain genetic make-up. At best there are strong correlations (but rarely with a mechanistic linkage).

I am pretty sure that carbon cages are meant and not diamonds. I.e. fullerenes or derivatives thereof that have surface modifications that enhance binding and uptake by cancer cells coupled to a drug payload. However, they basically increase the affinity towards cancer cells relative to healthy cells, but it does not mean that they do not affect healthy cells at all. You may want to google targeted drug delivery for details.

This is a bloody old thread. Note that for the effective use of grass or wood as food source for higher eukaryotes (including arthropods) a consortium of bacteria and protists are involved.

Well, the phenol extraction step is used to get rid of proteins. Another, longer, way to do it is to do protease digest and salt it out. For the latter NaCl also works. Other, non-chemical methods include the use of filters or dialysis and affinity columns.

Eh, just realized, if you are more interested in joining a group as opposed to leading one, not getting a PhD would be much better. This included e.g. analyst and technician positions (both in- and outside academia).

I know only a handful of people working in pharma companies personally, but it appears that they have mostly pharmacist rather than MDs involved in drug design. The ones I know of do the clinicals. Drug design in uni setting is somewhat different from pharmaceutical companies. Usually, the majority of the development money goes into the trials rather than into drug research. Also basic drug design is done only to a more limited extent within the big pharmas. Pandering to what one believe is ones strength can be dangerous if too narrowly defined. At the undergrad level (and to some extent this also goes for the grad and postdoc level) the perspective on the actual job be too narrow to be able to actually judge where ones strength may be. Also, if the interest is strong enough one is bound to become good at it. One has to realize that the actual job later on may require a completely different skill set than acquired in grad school, however.

Eh, I though I posted something but apparently lost it. In short: there are not many pure research institutes around that do basic research. In applied areas MDs are involved in clinicals but I am not aware of much else. Joining a group would is not a permanent job but more akin to a postdoc. Dual degrees are often tricky business and of limited value (not yet clear how that is going to work out). PIs themselves are too much subject to grants to be able to employ someone for a bit of random reserch (that does not have the prospect to be fundable). Also it is important to realize how the work looks like post-graduation. Just a random link towards that: My link

If you want to do research in a uni setting, an MD won't open more doors, but rather different ones. You are limited to certain types of research. My MD collaborators are basically all involved in epidemiological effects or are put on a grant to "provide expertise", i.e. they function more as consultants rather than researchers. However, a research path in unis generally involves getting tenure. For that you should familiarize yourself early how such a path look like. Also realize that not more than 25% of the PhDs (and less MDs) will end up in such a position.

1) Evolution is basically the change of allele frequency in a given population. Only under certain conditions (e.g. under the so-called Hardy-Weinberg equilibrium) evolution will stop. Hence, it is ongoing also for humans. What some of the posters may mean is that certain selective forces may be diminished or change. Others (as e.g. sexual selection) may be of higher importance than others. 2) Generally not. What you describe is basically Lamarckian inheritance and for the most part it does not happen. However, there is a limited area which may allow certain acquired traits to be inherited. But this is certainly more of an exception rather than the rule. 3) Nature operates in a continuum. There is no real cut-off in nature and while categorizations can make sense for certain aspects, it is always to a certain extent arbitrary. Some categories are better reflected, some worse, but none is perfect.

I think what was meant was the turnover rate of the enzymes themselves. E.g. protease activity that, in turn, can modulate other enzyme activities.

I had regulatory roles in mind, but yes, that is another good example.

Not precisely meaningless. In contrast to radioactive decay biological degradation is highly dependent and controlled by the circumstance (e.g. presence of nucleases, medium, etc.). It is not a material constant. But the turnover rate can be of high biological relevance.

Just a little update: http://www.world-nuclear-news.org/RS_Stabilisation_at_Fukushima_Daiichi_2003111.html

There are boatloads of protocols. I assume you want isolate chromosomal DNA? I would recommend a look into Sambrook: molecular cloning for them, if you got access to a library. Purification of nucleic acids from proteins is often used via phenol extraction. The DNA is then pelleted and rehydrated with a Tris buffer. A photometer can be used for purity control. However standard agarose gel will not allow a size determination of chromosomal DNA. It is far to big for it. An alternative is pulse-field electrophoresis.

Actually, it depends on what aspects of tissue engineering you are looking at. Individual mechanisms (e.g. proteins) pertaining to adsorption and cell-cell interaction are closer to molecular biology or chemistry, however in the broader and areas cell biological and cell cultivation knowledge are higher on the list. Other elements include biomaterials and biomechanics and, especially for the applied part, medical sciences.

Indeed. Persisters usually rise when AB treatment is discontinued. IIRC the presence of ABs and other stresses actually promotes the formation of persisters.

Simplified there are three aspects to it. First, the mathematical principles and generalized modeling principles, second the models that have been developed in the frame work of one systems theory or other and third is software development to do the numerical calculations. I am doing mostly the second part (i.e. looking and adapting existing models to my research questions, usually by using or adapting existing software/code) to supplement certain aspects of my research. While the first part is certainly best to build a solid foundation I am too much experimental to delve into it too much. If you want to develop novel approaches it would certainly help (but it would be rather ambitious). I can provide lit for applied approaches and models if you could provide information what you are interested in. I am less suited to evaluate basic principles.

Excellent. The blogpost was nicely written for laymen like me to understand, though with my knowledge I could not easily validate accuracy. Indeed.

Except from a microbial standpoint the toxin argument does not matter as what counts as toxins for us often can be considered food to them. The major issue is the chemical instability of arsenic bonds and the biological importance of phosphate bonds. A simple exchange would be incredibly tricky physiologically. Regarding appleseeds, unless crushed only a limited amount of cyanide will be released from the seeds during normal digestion. While technically correct, it would take quite a bit to be lethal. A few other food sources would be more efficient. It is somewhat well-known that rosaceae produce cyanide compounds, btw.