CharonY

Well, the problem is who do you think mostly claims "it is just a theory?" Someone who took time to look at the theory in detail or someone with a specific agenda but little knowledge? I think nervous is the wrong word. Bored and annoyed is more fitting and hence does not elicit little more than a kneejerk. Why go through all the trouble the upteemth time in detail for nothing? Of course, sometimes more legitimate questions may go unnoticed or misinterpreted due the unholy noise-to-signal ratio in fora.

Check out light-dependent reaction and/or photophosphorylation. In short: light harvesting protein complexes (that also define the optimum wavelength) use light to initiate an electron flow to NADH+. During this transfer and due to the associated split of water a proton gradient is formed that powers the ATP synthase.

Well there are different ways to pour and different reasoning for them, depending on amount sterility needs etc. Some of which really make sense, some less so. What I used to do is to pour stackwise, which is possibly the same way you do. I.e. one hand has the whole stack plus the bottom lid slightly lifted, pour, put lid back, continue with the rest of the stack. Now to your question I have not heard of flaming the media in the dish as a routine method, especially as there is a risk of melting the plate. However in courses it is sometimes done when pouring was so slow that some of the agarose started to harden, creating lumps.

As already said, networking has always been an integral part of science. Even before the internet. A forum is just not that best platform for it. Here maybe a handful of all the members are actually scientists with highly dispersed interests. As such it is clear that the majority of the posts will not deal with something that generate professional interest.

Public health care is definitely and probably a very strong element of health distribution. See it that way. Without a public system high-quality healthcare is generally only limited to the rich. By taking higher taxes from them, they help to pay for the poor. Who, incidentally have worse health than the rich.

Well, the price has been rising constantly for years. Delivery is slow, especially outside the US and about everyone is talking about a shortage.

First is always to troubleshoot the technical aspects (including lysis efficiency, measurement time etc.). After that you have to put some thoughts is whether there may be differences in you approach (e.g. cell line maintenance etc.). The description is insufficient to give detailed advice. However, how did you measure the enzyme expression? ELISA?Also I am confused on whether you measure enzyme activity or enzyme expression.

This discussion is becoming more philosophical than biological. If it goes further down that road I think it might be more appropriate to be moved there.

Yes, the respective function are usually encoded in the plasmid, in some strains they get incorporated into the chromosome, though. This then is either poor literature or cited out of context. Plasmids can encode additional functions that increase fitness, but it costs the cell to replicate. Of course, to survive the genetic elements cannot harm the cell too much and often only those genetic elements survive that actually are eventually of benefit, However, it is not that bacteria actively utilize every scrap of DNA there is. Quite the contrary, they have an elaborate restriction system that destroys much of foreign DNA that gets into the cell. In short, HGT does not automatically result in a fitness increase. Shuffling is an appropriate term if you go away from a species-defined gene pool, to a gene pool accessible to the respective mobile genetic elements. As they may pick up bits and pieces from their hosts they reshuffle the genetic content within their host range. The individual species may acquire traits that they did not have before. For HGT it is necessary to go away from species-centric viewpoint towards a gene focused one. Again the egoistic gene is a very simple model for starters.

The nucleocytoplasm contains elements that are most likely derived from archaea. There is a newer paper out there suggesting that the nucleus proper arose after the incorporation of mitchondria. Most likely the first eukaryotes did not possess a nuclear envelope, which evolved later from the endomembrane system. Note that the precise timing of the respective organelles are still under discussion, though.

Ah, the deliciousness of it.

It is not really an active process initiated by the cell (purposefully, whatever it may mean) in all cases. Some are (e.g. natural transformation, conjugation) but the above example of bacteriophage is an example of mobile genetic elements hijacking the cell. An example of egoistic genes, if you want. And they can combine. E.g. a plasmid may be acquired by conjugation but carries a transposon and the latter then jumps into the chromosome. In fact, one could also argue that conjugation is not done deliberately as the plasmids carry the function necessary for that. As such one could argue even plasmids, similar to viruses utilize cells to proliferate.

Pro- and eukaryotes have very different cellular structures. In fact certain organelles as mitochondria were bacteria once. As such it is of course almost impossible that bacteria possess such organelles. While there are in fact bacteria that proliferate intracellular in other bacteria, they pretty much destroy the cell with their presence. Note that in prokaryotes only transient multicellular states are known (e.g. fruiting body formation) whereas in eukaryotes obviously stable multicellularity has evolved. AFAIK it is still disputed how the first eukaryotic cell may have looked like, but IIRC it was assumed that it the first eukaryotic cell may have been a mix between archaea and bacteria. Also note that the first eukaryotic cells were very likely without mitchondria or plastids (mostly due to the comparisom of the timing when the nucleocytoplasm arose, relative to the ancestors of plastids and mitochondria).

HGT allows shuffling of genes between species. This is indeed a problem for taxonomic approaches. This is why most focus on conserved genes as e.g. the 16srRNA gene. Traditionally a new species was assumed when DNA hybridization between strain was less than around 70-75% similar (forgot the actual value). Phylogenetic trees with 16srRNA genes tend to correlate well with that. I disagree that we have to abandon the notion of species in bacteria completely, for most purposes it is quite useful. But it makes it indeed harder. One particular challenge is thus to distinguish the phylogenetically "old" backbone from more recent HGT events. There are groups that have specialized in looking into that.

The first part of the answer is correct, a dominant mutation is a mutation resulting in a dominant allele. I.e. an allele causing a dominant phenotype. Do not make the mistake with confusing it with e.g. enzyme activity, though. It is quite possible that the reverse is true. I.e. constitutively active variants are recessive alleles). Depending (in this case) on the underlying regulatory network.

The question here is really what probability is to be calculated. At the moment we are being sloppy. Let us assume that the question is how likely is an event to happen at least once after n repetitions with a given p for each indivudal trial. The probability of the event to occur at least once is simply 1- probability of it never occuring. Not that using that equation we do not use the probability mass (not density as it is binomial distrubution we are dealing with) function to solve it. I.e. the equation is only valid if the individual probabilty p is used, not P(x). However, if desired it can be calculated using 1-P(0), though it would require unnecessary additional operations (and result in the same equation). Moreover calling n a probabilistic resource is extremely odd and certainly not mainstream. I now suspect that the overall confusion is the result of incorrectly applying terms. I will try to clarify. If we denote the hit with a comet as success and take the number of hits after n trials as outcome, then the probabilty mass function indicates the probabilty of having precisely X successes in n trials. So we would use it, if we want to know the probablilty that in 5 million years (if we take each day, or month for example as a trial) the earth was hit precisely 4 times. The probability of each individual event does not change, but the probability of the number of successes is of course different. Note that we could also turn the question around and ask how many trials does it take that the even occurs the first time. We would then use a geometric probabilty mass function with X now being the number of trials. Using its cumulative distribution function, we could determine the probability of the even occuring after X trials.

I assume that you have continuous values and that the type of measurements is likely to be normal-distributed? In that case a Student's t-test is applicable. In short, it tests whether two data sets are from the same population or not. The null hypothesis here is that both are from the same population, and if the tests refutes it, it indicates a statistically significant difference between the two data sets. The actual calculation is pretty straightforward and can be found everywhere. In short, it is based on the means and standard deviation of the the data sets. Means that are very far are apart are more likely to be from different populations, whereas a large s.d. reduces it (as in a very flat distribution two values may be farther apart but still have a high likelihood of belonging to the same population). This is reflected in the formula. The resulting value is compared to the t-table and based on the degrees of freedom you can read there with which probability you can refute the null. In most cases a p of <= 0.05 is considered significant.

Adhesion is not a function of cell viability but mostly due to formation of the extracellular matrix on which the cell settle. Depending on the surface coating of the dishes certain cells can also settle there. However, a number of cell types, including neurospheres are permanently or transiently free-floating and do not attach under certain conditions. It is assumed that for certain developmental or regenerative functions these cells travel to a specific point in the body, where they do their stuff. If they undergo differentiation they usually form an adhesive tissue again, though.

Well, what job do you want? And what do you need to get that job? The problem is that at your level potential careers may be overwhelmingly broad and hard to assess. Now, there are still certain career options in the industry which also require a PhD. However, if you do not know what you want to do, one cannot really evaluate whether it is worthwhile to pursue one. It is definitely not a good option to get a PhD (or a MBA for that matter) just because. One possible thing you could do is to check job websites for biochemistry jobs just to get a very rough idea what is out there that you may want to do. Looking at real job description is usually more useful than listening to what random poster say, unless of course they have a career in that particular field. Also check out some career guides. Your experience up to now is unlikely to be comparable to the real thing out there.

Mostly not. It of course during the settling selective pressures can start to act, however the entrance into a new ecological niche is essentially a stochastic effect. It is well known that these and other effects are most likely driving forces of speciation rather than NS. The interesting thing in this paper is that they actually try to quantify it. Of course, once settling in occurs competition may start up again, but the main point is that the driving force is the movement into new niches, rather than having competition on that level.

In this article the authors provide evidence that tetratpod diversity is driven ecologically. So rather due to competition, the diversity was the result of conquering empty niches, a process known as adaptive radiation. Conversely habitat destruction is then likely to be the main element in destroying biodiversity. Sahney, Michael J. Benton, and Paul A. Ferry Links between global taxonomic diversity, ecological diversity and the expansion of vertebrates on land Biol. Lett. August 23, 2010 6:544-547; published online before print January 27, 2010, doi:10.1098/rsbl.2009.1024

Well, those specific markers can also be genetic. Only that population boundaries drawn around these do not necessarily correspond to"traditional" ethnic groups, but rather follows mating history, of course.

I am sorry, but this is just gibberish. A probability density function describes the likelihood of a random variable to fall within a given interval. An example would be, say, having a size distribution of kids in class and calculate the probability of a kid being between e.g. 175 and 180 cm. Note, that the larger the interval, the close we approach 1. The described example is much simpler and can be described with a uniform function and taking f(x)=const. In that case the probability would simply be described as by DJBruce (or simply the integral over the total time under consideration).

Has been posted a couple of times here, actually.

Even if folded correctly the protein-protein interaction with the transport system generally inhibits proper interaction with the substrate.