CharonY

It will be of lower efficiency than sticky end.

You may want to look at the Fulbright program (I do not know the specifics other than quite a few grad students are financed by it) http://www.iie.org/en. NSF and NIH are also obvious sources. I do not know what kind of funding may exist that are more specific for psychology (the mentioned sources are all not terribly specific to a given discipline). However, if you apply from overseas you may be limited to foreign exchange programs and especially many NIH and NSF fellowships are limited to US nationals or at least permanent residents. Also, you may need a letter of support from the department. However, I am more familiar with money sources on the post-doctoral level and above, so there may be slightly different rules for graduate programs. Certain fellowships as well as departmental resources are only available after enrollment/acceptance, obviously. However, it is probably best to check out available programs, pick the right field and school and then try to get the money.

Why shouldn't it be possible?

Many do not require you to make a full master, but often there is the need to complete a master's in passing as part of the doctoral degree. The most common differentiation are clinical and non-clinical programs, with quite a bit of sub-varieties. That depends on the school. Most want a GRE, some want additional aptitude tests, letter of references, statement of purpose etc. Foreign students also need to submit their TOEFL (most of the time). I do not know whether and which schools offer scholarship. The majority of available scholarships tend to be from other agencies. Additional sources are grant money from the PI (when one joins a group) and some department also finance students via TA positions. It is probably the best to create a shortlist of universities that you are interested in and start from there.

This is highly speculative. I am going to move it into the speculations forum (unless some hard data is provided at some point).

The position relative to the primers has a relatively low influence. Other factors are more important.

I would call it a physiological, anatomical or (more generally)a biological definition rather than a biochemical one, but it is, of course correct. However, even if bacteria penetrate cells, quite often they are not really inside the cell either. They are still separated from the host's cytoplasm as they are still surrounded by the host's membrane (e.g. after endocytosis).

There are studies that suggest that music preference is largely learned. Certain types of music are associated with certain emotions, for instance. There was a nice documentary (on Nova, I think) in which the brain activity of a researcher was measured, who loved Bach. When hearing that music large parts of the brains flared up. In contrast, listening to Mozart did little to overall activities. Of course the mode of association may transcend music styles, and for each person there may be different elements of preference. As with many things, the likelihood is high that much of it is based on early exposure. That being said, studies on toddlers indicate that very early on there appears to be a general preference for loud and fast music, that may get refined later. I do not recall all the lit, but some interesting stuff is here; Lamont, Ann NY Acad 2003 Huotilainen et al. Ann NY Acad Sci 2009

This is a gross misunderstanding. Generally speaking there is no species specific DNA per se. Since we all related in some distant way there are only relatively short stretches that can be considered unique for a giving organism. If we compare on genes (i.e. coding regions) the similarity between human genes and mice is, on average 85%. However, there are some that do not map to the genome of the respective others, while others are practically identical. Even taking highly conserved enzymes such as cytochrome C that basically all eukaryotes share, the similarity between human and yeast (still an eukaryote) is only around 70%. As such it is inconceivable that the 90% similarity exist on a broad scale between humans and prokaryotes. That being said, since our ancestors were prokaryotes early in time, it is expected that our genome was of prokaryotic origin. Due to the changes over time it is non-trivial to track those relics down, however. Nonetheless, simple homology searches reveal that roughly 40% of our genes show some degree of homology with prokaryotic genes. Note that the number refers to the number of genes sharing any degree of recognizable similarity and should not be confused with the percentage in the other examples above. On the sequence level they can be very diverse.

Also, what kind of culture vessels do you use?

I think the total free energy of the hydrolysis of PEP is roughly twice that of ATP. That allows the transfer of P from PEP to ADP. However, PEP has only one phosphate to offer. Where should the second come from?

It scales with ln(2N) (i.e logarithmic). ln(2E6) = 14.5, however ln(2E5) = 12.2. That would be 244 generations.

Under the assumption that it fixes, it will take about 290 generations. This model does not take parameters such as dominance into account. Note that time to fixation does not imply that it will really fix. It is just the average time that is required in case it really fixes.

I have not read the article, but you were describing the transfer of resistance genes in bacteria that live in foodstock. That means that there may have been HGT between bacteria. It appears to me that your assumption was that there was transfer between humans and other animals which does not appear to the be topic of the article. However, if you provide a link to the article in question I can check it out .

Even if it was dominant there would be chance that it becomes fixed. In fact, deleterious alleles can also be fixed, especially in small populations (remember, we are talking about probabilities). There are different models that explore the question you have, but I do not know it precisely off the top of my head. Kimura has developed models in that area, though. You may want to check his papers/books (unfortunately I do not have a copy with me).

Nice summary. I just wanted to nitpick that HGT in bacteria is technically independent on cell division. Thus theoretically (though highly unlikely) a mobile genetic element could spread within a (diverse) population without the actual need for reproduction (essentially an extreme model of selfish genes). Also HGT is not unknown in eukaryotes (including limited transfer of bacterial genes to their hosts), but as already stated the rate is much, much lower.

1) I generally try to keep my samples MS-compatible, so I generally use DTT rather than mercapto for reduction. Generally, I would not expect to have much of it left after the run, though, so it should not interfere too much with immunoassays post-blot. 2) That highly depends on the particular instrumental setup you have.

The website is lousy in terms of information, as it mixes up different aspects and levels of genomic organization quite a bit. In any case, a flat value such as 95 or 99% is not very helpful to draw direct conclusions, especially without a proper context. What has been shown, for instance is that coding regions differ by around 1-1.8% IIRC between chimpanzees and humans. However non-coding regions under much less selective pressure and thus the average over the whole genome (the sequence) amounts to the 95% shown by Britten. Note that despite the mentioned differences in genomic organization, the DNA-sequence is roughly 95%-98% identical (depending whether you analyze only coding regions or not). That being said, I am not quite sure what the OP meant. Genetic differences between bird species can be quite large, depending on how related they are. The same with apes, and other mammals for that matter.

It is a pretty standard technique. I am pretty sure that me and a couple of others on this board can help you out, if you got specific questions. For broad overviews obviously other sources are obviously better. Bioanalytical and molecular technique textbooks, for example (Sambrook is a standard). Also some manufacturers offer surprisingly nice manuals.

Yes, you do. Though it depends on the type of test you are interested and can be rather tricky. For instance, the alternative could be that the phototactic is stronger, weaker (i.e. one-tailed), or either stronger or weaker. However, in case of Fisher's approach an alternative is not even used to formulate the test. Here, the experimental data is tested against the probability that it arose from chance alone, assuming H0 is valid. However, in the ideal case the H0 and H1 are formulated in a way that makes it possible to accept H1 by rejecting H0. Though depending on the experiment there is also the chance that you reject H0 but cannot decide on H1. Also note that you do not accept the H0. You either reject it, or fail to reject it. In the latter case it just means that H0 may be a possibility (but so are others).

Separating Staphylococcus and corynebacteria can be done as described, but is often tricky. Very often you will find contaminants even after serial streaking. Manitol agar is generally already selective, but many corynebacteria (darn them and their hardy cell surface) are very resistant to a wide range of pH and osmotic challenges. Unless you know precisely which strains you have, I am not sure that there is a easy way with selective media.

You can be more specific by framing the null in terms of the parameters being measured. E.g. instead of "effect" you may want to posit that whatever being measured will not be influenced by light intensity (e.g. phototaxis).

Here some primers: U is indeed the activity (short for unit). You need to figure out/decide how much enzyme activity (how many Us in total) you need in your assay. With that known, you got the volume of your enzyme. Next DNA, here you got all the info. How many microliters of your DNA solution correspond to 6 micrograms? Then there is the buffer. 10x refers to 10 times concentrated. What concentration, should be in an assay (hint: it may depend on the enzyme)? With these quantities known you only need to fill up with water to the final 20 microliters. You may also want to check out the websites of restriction enzyme manufacturers, such as Fermentas or NEB.

With groups I meant the composition of people under a given PI (or, in short, the one who provides the money). However, also in biological sciences collaborations (resulting in multiple authorships) are often limited. Often authorship are shared not due to the actual work done, but e.g. by providing resources, such as samples, instrumentation, etc. Exceptions (more than in mathematics) exist, though.

This is incorrect. The rise of oxygenic photosynthesis is placed around 2.5 Gyr ago (studies that place it earlier are heavily contested). AFAIK the latest studies place cyanobacteria around 2.15 Gyr (and eukaryotes around 1.8 Gyr), but I may be remembering it wrong, it is just something I picked up talking with colleagues and I may be remembering the precise numbers wrong. But in any case it would be at best in the late Archean, way later than the first prokaryotes. Also nitrogen fixation has evolved earlier than photosynthesis, especially considering that the nitrogen fixing apparatus is very sensitive against oxygen (something that the early prokaryotes did not have to worry about). What you may have read is from a paper in the 90s (and which is erroneously propagated in many sources) in which it was claimed that records of cyanobacteria are way older. But this has been basically dismissed by now. According to molecular clocking mitochondria evolved earlier. Evolutionary evidence favors the assumption that the rise of the first eukaryote is bound to the endosymbiosis with prokaryotes.