CharonY

Simply put. Yes they do. More or less precisely as we do. The molecular basis of the diurnal clocks is to my knowledge very similar across almost all animals.

That's what I actually meant with live titer...

Generally a clean poster without too many colours tend to be less distracting and more informative. The details depend a lot on what you want to focus on, but put only those in that are really needed to convey your point. E.g. for technical presentations you may add methodical details but only present the data that are directly relevant for the data (instead of all optimization steps), otherwise focus on the results only and only flesh out technical detail when absolutely necessary or convey them verbally at the poster presentation. Diagrams are good if they are easily read and informative. It is annoying to have to read through dozen of legends only to find that the information could have been a single sentence within the poster. But generally diagrams are preferably over large text bodies. Keep the poster simple to read and do not toss the elements too much around.

Basically you would simply count the titer. Either count the whole (live and dead) titer and then count only the surviving part (either usind live/dead stain or plating and counting the survivors). You could also simply split a culture and treat one portion and compare the live titer in each case.

Why "should" it? Bacteriocins, however, are interesting antibacterial agents in that regard. They only kill off closely related bacteria (not carrying the required resistance genes). With that those that possess the bacteriocin and resistance genes kill off specifically those that are similar to themselves (and hence are likely competition in the same ecological niche).

You are wrong. The mere sequence does not directly convey information about what or if they encode anything. This various algorithms are being employed to predict ORFs out of the naked sequences, however, they are still only an estimate unless being experimentally validated at some point. You can imagine the sequence as a series of letters in a foreign language, and it takes enormous work to correctly read the words out of it, and even more to make sense out of these words.

What about it? Yes. Generally these changes are either caused by loss of genes (the more common phenomenon) or gene acquisition. However, the number in this paper is based on an estimation and is by no means the result of a 1:1 comparison of the complete respective sequences (which is technically rather tricky).

So straight couples who decide not to or are unable to get children should not be allowed to marry either?

No, at least not if you are plating from a homogeneous culture. The colony is simply formed because the bacteria are diluted on the plate. That is you usually dilute it until there are only single bacteria on the plate, which then start to divide. Each colony is the result of continuous division starting from (ideally) a single bacterium.

First the semantics: BSE or TSE are conditions, not the agents themselves. Also they are caused by prions, and not by viruses. As such they are not successful per se, as they do not replicate in the traditional sense but only change the form of existing prion proteins to their malign form. The prevalence of BSE (and scrapie) compared to e.g. CJ is likely due to the fact that cattle were fed contaminated meat-and-bone meal, something that does not normally happen in nature. That and of course the media coverage.

This is not easy to answer. First question would be whether you want to stay in US. Getting a job on H1 visa are, if I recall correctly, rather tricky as it is coupled to your current contract. Working in the private sector usually require you to get a specialist greencard (or equivalent). If you want an academic career a PhD is usually inevitable. Have you talked with your supervisor?

Not in this context.

Zero. As mentioned, bacteria are themselves (basically) immortalized cells. Viruses will, at best, reduce their viability or slow their growth (unless transduction occurs, but then then virus is incomplete). It is not that cancer cells are necessarily defined by their kinetics (growing as fast as they theoretically can) but rather the mere fact that they do not stop proliferating.

Edit: I am writing up garbage at the moment. In any case, it is not that necessarily so that B. anthracis [\I] only germinates in macrophages. Other factors might also trigger germination. Generally bacterial spores react to presence of nutrient, quorum sensing cues, or certain ions, though I am not sure which cues from the host cell are actually triggering B. anthracis germination (there is literature about them available, I just have not read them). As such I am not currently aware if the same germination stimuli can also be triggered by other cells that may have phagocytosed B. anthracis spores. On the other hand, macrophages tend to be the first actually encountering them, thus the bulk (if not all) of research has been focussed on this particular way of infection. Given the fact that the way of entry of the spores does have an impact on the virulence, it is is likely that germination via macrophages is the primary route (at least from the viewpoint of a disease onset). Also, normally infections do not occur with vegetative cells, but with endospores thus entry of vegetative B. anthracis cells is rather unlikely and does not cause diseases. In other words, for the disease the the bacterium indeed enters the body as a spore and has to germinate before actually causing any damage.

Well, without the sequence you won't know what fragment sizes to expect. Assuming perfect restriction and depending on the combination of restriction you can get some information regarding the DNA you cut, though. The basic question is whether you got linear or circular DNA, then take a digest to map out the overall size and then map the fragments from each digest back to the original DNA fragment (as the sum of all fragments is always the molecule size).

To be precise, mitosis refers to the separation of the nucleus not that of the whole cell (though that is what usually happens).

Darn I made a lengthy post and then apparently it did not get posted. Just a short recap: From what I have seen so far (I had visited physicians and had to have blood analyses done for the same condition in the US and Germany), the quality was equal or even better in Germany. While I did no see much of a difference on the primary care level (I assume the individual differences to be higher than the differences between countries), I have to add that I had an average waiting time on most doctors that I called before I could get an appointment as a new patient. The longest I had to wait for a specialist (not primary care ) in Germany was one week. For primary care physicians my average wait time was around half a week. Also in Germany I had not only faster and cheaper access to specialists. but I was also not limited to whom I went. In contrast I could only visit those that were in my plan. Also in my experience the German specialists were better. I did read up on recent research beforehand and could discuss it with the German specialists (two different ones in different cities), whereas in the US they tended to be upset when introducing the new data (also only with a N=2), or trying to discuss some fine points (a bit strange considering that I live in a University city with a lot of academics). At the very least, at least in this area I could not see anything in the US system to be superior, neither quality of the medical specialists, nor treatment. However one of the biggest difference was the bloodwork. In Germany either the primary physician took it and sent it in, or the specialist (or hospital) did it directly and I got results in 1-3 days. In one case I even got a phone call in the evening the same day, because I mentioned that I had to attend to a conference the next day. In the US I am limited to certain labs (according to my plan), I get results for precisely the same tests roughly a week later, and the first 6 or seven times they always screwed up at least one of the test. For instance by doing the wrong one, or testing the same value twice (one by a cheaper by inaccurate means and a second time with the one normally used) and then "forgetting" a parameter that they actually should have tested. Beside that apparently the communication with my plan provider was not optimal as it may be the case that for some obscure reason I may have to pay for 400$ for a bloodwork (that I incidentally could have done myself with a ~60$ kit) by myself. I assume that this will eventually be resolved, but again, I never had that kind of hassle in Germany. (Did I already mentioned higher co-pay here..?) I did heard a number of times the argument that the US system is more expensive, but also has a higher quality. Is there any statistics at all that supports that notion? Mostly I hear that it is sometimes even inferior. I would like to have a comparison with Japan, for instance, which has IIRC one of the best medical infrastructures of the world.

Well I have been in the US and the German system at least. Based on that I have to say that in Germany I have to pay less and at least for what I needed the treatment in Germany was better. I do think that the German system (mandatory insurance for everyone, either private public) is more expansive than the UK system, however I the overall cost for my coverage in the US is roughly four times the amount of that in Germany (for my income group).

Well, it really depends on what you want to look at and what really you want to demonstrate. If you just want to run a PCR you could even use random primers (essentially like a RAPD, see Welsh, J. and McClelland, M., Nucleic Acids Res., 1991, 19, 6823–6831). Its use for plants is documented in: Tingey, S. V et al., RAPD Technology to Plant Breeding (ed. Neff, M.), ASHS Publishers, Minnesota, 1993, pp. 3–8 and Williams et al., Methods Enzymol., 1993, 218, 704–740. If you got the sequence of the plant(s) you want to identify it is obiously even easier (align sequence, build primers based on conserved seqs). A database of potential plan mol. markers is documented by Rudd et al., Nucleic Acids Res. 2005 33(Database Issue):D628-D632

Yeah that is basically the answer, I think, though the OP is misleading. I think this is homework and I assume what he/she meant was that the insert was digested HindIII/XhoI and the vector was digested HindIII/SalI. It was not, as the post implied, first cloned and then tested by double digestion, as the latter would probably not make much sense. The important bit here is that SalI and XhoI have different recognition sites, but produce compatible ends (as In the scenario outlined by Sceptic). And I assume the confusion in the OP was derived from the fact that the "clone" was used erroneously here. (Actually I have used similar questions in exams before)

No. SNPs are single nucleotide polymorphism. That is single base changes on the same locus.

Actually the integration of DNA in the host cell would not have much of a consequence on a multicellular organism. Especially if you can target cancer cells specifically. While there are markers for cancer cells, it is often more a matter of amount (of marker recepetors, for instance) rather than the mere presence of course, as cancer do not possess novel genes compared to "normal" cells. Also there is the usual problem of proper dosage application etc. of viral therapies.

Actually we are not even close to a billion genes. Moreover, to date there are only few examples where ethics really inhibit science. Actually, the only one I could think of is the stem cell research controversy. Doing animal experiments as humanely as possible may prolong the protocols a little bit (paperwork beforehand tends to be worse), yet I consider that a fairly small price.

One possible scenario: presence of nitrate causes nitrate reducers to outcompete methanogens, thus indirectly reducing competitivity of methonotrophs.

This bottom up approach is being used in a limited manner (partially due to above mentioned computational limitations), however, even if it wasn't the knowing the structure does not necessarily confer sufficient information about function. It will obviously only work with structures of already known functions.