CharonY

Well, in theory bacteria do not classically age, but they die for a hosts of other reasons of course. It is in theory possible that upon a certain point a bacterium may accumulate enough mutation so that it eventually dies from it, but then they are incredibly robust and even curing certain bacteria from a large number of genes does not necessarily cause them cell failure. On the other hand they may then die from the inability to process certain nutrients, increase susceptibility to certain stresses and so on. In the end it is more likely that they die from other reasons. The same also goes for immortalized eukaryotic cells like tumours, for instance. It is hard to track individual cells during several life-cycles. though. But of course what happens on the single-cell level cannot be easily applied to a whole multicellular organism. In the latter survival is dependent on a unbelievable numbers of things not going wrong.

Well, as far as I remember the video he did, if only roughly. I did not like some of the more graphics filled slides, though. The principle of trying to be remarkable is sound, however using Robin Hood AND a Chihuahua was a bit much. It is better (but harder) to try to achieve humour within the actual scientific part of the talk. I do remember a talk from a british prof. about a ferric uptake regulator (FUR) in bacteria. Some bacteria did not have it. So he put a small image of a Fur-less dog beside them. That was fun.

Yeah, but as I said, even if you can get hold of them, they are too dangerous to use them at home.

Well, start off with the genotype of the parents. You know their phenotypes, so you just have to associate each phenotype (eyes and tail type) with the given genotype (aA or Bb).

You would need to post more information to get replies. Including available equipment maybe.

Experiments with human cell lines (or even cultivation) require a biosafety level 2 lab (mostly due to the danger of viral infection).

Well, mitochondria are a good example of bacteria that have evolved (in case someone mentioned it already and I overlooked it). Moreover, there are bacteria that have multicellular part of their life-cycle like e.g. Myxococcus xanthus. The problem with long-time bacterial evolution is that they simply do not leave us fossils to recognize changes over long time scales. In theory it should be possible to see the transition from one bacterial species, however it would require the sequencing of single cells, which, while in theory possible, is quite complicated to do.

Not to mention very toxic.

That is pretty much wrong. Many had resistances to natural occuring ABs. You have to understand that often only minute mutations (sometimes as less as a single nucleotide exchange) to confer the resistance. In other words, all kind of potentially resistant strains pop up all the time. However, this mutations often do not occur in significant numbers to be noticeable, unless you change the selective pressure so that those carrying the mutation get a selective advantage over the others. In other words, once you pour ABs over them, those with those mutations suddenly pop up. Otherwise they remain numerically insignificant. The only matter of induced evolution, if you want to call it, is the so-called error-prone repair system, which increases mutation rate. The rest of the argument is thus pretty much based on wrong assumptions.

Severian wins. Hands down. The only thing I could show are a couple of MS. And maybe the AFM (but I have seen calculators that look like more).

AFAIK the actual sensations are quite different. For instance, some may associate numbers with a certain landscape, other associate them with sound, or colours, for instance.

Well one could tell horror stories without end on every step in an academic career. Most would sound pretty similar and revolved around - lack of money -lack of time and therefore -lack of sleep (imo the worst part in the long run) -to be completely at the mercy of the advisor (can be good but if it is bad it is really bad) It mostly depends on what you want. If you just want the degree and leave academia it is somewhat easy to ride through it. However, if you really want to go through all the bad times to get a position in academia it is far more haunting as you will get frustrated even more on every mistake you make and every bit that might leave you behind the competition. And then it will get worse if you do your postdoc. But the single most important thing is simply this: find the right group. If you are lucky this might boost your career to no end. If you are unlucky it may very well end it. Make no mistake, it is almost impossible to make a career in academia just with ones own ability and resources (at least not in the practical sciences). One has to be extremely brilliant to do so (and so far I have not met a single one that may qualify for it). But in the end, for some reasons, if everything is right, it can be the best time in your life. This is the only time one can do research somewhat more carefree.

You should be sure that the agar plates you use are able to capture a significant amount of skin colonizing bacteria. Either that or use a variety of media. If you did not, you should discuss what bacteria are able to grow within the time frame and under the condition you cultivated and whether this includes a significant bias or not.

However, quite regardless of what is actually written in the paper I would probably ask something completely different: are there any reports which highlight that the massive use of triclosan or any other desinfectant has any beneficial aspects in normal households? The need of desinfectants in crititical areas as hospitals or labs are pretty obvious, but why incorporate it in anything else?

Weeeell, in a way bacteria (or other prokaryotes) are similar to cancer cells as both are in theory immortalized cells which can proliferate endlessly...

Well, in the strictest sense a strain refers to genetically uniform entities. As such in theory a single mutation would be sufficient to classify it as a different strain. Note that this is not really a taxonomic distinction but rather is used for practical distinctions.

The immune systems recognizes specific structures of the viruses (antigens, this term is not specific to viruses but to anything the immune system recognizes). If the genes for the given structures mutate, the resulting structure might be altered in a way that is not recognized by the immune system anymore.

Ahem, Craig Venter's journeys were anything but a success. At least from the viewpoint of environmental (micro-) biologists. Most thing that the produced a data dump hardly useful for anything. There are however similar approaches that were more successful (and took more care during the sampling procedure). How to do that? Fairly simple. Just go and take samples, record all relevant data of the sampling point, think about proper storage procedures, got to the lab and analyze it. This is, actually traditional research in the biological sense. The only tricky thing as always is funding. But the procedure is absolutely the same as with other research, write a grant, apply for travel money etc. If you are not as rich as Venter and want to apply for the money for an own research ship, you are outta luck, though. Few companies (as stated above) would actually finance a research expedition, unless you happen to have longer (research) bonds with them and have a very specific proposal. Just going out and taking samples doesn't give you any grants. Regardless from which sources.

Well, the white paper has essentially a simple negative statement: there is " no evidence of acquired bacterial resistance developing by triclosan." Of course they simply disregard the problem of the increase of a resistant population (as opposed to non-resistant strains acquiring a new resistance). While the spread of AB resistance is often more of a concern than merely the propagation of resistant strains, the numeric increase or already resistant strains should not be totally disregarded. But except this point, the only thing one can really do is to check whether the cited literature does in fact agree with that white paper. Chances are that they do, but maybe there also some side conclusions that are note detailed. The next thing to do is to state a counter hypothesis (which has been only done implicitly). For example: - triclosan use leads to spread of resistance against it - triclosan use increases the titer of resistant strains Then it is only a matter of doing the experiments, or more likely, search the literature to validate this. As it has been in use in all kinds of desinfectants, deodorants, toothpaste etc. there are scores of papers out there. Chances are, however, that there are not that many around which show that triclosan use really has an impact. At least just on top of my head I have not literature ready that demonstrates a a spread of desinfectant resistance (as opposed to defined AB resistance). Also I am not entirely sure about the mechanism of triclosan resistance, I only think that it was not a single gene contributing to the resistance and contrary to what is stated fabI overexpression was not the single source of resistance. Due to lack of time I am not able to read all the papers available, however if anyone has any questions I'd be glad to fill in as much as I can.

Actually this is only true for infinite time frames. Normally the fixation probability scales with s, but depending on what factors we allow into a model the allele might well get lost prior fixation. So, not in all cases do beneficial mutations persist. On the other hand, alleles do not necessarily need to be fixed to play a role...

It sounds to me that you have to read up the basics of separation methods. I cannot (and also do not want to) give you an ad-hoc lecture here. Just some basic infos, for real understanding you should look them up in more detail in textbooks for bioanalytical techniques (check your local library). In very short: electrophoresis is a technique to move charged molecules. For protein separation polyacrylamide gels are used that function as sieves. Larger proteins move slower through the gel than smaller ones, hence you can separate proteins according to their size that way. Of course you have to mask the endogenous charge of the protein first, but let's not confuse you too much. For protein separation via chromatography normally HPLC (high performance/pressure liquid chromatography) is used. Essentially proteins are moving in a mobile phase through a column packed with the stationary phase. Depending on what the stationary phase consists of, the proteins are retained according to specific property (e.g. charge).

One general problem is that according to one of the basic tenets of the modern synthesis "The durable units of evolution are species...". However, it is clear that on the prokaryotic level there are in fact no clear-cut species, except by drawing arbitrary lines. This however can clearly not be a fundamental unit of anything. Accordingly, declaring any lineage special does even make less sense. An additional problem is that genetic analyses do not give easy answers either. Especially HGT is a nasty thing to consider. Finally I have to add that most current taxonomic studies place birds clearly in the class of reptilia.

Explain what? I do not see a question...