CharonY

My main question would be whether it is really true. I would have expected that the majority of the AB would not reach the bacteria at all and gets secreted directly. But for fast detection of ABs I would probably try to develop an ELISA system. These are fairly easy to use and can be done even small labs.

Uhm you do not need to acquire a P. aeruginosa strain from hospital to have them AB resistant. Basically all are. The reason is likely the high abundance of exporters found in them that throw everything out before it can harm the cell. One should keep onself clear from this bugger if one has a compromised immune system or have specific conditions that may allow infection (e.g. cystic fibrosis).

Moreover telomere length are also a form of cell regulation. As already pointed out, loss of such a regulation can result in cancer. And also to nitpick, not all immortalized cells are from cancer lines. But all cancers cell lines are immortalized.

Well that and the fact that IIRC the metabolisation of crude oil required a dioxygenase at some point, (i.e. the process is aerobic) and also very slow and rather inefficient. As after all this time there are still oil reserves it indicates either that the bacteria able to metabolize them are pretty young (but there is not much evidence for that) or that their metabolization rate is overall lower than the actual production rate. So without further involvement it is likely that the oil pool would slowly increase over time whereas the bacterial activity would only slow down the process. Human activities on the other hand utilize the pools faster than they are regenerate so they are not only accelerating a process, but in fact reversing it.

P. aeruginosa is an opportunistic pathogen, so be careful. Also I have to add the caveat that if you isolate bacteria from environmental samples you cannot assume GRAS status, as there may be infectious in between them and there is always the chance to increase their titer to dangerous numbers. This is especially true for bacteria isolated from humans, even if it is only the skin. It depends on countries and then even on the respective local biosafety regulations, but often if you cannot state with certainty what you got in your raw sample, you will have to treat everything as potentially infectious (with all safety measures that have to be taken etc.). That being said, there are number of interesting soil bacteria. For example rhizobia (e.g. Sinorhozobium meliloti, Rhizobium legumniosarum, Mesorhizobium loti they induce nitrogen fixing root nodules in their respective legume hosts. A simple class experiment would be infecting the respective legumes with the given bacteria and see their growth increase compared to non-infected plants. Corynebacterium glutamicum an industrially relevant amino acid producer, Synechocystis photosynthetic bacterium. Shewanella oneidensis it is known to dissimilatory reduce about anything. Myxobacteria, e.g. Myxococcus xanthus it forms fruiting bodies and hunts other bacteria. Just to name a few. Make no mistake though, creating a pure sample out of an environmental one is quite a pain in the lower back. Even if you see a nice uniform colony upon microscopic investigation one can find that it is not that pure after all. I remember a grad students whose job was to isolate bacteria with a specific metabolic ability out of anaerobic samples. Took ages until he realized that the co-contaminant was there because it was smaller than the sterile filter he used....

A) Any potentially infectious bacteria are at least BSL2. This includes all S. aureus strains, regardless of resistance. Moreover, if you try to isolate from human samples you can cultivate a host of potentially infectious bacteria. Again, do not do it without proper training. That is, it is well outside the scope of a highschool student. Just trying to amplify something from human skin is well outside of safe and careful. B) The media is non-bacterial matter. And some media are literally dirt. Only sterilized dirt.

What is the weight of one plasmid?

The graphic alone is not sufficient data. At the very least one have to include what was used as a marker. Ideally refer to the publication please. Just to add, what generally is depicted are certain allele distributions or microsatellite studies. While they show the distributions of the markers in question they do not validate a notion like race per se. Also I have to add that K-means clustering essentially groups your data into K groups. You can either estimate K a priori, or by using calculations as indicated in the OP. They means to estimate K are not undebated, though and often depends on the application of the clustering. In this case, for instance it is likely to be sensitive regarding the genetic markers used. Just from the wording I am somewhat sure that it was ripped out of a legitimate study and "race" was subsequently inserted. Maybe search and replace of population with race.

If anything redundancy is a point in favour of evolution. Created things usually tend not to have too many of those. I mean how many times did you shirt lose two buttons whereas there is only one additional spare was to be found. Not to mention the lack of thread, needle, a coffee, a hot meal, a non-time limited research position, a few mills to set up a lab, donuts and fresh air?

What kind of paper is this and what are the main points?

If you are talking about sequencing a genome, nowadays it would take maybe a month. If all runs work perfectly it may cost less than 100k in sequencing kit costs. To generate the sequence with sufficient coverage using a next gen sequencer (e.g. 454) that is. The assembly would take somewhat longer. But everything could be easily done within a year nowadays. But yes, a simple paternity test would generally not reveal any medical information. Of course the same material can used to search for known diesease markers, though, which is only moderately more expensive (if at all).

Uhm guys, you are aware that are biosafety 2 pathogens? Not that something to play around with (without proper training at least). I am not sure what you mean by that? Even a oure (clonal) culture of pathogens is pathogenic (more so actually). Not totally. It has some historic reasons, but even then they were not randomly selected. Main reasons are the easy genetic access to to E. colis and fast growth combined with easy cultivation.

If you really want bioluminescence you would just clone the luc (luciferase) gene. However you would need an in vitro assay to really see that. Probably Ecoli suggestion is easier, as you only need to excitation light of the proper wavelength (around 390 ish nm). a) you would not need the proteins themselves, you would only clone the genes. This is most easily done either by buying a plasmid with the genes already cloned in, or, if you want to clone yourself, you will need everything to do a PCR. b) the whole cloning part is. The GFP or Luciferase assay can be done in vivo as well as in vitro. c) it depends on the vector. Ideally you would have two markers (selection and counterselection) then you only cultivate them twice (once for selecting for vector and insert, once more for the actual test). d) PCR to amplify gene of interest (requires DNA with gene of interest plus suitable primers), cut the vector (or use a TA vector and a polymerase that does T-overhangs) ligate vector and insert, transform cells with it, select for vector, select for insert.

Is it really illegal to do a test? I thought it was only not usable in court?

Actually they are not the same thing, though admittedly they are often used interchangeably. Protease is the generic term for all peptide hydrolases which includes endo- as well as exopeptidases. A proteinase is another term for an endopeptidase. At least it was traditionally that way. Since them it has become muddled a bit.

Indeed. And in fact the Maths makes it far easier for physicist to discuss things, even if they are from different disciplines. Different disciplines in biology have a harder time to communicate with each other (I have been in both situations while working with physicists and microbiologists/ecologists).

Yupp, I take it back. Spermatozoa do stain. Though the mechanism appears to be a bit obscure (they can be either positive or negative, depending on chromatin condensation). But as already mentioned, there is no way to confuse them with the bacteria in question.

Please provide an example that we may discuss.

Yeah, that would be good. I kind of misread the OP- I kind of thought the question was what the difference in establishing the lineages were (sucks not to be able to read). Differences are to be expected, of course, but "consistent" differences are unlikely.

The virus particle itself outside the body is not likely to maintain integrity for very long. The maximum is around a few weeks in humid environments. But inside the body it is a different story. Though of course the stables form is the one we all carry around with us: integrated into genomes.

They are mathematical models based on current available sequences and include factors like e.g. mutation rates.

Reproducible. In that case is it possible that the films are no good anymore? You could try and expose a film and develop it to see whether you see a similar pattern on it.

Well, I have not used dendritic cells myself, but with older, almost apoptotic cell cultures I used to get far lower yields, too (roughly half of active cells). But absolute quantities are hard compare, of course, at least if not normalized to cell numbers.

Actually it looks a bit like something was on the film, or the developer was not stopped evenly, something like that. Is this reproducible?

This is homework, I'll move it. Wheee Tris buffer!