CharonY

Based on current behavior of a number of the big pharmas, my bet is that they would leverage their lobbyists. Unless there is such media hype regarding that treatment that it would be hard for them to succeed. I am not sure regarding fairness, since this is not what corporations are there for. This is generally a bit of an issue in overall health care. Of course, patient outcome should be paramount, but much of the infrastructure requires corporations and those are obviously profit-driven. This is not always a bad thing, as they can leverage their capital to e.g. conduct clinical trials. What I think that is more important is to cut ties between regulators and the corporations, so that that kind of lobbying cannot happen. But considering how humans work, I assume it is a pipe dream.

Kind of relevant Linky

I think one question is the complexity of the treatment and whether there are any kind of risks involved. If it is easy (i.e. one does not need any highly specialized equipment/drugs) to do the treatments and it is safe, I would think that it would be relatively quickly adopted by hospitals. If there are any risks, I would imagine that companies that have specialized in selling and producing insulin would lobby heavily to at least delay the approval of this treatment (so that they can re-orient themselves). If it requires specialized drugs, but the profit margin is low, then it may take a while until a company sells it, unless, of course, the aim is to hurt a competitor who is heavily invested in diabetes control.

Yes, Jimmy is right.

For most purposes I use WoS, I have hardly used SCOPUS, so my knowledge on that is limited. What I like about WoS is that you can easily find which papers have cited a particular paper, which makes it easier to catch up on a given topic. I do not know whether SCOPUS has that feature.

Tricky thing, that. Truth be told, if you start off with a gene with unknown function your chances are low that you will be able to find its function. To give some perspective, the genetically best characterized organisms, is probably E. coli. Each (non-essential) gene has been knocked out at one time or another and even essential ones have been characterized (e.g. by rescue methods). Nonetheless, around 20-25% of its genes are still of unknown function. If you pick a random uncharacterized gene in humans, chances are very slim that you will find the right cell line and condition to elucidate its function.

Also, certain types of corruption may not be perceived as strongly as corruption as others.

I think it can, as a general term. But obviously not if you are talking about "active transport across membranes", which would be a more precise description to begin with. Again, definitions such as these are highly context dependent. I would not put them into the same category, but the term "active or passive transport" is not precise enough, either. It is just a convenient distinction in a given context (and thus a convenient exam question), but quickly becomes imprecise when venturing out into other biological contexts. For instance, does pumping blood qualify as active or passive transport? From the viewpoint of transport into cell the active part plays no role. It only does active circulation. But from the viewpoint of moving cells and other metabolites throughout the body it is.

I would suggest not to remove a change immediately if it is not a "real" word. A bit closer to real evolution would be a population which contains several copies of each word, or may be even several words concatenated as a string. Then if the mutation results that one or several of the words change to a meaningless word, decrease its frequency in the next generation, but do not eliminate it (yet). That way mutations can accumulate.

The simplest way would probably a PCR assay. pCMV and pGlow both have Amp resistances, I think. I assume you are testing it in an eukaryotic cell line? It is probably less of an issue, but IIRC pGlow is a pUC derivative that belongs to the same compatibility group as the pCMV vectors (both derived from pMB1). So they would not replicate in the same cell. But again, that is not an issue when measuring transfection into eukaryotic cells. However, in most methods co-transfection occurs at a lower rate and the smaller vector can outcompete the larger ones.

Yes, precisely. You have to think using semi-log scale, though (just plot it and you should see).

Do you know what a ladder is for?

For a 2% gel you need to know the weight of 50 ml water and take 2% of that weight in agarose. There are different types of loading buffers (though with overall similar to same composition). As a rule of thumb X-buffers are used in 1x final concentration (though in cases of some universal buffers, they are not).

It is a matter of context and level of transport. The transport you think of is generally a transport across membranes (short distance transport) whereas vesicle based transport is a means of long-distance transport. From a physiological viewpoint both are transport processes, albeit in very different contexts.

Have you validated the presence of both vectors in your cell lines?

More importantly, RAPD is often not trivial to interpret and has often a low resolution. More detailed sequencing-based approaches found quite a few differences (Edwards-Ingram et al 2007, AEM) probably relevant to their different probiotic effects. However, overall similarity still suggests (afaik) that both are most likely just one species (but then species concepts in single celled organisms is often a tricky business).

Wait, do you imply that there was a part that made sense to you?

This is a tricky question in my opinion, and does (again, in my opinion) not have a simple answer. Bacteria under stress for instance, can induce an error-prone repair system which will increase their mutation rate by quite a bit. In addition, mobile genetic elements also act as mutagenic agents, which different organisms. In eukaryotes, different cell types have different mutation rates. Based on that, mutation rates are only rough estimates and are highly dependent on the organism, even the tissue within an organisms and their overall exposure to mutagenic agents. In single celled eukaryotes mutation rate estimates are going to be higher than in more multicellular ones, for instance, as only mutations in the germline are going to be detected (so, it is also slightly a matter of how mutation rates are estimated. Overall, however, due to the fact that they are all single-celled, plus overall higher exposure to mutagenic agents (including mobile genetic elements) plus higher potential of horizontal gene transfer (of which the before mentioned MGEs also play a role) plus error prone repair systems I would think that on average, the estimates for prokaryotes should actually be higher than for eukaryotes. Edit: Repair mechanisms in proakaryotes are actually pretty good and mutation rates are generally adjusted for generation time, so these two answers are not really relevant.

Depending on how the cell gets into the cell (e.g. whether via endocytosis) I would assume that common degradation pathways such as ERAD or endosomal degradation take care of the virus.

The general pathway is that the mosquito is infected with a virus, which they then can transmit. So it is not the same as direct blood contact. It depends on how well the virus survives (and propagates) within the respective hosts and vectors. HIV does not remain functional after passage through mosquitos, for example.

Sounds like ultrafiltration devices indeed. I generally only use small-sized ones (i.e. for molecular biological stuff), but the same membranes can be also bought in custom sizes. One problem that you will have is clogging, if you intend to do it for any extended amount of time.

I would try to hunt down the original recipe.

In addition to that why should bacteria in the stratosphere have originated from space? AFAIK identified samples were for instance Bacillus and Janibacter species. And the evidence such as mentioned radio spectroscopy or the claimed fossils of extraterrestrial cyanobacteria are just too weak to have any value (*cough* artifacts *cough*). And finally, quite a bit of that kind of stuff is published in a junk journal/website (journal of cosmology or something like that). Also, Wickramasinghe (in addition to some others) are rather well-known to be the main proponents of panspermia. Nice theory with little evidence and even less explanatory powers. Also, apparently they think that evolution is driven by the influx of extraterrestrial viruses (of which they claim SARS was an example of, don't ask me). What makes it worse is that quite some effort have been put into promoting this notion, efforts that should have been put into gathering and critically evaluating evidence. Finally, things like this fake journal and stuff like the wiki pages as well as the OP here, just cheapen their academic achievements. In the realms of cosmology, I mean. In the area of biology I am rather dubious about their contributions.

You mean like parasitic bacteria? Yes. But in contrast to mitochondria their evolutionary fate is not coupled. They can (and usually will) spread from host to host. Mitochondria do not have a free-living state anymore.

Unfortunately, no. You will need to know what the concentration of the 4x Tris is. That is why using the x-notation is useful in lab (e.g. if you always have the same concentration for the stock and then just dilute it down to 1x), however it is worthless for documentation since it could be anything.