CharonY

In principle yes. I think for this database it is decided on the type of experimental evidence (e.g. using mutant analyses vs DNA binding assays).

I am not familiar with that database, but from the looks of it it appears that physical are include e.g. protein-protein or protein-DNA interaction (i.e. actual molecular interaction) whereas genetic interactions are apparently mostly based on mutational analyses or dose investigations (e.g. effects of over- underexpression). I expect that in some cases there will be considerable overlap.

I think the terms are only very loosely defined and you will find these are similar terms pretty much describe the same thing, depending on whether you come from the biological or e.g. the bioinformatics side. They can be used to distinguish certain finer points depending on the way the network is built. For example the whole network can be based only on genes, i.e. you ignore the subsequent transcription and translation steps and potentially also involved metabolites. In this genes you would have genetic interactions mapped but you may not be able to read out the underlying mechanism of regulation. Or you can add protein information as well as level of regulation (which is more common when the term gene regulatory network is used). But again, these tend only to be strict terms in a very small area in specific sub-disciplines. In common scientific usage one has to provide more context to explain what precisely is meant. The question about inference is a fantastic question and I could write whole assays about that subject (which I should not due to time constraints). But to put it simple, it is one of the big challenges, how can genomic (or omics in general, i.e. transcriptomics, metabolomics and proteomics) information be used to inform us on physiological consequences? The question is pretty much still open and there have been all kinds of approaches (often summarized under the banner of systems biology). However, there is still no clear consensus what the best way would be. Modeling techniques have seen some popularity and while useful for either simple networks for which we have a lot of biological information, they tend to be less useful for complex questions. In the end, most of the time a clever experimental design is needed to really figure what is going on, with genomic information being just a part of it.

I think this is close to the likely mechanism. However, I would assume that not any swelling is the responsible but the cell damage that a highly hypertonic solution may cause. Nerve signalling tend to get sensitized upon tissue damage (i.e. the wound) and I would speculate that the presence of salt or other harmful compounds would exacerbate this. In addition electrolyte sensing receptors may add to the overall response, i.e. further stimulating nociceptors.

Ah yes, if the color is really dark it is possible that the temp in your bottle is getting a few degrees higher (IIRC autoclaving glucose solution for 30 mins at 125+ caused strong discoloration, whereas at lower themp and times it was much less apparent or absent). However, if that happens it is probably a good idea to filter it. That being said, yeast (and certain less finicky bacteria) appear to grow OK on plates even when caramellization occurs (though it may depend on degree which is a bit hard to compare, of course). and colonies did not appear to be very different. But if you do test growth parameters or for more defined experiments you certainly should eliminate those variables. In addition I should note that sugars can undergo the Maillard reaction with amine groups if present in the media during autoclaving. Again, if precise growth parameters are needed, addition post-autoclaving would be wise.

Relative to what? The vast majority of labs are autoclaving glucose in the broth so there is probably not a fundamental issue. And I am not even sure that at the regular parameters for autoclaving (121C, 15-25 min) significant caramellization occurs. Of course one could just test it with sterile filtered glucose solution instead, but I would be surprised that on plate you will spot a lot of differences (maybe more so in liquid).

One thing that may be confusing is that the US systems is heavily based on agreements. This quite the contrary to the parliamentary system in, the Netherlands or Germany where you have a ruling party and an opposition, where you basically expect that the opposition is, well, opposed to almost anything the ruling parties decide. So for many US citizens it mostly looks like that their two big parties are not able to agree on something, which is also somewhat perpetuated by the media due to their desire to appear neutral on that matter. Re-election is legally probably not an option and even if it was, there is a good chance that it would change little. Those opposing ACA are probably elected because of their stance. Hence for them this is probably a good way to show their constituents (remember, congressmen are not elected by popular vote across the nation) that they fight for them and is standing up to the evil government (or something on that line). But the key point is really that the power struggle has a completely different structure than in Europe and is often within, rather between party lines.

Uh, two-year necromancy?

There are numerous issues with that with one being liability. If you get injured on the job you are generally taken care of. But if you are not actually on the job, but it happens in the facility, well that is going to cause problems. Another one is security. If you are not on the job your access to certain areas will be automatically revoked for the time. Again, it would be a liability issue when someone has access to dangerous, classified or similar material while technically not being on the job. Tangential to federal wages: I vaguely remember a CBO report indicating that below a masters the federal compensation (wages+benefits) are on average higher than in the private sector. At masters and above the trend reverses. One of the reasons I presume is that federal agencies are not able to squeeze untrained labor that well (i.e. there probably regulations to limit use of part-time or temp worker that go without benefits). Instead they have to outsource to companies that do that. Still, missing paychecks on the lower bracket will hurt, no matter what.

Federal programs that are deemed essential will continue, this will include staff that keep expensive machinery running, from what I heard. Most labs are likely to have reserve funds to pay people internally. However, researchers working on federal programs are likely to be furloughed.

I think this misses the broader topic. The fact that faculty positions are replaced by adjuncts and the fact that the latter are paid a pittance for their work. This is especially an issue in humanities as there are not as many postdoc type positions which are also a type of waiting position for until one decides to seek a different career or finally lands that tenure track position. However, postdocs are at least paid better (though not terribly much all things considered) and they get benefits. The big issue is that adjuncts have basically no say in this matter and the question is whether forming an union (which in some cases is not allowed) would improve that situation. In many ways the career path of a scientist is often broken (as compared to a "normal" career) with many abusive steps in-between, if one is unlucky. The situation is only going to get worse with more and more students and graduates and less funding for science and teaching.

First of all, as the name it implies it is is not a structural protein but an inhibitor of a serine protease. Also polymorphisms are not anomalies, there are simply genetic variants of a particular gene. The vast majority of existing alleles are do not result in dysfunctional proteins, as they would likely be selected against and thus eliminated from the population. Allelic variants can have different properties in terms of expression or activities, though.

I think dementia (and their causes) should go high on that list, too. Especially if friends and family is involved it is in some ways worse than cancer. At least in the latter case the person you know and love is still there to the end. And it is really bad when the person has moments of clarity and realizes his/her situation.

I realized that I misread the post. For some reasons I assumed that that the primer were derived from chicken rather than cauliflower, which pretty much invalidates my post. In that case it really depends on the primer how to interpret what you see. I.e. what area is targeted as they are highly conserved regions in beta-actin genes which could yield identical results across species. I.e. using the correct primers you could either amplify a region that is conserved across species or specific for only closely related ones. For that you would have to know what fragment size to expect. Considering that you ran a high-percentage gel (as seen from the marker) I now suspect that the smaller fragment is indeed the expected one. As there is a bit smear up to the top, is it possible that you either contaminated or had a large amount of DNA in your PCR reaction? The alternative is, as Tridimity mentioned unspecific amplificates (of greater length that is).

I would actually be surprised if there are any structural differences. On the extreme ends of the spectrum (of whatever parameter we are testing) I would expect maybe slight differences in the activation patterns (e.g. due to the way a problem is being perceived and subsequently solved) but I am not certain that there would be anything detectable on the (sub-)cellular level, for instance.

Why do you think that this is a Southern? The simplest explanation is unspecific amplificates. Note that the size is fairly low (in the low 200). If the run was not stringent enough there can be some products there. Note that there is something even lower, which are likely primer dimers (depending on their length). Of course there is also always the risk that there are just by chance sequences somewhere that allow that. But considering you see them in both I am pretty sure that they are typical artifacts. They are also stronger in the cauliflower because the specific target is missing that would outdilute the primer for the PCR reaction.

It is possible to grow certain neural cultures. The key is often onbtaining them from (rat) fetuses or very young rats. In these cases hippocampal cells can be stimulated to grow and proliferate. Hoever, in contrast to immortalized cell lines there is only a limited life time to them (afaik).

The protocol is not quite clear to me. What precisely do you with "the bacteria are not growing after I incubate them for three hours."? Do you mean after harvesting the bacteria from plate or liquid medium and incubating them in pure buffer? If so did you grow them again in media (full/minimal?). The source of the confusion is that incubation also refers to regular growth conditions. And thus is kind of contradictory.

Precisely. Trying to replicate this on the cell line level is needlessly complicated.

As an update to the Syrian chemical weapon stocks: Source

It should also be added that the sugar found in e.g. apple is not purely fructose, though it reaches around 50% of the total (simple) sugar content. Other sugars do include gluclose, sorbitol and sucrose, for example.

You are preaching to the choir here. Quiote a bit of my work is in the area of proteomics and single cell analysis and there is quite a lot of things going on that are hard to interpret. I am convinced that more fundamental cellular research is necessary before we can properly interpret and intervene in cancer processes. Unfortunately the funding agencies are more focused on the applied side. At least hypoxia investigations have gotten some traction lately, but I feel a more integrative approach is needed. That is probably quite a different discussion, however.

What? How do these two things relate to each other? We do have neuronal cell lines, which are clonal, but obviously this is quite a different goal than to clone an organism. To enucleate a neuron without damaging is likely to be trickier than a germ cell line, but again, what would be the purpose of it? If you want to have clones of a cell it is easier just to grow them. In addition to what Ringer said, also proteins for general metabolism, energy conservation etc.

This is blatant nonsense. You could use the same argument to argue that chimpanzees were made by aliens. In essence it is a proud display in failing entry-level genetics. But to answer OP: No.

To be fair, your description actually mixes different types of research directions. For example it is mostly microbiologists that look at biota, even in humans. There is certainly a certain overlap, depending on the aspects of human/microbiota interaction. Human genetics has usually different directions, some that may be medical, some that are not. But with few exceptions (a handful of groups maybe) there is little overlap. Also there is the question what you look at, e.g. genetics on the population level, or genetics on the molecular level. With regards to the the actual career, most fundamental biomedical research is conducted in universities. Some is done in companies, usually for applied research (including development of products). Research teams may contain technicians (usually master's degree) as well as researchers with a PhD. In academia there are few permanent positions that are mainly involved in research. Most tenured positions involve heavy teaching loads. And these are usually very competitive. Being actual in the lab tends to be a phase during your career that you have to grow out of to a certain extent (unless you go the technician route).