CharonY

From what I have heard it appears that the career path in biomedical engineering is somewhat less clear (considering that it is a relatively new discipline). For pharma students there are the typical options that still exist. Biomed engineering sounds fancy, but jobwise they still lack their own strong niche. Due to the dual nature of it, they tend to be less specialized and especially in research positions more biological or more engineering-oriented disciplines are better established and have an edge there. Engineering as a discipline is very diverse, though and there are plentiful established subdisciplines apart from biomed, obviously. At this point it would be best to figure out where your priorities and interests are.

Ribozymes, not ribosomes. Ribozymes are essentially RNA molecules with catalytic properties (i.e. independent of proteins). Also you got it backwards in terms of efficiency. Now, due to complex cellular systems the required mechanisms are in close proximity (including specialized compartments, when thinking about eukaryotes and to a certain extent prokaryotes, too). Just putting everything into a big pot would dilute everything. There is no strong consensus how early proto life could have been. Many favor a nucleic acid system, though there are proponents that postulate peptides as early replicating units. The mix of the two is almost certainly something that evolved later.

It is more a matter of convenience. You could clone it into the MCS, but then you are limited in how you can clone in the subsequent protein to create the fusion. But functionally, if you get the stuff in frame into the construct you should be fine.

Normally you would want to clone the PTD in first and the create or clone in an MCS after that. That way the plasmid is more convenient to clone fragments into. Also you would want to avoid cutting out the PTD when using restriction enzymes. So often e.g. a PCR construct with the PTD is created that can be ligated into the original vector, often in a way that does not result in a restriction site (unless you want to be able to remove the PTD sequence, then it should be a enzyme not present in the downstream MCS).

The evidence (e.g. DNA codons) strongly suggests that all known organisms (i.e. including archea and bacteria) share a common ancestor. It is of course possible that several proto-life forms evolved but only one group survived. Current mobile genetic elements depend on relatively highly complex protein systems to facilitate their spread. Early mechanisms were likely much simpler (more in the form of ribozymes, for instance).

What is a good strategy to derive physiologically relevant answers from omics based experiments. More specifically what would be the ideal workflow to reduce false-positive detections in quantitative analyses on the one hand and derive predictive models on the other. Also what do you think are the implications of population averaging in proteomic samples?

After a few hours you will experience wonderful diarrhea.

Actually this is close to the standard theory for the origin of eukaryotic cells. In fact, the similarities found between archaea and eukaryotes was one of the big problems placing archaea properly in a taxonomic model. Current assumption based on molecular data posits that early eukaryotic cells were derived by association of distinct archaeal and bacterial partners. Also note that archaea and bacteria are both prokaryotes.

The important bit is generally that the whole construct is in-frame. I.e. if you translate it, you should get the correct overall AA sequence. Small aberrations are often not avoidable, but especially in those linker regions they tend not to be crucial (though as usual with recombinant protein expression there may be exceptions). If the additional base pairs result in frame-shift, the whole thing won´t work, obviously.

That is interesting. While I knew that Northerns and Westerns are derived from Southern, I was not aware that they are not capitalized (in publications they generally are). As a comment to the blot: the process takes at least two steps. The first is a standard gel as described above. In the second step (the actual blot) the proteins are transferred and immobilized on a membrane. On this membrane immunoreactions against target proteins are carried out, detected and quantified (if applicable). Molecular compositions are not detectable by these means. The method gives two information. 1) Molecular weight (as assessed by the gel based separation) 2) reactivity to antibodies in question (technically presence of epitopes).

I have not read the papers, but often it does not make much of a difference whether the start codon is introduced or not. Sometimes the additional methionine (especially the sulfur residue) may prove to be problematic, but usually one just has to clone in-frame. The UTR obviously has to be removed, otherwise you would introduce some random aa sequences.

Flu vaccines are usually live or inactivated viruses. I.e. they require the strain to develop a vaccine. [The selection of the strains for the seasonal vaccine is based on known spread. IIRC H1N1 (the one that caused a pandemic 2009) was in the 2010 and 2011 vaccine. For some reasons I overlooked that you actually cited that from the CDC website] The first step is usually isolating a new strain from the wild and then develop a vaccine. Having e.g. identified crucial parts of the genome for the spread between humans as a template, can improve the detection, as well as monitoring of spread. It can also accelerate the production of attenuated viruses (though that is usually not the most time-consuming part). With the average of 50%, do you mean how much of the population is being vaccinated? A quick google search shows that in the US the average is indeed below 50%. Though it varies a lot and of course it depends on local rate that determines spread and especially death rates. Elderly and children are most susceptible and here the question is how high the vaccination rate is in a given school, for instance. However, for vaccination morbidity rates are often not a good measure as the goal is usually to limit spread. The reason why H1N1 caused a pandemic (whereas other strains did not) was the lack of immunity within the populations.

That would be quite an extensive list. I am afraid that for a true exhaustive list you would have to got through lots of reviews. Also note that many differences are only inferred e.g. by identifying expression differences. They may not be "true" differences or false positive detection. Also, individual differences may not account for much alone (only in conjunction with other changes). These are among the reasons why diagnostic biomarkers are so hard to validate for cancer.

Dalton is synonymous to atomic mass unit (1/12 of 12C) as mentioned, this is not precisely the same as the mass of a proton (and with increasing mass the error become bigger). Again, it is a measure of mass, not size.

I am still waiting for the hounds...

You should look into curve fitting. Also more than two values to properly calculate averages and standard errors (or deviations) would be useful...

Group selection has been shown to be formally equivalent to kin selection. Hence, with the exception of a few remaining proponents, group selection has been essentially abandoned. And the selfish gene explanation fits nicely under the umbrella of the inclusive fitness theory, which is the basis model to explain altruistic behavior.

Let me guess... mathematics (they and sometimes theoretical physicists play by slightly different rules)? However, all institutes require that intellectual property is signed to the employer (i.e. uni institute etc.). Many have the right to prevent you to publish if they wanted to (though almost never enforced). It is most obvious when e.g. patents are issued. The institute holds the right, but may extend it to the PI (and other people involved). In almost group based papers credit goes to the corresponding author (everything else is a spill-over by association). And again, publish or perish is the game for most of us...

Well, it is academia, isn't it? I do not really think that nationality plays a role here. Usually such cases are handled by an ombudsman. But especially when different groups are involved, the first one to publish has won. And it is a rare thing even within a given institute that a junior scientist will have any claim to property. Ideas generated belong to the institute and the PI (in that order).

I have no clue where the government plays a role here. They advise no to publish, but the journals can do what they want. Also the work was carried out mostly in the Netherlands (though there are collaborators in the US) and is an independent group in Japan working on this, IIRC. So which government is now doing what? As you can tell, I do not understand the line of reasoning here. My personal opinion is that bioterrorism is a relatively poor argument when it comes to pathogens. They are, as a whole, rather inefficient. Blowing something up creates much more immediate sense of danger and fear (a goal of terrorism) rather than something that may or may not have been man-made. Compare for instance the anthrax mails with the regular deaths we have in the US due to seasonal flu, Salmonella outbreaks or Clostridium poisoning. It would be easier to claim responsibility for the deaths due to contaminated food rather than try to get spread the agents on your own. Seriously, in the US alone Salmonella is responsible for over 500 deaths annually (and still there is resistance against control programs). Where is the panic and outcry here?

I disagree with you disagreeing.

This may be correct, but the next logical step is figuring out the mechanisms behind it and how whether they affect potential epitopes. Last time I looked there were flu vaccines around. And strain analyses are routinely conducted to estimate which strain is going to hit next. Vaccines are produced accordingly. Your main argument is apparently that vaccines are useless against flu (and therefore research into mechanisms is does not bring any useful information), however the fact that there are seasonal vaccinations around somewhat weakens the point, no? You may be thinking of lifelong immunity, this may not happen with flu, but that is beside the point. The idea of immunization is to prevent large spreads throughout the population. High mutation rates are therefor not a dealbreaker when it comes to viruses. The important bits are identifying epitopes and their variations (though much is done on a far rougher scale). There are a lot of issues with developing an HIV vaccine which I cannot cover in a short post, but they are not limited to the mutation rate, but also include e.g. raising a decent immune responses from inactivated viruses (however there are a number of trials for HIV vaccines right now). In contrast, seasonal flu vaccines are routinely derived from inactivated strains which generally requires the isolation of the strain to begin with (thus having the strain already at hand, accelerates vaccine development and testing). Again, mutation rate is one issue, but does not render vaccines useless. Think about polio (also an RNA virus). Regarding mutation rate: that rates are not dependent on population size, however a larger pool increases the probability of a given mutation to occur (essentially like throwing a die more times). Assuming a large pool of flu carriers it definitely increases the chances of certain recombinations to occur within a given time frame.

Hah, not that unusual, tbh.

If that is the work I am thinking of, there is a definite good reason for this research, and I am not talking about bioterror or something like that. What they did is introducing alleles in H5N1, which already exist in nature, just not yet combined in a single strain. The goal was to find out, how many changes are required to result in a strain that can be transmitted between humans. There are two reasons why this is important. First, to evaluate the likelihood of that occurring in nature. Remember the first outbreak, when people claimed that the warnings of this strain were overrated because it was not transmissible between humans (and thus declared it alarmism)? Well, this study provides how many allele exchanges are necessary. I think they have not yet published, due to ethical reasons, but they mentioned that it was only five or so. Thus, I would think that this work is important as it shows that a limited number of recombinations can result in this precise strain in nature. The second important bit is closely related to the first is what CaptainPanic mentioned. If it is only a matter of time that the virus may pop up, isn't it better to develop a vaccine beforehand? And for that, this strain is also needed. Will the vaccine work? Well, the question here is whether further mutated strain are A) still able to transmit between humans and B) be more virulent. And again, to analyze that one has to know what actually are the factors leading to transmission. To be honest, I was pretty much on the fence, too, when the information started to pop up. However, in the end I think the likelihood of the recombinations/mutations are going to happen anyway that I prefer proper research before it really hits.

I do not think that it is matter of independent thinking. Of course there are examples, in which controversial opinions, that eventually were proven true have led to marginalization. But these are more exceptions than the rule. Sometimes certain people are so obsessed with certain aspects of nature that their social skills may suffer. More often than not, however, successful scientists are often also excellent networkers that are highly skilled (if not gifted) in social interactions. The reasons is that a part of the job as scientist is to communicate science. Every good scientist is expected to explore the unknown and hence, any new idea could be considered controversial. However, in cases where new ideas throw established knowledge overboard, without a strong empirical foundation to support it (an issue in inter and multi-disciplinary sciences) it is (and should be) faced with strong skepticism. Another important aspect of science is the hunt for truth. Ideas are cheap to throw out. The challenging part is figure out which of them reflect nature best. In the end, it takes more time to figure out where one was wrong then to throw up something different. This is something that is plentifully documented in our very own speculations forum here.