CharonY

Well it all starts off with a good experimental design, obviously. Which does include the use of proper controls and choosing or developing the right protocols for the job at hand.

In a way, yes infecting oneself in low levels may strengthen your immune response against a full-fledged infection. This is how the immune system works, but that is not what the OP was asking. However, you may be a bit misinformed what adjuvants are. They increase the immunogenicity of a vaccine, for example, by making your immune system respond to the injected antigens more strongly. But they do not work alone. So again, it would not be a boost of your immune system, but rather increasing the effect of a vaccine.

Also functional proteins are not rare at all. Synthetic biology approaches demonstrated that synthetic peptides with more or less random elements of alpha and beta helices (IIRC) have the potential to catalyze simple reactions. Albeit with far lower efficiency than those that have arisen during evolution, of course. The existence of protein families and the prevalence of certain proteins is just another indicator of common evolutionary origins. And as Sisyphus pointed out, no-one argues that there was just a random event and oops there is life. There must have been conditions that favored the existence of simple self-replicating biomolecules as a first step. Or maybe there were several first steps, so to say. Arguing from ignorance is not helpful.

Actually not necessarily. Organisms with very high number of genes do not express them all at once. In fact, depending on the condition of the cell (and environmental condition of course) the cell may just express genes necessary for basal metabolism and shuts down the majority of its genome (as there is no need for their expression). Thus, the actual transcriptome or proteome of an organism does not correlated directly with its genome size. Of course, one could argue that due to leaky regulation there will always be a few transcripts, but that was not really the question. The point is that the genome is static, the expression is dynamic and the only connection is that a larger genome potentially allows the expression of more genes.

This essentially disqualifies an academic career. However, qualifications are only a small part of the package, first you should work out your career plan and then look what qualifications you may need to achieve that. I do not believe that we have got many members that could help you with that, though. Probably you should look for job advertisement and delve a bit deeper into the job market.

If we do, it will likely still be based on existing templates.

Well, there are biochemical differences in terms of activity (including, but not limited to cell proliferation, cell motility and so on). But as the cells are part of the body (rather than external agents) there will be no qualitative differences in composition, but only quantitative.

A simple explanation is that the temperature is so low that it binds at random positions spread out through the chromosome. If they are too far apart and/or the binding is random enough you will not amplify anything, either. (37 is really low for a standard PCR).

The problem with throwing antibodies on it is the following. Genetically the cancer cells are identical to normal cells, except for the mutations. Antibodies, however, act by binding to antigens, in this case surface proteins of the cancer cells. Since the proteins are identical to other cells in your body, the antibodies will also bind to those cells. The affinity to cancer cells may be stronger, but you cannot simply flood the body with antibodies as it will result in adverse reactions to your healthy cells, too. A bit akin to autoimmune responses, maybe. That is why you cannot vaccinate against cancer cells, they are basically still your own cells (you can vaccinate against viruses that may cause certain types of cancers, though)

You must have misread. There are 20 basic codogenic amino acids, but not all of them are essential. The central hub of synthesis reactions (not only for amino acids) is the TCA cyclus. Look it up.

Actually the mechanical, physicochemical and also often morphological properties are often quite different (and not only proliferation rate). For instance, cancer cells can become motile, requiring a massive reorganization in the cytoskeleton.

The quotes you posted have quite a bit of misinformation in it. Cancer cells are for the most part normal cells that mutated for a reason or another (including virus infections) that resulted in a deregulation of their proliferation. Thus the assumption that you already start out with cancer cells is half-wrong. They eventually become cancer cells. The second quote is also wrong as it simply would not work. Cancer cells are your normal body cells, but are deregulated. That means that all the surface proteins it carries will be found in a couple of other cell types, too. What is different is will be the amount of the proteins, which is why they can be biomarkers (though most are not very good diagnostic tools).

Cell division itself involves a massive cellular rearrangement catalyzed by big changes in protein expression. If the needed proteins are not synthesized cell division is not initiated.

The estimates are out of context and I cannot easily comment of them (i.e. do you refer to total mutations in the total population, etc.). However, mutation itself is not a driver for evolution, but for diversity. During your life you accumulate mutations arguably in most of your cells. Especially ova are vulnerable as they are formed very early and accumulate mutations over time. Thus almost inevitably all kids are mutants of some sorts. Cells simply do not stay pristine forever. However there is no immediate selection as the vast majority of mutations will not have any effects at all. So they just sit there doing basically nothing until it affects the genetic network in some tangible way. Even then we do not have a sudden fixation (usually) but at this point population effects kick in. Nonetheless, even before the phenotype arises there may be plenty of alleles around that by themselves are neutral, but may, in some combination result in them. There is a nice recent paper that illustrates that a bit more: Bard J (2010) A systems biology view of evolutionary genetics. Bioessays 32: 559-563.

IMO it is pretty much common knowledge. For simplification purposes sometimes (maybe too often) free diffusion is assumed. However, it is well known that the extra- as well as intracellular matrix will have effects on Brownian molecule movement. As it is one of the more complex and yet poorly defined (as few methods exist that allow any kind of measurements in that scope and they usually are not too accurate) it rarely makes it into textbooks. It is assumed to be a kind of common knowledge that only comes into play when necessary. The author is a bit overplaying his hand by highlighting things that are not as obscure as he may want others to believe.

And I suppose you do have good references for these assertions? I mean, ideally more than the opinion of an astronomist who has more than a fair share of controversial views?

For the pure physical aspect no limit is currently known. It would require more packing, scaffolding and possibly subdividing into more chromsomes but to my knowledge there is no information that would prohibit a given genome size. And Cypress, you were first talking about gene expression. You do know the difference from what is being asked and discussed, I presume?

The problem with popular books is that they really do not help in a science curriculum. They are more about digestible narratives than providing the basis concepts and fundamentals that you need to eventually build your understanding of a given topic.

As long as the cell line replicates (i.e. immortalized cell lines) there is no obvious reasons why knockouts should not work, though some may be less amendable to genetic manipulations.

For what it's worth, China is pretty much taking a lead in the use of renewable energies. Less for ecological but rather due to economical reasons, obviously.

I n short, you have hidden Jews in the basement and Nazis come knocking on the door asking whether you have hidden someone. Answering truthfully would result in the death of the Jews. The dilemma is based on situations where answering truthfully results in greater harm than lying.

If there is nothing to substantiate your assertions it is just pure speculation.

I would like have a discussion point proposed here. Otherwise it is just a rant, and we do not do rants here.

I see. It could be easier to produce strains that express the individual proteins, though, and make cross assays to identify combinations that do something. You will have less problems in producing the strains as well as have less trouble possible cross interactions (e.g. promoter competition) within a strain that may give erroneous results.

Define social cost in absolute terms, please.