CharonY

Just as a remark, it would not work. Anything strong enough to hydrolyse virus RNA would also affect normal cellular RNA. Also, the cell dies (if at all) when the virus leaves the cell. Not when it enters it (would be kind of ridiculous). And so on...

I am not sure if I missed something, but aren't these reports not actually in agreement in each other in saying that sucrose, fructose and high-fructose corn syrup elicit similar responses? And btw. as far as I am informed sweeteners do not increase the craving per se. The foundation for this is laid far earlier, i.e. in early childhood. While there is basis preference for sweet products, a diet on sweeter baby products (or vanillin for that matter) will increase the preference for the same later on in adult life.

Actually it is both. They increased the amount, people bought more of it, they increased it more, rinse and repeat. While the industry had a significant part in it especially when they started adding it into baby food, it is the consumer who showed a preference to buying it that continued the cycle. When I arrived in the US my cravings for sweets actually dropped dramatically as the stuff here is much sweeter than I was used to.

Actually the mail in the OP is wrong in several ways. I have no time to comment on the all at the moment, though. What is true, however is that a high amount of high-fructose corn syrup is bad for you (wouldn't have thought that, would ya?). But surprise, before corn syrup was used, other sweeteners, especially sucrose (a disaccharide of fructose and glucose) was used. And in most studies the effect of corn syrup and sucrose is similar. In other words, it is not corn syrup per se that causes obesity, but the overall increased consumption (plus a vast number of other changes in diet and calorie burning). I believe that I read somewhere that a few decades ago less sweeteners were used but that Americans have somehow gained appetite for sweeter food (and the food industry was happy to oblige).

That is not what a retrovirus is. All viruses add genetic information (their own) into their hosts. Retroviruses however do not have their genetic information on DNA, but on RNA. So they need a mechanism (reverse transcriptase) to write RNA back into DNA, before integration into the host genome. Hence the "retro".

I feel dumber every day. Does that count against the average?

They do not create a merged bacterium, but they can introduce new genetic material into their host cells. Either virus information (which is part of their infection process) or from a former host, usually due to erros in packaging the genetic material. The latter is referred to as transduction. Obviously, if a cell gets co-infected with several virus strains it is easy that they may get genetic material from the the other virus. Depending on what has been swapped there may be no or only subtle difference, but other things like e.g. extended host specificity may be one of the outcomes. Swine flu is such an example as it appears to carry material from avian, swine and human influenza virus strains.

Actually recessive alleles generally stay in the pool even if they are selected against, due to the masking of the dominant alleles.

It all depends on the enzyme to be produced. Many eukaryotic proteins require modifications that bacteria do not add to theirs. Also often specific chaperones (special proteins) are needed for the correct folding of the proteins. While bacteria have of course a lot of heme-proteins, I am not sure whether hemoglobin (which consists of four subunits) would fold correctly. I actually think it may, as. if memory serves correctly, it folded via self-assembly.

Precisely. Especially as some possess extremely vile plasmids carrying extraordinary evil genes. Can we close this thing?

As viruses do not live it is not possible to kill them. You have to know that once a virus enters the cell most of the time they inject nucleic acids and proteins. Targeting them would inactivate the virus. It is easier to prevent viruses from entering the cell by manipulating the entry point (often a receptor of the cell). This only works in single cell models, and not in whole multi-cell organisms, though.

I am actually kind of surprised that there was a response. This kind of posts tend to be hit and run, usually.

The genetic code is realized by those tRNAs (together with the right coupling of the respective synthetase). In a given organism all cells share the same genetic code. That is, all have the same complement of tRNAs.

As GDG mentioned, viruses can contain a number of enzymes, however proteinbiosynthesis is carried out by the host cell. Moved to homeworks.

Brandon, I am sorry to say, but your post makes little sense. RNA does not read codons. The only pairing relevant to codon generation is the antisense pairing of tRNA. And it surely does nothing with regards to DNA replication. You are mixing up transcription, translation and replication. Badly.

About 45s after we see smoke emitting from his ears for maximum effect.

They are not called differently, they are just different level of hierarchy. Think of it that way. The chromosome is always the whole structure, regardless whether it consists of one or two chromatids. Likewise during the S-phase (you really need to read up on cell cycles, it is basic knowledge) it is more correct to state that the chromatid replicates rather than that the chromosome duplicates. Because the result is still one single chromosome, only that it consists of two chromatids again. I know wikipedia describes it differently, but in my opinion that description is rather messy. The confusion arises from the fact that chromatids, once separated are referred to as chromosomes, as each cell requires to have the full set of chromosomes. Referring to them as single-chromatid chromsome would be more precise. Use this as starting point and revisit your assumptions once more.

De novo in the lab? Reasonable? No. But if you mean that man-made conditions have increased the chances for its rise and spread, then yes.

The pdf in the OP is unfortunately appears to be only supplementary to the main (meta) study. One of the studies they are refering to is: RC Bailey, S Moses and C Parker et al., Male circumcision for HIV prevention in young men in Kisumu, Kenya: a randomised controlled trial, Lancet 369 (2007), pp. 643–656 In the same paper some nice references about proposed mechanisms are given: Patterson BK, Landay A, Siegel JN, et al. Susceptibility to human immunodefi ciency virus-1 infection of human foreskin and cervical tissue grown in explant culture. Am J Pathol 2002; 161: 867–73. Donoval BA, Landay AL, Moses S, et al. HIV-1 target cells in foreskins of African men with varying histories of sexually transmitted infections. Am J Clin Pathol 2006; 125: 386–91. McCoombe SG, Short RV. Potential HIV-1 target cells in the human penis. AIDS 2006; 20: 1491–95. O’Farrell N, Morison L, Moodley P, et al. Association between HIV and subpreputial penile wetness in uncircumcised men in South Africa. J Acquir Immune Defi c Syndr 2006; 43: 69–77. Weiss HA, Thomas SL, Munabi SK, Hayes RJ. Male circumcision and risk of syphilis, chancroid, and genital herpes: a systematic review and meta-analysis. Sex Transm Infect 2006; 82: 101–09.

Actually the distinction is not based on size, but on the existence of essential functions. In other words, if e.g. non-redundant housekeeping genes are located on a plasmid, it would be considered a chromosome. Vosh, only the gametes have 23 chromomsomes after fertilization (fusion of two gametes) you got 46. However, each chromosomes consists of one (before S phase) or two sister chromatids.

Well officially I do have 15 days per year holiday time. For some reasons they disappear when I look for them. Unfortunately I am still middle management in a research lab, meaning that if I am not trying to get grants or writing papers, I have to actually run the lab and beat up students. As my wife has a similar job we hardly find a day that we could take off together. But anyways it is very hot here in the summer, well above 37 C and interestingly a lot of faculty are on "research travels" during the summer...

Well, that is always the case.

So it boils down to the assumption that there are specifics in the US not found anywhere else in the world? Jackson, you do provide arguments I am not able (with my limited knowledge) to deduce whether the points really address the issues. I am not saying that you may not have a point somewhere, but it is hard for me to see what you want to convey. John tends to address specifics and elaborate on it, making it easier for me to understand. This is not meant as criticism it just appeals more to the way I analyze things. At this moment it may be easier to limit it to a comparison of the Australian system, however, it has to be noted that no one is advocating a 1:1 carbon copy of it, and there are plenty of other systems around. I am a bit limited on time atm, however just to address your first point: you mention that This is not true to my knowledge. You only cannot be refused in the emergency room, but I am pretty sure that it also applies to Australia. You also stated that they have then to pay for treatment out of pocket. However this is also true in the US. If I am not insured physicians can deny treatment unless I go to the emergency room. And if I do, I have to pay out of pocket (if I am not insured). So I do not see anything here right now that justifies additional costs in the US (if that was your point). Edit: with knee-jerk I was essentially referring to other sites in which the it was argued that it is bad because it is socialism. And then everything went downhill from there. I was not referring to any particular post here.

Please start only one thread per topic.

Ah I see. Sorry for the misunderstanding. Sounded like a knee-jerk response. But without further data it is hard to evaluate.