mattbimbo

you could try an antibody based method for detection of DNA-aflatoxin adducts.

this statement is dumb. try considering the evidence for the endosymbiotic origins of eukaryotic cells. the evidence actually points to multiple endosymbiotic events.

by nonspecific immune responses i assume you mean innate immune responses. one great thing about the innate response is that it is very fast. adaptive immune responses take weeks, to months, to develop, while innate responses are immediate. furthermore the adaptive immune response is built on top the innate response. for instance a bacteria enters a host, this triggers an innate response that can limit the growth of the bacteria (remember a bacteria can replicate in 20-40min which is very fast). the bacteria are opsonised with complement and taken up/eaten/phagocytised by cells such as macrophages and dendritic cells. these cell types can not only tell when they are eating bacteria, which actives them to produce signals to attract other cells, they also present antigens on their cell surface. this is the basis for the adaptive immune response where B and/or T cells recognise the bacterial anitgens presented on the surface of the phagocytic cell. does this part way answer your question? my advice would be to look at how phagocytic cells link the innate and the adaptive immune responses. i can find references if you need but a standard text book should do. you are asking good questions - in the future you might want to consider the relationships between the immune and the nervous systems.

not sure the links in my last post worked, anyway here is another recent paper. i just discovered that drosophila lack a telomerase enzyme, and that RTs from retrotranspons can extend telomeres in this species.

retrotransposons contribute enormously to plant evolution. as i mentioned before, telomerase has reverse transcriptase (RT) activity, indeed telomerase is thought to have evolved from a RT.

hi dak, you may find it interesting to consider RNAinterference. and VDJ recombination.

. Interesting point. What if a new and fatal disease evolved that was beyond our ability to cure despite all our knowledge and technologies? Let's not forgot, all life forms are evolving.

i love the complement system. it will you take some time to get your head around all its subtleties but it is well worth the effort. the complement system is one of many examples which reveal how extracellular signalling involve cascades of protease reactions. as DrZoidberg writes, the formation of C3b is essential for activating the complement cascade. C3b is a protein fragment of C3, but it is very unstable and undergoes self-proteolysis to another fragment called iC3b or C3d which is inactive, thus limiting the extent of immune responses. there are also special cell surface proteins, eg CD46 and CD59, whose function is to increase the rate of C3b decay. interestingly mycobacteria coat themselves in iC3b so that they are taken up by host cells. interestingly the proteins C3b and C5b have domains homologous to alpha-2-macroglobulin, the archetypal extracellular protein dustbin. i could go on for hours - hope this helps.

R why not ask whether the laws of thermodynamics or the speed of light are widely accepted by the public.? has anyone ever been able to accurately predict what the public will or will not widely accept? isn't that the more scientific question? since science is partly about predicting future events.

there is an assay used to test for reverse transcriptase (RT) activity in cells. i have known a few scientists who thought they had found this in primary lymphocytes. however i later learnt that telomerase can also give positive results for RT assays. not sure how true this is, since i haven't done any experiments like this. i am just trying to point out that when it comes to reports of endogenous RT activity in cells, you should check that they have the right controls.

good point - let's not underestimate the public - perhaps this is what the public percieve too. as a scientist, i would expect that if all the evidence, the fossils, the DNA sequences, etc, were put before the public that they would grasp evolution theory. but this hasn't happened and we have failed to understand why. many factors may be at play. if the public already have a general perception that the evidence, and perhaps all evidence, is biased then the chances of them grasping evolution theory will be less likely. if members of the public have struggled in their education would it be suprising that they are distrusting of scientists, the winners of the same education. these are just a few possible explanations which i think can illustrate why asking people to be more scientific is doomed.

does this make the threat any less real? bjaminwood, could you explain why you percieve/contrive evolution as a threat to your religion? what do you think of the earlier comments in this thread that reglious beliefs are a psychological defense mechanism?

well i just had a look and this is wrong, the highest i found was 1% for cleft palettes and 0.3% for syndactyly. do you live anywhere near a nuclear power station perhaps? i take it mrD that you have now dropped the early statement that genetic damage contributes to homosexuality.

i hope they are sure that the snake hadn't swallowed the front end of a frog.

yiyun li ls a chinese writer, with a degree in molecular biology and a PhD in immunology. a great writer in my opinion, in this short story she describes the public execution of a woman in 1978 and the public taking of her organs.

i think you are going to end up with a long list of virulence factots. i thought i'd let you know that yeasts and mycobacteria also produce virulence factors. i thought charonY's comments were very good. one could argue over definitions regarding virulence factors, especially in the context of viruses. for instance strains of influenza can be fatal to their hosts, now are these strains more virulent than other influenza strains which does not cause death to their host? surely by killing their host, the first strain is in fact reducing its chances of survival.

this and this and this should get you started.

that i seriously doubt. and anyway the breakdown of fat by lipolysis is not the whole story, the fat can then be converted to glucose, known as gluconeogenesis. perhaps you should try reading about futile cycling.

never heard of marilyn munroe? or the many other actresses who were given drugs to reduce weight. very big in the 50s.

well they could still smoke, spliffs too, they just wouldn't get the nicotine related effects. my initial opinion is that it is a parents choice.

thanks for the posts. what is RIP? have you never looked up the meaning of swansonts/supreme canuck signature? the idea of a tiny balrog was inspired. i am still curious to learn whether the semantic web will make a difference.

they are called non-enveloped viruses, the particles are stable in the open, ie air and water, while enveloped virions are predominantly internal. lock/key pretty much sums it up. in an immune response, antibodies can bind to the virus particles thereby 1) inhibiting their uptake by the cells which the virus targets and 2) facilitating their uptake by immune cells such as macrophages. it can seem complex but it is just another variation on the lock/key interaction.

deux ex machina please, vegrandis balrog

simple questions: how long will it be till i can have a creationism-free search engine? will the new semantic web really make a difference?

yes and no, one gene can be modified in many ways due to RNA processing etc; there are genes, give me time to remember them, which have over 1000 splice variants. (note, 1000 genes is about 4% of the human genome) do i rightly understand this? if a condition/illness involves a large number of genes, you expect it to occur randomly and with the observed frequency of 10%? but there is a fair body of evidence for the determination of sexual orientation in the womb. suprisingly this never came up in the recent thread on circumcision.