Variola

Yes that is true, but some standard toxicology to prove x causes y which causes z will be a starting point, and presumably one of the next goals. The paper in itself, despite the support of other research findings is not enough to make me start worrying just yet. Some comparable tests to examine ordinary non-organic ( although BT is considered by some to be organic) maize grown in the traditional way against the GM maize would be more relevant I think.

I think it is too early to say the EU have been right, there are a few holes in the research, as with most research you can't cover it all, and that is reflected by the authors in the discussion. Briefly- a few points to bare in mind. There are trace amounts of pesticides in most non-organic foods we consume. the ordinary levels need to be compared to those contained in GM crops. The food we eat is usually processed, not many folk eat maize/corn straight from the field! Therefore the diet containing GM foods of a rat and a human would be very different. Processing can alter the structure and bioavailability of a chemical. Following that is the level of GM crop fed to the rats, if it was an exclusive diet then it would contain levels much higher than in a normal rat, or human diet. Despite being good animal models, there is still a vast difference between rat and human physiology. This study needs proper biochemical analysis before it carries any real weight, saying there is a possible causal link, without the biochem to back it up is not enough, not to convince me personally anyhow. The authors discussion is reflective of their study though. I dunno..... maybe I am just erring on the side or caution..... or I am getting too obsessed with seeing Biochem..... lol!!

You are welcome

Yep and we are mad enough to be studying it.....!!!

Hiya B cells, in their normal state are about 10-15 micrometers in size and T cells are about 7-8 micrometers, so they are smaller. That is only general though as you have to account for different types of B and T cells and what they are doing. Ref: Err.. my lecturer from lecture 3 handouts that I happen to be revising at the moment

Hiya This is slightly out of my depth, but I can answer a few point that might help. There are usually more than one receptor for a type of interleukin on the cell surface, however some interleukins, when they are bound cause the cell to express more receptors of a particular type of interleukin, and so increasing the chance of binding and activating intracellular signalling, the cast of IL12 i is the JAK_STAT pathway. It can also induce the decreased expression of other IL receptors, and sometimes cause the intracellular deactivation of other IL receptors. ( you would have to check exactly how as I can't remember!) *As I understand it, T cells are all or nothing when it comes to IL signalling, which means they don't usually have two conflicting cytokine signals while being in an 'undecided' state. In other words, they usually receive a signal from one IL receptor, and they go down that pathway doing whatever they need to do, unless they get a signal telling them otherwise, often from a regulatory T cell that dampens down the immune response. Plus it is not always just a single step signal, IL12 for example induces naive T cells to become Th0 cells, and then only after that to they become Th1 or 2 cells depending on what they encounter Affinities are usually defined by the structure of the receptor, and with T cells the arrangement of alpha and beta chains whilst they mature in the thymus, therefore they will need very little of one cytokine to have an effect and a much higher concentration of another. This affinity regulation is important so the cell responds competently to the given situation. So if the concentration of two cytokines were the same, it would not matter as the key receptors with their own affinity for the cytokines with determine what happens. *Denotes someone may give you a better or more correct answer to this one! HTH

Hi I am not totally sure what you mean, but I will give it a go. T cells are restricted to MHC1 or MHC2as they both have other functions other than to recognise self/non self, there is a fine balance between the innate and acquired immune system. It is common to think of them as two different systems, in fact we are often taught them separately, but really the actions of one affect the actions of the other. Your 2nd question I am not too sure what you mean. MHC class molecules structure vary a lot from person to person, hence we often have problems with organ donation and rejection. For the T cell to be niave enough to recognise a different MHC it would have to be caught in its CD3/CD4+CD8 state before progression through the thymus. Assuming you could still induce the T cell to mature in the same way as it does in the thymus, but present a 'foreign' MHC mole to it, then in theory I suppose you could. But the maturation is heavily checkpointed, particularly at the CD4/CD8 expressing stage by the positive-negative restriction. You would have to ensure the cell got the signal to survive and the signal not to apoptose at both stages. But assuming the cell wouldn't be fussy and happily induced into a CD4 or CD8, then the experiment would I suppose need to use a control sample of the same T cells 'trained' on their host MHC moles, as they would normally. Then to check for binding affinity..... well there are several methods you could use.... GFP conjugation plus fluorimetry perhaps? and sandwich ELISA too.... ?

Yep agreed. And he will never be as good at creating life as the masters themselves, the bacteria. I'd like to see more work on how the 'new' bacteria cope with different growth conditions, how the up or down regulation of genes is comparable and of it exhibits any different growth forms. That, IMO is where we will learn most from.

I trailed my towel around Uni with me on Tuesday, I got a few looks Especially is mine is a red and white one with "Don't panic" written on it.... in large friendly letters

Really this is not creating new life from scratch, this is building from a blueprint. The genome was already known, all Ventor has done is create the entire genome from scratch and make it function. Don't get me wrong, I am seriously impressed with the techniques they used for building the genome, transfection and the methylation, but any talk of creating new life or playing god is poppycock. If he had built an entirely new genome, or even part of a new one, and made it function without problems I would be more concerned about the impact. But it is way way off anything like that. The techniques they used, although impressive are time consuming and prone to faults with quality control. Merged post follows: Consecutive posts mergedGood article http://www.newscientist.com/article/mg20627622.600-special-report-where-next-for-synthetic-life.html

Yes good point, linkage disequilibrium studies and the like are pretty reliant on healthy volunteers. I have wondered before how they managed to get such a wide range of genomic data. Diseased patients samples are much easier to come by because they are under medical monitoring.

Mine? I love microbiology! Not too original but that's it.

I agree, I read the paper this morning. I was really impressed with the techniques they used, particularly the methylation. However it isn't that much different to what they did before, except they build the genome from scratch but based on a blueprint form a species related bacterium. we have been changing the bacterial transcriptome for years If they had synthesized a new genome, or even part of a new genome and made it functional, then I would call it more of a breakthrough, but the hoo-hah over ethics and the possibility of biofuels is pie in the sky.

It is worth bearing in mind that WBC count can tell a moderate amount about what type of infection you have, simply by looking at which type is raised and in what ratio to the others. Or if you are expressing a particular type of antibody, or it can give some indication of any bacteria in the blood, not necessarily septicemia. It can also be used to assay the response of the immune system, and the possibility of sepsis occurring or has occurred.