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What seems odd is that he has picked up from the PACE follow up that there was no long term benefit yet that is not how the paper he quotes presents it at all. And he seems oblivious to the much more obvious problems with the original PACE results - not just the re-analysis but the uselessness...

This looks like a muddled review by a junior doctor who has not himself quite worked out what he wants to say. It mentions some of the issues patients have with treatments but makes no constructive analysis. The account of PACE is still woefully inaccurate. This reminds me that maybe ME...

He interviewed me when we got the results on rituximab in RA. He seemed to have no interest in science whatever. Mostly in free lunches.

@Awol, I very much agree that IiME have made a huge contribution to the field. But I based what I had said on facts, not opinions or assumptions. I think the Facebook messages were badly misjudged in style and content. Maybe we should leave it at that.

It seems that I am damned if I do and damned if I don't. I tried very hard to help IiME with research strategy. Unfortunately I think they have made a number of unwise decisions of late. I am very sorry to have to say that but I have deliberately made no comment about this for a very long time...

I have facts at my disposal that I would prefer not to have to air here. I don't want to name names of people who have been treated badly in my judgment.

I agree that for multiple small effect genes these might not make it to the ten best bets. However, I am a bit sceptical about lots of small effect genes pointing up a pathway. The genes that have helped us in rheumatic disease have been rather large effect ones. Maybe there are examples for...

I actually think the problem is more serious than this, @Andy. It may sound crazy but recruiting people who join support groups may just end up identifying a genetic risk factor for joining support groups. You then spend five million pounds studying something that has nothing to do with ME...

I don't really buy this, Simon. Obviously the bigger any study the better but I see no problem with making use of the current study as a primer to look at replication in relatively small cohorts. The 'significance' of findings on the GWAS is not really relevant since it is an artificial...

Absolutely possible. Rather than doing a huge study next I would pick the ten most correlated mutations, regardless of whether or not they reach significance in this study, and go to the DNA we have from the ME Biobank and see if they are confirmed. If you only test 10 mutations rather than...

I think the statement is based on other research - probably studies of monozygotic and dizygotic twins, which can be used to give an approximate estimate of heritability. Twins are assumed all to share environmental factors but monozygotic twins share more genetic material.

Actually it is more extreme than that. The paradigm of genetic searching in unravelling disease is ankylosing spondylitis. Around 1974 Bluestone's research lab decided to see if there was a link between gout and tissue type. Nobody knew what tissue the meant much at the time except that it...

Certainly for the people that matter in terms of having a chance of doing something useful for ME, I think IiME's comments are out of order. If the political landscape is moving on and a number of researchers are in London then it makes sense and is right for PWME for researchers to talk...

That was certainly true ten years ago. What I am not sure about is whether the technology is now so powerful that it would be relied on to pick up the disease gene in disequilibrium too. Simon may know. Chris will obviously know. Interesting point.

To a first approximation I think yes. But as indicated, there may be caveats.

I think that is an interesting question. Maybe Luis Nacul, (and others) who assessed patients for various criteria, could extract that information.

I was talking to Chris Ponting about this last week. Take inflammatory arthritis. It is three times as common in women as in men and has a genetic association with HLA-DR4. BUT hidden within that it runs out that there are two groups of diseases. One is rheumatoid arthritis, which links to DR4...

I think if an amino acid is not conserved across species for a very basic protein like prolyl hydroxylase it suggests that the amino acid is not crucial to the protein's function - perhaps an optional link in a chain that just contributes to framework structure. That would allow a nematode to...

The review was accepted on January 7th. So it may now be out of date.

This is certainly very interesting. My first question is whether the genetic risk estimate and the link to the prolyl hydroxylase gene are the same in men and women. They will quite likely either be pretty much exactly the same or obviously different. I think that would tell us something very...