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The difference is to some extent semantic but mutation implies a variation from a standard form of the gene. There are no standard forms for MHC Class I and II genes - they exist in a wide range of variations or allelotypes, all as normal or standard as each other. Even variant tends to imply...

Something I learnt as a rheumatologist is that 'not-quite Marfan's' or what is often called Marfanoid has nothing whatever to do with Marfan's itself - which you either have or do not have. A Marfanoid body is well within the range of normality. The deformities of true Marfan's are quite specific.

B27 isn't a mutation as such. It is just one of many forms of HLA-B. It probably exists because it seems to be better at protecting people against certain viruses including against clinical AIDS.

No, that is my pet metaphor for the current discussion. There is a vast literature on TGF beta binding protein and matrix. But as I have said, very little seems to have been written on clinical relevance other than my paper on Ankylosing Spondylitis with Archer and Bowness in 2000 in Immunology.

The MDs won't know who wrote the papers because they are just parroting what others parrot - it is a meme. It goes round and round medical meetings. It sells private practice. There is no evidence of over-representation of a hyper mobile phenotype that I know of. Doctors believe what they hear...

I am afraid I see this as pseudo-academic voyeurism. The historical stuff is all plain wrong anyway.

Elastic fibres are associated with fibrillin fibres. These have repeating units that tie in to a TGF beta binding protein at regular intervals if I remember rightly. Elastin tends to stay put once laid down - which is why we go wrinkly with time - we do not refresh our elastin. I am not so sure...

That is just because they are all parroting two very weak papers by Peter Rowe and Hans Knoop - yes the very same biopsychosocial Hans Knoop we all love to disbelieve on every other count!!

To be clear, ECM covers collagen and elastin and everything else supporting the cell. The signalling molecules are not on the EDS affected fibres. And anyway, the abnormalities in EDS do not change throughout life. ME/CFS would not be due to an abnormality of ECM itself but some change in the...

Of the cocoon that the cell occupies - the tissue matrix.

The writing on the wall.

Waiter! My word salad is incompletely medicalised. My apologies, Sir, I will bring another one. And another.

Perhaps, to be agreeable, people might be agreeable to agree to disagree? According to Google disagreeable does not have the equivalent two meanings - only two nasty meanings.

It is useful to see who attaches their name to papers so poor that they should be ashamed even to be acknowledged on them.

That isn't actually the case. People spent years looking for viruses that might cause 'ME'. When retroviruses appeared they looked for retroviruses and claimed they had found one. People have claimed to find abnormalities in metabolism and NK cells and goodness knows what. Even Simon Wessely...

There is a lot wrong with the medical profession but not this. The reason there is nothing to treat ME/CFS with is that there are no clues as to what to do. It is an illness with a mechanism that so far we have no understanding of. It is a bit like saying why didn't Peter Higgs find his Higgs...

The implication is that there is useful care that the NHS is not providing. There isn't. But I think it is an important point that the NHS is not even attempting to provide competent advising and supporting staff. If ME/CFS is real like diabetes is real then it should be handled by the public...

I am afraid that I totally disagree with this @butter. The reason progress has been made in Parkinson's disease is simply that for over a century people have known where the structural pathology is. So there is a lead. In ME there is no lead. Money is no use if you do not know what to do with...

It is an important milestone that was well aired in the pre-S4ME days. I think it was presented in Bristol in 2014. TGF beta should probably be taken seriously. The conclusion is fair but only in the sense that serum levels are clearly not the whole story. That would not be at all surprising...

That appears to be non sequitur to my quoted comment, Peter, which was that most of these studies turn out to be artefact. They are not for generating hypotheses, they are for testing them. The idea that post-infective disease is due to autoantibody is sixty years old and has failed to show any...