Search results

I know that I raised it as a plausible-sounding connection ages back but i had no evidence base. We might even have mentioned it in the FcR1 paper but probably not.

My biggest concern is that if patients engage both with a private service of this sort and the NHS for things like feeding support via PEG or IV line then there are very likely to be conflicts of opinion and problems with trust of the sort we have heard of before.

I would like to send a draft of the suggested service format to the others on the ForwardME service group on Wednesday morning. I think we may have a meeting in the afternoon and we had talked about proposals for a service format last week. I can say that it is something that has arisen on S4ME...

I know of one, at least interested. But there won't be many.

I am not surprised. Why would a doctor want to take up a job in a clinic with an airy-fairy name that sounds as if it might be closed next month? And why would they want to join a clinic full of physios and psychologists? This is why the 'community rehab' model is a dead duck.

I am not sure what you think might be different. If you are using an array of human proteins then ALL the antibodies binding are autoantibodies - because they are binding self proteins. That is what we mean by autoantibody. There is nothing 'abnormal' about an autoantibody's structure or...

And nobody really knows what the assays mean in clinical terms.

It is very rare to use functional assays. They are usually totally impractical and very open to variation in results. It is very hard to know that a functional effect is actually due to a specific antibody unless it is backed up by a chemical assay (ELISA, Western blot, etc.). I have not gone...

I don't think any of the patients I came across with Sjögren's had high IgG. It is associated in some cases but not most. Sjögren's syndrome is basically dry mouth and dry eyes with evidence of lymphocyte infiltration in salivary glands - which may be biopsy evidence or circumstantial evidence...

Yes, they do. It would be good if useful research came out of Dr Kane's service but I am not aware of any such research. It is not clear to me what she can offer that has a realistic chance of doing more good than harm and that is not already available.

Nobody knows very much about this, I suspect. There are probably data that narrow things down to an order of magnitude or two for Kd but one might expect the system to be pretty precise on this and as you say it would make sense to be over-cautious. The 'physics' both for B cell selection and...

If you use staining of tissues you are likely to pick up antibodies to any protein in those tissues. People have screened pretty much every tissue looking for autoantibodies. SO these assays contain all tissue fixed proteins. If the protein is circulating then it should run out on an SDS-PAGE...

Maybe they aren't there. I think jnmaciuch and I would agree that they probably aren't. If they are there then they might still be hard to find for very complicated stereochemical reasons. That said, most autoantibodies we now know about can be identified either with tissue staining techniques...

Assays differentiate antibodies to foreign antigens and antibodies to self antigens (autoantibodies) simply by starting with the relevant antigen and measuring what sticks to it. Autoantibodies are normal antibodies in any other sense. We all have autoantibodies that don't happen to do much...

That sounds sensible, forgetting about any relevance to DM, which I find hard to credit.

From the abstract i cannot make much out. They would do better to avoid vague terms like immunomodulatory or immune function.

I agree. It will be ridiculously cheap in comparison to most other disabling diseases, however one does it. But the Suffolk experience may well provide the costings. It has been argued that commissioning from a hospital will be more expensive than from a 'community' authority. That may be true...

As Jo Cambridge pointed out in the 1980s, dermatomyositis is different from polymyositis (another autoantibody-associated myopathy) in that there are significant numbers of B cell sin DM tissue but not PM. T cells go in to any inflammatory site so tell us nothing much. B cells don't, so there...

The experimental conditions are so artificial that I think it is very difficult to judge whether this has anything to do with what happens in the disease. These muscle preparations aren't even vascularised, so all sorts of complex immune signalling systems will be upside down.

Yes, I think he has always tried to be accessible.