Search results

Can you explain that in plain English. What would be obvious? Surely we only 'know' about what happens in standard situations with healthy controls, which might not happen for all sorts of reasons with patients?

Interesting to see this paper. The points that strike me: 1. The increased association with NHL is not that great at 1.29. It is potentially of scientific interest but tends to suggest an indirect or spurious link could be involved. 2. The CFS rate of 05% seems high. 3. The use of medical...

I don't follow that. If it shows up on the graphs as the result that we see then it does. I realise things are complicated but as far as I can see at the moment it is possible that increased ventilation occurs at a lower work rate in the second CPET for PWME because of some inhibition of that...

Are you sure? It seems to me a bit odd to do a CPET two days running to show reproducibility. I would expect in the context of ME to leave it for a week or two at least before trying again. I thought it was a deliberate attempt to demonstrate fatiguability - which after all was supposed to be...

When I have flu I don't actually have a choice. I collapse shivering if I try to do anything vigorous. But my point was exactly this - that to overcome feeling so ill you need to be in a very particular mental state supported by adrenaline and cortisol and goodness knows what and that may matter.

That sounds a bit weird. I thought the post of doing it twice was to show a difference?

Another interesting example of the CPET not correlating with PEM in time scale - but the other way around. I go out of my way to be sceptical because it is the way to get debate going and I am happy to believe that there is some consistent finding on the 2day CPET of relevance to what is going...

Yes, I agree with all your points, but there remains the key point that if we are tracing a complex series of cause-effect interactions then it is unwise to assume they can be treated as a simple; 'exertion'>>'PEM ' relation and interpret findings as if it were. The 2day CPET is often quoted as...

Agreed. And I can see the logic of the original experimental design trying to show a dip in function on day 2 by looking for maximal performance twice, studying people who are bad enough to show an effect but not bad enough to find it distressing. But if the aim is to study metabolic changes...

Actually I don't think I could. I think I would vomit and collapse on the floor. Over the years I have looked after people in hospital with all sorts of reasons for feeling acutely ill and I am quite sure they could not get on an exercise bike and start pedalling. I have assumed that PEM feels...

I think this is highly possible and I think it is worth discussing in the context of this study. I understand the desire to keep discussions in pigeonholes but my brain is a bit too old to keep dotting about threads once a line of thought has started!! Breathing patterns are very much affected...

Absolutely, I do hope someone takes this on. I heard yesterday that my wife's cousin has an app linked to a sensor in her ski boots that tells her how good her turning technique is in terms of edging the ski and weight alignment. I get the impression that making a device that would demonstrate...

But wouldn't they then be considered to have PEM? My understanding is that the reason for doing a 2 day CPET in ME is because it is expected to pick out a very unusual situation of feeling ill hours or days after the exertion whereas in other conditions feeling exhausted occurs at the time and...

It is isn't a matter of doubting willingness to do the test properly. It is recognising that if you are feeling ill you may be in a mental state that affects repeated tests differently from healthy controls. And if you are worried that you will not be believed that may well affect mental state...

Yes, I guess that if ATA 188 worked it would suggest that MS lesions are specifically mediated by EBV infected cells. But it would be a pretty big coincidence that rituximab works comparably well for all sorts of autoimmune disorders where there is no particular suggestion that EBV infection of...

It looks fatuous. People having trouble after Covid are defined as people having trouble after Covid that isn't something else. It is a bit like defining 2022 disease as people who are ill in 2022. It is heart sinking to see what is supposed to be a top level academic unit producing guff like this.

Can you give a reason for saying this? As far as I can see ATA 188 kills B cells, so if it works either explanation would fit. It doesn't look as if there are any firm data yet. The blurb looks fairly simplistic immunology to me. That does not mean that the drug will not work but I don't see...

This is an important point. Studies of treatments are only valuable if they are generalisable to new populations. 'Individualised, integrated multidisciplinary care' or whatever is by definition not generalisable, unless it invokes evidence-based indications as to who will benefit from which...

I think that is very unlikely. The presence of EBV in our B cells generally has no consequences. It just sits there. If it proliferates the B cell is killed. In all autoimmune diseases something else has happened to the B cell population that is not removed simply by temporary removal of EBV...

Ocrelizumab is essentially the same as rituximab. Its effect on MS probably has nothing to do with depleting EBV though, even if EBV is a necessary factor in genesis of the problem. The drugs remove the B cells that give rise to antibody-secreting plasma cells in brain. The problem about using...