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If dara turns out to really work like in the pilot it will be close to a silver bullet for at least a subset of pwME. The psychobehavioural school cannot demonstrate any significant improvement at all in a decent trial, let alone anything close to what the dara pilot showed. I fail to see how...

On a related note, do we know if Altmann is aware of the CD38 finding in the Mensah/Armstrong/Cambridge study? That might be a good one for him to try and replicate.

My issue is that Wirth has done no basic research in ME/CFS, has only published hypothesis papers, and has gone straight to drug development. If it turns out to work I'll be over the moon but I can't bring myself to get excited until I see some solid science behind it. This guy Ussher also...

Where did we land on the possibility of preliminary results being announced/presented before all patients have completed the 72 week monitoring period? I think we were generally of the opinion that the given date of 2029 was probably the worst case scenario for preprint publication, and 2028...

Is it possible that these antibodies are a) pathogenic and b) killed by dara but not rituximab (i.e. anti cd38 but not anti cd20)?

Is there currently any way to get an up to date novavax shot in the UK?

What video was it you showed her, out of interest?

The thing I'm currently feeling trepidation about is the upcoming severe patient case study. If the severe patients with higher NK cells don't respond I'm going to find that difficult to cope with. Of course a handful of unblinded patients isn't exactly definitive proof but if they react like...

Ah right, I think this question was saying could PEM be caused by different things, rather than PEM causes different subtypes of symptoms. As to what you said yes I think were in agreement.

Can you explain why you think this? I'm not sure what makes this more likely than there being a single upstream cause of ME/PEM. I'm not dismissing the possibility here, I'm just interested in your reasoning.

In terms of hypothesis I'm pretty convinced by the idea of an immune signalling loop perpetuating ME/CFS. In terms of specifics I'm not really qualified to judge but I find the idea of JE et al's T cell and IFNg mediated hypothesis, jnmaciuch's interferon/mtDNA hypothesis, and the idea of some...

I saw it quoted on Bluesky the other day iirc. I think it was a screenshot of a twitter post. Pinker sharing an article about 'patient activists' harassing CFS researchers etc. If I find it again I'll link it.

Given Steven Pinker's promotion of the dangerous 'militant ME patients don't like good scientific findings' myth, I don't think he is the person to be handing out lessons in this area.

Is this study the basis of Younger's recent claims about heterogenaity in ME/CFS? Because this does not seem like nearly strong enough evidence to make the statements he's been making.

That's sort of what I'm getting at. We have good researchers in Edinburgh, good researchers in Fluge and Mella, some very good researcher members of this forum I could name. If we could get them collectively even half of Polybio's funding it would change things significantly. I just wonder if...

This study just shows how badly we need a much bigger whole genome sample like SequenceME

I was probably thinking of this in the Zhang thread, so I was kind of in the right ballpark!

No in fact I think he said in his hypothesis thread that therapeutic experiments might be crucial to proving or disproving it (but I've already misquoted him once lately so don't take my word for it!)

@Jonathan Edwards do you think Anktiva would risk revving up T cells and making things worse in a similar fashion to Checkpoint inhibitors if your T Cell hypothesis is correct?

I've said before, I think this is a false binary. We need the basic research and the clinical trials. With sufficient funding we wouldn't have to choose. Good quality research would entail doing both stuff like the anti-cd38 trials and SequenceME.