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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.

Oh, I just checked the treatments section of your hypothesis paper and you're right, you didn't. Don't know why I thought that. My mistake!

This is a big reason why we need real clinics - they can do this sort of tracking of patients with ease. A ten year study of pwME who are not on any treatment would be confounded if an effective drug were found e.g. if dara works. You'd see a massive amount of participants drop out to try the...

I just want to say - I feel really weird about this situation. I am so happy Whitney is talking again, and it was a really emotional thing to hear his voice. But this Leisk guy gives me so many red flags I can't even begin, and I am very worried about the perception that OMF supports JL leading...

Related question: is there any reason we can't aim for Polybio levels of funding for good quality ME/CFS research?