Search results

Yep, at least. I wonder if there's a smaller number than 24M where they would still do the whole trial, just with fewer participants. Maybe they've already reached that smaller number since they're talking about starting treatment in September.

Here's what they said they were at on August 26 (about two weeks ago): https://www.me-foreningen.no/me-fondet-over-1-million-og-er-pa-na-facebook/ (Text from auto-translated version)

Thanks. Am I understanding right then that even if covid specific plasma cells were injected into the brain but not actually specific to anything there, you'd still see the bands show up from their antibodies?

Doesn't MS require the antibodies to be specific to myelin? If they are just regular old COVID antibodies, you wouldn't expect myelin to be destroyed. Maybe just antibodies gumming up the works, but not actually binding well to anything. Sorry, I don't know what oligoclonal bands terminology...

Yes, not the antibody distribution independently, but the plasma cells get deposited in the brain during an infection. They spew out antibody there, potentially causing issues with neurons.

It's possible. I can't construct a good argument that satisfyingly refutes that, just intuition that may very well be wrong.

I agree. The specifics of your paper were somewhat over my head. But maybe nothing to do with the specific type of antibody, but instead something about location? Is it possible maybe the normal covid or EBV antibody LLPCs somehow find their way into the brain and set up camp after an infection...

Ok, yeah, rituximab might have been nothing, a wrong way to try to replicate cyclo. But I think it is likely that whatever explanation dara offers, it will have to explain why cyclo causes a response as well. Yes, it was possibly an unrelated placebo effect, as we've seen with lots of...

Yes, I'm only referring to the phase 2 trial, and assuming the phase 3 trial was underpowered to replicate the effect. But it does make more sense that cyclo would be the drug with the common mechanism, since it was the one that started this whole thing.

Oh yeah, I don't think there's any reason to care much about proving rituximab works with giant sample sizes. It clearly isn't very effective. I'm just saying that I think there is reason to believe that either cyclo or rituximab (or both) actually affects some mechanism that improves ME/CFS...

Right, if you have a booster. But if dara wiped out all LLPCs, would tetanus antibodies quickly be automatically re-made? If some wonky LLPCs got made when a person got a COVID infection and which cause ME/CFS, but without a persistent antigen, I wouldn't expect them to quickly be replaced if...

Can you link to something saying disulfiram depletes LLPCs? I can't see anything about that from a scan of those threads or a search.

Doesn't this replacement with new B cells require re-exposure to an antigen? I was thinking that the LLPCs are created originally for some reason, but that the antigen is long gone if it ever existed, since there aren't signs this is a typical autoimmune disease, so there'd be no reason for the...

I'll need to re-look at that. I might have misremembered the improvement being more impressive. Okay, if they're both just killing everything, that makes B cell specificity less convincing. Yes, I was going with the idea that higher efficacy is probably the explanation for the difference due...

I know discussions about how antibodies don't make sense have happened a million times probably but it's mostly been hard for me to understand. Can someone say why what seems to be simplest way to look at the results we see is not the most likely: that the mechanism of action of dara is due to...

Oh sorry you're right, I totally skipped over that both the MM studies in that thread are about bone marrow NK cells, not blood.

Oh yes sorry, just saw your post. Yes, that was incorrect to say it was the NIH study.

The Fluge paper looked at "CD16/56 positive NK cells" and found higher baseline levels correlate with recovery. From multiple myeloma paper: So they seem similar. I don't know the implication of the difference in the ME/CFS study also including CD56 though.

The way I always assumed it worked, though I could be wrong, is that the analysis finds relatively few harmful variants in the actual sample. If they found, say, that participants 1 and 2 have an LoF variant in DLGAP1 and participants 3 and 4 have an LoF variant in DLGAP2, then the machine...

In Article History, I don't see an update on September 6 (though I see the article does say that date for some reason), but it did get updated on July 10, 2025 to switch from describing some old criteria to describing IOM, so now post-exertional malaise is included. Maybe the September 6 update...