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Yes. 1. Cytokines elevate during acute infection and stay elevated for several months. This might resolve itself or number 2 happens. 2. Cytokines prime B cells to more rapidly produce CD38 when activated. 3. Rapid CD38 activation leads to altered BCR and you get skewed pathogenic long live...

So rather you'd be looking for epigenetic changes? What if the autoantibodies targeted orexin pathway or CRH neurons? Similarly to African Sleeping Sickness but antibody induced and not the parasite. I think that alteration might set up a system to perpetuate the B cell priming of CD38.

Oh right. Sorry @Utsikt, thought you were asking what I originally meant by inflammation. My initial thoughts were on pro-inflammatory cytokines are what we see elevated in the 1-3 month post-acute COVID patients. But you're both right, no signs of inflammation needed. The cytokines themselves...

These might be useful: https://pubmed.ncbi.nlm.nih.gov/24108696/ https://pubmed.ncbi.nlm.nih.gov/29944759/

Also the original work on Fibro where I think they got the idea. Do we know if pain was a major improver in the Dara trial?

I also think the fact that bigger response in those with higher baseline NK cells suggests getting to the pathogenic plasma cells and destroying them is the difference, rather than clearing antibody alone. Do we know that plasmapheresis didn't provide immediate relief that was unsustained?

Wasn't it the pain profiles that were most clearly transferred in to the mice? Just from memory.

Well from the early long COVID literature, especially when they were including patients at 1-3 months post-acute, they all seemed to show elevated cytokine profiles. This is what my mind was thinking of when I said inflammation in PVFS. The idea is that this ongoing inflammation may be part...

I'm talking about the inflammation that occurs during acute infection/injury in this context.

It could certainly for the FcR1 idea. It's in the same vein really. I've recently been playing with the idea that PVFS or an elongated acute infection may actually be the trigger point for ME/CFS and that the mechanism of ME/CFS is produced by that elongated inflammation event as part of the...

@Jonathan Edwards Could this be a reasonable pulling together of different findings: CD38 functions as a key co-receptor in the BCR complex, associating with CD19 and modulating BCR signaling by lowering activation thresholds, enhancing calcium fluxes, and amplifying responses to...

I agree with you, it can be confusing Yeah OMF supported for a couple years when it was an in person conference in 2017 and 2018. It's now an online working meeting and it is entirely different. OMF never supported the working meeting. OMF promote every conference on ME throughout the year...

If you guys can find anything supporting Leisk from the OMF social media then that's a different story but I do not believe OMF have anything to do with Leisk. Leisk has a relationship with Ron, Janet and Whitney. I don't even think Ron and Joshua collaborate on a research project. If they did...

That's not an OMF symposium. There is no OMF logo on the agenda. That is run by Stanford alone, has been since the pandemic (2019) I believe. Only the in-person conference they used to do was OMF. It changed to an online only meeting.

My take on this (which may be wrong) is that the chart is adding those that got 4 DARA to those that got 7 DARA. The chart timeline on x-axis is also not linear so it's confusing to the eye. The IgG for the 4 DARA may have went up at the same time as the IgG from the 7 DARA went down. The chart...

I think the rapid increase in CD38 is because the b cells were primed in ME, primed because of chronic stress signals from cytokines or something else (perhaps even genetic) In vivo it may be that ME create more short lived plasmablasts in response to even mild triggers for B cell activation...

The healthy controls population was used because that's what has been used in other mgwas studies. Wanted to show that there are many genetic links to metabolite changes. Reducing the number of controls isn't helpful, if anything we should look to raise number of ME/CFS patients. We are bummed...

Often clinicians don't make it to authorship but they still help with studies. Depends on the level of help.

I believe Kaufman has helped with Rapamycin and Abilify studies. I don't think he's involved in a CCI trial no. The Oxaloacetate trial was fine. Do we know of any published RCTs in ME/CFS that were done any better? The common failing is low funding and a poor outcome measure because we simply...

I have known a couple people to be significantly helped. From wheelchair over years to walking several km daily after recovering from the surgery. And it's been sustained over years. I know more that have had surgery, improved and returned to pre-surgery state. That is knowing patients, not a...