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You might be interested in this study on ME/CFS that did not find differences in T cell receptor repertoires: Comparison of T-cell receptor diversity of people with myalgic encephalomyelitis versus controls, 2024, Dibble, Ponting et al

Don't you have to know what antibody you're looking for? Surely an assay can't contain every single human protein, so it doesn't seem like failing to find autoantibodies with these assays would be evidence that there aren't any clinically meaningful ones.

The blinding is interesting. Each patient received the placebo first, then the low dose at the next visit, then the high dose at the visit after that. The patients were unaware of this schedule, but the research personnel weren't.

It seems to me there should be a whirlwind of research following up on this. If low level sarin exposure from a war can lead to a chronic condition like GWI, and it has taken decades to unravel that association, how many other associations are there that we don't know about yet between sarin or...

It should be noted that there was a comment published which brought up a potential limitation of the study: there was no matching for ancestry between cases and controls, and thus the association between GWI and allele frequency, which varies with ancestry, may be due to ancestral confounding...

This seems like a very compelling study. It's honestly one of the most exciting papers I've read because it provides strong support for a very specific lead. The study found a strong gene-environment (GxE) interaction between exposure to sarin gas and the PON1 Q192R allele, which is known to...

Health Rising: 'Is the OMF’s ME/CFS BioQuest Study the Study We’ve All Been Waiting For?' Article includes an interview with OMF's Danielle Meadows.

There's a comment, but the details are behind a paywall: Comment on “Association of Symptoms of neuropsychological long COVID with imaging and plasma biomarkers” Shukla, Ankita; Brahma, Pratyush Kumar; Rajput, Dharmendra Singh Web | DOI | Journal of the Neurological Sciences

Association of symptoms of neuropsychological long COVID with imaging and plasma biomarkers Highlights • Neuropsychological long COVID i.e. “brain fog” were investigated by biomarkers. • Cognitive impairments related to abnormal rCBF in the occipital lobe. • Psychological symptoms related to...

Another resource that helped me understand: The Intuition Behind Confidence Intervals

Distinguishing post-COVID from long-COVID in adults: Development and validation of a biomarker signature using targeted proteomics and machine learning in a cross-sectional observational study Background COVID-19 can have diverse clinical manifestations, ranging from asymptomatic infection to...

Some discussion about antivirals has been moved to: Antivirals as ME/CFS or Long Covid treatments (e.g. valacyclovir, valgancyclovir, amantadine)

Very cool. I notice that the link you provided seems to already have a DecodeME custom track with variants.

Auto-translated section mentioning genetics, with bolding added:

Hi @nafione, welcome. We have a thread for that study: Evaluation of a Gene–Environment Interaction of PON1 and Low-Level Nerve Agent Exposure with Gulf War Illness..., 2022, Haley et al But it looks like most of the discussion for that study was on the general gulf war illness thread: Gulf...

Now published: Web | DOI | PDF

This is unclear. What does it mean for physicians to be in "contact with clinical problems that can inform ME/CFS care"? Add comma before "off-label" Add comma after "ME/CFS" Agreed. This part stood out as the easiest to misunderstand. I think it should just say or summarize the advice right...

Posts about a GLP-1 related anecdote have been moved to: Ozempic, tirzepatide and other GLP-1RAs - impact on ME/CFS

Acute inflammation and fronto-striatal connectivity in the transition from acute to persistent fatigue after mild COVID-19: A longitudinal fMRI study Background Persistent fatigue is one of the most common and disabling sequelae of COVID-19, yet its neurobiological mechanisms remain poorly...

Why does figure 12C differ from 12A, in terms of CD3 distribution? In 12A, there's a cluster around the 0 mark on the y-axis. But there's no cluster there in 12C.