This is mentioned here in this documentary (38:20):
Scheibenbogen later commented on this:
https://www.healthrising.org/blog/2021/09/16/autoimmune-options-chronic-fatigue-syndrome-scheibenbogen/
I heard people suggest that the dosage might be different (and that the Norwegian trial couldn't provide the dosage because of lack of funding). Not sure if this is true. Here's what I could find online:
Fluge et al. 2011 (pilot RCT, n=30)
Rituximab 500 mg/m2 given twice two weeks apart, with...
I also wonder how this relates to the study by @chillier which found no difference in oxygen consumption rate when ME/CFS serum was added to myoblasts. Do these studies contradict each other?
Yes it looks interesting but it seems that this is not for LC in general but for a relatively rare complication called 'Multisystem inflammatory syndrome in children (MIS-C)'
This page says:
https://www.mayoclinic.org/diseases-conditions/mis-c-in-kids-covid-19/symptoms-causes/syc-20502550
The first sentence is:
This also looks strange, perhaps written by an AI?
The first author Martin Toby published a case series on chronic symptoms following EBV in 1982 in the Lancet.
https://pubmed.ncbi.nlm.nih.gov/6119490/
The link to sickness behaviour is interesting, thanks for highlighting this!
If I understand correctly this was only significant in the female-only comparison which had only 34 ME/CFS patients and 27 controls.
I think it means that most common allele (C, which is present in 62% of the...
Interesting but wouldn't a decline in neurotransmission result in muscles or cognitive abilities no longer functioning? In ME/CFS the end results always seems to be feeling awful. So instead of normal functions shutting down, it suspect it involves some feedback signal that is turned on too...
It's a bit unclear but it seems that they used this model to see how these factors influence SMPDL3B but that they didn't use it for group comparisons.
Interesting thanks.
I wonder if they split the control group in group A and group B and do the same analysis on these groups (rather than ME/CFS versus healthy controls), how high the predictive power and AUC would be.
The research team of Unutmaz at Jackson Laboratory has made all of their data public following the BioMapAI publication:
https://github.com/ohlab/BioMapAI/tree/main
I have no idea how they came to this result. They mention it in the text and have a Figure 5 explaining it but I don't see how this came out of their AI model. Perhaps it's based on further correlation analyses within each group?
This graph (Extended Data Fig. 3) is also interesting as it shows the most useful biomarkers for each of the 12 symptoms outcomes. These are based on SHAP (SHapley Additive exPlanations) values which indicate how much each feature contributed to a specific prediction.
Rather than just predicting ME/CFS versus control, the model could also estimate symptom scores such as subscales of the SF-36. It seems that the immune data was most useful for prediction physical functioning and general health while info on gut microbiome was useful for gastrointestinal...
Supplementary table 3 gives some more info about the predictions. Using all datasets (metabolomics, immune, microbiome, etc.) the BioMapAI had an accuracy of 72.5%. Precision was 0.71 meaning that approximately 7 out of 10 participants predicted to have ME/CFS actually had ME/CFS.
On the...
Yes looks like its relatively old data. Patients were diagnosed in 2013–2018 and ethical approval for the study was given in 2016.
Weird result. No difference between steroids but almost a total lack of correlations among them in the ME/CFS group. Unfortunately, the authors couldn't give an...
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