Search results

Eventually found the map: https://www.journalslibrary.nihr.ac.uk/sites/journalslibrary/files/journal_data/BTBD8846/NIHR136262_supp7.html I could not use "Filters" on the page to arrive at the "11% of studies only included people with postexertional malaise" - using CCC I see 170 on the map...

I certainly will, eventually ... takes time to go up these learning curves. I especially want to understand how these GWAS/WGS studies will infer possibly quite complex genotype-phenotype associations, and the corresponding multiple-test-corrections (dull statistical questions, but vital...

Thanks so much - the "Efficiently Analyzing Large-Scale WGS Data" video is really helping.

Epistasis (gene-gene interaction) seems an attractive hypotheses to explain at least part of GWAS "missing heritability". Is there a clear winner these days on how to do this? I read of efficient enumeration methods, random-forest and other ML methods, Bayesian methods, etc, but want to only...

I guess I want to "look at" those technologies which GWAS results would prompt researchers to reach for next, in order to discover higher associations with PWME phenotypes. I read about Next-Gen GWAS methods, rare-variant-analysis etc, but as a non-scientist am confused as to which learning...

Non-scientists like me are only now learning about the GWAS "missing heritability problem" (rare variants not on the GWAS arrays, epigenetics (SNPs affecting only gene expression), SNP/gene interactions) etc. I now have a better sense of how slight (but very important) a clue a significant SNP...

Low SNP frequencies surprised my non-scientist eyes; for example, directly genotyped tagSNP rs115523291 had: a) Norwegian allele frequencies of 2.5% and 0.4% for MECFS/normal, P=8.5X10-07 b) UK 1.0% and 0.9% P=0.03 I take it...

May I give my non-scientist takeaway? a) interferons IFN make people feel lousy b) pathogen --> IFN secretion by macrophages ... some pathogen stimulates macrophages (eg microglial cells in the hypothalamus?) to produce itaconate (by expressing IRG1/ACOD1 enzyme) ... this occurs mainly in...

We (society and medics) have surely evolved past all that. Fashioning psychosocial labelling seems to be backwards-looking and, in a way, actually reinforcing the very stigmas etc they profess to want to address. I can't see any benefit of this sort of labelling; to anyone.

Thanks - I guess if T cells are somehow impaired in ME then creating more impaired T cells is presumably not helpful for PEM.

Surely high-intensity exercise is very detrimental for ME?

High EBV but normal anti-IFN-1 autoAbs seems to support one pattern I keep coming back to: Epoch1. Prior to infection a) stress and “over-doing” things causes HPA activation to create sustained cortisol elevation b) high cortisol (initially may enhance innate immunity) if sustained can inhibit...

Could "trained immunity" not be triggered also by autoimmune disorders?

I noted that another thread "Defining trained immunity and its role in health and disease, 2020, Netea et al." elicited little response. Is "trained immunity" unlikely to be relevant to ME, and if so does anyone know of a good resource that explains/highlights why? Thanks so much.

Do you think "trained immunity" is unlikely to be relevant to ME, and if so can you highlight the main issues? Are there other studies that do a better job of characterising the relationship, if any, between ME and "trained immunity"? Many thanks - I am keen to travel up this learning curve.

While I have no scientific credentials in this area, I am alarmed to read Stressing ME mitochondria on the basis of a tenuous non-hypothesis implicating mTORC1 strikes me as a very bad idea.