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something seems to be going on with cell survival processes in circulating PBMC in both ME/CFS and LC - stay tuned (and in pre-empting the Jonathan Edwards/Snow Leopard "PBMCs aren't doing anything" reply, I'm not saying that it's driving the disease but there is a detectable feature here. The...

even if there is no ME-specific mechanism I am certain that HLA alleles would contribute towards ME/CFS susceptibility even if it is as little as increasing one's tendency towards experiencing more severe illness with eg viral infection. My reasoning is that particular HLA alleles associated...

If this is the TCR-funded Deakin work I would guess that the workflow is phenotype cells (as far as we know, RNA seq) -> blast them with an array of accessible drugs -> see what worked best in "reversing" the phenotype. It seems like a discovery approach How the final step is determined is...

I can't see anything about blinding/placebo on the poster Rapamycin is a bit of a nasty drug so I would be cautious until we have clear evidence of efficacy fingers crossed!!!

Could be commercially sensitive

a useful tool if looking at specific enzymes is protein atlas. If you have specific lipids in mind and can trace back to a protein of interest, that's one way to make sense of things. one example for a relevant enzyme: https://www.proteinatlas.org/ENSG00000100596-SPTLC2/tissue In this example...

if we read this in good faith there might be nuance lost in translation. it's possible to me this paper is telling us about the specific role of a particular protein in relation to particular outcomes, some of which may be relevant to ME as common symptoms, but ultimately may not recapitulate...

general comment some things, particularly lipid metabolic pathways, are very variable between tissues (whether relevant enzymes are even expressed or whole processes even occur varies massively with the tissue or cell type) so studies done in eg circulating blood will have to kind of be...

They have transfected mice with (human?) PKM2, plus overexpressor and knockout groups, and then made them to do exercise. How is that ME? ?

thanks, I didn't know PR pre-dated s4me. I had actually forgotten about it since I haven't really looked there very much

Two leading experts sounds good to me. I look forward to whenever your ideas are out there so that they can inform my own research ideas in a similar vein When we both have the ideas solidified we should have a future, detailed chat (long overdue) - - If it's something we can feasibly...

Ah there mustn't have been a thread for this afterall. The paper stood out to me yesterday and I couldn't find a thread for it (when I made the other post about cytokines, I did indeed have this paper in mind)

Are we aware of any consensus in these areas in ME/CFS (no matter how small?) What do we think about the TGF-β angle in 2025

Generally yes but lit reviews are a little different as they are often an entry point for new readers. Since they are discussing other illnesses too, this is context that may explain the choice to describe ME/CFS as well.

These bits led me to believe (I think fairly) that you were referring to ROS in disease in general, as well as human disease research in general. I agree with this, it just didn't come across that way with the broader things being said so I made broader replies. It depends on which form of...

I initially began my reply by responding point by point but it became pretty clear that there’s a central issue here that it would be more efficient to address directly: what you are discussing is in the context of inflammation research and based on knowledge largely pre-2000. I was not talking...

"Oxidative stress" would generally be referring to a biological scenario that involves increased likelihood of damage to molecules usually by accumulated reactive oxygen species yes It is one of those phrases that is wielded often and probably too loosely (which phrase in biology isn't? alas)...

the abstract explains what they are meaning "Using a combination of flow cytometry, bulk RNA-seq analysis, mass spectrometry, and systems chemistry analysis, we also observed aberrations in ROS clearance pathways including elevated glutathione levels, decreases in mitochondrial superoxide...

Can study them inside live samples from patients - easier or harder depending on the tissue of interest. We have done it in circulating immune cells, primary fibroblast lines and immortalised cell lines. Others have done it on immune cell subsets and muscle biopsies

"mtDNA analysis from muscle at 46 years of age revealed the m.8753_16,566 deletion with <10 % heteroplasmy. The deletion was larger than in patients with KSS but encompassed the entire ATP6 gene associated with complex-V of the respiratory chain. An abnormal complex-V band was detected in the...