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PC's were some of the top differences between ME/CFS and Controls in Karl Mortens metabolomics work measuring ~10,000 metabolites. This is a slide from his 2018 New Zealand presentation. I think the work was written up in an ME Association report but I've no idea where to find that.

Some more info from the web page.

Professor Robinson has contact information here (link) if you want to have a discussion and clarify some things about this lupus study. I hear he is one of the "good" guys for looking into understudied diseases and "rare" disease patients. I get the impression he really wants to make a...

Prof. Akiko Iwasaki created a thread on X to summarise the paper 1. A groundbreaking paper by @younis_sh1 et al. @stanfordimmuno provides an answer to the long-standing question about how EBV infections are linked to lupus. A short thread to explain the key findings. 2. The authors developed...

This section seemed key to me. Interesting to see insulin signalling, synapse, and muscles come up yet again.

Funding The Amar foundation seems to really believe in the work of the Hanson lab. Dr Hanson has mentioned in webinars that NIH funding didn't provide enough to process as many samples/tests as she would have liked and that she is grateful for the Amar foundation to cover some of this gap.

Some good news. Dr Cliff's funding was renewed on 2nd September 2025 for her HHV6 / T-cell project. https://reporter.nih.gov/search/XeO6cAqjak2ry0akmjFQeg/project-details/11159442 The is also good news for the Cure ME Biobank team as they rely of Dr. Cliffs lab at Brunel to process samples...

I see a BTK inhibitor has recently been FDA approved for chronic spontaneous urticaria. Chronic spontaneous urticaria is primarily caused by the activation of mast cells, which themselves are derived in bone marrow.

I see that TLR7 is also associated with Sjogrens....... https://pubmed.ncbi.nlm.nih.gov/34108972/

Impressive work @forestglip. Can you look to see if you can find any datasets for Sjogrens. It's a CNS disease with some overlap to ME/CFS such as small fiber neuropathy. This Sjogrens GWAS meta-analysis abstract also mentions RABGAP1L...

From the Mark Davis talks a few years ago he was thinking ME/CFS could be something like this and was interested in differences in KIR+ cells. Apparently it is normal for these types of immune cells to be very active during infection and they should turn off after the acute infection is resolved...

The tracer is DPA-713, a second generation tracer designed by Dr James 20+ years ago. She really seems to know how to design tracers with a long track record of developing different ones since then. What I learned today from the symposium is that the PBR/TSPO receptor lives on the...

I am posting this paper because the Zhang et al WGS paper and the DecodeME GWAS paper both highlighted the genetic involvement of the central nervous system and immune system as key in ME/CFS. This paper can help us better understand the neuro-immune interface.

Neuro-immune Interactions in the Tissues Abstract The ability of the nervous system to sense environmental stimuli and to relay these signals to immune cells via neurotransmitters and neuropeptides is indispensable for effective immunity and tissue homeostasis. Depending on the tissue...

If there is persistent T cell activation would we expect to see more gramzyme B and perforin in the blood? I think from studies certain T cell types don't make as much of the two when tested in the lab. According to the Selin lab only a subset show gamma-delta T cell differences. I suspect...

X is blocked on s4me for me so this was the full quote on X giving context. "We also want to take a moment to acknowledge the recent shooting at the CDC and send our heartfelt support to our colleagues there as they process and heal from this tragedy. Our thoughts are with all those affected"

The video that was shown said they were white blood cells in the capillary. They should in fact be red blood cells. The capillaries in the video look pretty good to me, and the technician also said pretty much the same. So the comment about abnormal results doesn't seem appropriate for the video...

I think the GWAS arrays were specifically designed to focus on protein coding genes. Just like Whole Exome Sequencing. It's only relatively recently that Whole Genome Sequencing has become more competitively priced for full coverage, but still more expensive than GWAS arrays.

This is a very big project on it's own, on top of a SequenceME like project. You would likely need to carry out individual proteomics & RNA / western blot / sanger sequencing etc to confirm the gene is in fact causal. The most important part is to have clinical centers the patients identified...

So why don't they show a data comparison between GRCh38 variant rs35306732 13:53194927 (paper) and GRCh38 variant rs1923773(P) 13:53176219 in DecodeME dataset only to show that comparing rs1923773(P) to an external data set is even valuable? They must have the data. Perhaps they did. I don't know.