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Looked like an interesting paper on data driven drug discovery for chronic pain using a proteome-wide association study (PWAS) and things like gene ontology enrichment analysis on UK Biobank data (protein and genetic data). They used machine learning with a proteomic-based score and clinical...

Diagnosis, Prognosis, and Drug Target Discovery for Chronic Widespread Pain: A Large Proteogenomic Study Li Chen, Eoin Kelleher, Ruogu Meng, Duanke Liu, Yuchen Guo, Yunhe Wang, Yaqing Gao, Zhe Huang, Zhu Liang, Shuai Yuan, Chao Zeng, Jun Ma, Yanhui Dong, Anushka Irani, Guanghua Lei, Junqing...

Excellent question @Yann04 and zi share the feelings about the value of S4ME. And excellent summary from @Hutan which I think describes a lot of my journey through going along with things to accepting the reality I knew earlier than those around me. How will people know when the real deal...

I hope it’s all or mostly correct! Yes, it can do things without killing cells, like the calcium, signalling and metabolic transfer changes I mentioned (see the wikipedia page for more info). But I don’t know about ME/CFS. It’s probably unlikely these other effects would be the sole route of...

Yeah, it’s covered in the paper, but I’ll try to expand on this a bit. Daratumumab is a CD38 antibody, so binds to CD38. CD38 is found on many immune cells but is particularly highly expressed on multiple myeloma cells. When it binds to them it can have various effects including - tagging that...

Yeah, there’s bound to be some differences in context. But if daratumumab ends up being the real deal and we can leverage all that work and research to help efficacy for ME/CFS that would be great. Understanding the complete mechanism involved would help.

Really interesting, thanks @ryanc97 Link to the full paper From a quick scan… a few bits that stood out to me And that daratumumab itself changes that makeup In closing they say This seems to indicate the characteristics or quality of the NK cells as much as the quantity is important...

Interesting to see that Solve ME/CFS were involved. I wonder how much input they had on the design? An organisation which exists to promote TMS was also involved in funding the article (but not the research it seems). This from the Acknowledgments

Deciding what should be degraded in the cell or ejected from the cell is one area I thought about. And some cells deliberately chuck things out for other cells to take care of for them I believe. But cells which normally take care of their own rubbish may decide not to or have their own internal...

Thanks, the idea of things being a localised amplifier and only ‘spilling over’ in certain circumstances is interesting. There’s a few things in DecodeME that also showed some genes related to mitophagy and mitochondrial antiviral-signaling protein (MAVS) and how cells respond to RNA that...

A couple of useful quotes And in closing they say this So it seems to be an area with people interested, but not well understood, especially in humans, and not easily measurable. Hmm

A Guide for Studying Mitochondria Transfer Tiash S, Brestoff JR, Crewe C. Abstract Mitochondria can shuttle between adjacent cells or travel to distant organs by breaking away from the parent cell and entering circulation. Here, we briefly review the state of the mitochondria transfer field...

The author and their family no, but the paper and its editors I think there it is absolutely right they are challenged. This is written in a personal way by the author for obvious reasons but it is being presented as fact, as a news feature so having journalistic rigour. The author...

Maybe they should have got their science or health editor to take a look at this before publishing it eh I feel for the girl and her family and there is a good article to be written on their experiences and how they have been failed, but publishing what seem to be more lifestyle pieces like...

Microvesicle-transferred mitochondria trigger cGAS-STING and reprogram metabolism of macrophages in sepsis Ji T, Zhao T, Long S, Wei C, Cheng D, Chen J, Kuang L Abstract The inflammatory cytokine storm is a hallmark of sepsis and is highly correlated with organ injury. Therefore, inhibiting...

I’m very much in learning things, seeing possibilities and throwing stuff at the wall and seeing what sticks territory. Which is very fun. But find piecing it together into something cohesive or articulating it is much trickier. I’ve made some notes though. So they’re not fully formed or...

Not explicitly no. There’s so much in there. It’s really useful to see what someone more familiar with all this sees as relevant or important. Yes and no. More potential fragments of mechanisms or involved pathways. Probably all a bit hand wavy!

Thanks! Well, I got there in the end and am now all aboard the mitochondria and IFN Type I hype trains. Or maybe it’s more accurate to say I have a better appreciation of your interest in these areas than I previously did :) Today a whole bunch of things you’ve said this year sort of slotted...

Presumably the sort of thing it should be easy to compare with DecodeME data, this is 2261 and DecodeME has 10x as many people’s data including comorbitities and for many, NHS records.

After some more digging there could be a link to Type I Interferons too, which has been of interest to people. We’ve often asked how signals are passed around the body especially as we haven’t seen them. How can this be interferon mediated with no measurable systemic IFN changes? Well what if...