I can’t 100% remember what I checked or where I said it but I think it was my PBMC data…without knowing which populations were shifting in what ways that comment shouldn’t be used as grounds to dismiss anything
yep
I remember reading an article saying they planned to look at morphology as well
I didn't see anything about blinding but the only results were a few images, nothing quantitative. Small sample, clearly done in not a lot of time by an undergraduate student (understandably, probably with no...
I personally would not run too far with this idea. An event that we know little about that is enabled by cells staying in contact for hours doesn't seem like fertile ground to me.
Seems like this was a project as part of a bachelor's degree but we will need better evidence of serum effects on mitochondrial morphology than individual images. Are Audrey and Charlie still doing the replication attempt on this? (Prusty's work or whatever it was) @chillier ?
My gut is that I...
Regarding this line of investigation it is whatever mr dmissa can get funded, grant apps are submitted and fingers and toes are crossed
The idea is to screen primary cells from pwme for mitophagy abnormalities while measuring the activation and downstream outcomes of different signaling...
I forgot about this recent one from the melbourne uni team https://pmc.ncbi.nlm.nih.gov/articles/PMC11599898/
gonna move to that thread now. I think it is the missing link I was looking for.
My guess is that there is no clear abnormality in cholesterol or other lipid markers in routine pathology testing in pwme right?
I am very interested in this particular issue and trying to piece it all together. I have a model under construction of how something might be going wrong here at the...
CD38 mRNA is down in bulk PBMC RNAseq data I have from ME/CFS and Long COVID w/PEM versus healthy and post-COVID controls. not sure if this helps anyone's thinking but thought i'd throw it in (may be explicable by cell type proportion shifts)
Yeah look, this might all be a case of incomplete contentions coming across, from different people, in combination. This is one weakness of jumping in to a forum thread late. So I thought I would just set the record straight on my own opinion because I did involve myself, and realise there is...
This is something I want to get some $ look at on the side. Our lab has pioneered intracellular calcium flux measurements for like 40 years now or something.
I have just put in a proposal tangential to this idea while combining some clues from DecodeME and also our fibroblast lines. Fingers...
Hundreds of bedside one on one interviews with patients.
Because my real life friend tried something in isolation that moved her from housebound to able to work part time with pacing, and yes she deals with PEM and does have genuine ME/CFS.
The point I am making is only that for interventions...
POTS? Managing POTS seems to be one of the most common pathways by which people gain some improvements in quality of life. I'm not saying it's addressing the other features but it does help.
Edit: I see there was more discussion on this. Fine, whatever you want to call it. Orthostatic...
Would these not be among what this is used to attempt to aid?
In the abstract David even says "it is unlikely to be a stand-alone solution"
Nobody reasonable is saying that the problem is going away. The point is that some benefits may be attained in particular symptoms in particular people...
I have not designed anything in this space yet. I have just finished a proposal to check for dysfunction in processes relating to one of the DecodeME genes. I will have to design a “basic science” project later in the year which I may use to try to fill holes in our fundamental knowledge that...
What was the evidence put forward in favour of inflammation?
Do you think this frequent source of disagreement is an issue of language specificity? My sense is that use of the word inflammation has drifted (whether appropriately or not) away from its classical definitions.
I have no investment in muscle studies, but I have spoken to several moderate-severe people with ME/CFS (CCC, diagnosed by a CCC author) who used to be athletes and describe their pain as being the "lactic acid build up" that they were used to as active athletes, which I interpret as meaning...
I am intending to look along the lines of how specific mechanisms that may lead to altered ER-mitochondria interactions (including by biogenesis or phagy of either, lipid content of or lipid shuttling by either, calcium storage or mobilisation, etc) may interact with activation of or signalling...
What’s this in relation to? Sorry, I don’t have time to catch up on the whole thread and study yet, but I don’t want to miss whatever this was referring to on the off chance it’s important given that I have hundreds of these cell lines in the freezer
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