I don’t see how to fairly title the paper as it is based on the data presented. There is little use acknowledging “what would be important in future” while the current absence of it makes the main conclusions and title of the paper unsupported.
“Shift in respiratory profile of PBMCs from people...
It has its uses (mostly to suggest starting points) but yes I wouldn't accept what it says without verifying specifics. I put the decodeME genes in there as an exercise to test its sanity and the very first gene summary had two completely fabricated factual inaccuracies.
Sadly I don't know what can really be drawn from the study in terms of mitochondrial function differences
There's no mention of PEM, and they're reporting negative proton leak values which means they have larger OCR values at the end of the assay than post-oligomycin, which doesn't really make...
Not on my best form today but seems fine to me!
This is a very ambitious question that I’m not sure we have the answers to, but I am not a mitophagy expert. Starting points might be 1) Can heteroplasmy and mitochondrial contiguity interact to produce localised “mitochondria” of different...
Patient muscle homogenates or isolated mitochondria showed variably decreased activities of the mitochondrial respiratory chain complexes as well as decreased mtDNA content. Cultured skin fibroblasts had reduced maximal oxygen consumption rate and increased fragmentation of the mitochondrial...
There is a lot of talk in this thread about muscle culture and seahorse etc, I haven't gotten to read the paper yet but useful things to look into would be a) whether activity matched controls b) passaging/handling of the cultures (primary muscle cell phenotypes change with doublings - is that...
We have a student in the lab doing this, I sat down with her and went through it a few days ago, actually. It was pretty objective and automated. That mito morphology package was part of the workflow, i just dont remember the full suite she was using. So it's possible this work here is also...
There is a lot in here that will take me a very long time to parse in detail, but I met Sheeza last year in Oxford and I was impressed with her technical understanding. Good to see the work accepted
"Although acute and chronic infection require and consume considerable ATP, people with both long COVID and ME/CFS have a reduced capacity to generate ATP from oxygen, glucose, fatty acids, and amino acids."
Citation: prior review where they have a table of very broadly combined evidence from...
nor do classical genetic mitochondrial diseases seem to produce PEM (as we know it in ME/CFS), as far as I am aware. Of course this comparison is to a degree confounded by developmental issues incurred by inborn mitochondrial dysfunction but still.
my guess is that most of us are constantly wrong and that a key difference maker lies in how receptive to argument and vigilant against bias one is
this is to say: don't shy away from papers unless it's for a health reason! In theory everybody should be capable of getting at least the gist of...
Sure. I agree on all fronts. I was going by my first impression, having looked at the graphs, so I'm not sure what their internal framing was for the questions being asked - your take is probably more well informed than mine :)
If you are hypothesising differences in each one, individually, do you need to? I probably wouldn't apply it in this case if I was the author, I would see it as 6 different experiments, each having 5 groups
I would not refer to it as different diseases, but if something is progressing there may be different components of the contributing processes becoming more or less deranged or consequential as things get worse.
Now that it's published I am having a proper read. I am writing an experimental paper at the moment that is likely to have a section very relevant to some of the results (results specifically, interpretation is trickier). Still cooking but interesting.
Onto some specifics from this paper that I...
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