This may be really silly, but I can’t remember if you mentioned if breaking the feedback loop you’d think the body would find homeostasis?
I was wondering if the new OX40L antibody target class (amlitelimab not out yet) would be enough to break this feedback loop. This also may be a silly question…
I have to stop looking at this paper, but how did they choose the cells here? Seems like it could induce a lot of bias....
"1042 A. Representative confocal microscopy images show mitochondrial architecture in primary
1043 HUVECs expressing stable GFP within mitochondria and exposed to 1\μg/mL...
It's a bit unclear in the abstract, but I believe all the images and mitochondrial data were done on "primary human foreskin fibroblasts (HFFs) and 117 primary human umbilical vein endothelial cells (HUVECs)". They were just saying the reason they did all of this in the first place is because...
This is exactly what my colleagues said when I showed them old papers. I don't even think I'll show them this one, as it will just make them jaded toward ME/CFS research in general if this is what we're funding and talking about.
They were also surprised at the poor level of science happening...
I’ve worked with a lot of molecular biologists and translational immunologists (I’m an engineer, not biology but catching up). I’ve showed them prustys papers in the past and basically they were not too excited, he does a lot of correlations and throws a lot of jargon in to obscure. The last...
"IgG-induced mitochondrial fragmentation was not detected in the whole ME/CFS cohort. Only a subgroup of patients induced strong mitochondrial fragmentation"
Then goes on to say it was only in the women subgroup. How many women were in that subgroup?
This paper has a lot going on…
All this seems to be built on reference[14]:
https://www.s4me.info/threads/elevated-atg13-in-serum-of-pwme-stimulates-oxidative-stress-response-in-microglial-cells-2022-gottschalk-et-al.27343/
Where it was discussed the levels were “off” only of in two patients…
Has anyone ever tracked infection precedence in ME/CFS before becoming sick? I would say I was “the sick kid” in my teens and 20s… food for thought if others were like this
I’d like to echo this, but only after EBV. As a kid I got sick a normal amount of times as other kids. I actually don’t think I ever got strep throat as a kid.
After having EBV in my teens I was sick ALL the time, mainly strep throat, which I’ve discussed probably triggered my ME.
The thing is though Jared presents himself as a beacon of truth for ME/CFS. He constantly breaks down other studies for scientific rigour, i.e. he ripped apart the rapamycin study. It’s a bit different than a tabloid presenting “the cure to Alzheimer’s”.
He has a small niche audience that...
I don’t even know what to say we’re now taking a 5 minute video of an unsubstantiated claim running it through LLMs and reporting it as news .
It’s like a game of telephone….
Wow, that first gene RABGLP1 and its strep association. I’ve always struggled with strep throat after getting mono in my teens. Then my 20s my ME/CFS started after a strep throat infection did not fully clear from 1st round of antibiotics, sat with an infection for 2 weeks, before getting a...
Great it’s on the front page of the /r/CFS subreddit…. If this turns out to be a nothing burger it’s just going to add more confusion to the root cause landscape. Though im hoping that real peer reviewed data is presented soon. I’m not against this research, I’m against overarching...
Why come out with these statements without even giving a clue of what statistics are… irresponsible imo as people are already sharing this video saying ME/CFS is conclusively a case of neuroinflamtion.
I know YouTube incentivizes posting regularly but yikes huge statement to say without any...
I wonder if this is why some patients find PEA helpful, as it helps create allopregnanolone
Edit: this slide is referencing pregnenolone where I am thinking of a different molecule pregnanolone. Allopregnanolone is a metabolite of pregnanolone
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