1) Professor @VirusesImmunity about Long-Covid being a functional disorder:
"What we're saying is that #LongCovid at least,
what we're able to already obtain data from patients is that we can explain 94% with accuracy, 94% accuracy long COVID just by looking at the
2) immunological factors alone. So to me that
says that this disease is driven by, you know, something, or immune response to the infection or something else that's triggered by the infection, and we don't need to invoke other hypotheses to explain it.
And that's why, you know,
3) if the functional whatever, you know,
hypothesis is true, I'd be happy to see the evidence of whether, you know, there are parameters can explain with accuracy #LongCOVID and whether that it's going to lead to some kind of a therapy. But that's not what we're seeing, I think,
4) in looking at the biology. And if we can't explain anything, looking at the biology, that's one thing to
sort of invoke other kinds of explanations, but WE DON'T NEED TO."
#LongCovid #pwME #millionsmissing
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1) "Her dogged efforts led to a new scientific discovery at the National Institutes of Health and a promising new line of research that may end up helping many other people with chronically fatiguing illnesses, possibly including #longcovid."
2) very excited about trying” drugs to treat the problem identified in Twinam, said Paul Hwang, an @NIH researcher who led the work."
"Hwang brought Twinam to Bethesda in 2017. During a battery of tests, a curious result popped up. Twinam’s calf muscle took a long time to
3) replenish an energy-carrying molecule after a short exercise session. In other patients with Li-Fraumeni syndrome, this molecule regenerates in an average of 35 seconds. In Twinam, it took 80 seconds.
1) When I die many of my healthy friends and colleagues will write how I was plagued and hampered by my disease. Some might even see this as a failed career, but you never stop being who you are. Even when you're ill you remain the same person and artist.
Plus they might have no
2) clue what we patients have accomplished from our beds. We have succeeded in so many things. Especially considering our disability it deserves all the praise it can get and so much more. Although I was lucky to still dance for a good chunk of my career I had to stop
3) prematurely. I might not have reached goals I wanted to in regards to my work, but I still very much feel I succeeded in life as a whole. I hope people will get to see and remember me by that as well. I'm very much proud to be me, even with the ME.
1) "Now, researchers have identified a protein that’s present at unusually high levels in the muscles of people with #MECFS and that disrupts cells’ ability to generate energy. The findings, reported today in the Proceedings of the National Academy of
2) Sciences, could point to new therapeutics for this condition and for illnesses that share similar characteristics, such as #LongCovid."
"It’s not clear what causes high WASF3 levels in the first place. Hwang suggests a role for endoplasmic reticulum (ER) stress—a dysfunction
3) of membranes that help the cell fold up its proteins. Viruses can trigger ER stress, perhaps explaining why #MECFS and related conditions often arise after infection. (S1 told Hwang her fatigue started after she caught mononucleosis as a teenager.)
1) The results made it clear that exercise was indeed causing #MECFS patients’ guts to leak – spilling gut bacteria and food contents into the blood. One side of the immune system – the antibodies – leapt into action. Another side – the early
2) inflammatory immune response that’s designed to quickly neutralize the invaders – did not, however.
Plus, an anti-inflammatory factor called IL-10 that both knocks down the early immune response and interferes with glucose metabolism in the gut was elevated in #MECFS.
That
3) set the stage for the last finding involving impaired energy production. We usually think of energy production in terms of exercise, but when the immune cells find an invader, they need to ramp up their energy levels dramatically in order to combat it.
All subjective outcome measures. The actometer that was used at the beginning of the trial to assess patients activity that could've provided objective evidence of
2) improvements was not used? Neither right after the trial or at 6 months. Sounds very familiar where with studies in "CFS" and QFS the disappointing objective outcomes measure never seem to match the "positive" subjective outcome measures. So what do those physical function
3) questionnaires really mean?
Patients might simply report improvements because they received more attention than those with regular care that didn't. We all know the care that people with #LongCovid isn't that great in the Netherlands.
1) Conference abstract: "All 62 patients demonstrated preload failure (pRAP < 6.5mmHg). Of this group, 54 patients (87.1%) fulfilled NAM criteria for ME/CFS, with 32 testing positive (59.3%) for small fiber neuropathy (SFN) using either morphological and/or functional testing.
2) Significant correlations were found between pVOg and both AH (r=-0.439. P<0.05) and AETCO, (r=0.474, P<0.05) during TTT. The same tilt table variables were found to be significantly correlated with pQc (r=-0.365, P<0.05 and r=0.351, P<0.05) from the iCPET.
It should be noted
3) that 8 of the #MECFS SFN patients (25%) fulfilled diagnostic criteria for postural orthostatic tachycardia syndrome (POTS) based on the tilt table test.
Decreased oxygen uptake and cardiac output at peak exercise during iCPET correlated with a greater change in heart rate and