I think you untangled what he's said here correctly, however he previously also said that the missing protein biomarker correlates with disease severity which doesn't really fit the above picture IMO.
Prusty talks about his upcoming research on a podcast
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So in that example they are suppressing some part of overactive immune system ( speculated to be involved in covid mortality ) by use of an artificial antibody ? is that actually relevant to our situation with CFS ? i'm not seeing the connection with prustys thing.
Rebecca under the papyrus
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Yes, i was wondering about this, too. My desription is based on him saying that he won't talk about the missing protein this week. We'll see, I guess.
Edit: I edited my above post to add that.
The only connection I see to Prusty is that he recently said that the problem (or one of the problems) lies in the complement system. That is exactly what this monoclonal ab adresses, however there are several other pathways and mechanisms in the complement system.
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Rufous McKinney
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I wrote a snide remark about the fact that us hapless victims certainly have more than 15 minutes available but then I erased it........
I signed up when you posted this and never got an email. Now it's closed
Same hereI signed up when you posted this and never got an email. Now it's closed
Hopefully everyone is so dialled in they don't have time. Lol. But I am wondering what's going on
I found something from the conference I think https://www.tagesschau.de/wissen/gesundheit/mecfs-post-covid-scheibenbogen-100.html
At the conference in Berlin he was talking about fibronectin.
I did not understand much about his talk but it seems that both plasma fibronectin as well as celullar fibronectin is increased in ME/CFS.
I attached the relevant slides. Sry for the bad quality.
Here's what chatGPT gives me on fibronectin:
Fibronectin is a glycoprotein that plays a critical role in cellular adhesion and the organization of the extracellular matrix. It is found in many tissues and body fluids, including blood, and is involved in a variety of biological processes such as wound healing, embryonic development, and tissue repair. Fibronectin is produced by cells such as fibroblasts, endothelial cells, and platelets, and is composed of repeating structural domains called type I, II, and III modules. It interacts with other extracellular matrix proteins and cell surface receptors to mediate cell adhesion, migration, and signaling. Dysfunction in fibronectin can lead to various diseases and disorders, including cancer, cardiovascular disease, and fibrosis.
I did not understand much about his talk but it seems that both plasma fibronectin as well as celullar fibronectin is increased in ME/CFS.
I attached the relevant slides. Sry for the bad quality.
Here's what chatGPT gives me on fibronectin:
Fibronectin is a glycoprotein that plays a critical role in cellular adhesion and the organization of the extracellular matrix. It is found in many tissues and body fluids, including blood, and is involved in a variety of biological processes such as wound healing, embryonic development, and tissue repair. Fibronectin is produced by cells such as fibroblasts, endothelial cells, and platelets, and is composed of repeating structural domains called type I, II, and III modules. It interacts with other extracellular matrix proteins and cell surface receptors to mediate cell adhesion, migration, and signaling. Dysfunction in fibronectin can lead to various diseases and disorders, including cancer, cardiovascular disease, and fibrosis.
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junkcrap50
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FYI there will be summaries and recordings of some of the talks.
BrightCandle
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I am not sure quite what to make of that talk. Fibronectin is elevated and correlates with the disease. We also have a few key IgM antibodies that are low that determine Severe v Mild/Moderate and health controls. HHV6 seems to be in there disrupting the cellular cytoskeleton which is maybe linked with the Fibronectin being elevated. The fibronectin seems to fire up all the IgG response and immune response.
How big were the samples sizes seems like a key question once again.
BrightCandle
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This was all small groups of 10 or so people by the looks of the dots.
Ten people with ME/CFS in total or 10 severe, 10 mild, etc., do you recall ? 10 in total is an almost negiliable number.
I always wonder this about studies when it's not clear. Someone with mild or moderate improving is pretty meaningless outside of a DB-RCT because it seems many people mild or moderate will improve if nothing is done and they just take it easy. Severe, in my opinion, seems like a different beast. There seem to be much fewer credible reports of someone with severe ME/CFS for years then improving significantly with treatment. Most of what I see discussed is, "I went from being bedbound 22 hours a day to being bedbound for 20 hours a day." Admittedly a big quality of life improvement, but still totally disabled.