Prusty talks about his upcoming research on a podcast
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I think he said both plasma and cellular is elevated. Cant remember what source i heard that from though, maybe it was in Tess Falors live tweets.
In Isabel Ramirez-Burnett Tweets it says "Both cellular and plasma fibronectin is increased in mecfs", however from there onwards it isn't clear when he is talking about what, the same holds for the interview. For the nIgM I think we can maybe assume it's lower for the set of pFn and cFn. We'll have to wait for the paper for the proper details.
I believe this is the study Prusty was referring to in connection to Fibronectin: https://pubmed.ncbi.nlm.nih.gov/34024298/. It has a very similar flair to his finding (apart from the nIgM finding) and argues that Fibronectin could be a better biomarker than an PCR-test for Trypanosoma cruzi as it measures treatment effects better (since PCR doesn't asses tissue damage and cardiac alternations). They saw that in T. cruzi a cysteine protease (the major enzyme on this illness that causes protein degradation) degrades fibronectin during infection, and this may play a role in host cell invasion.
They looked at 2 things pFn and dFn (fibronectin degradation fragments, something like fibronectin is being broken down). It seems like cFn levels weren't relevant to their results (or maybe it's harder to test for). Their main results were mouse studies where they observed, that:
In the acute phase pFn went down and pFn stayed decreased in the chonic phase of the disease. Looking at the dFn levels they showed that treatment can reverse degradation of fibronectin in the acute phase, but in the chronic phase it can only halt the degradation. They were able to show dFn correlated with disease severity. Their conclusion was that fibronectin degradation can be a biomarker for cardiac tissue damage.
Relevant to us they state "These results warrant the development of easier and more quantitative tests to measure fibronectin degradation, including as ELISA or immunochromatographic rapid tests for the point of care monitoring of disease progression and response to treatment in patients. Fibronectin is present in blood at a relatively high concentration of about 0.6 mg mL−1 in mice and 0.3 mg mL−1 in humans (Mosesson and Umfleet, 1970; Zardi et al., 1979) supporting the feasibility of such tests. On the other hand, fibronectin degradation may not be specific to T. cruzi infection as it is a target for other pathogens (Speziale et al., 2019), and this should be further investigated."
So maybe this team has already developed fibronectin tests that could be relevant to us. It should also be possible to assess our dFn levels. None of this is specific, but could be made part of a biomarker platform.
They looked at 2 things pFn and dFn (fibronectin degradation fragments, something like fibronectin is being broken down). It seems like cFn levels weren't relevant to their results (or maybe it's harder to test for). Their main results were mouse studies where they observed, that:
In the acute phase pFn went down and pFn stayed decreased in the chonic phase of the disease. Looking at the dFn levels they showed that treatment can reverse degradation of fibronectin in the acute phase, but in the chronic phase it can only halt the degradation. They were able to show dFn correlated with disease severity. Their conclusion was that fibronectin degradation can be a biomarker for cardiac tissue damage.
Relevant to us they state "These results warrant the development of easier and more quantitative tests to measure fibronectin degradation, including as ELISA or immunochromatographic rapid tests for the point of care monitoring of disease progression and response to treatment in patients. Fibronectin is present in blood at a relatively high concentration of about 0.6 mg mL−1 in mice and 0.3 mg mL−1 in humans (Mosesson and Umfleet, 1970; Zardi et al., 1979) supporting the feasibility of such tests. On the other hand, fibronectin degradation may not be specific to T. cruzi infection as it is a target for other pathogens (Speziale et al., 2019), and this should be further investigated."
So maybe this team has already developed fibronectin tests that could be relevant to us. It should also be possible to assess our dFn levels. None of this is specific, but could be made part of a biomarker platform.
https://www.jacc.org/doi/10.1016/j.jacbts.2016.06.004
For those of us with that vascular asthma sort of tightness,especially in the neck, this anti purigenic targeting of the cartoid artery may help resolve some of the vascular issues?
For those of us with that vascular asthma sort of tightness,especially in the neck, this anti purigenic targeting of the cartoid artery may help resolve some of the vascular issues?
Judee
Psalm 46:1-3
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Did I just found a connection with the clotting and platelets theory ?
I also read something regarding microvesticles and possibly low IgM. It sounded like clotting.
I couldn't remember the terminology but another thread title reminded me. I'll try to search later for the actual study 'cause I still don't remember the wording.
Edit: Here it is: https://ashpublications.org/blood/a...al-IgM-antibodies-inhibit-microvesicle-driven
Natural IgM antibodies inhibit microvesicle-driven coagulation and thrombosis
so if IgM is low...?
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Has the coagulation factor X/Xa, which is somehow the problem here and is the thing with which the nIgM LR04 competes and in turn lowers coagulation, been looked at before in ME/CFS or LC research? (I don't really find anything relevant, I can find someone mentioning it for acute Covid, but not specifically or very relevant as by now anything that exists has been mentioned in connection to acute Covid). In Pretorius' work for example factor XIII seems more relevant.
Rufous McKinney
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Dr. Aguirre-Chang posts alot of info on micro-clotting, how to determine if you have clotting trouble, and protocols for clearing it. Have you looked at any of that info? I think he has posted some of it here in PR.
Countrygirl
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https://www.healthrising.org/blog/2...RF2QkCoMqWBBxmZHqfNw7rvkABcgYS-MDd2_SMWleh4eo
Prusty on Herpesviruses, Messed Up Mitochondria and a Biomarker for ME/CFS and Long COVID (?)
by Cort JohnsonA couple of weeks ago I commented about MBL and its possible connection to Prusty:
Well here's the possible connection: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354681/.
Well here's the possible connection: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354681/.
Rufous McKinney
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My GP said he thinks it's HHV-6 the likely cause of my low grade B cell lymphoma.
Rufous McKinney
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really outstanding summary....overview/ THANK YOU
the Discussion of sudden versus gradual/slow burner onset...is interesting. I was mildly SOMETHING for decades; but when I got MUCH worse that seemed to occur quite quickly....withim a few weeks.
I Like this theory because it's consistent with The Flow being impaired. I'd like to Go With the Flow, but something is often interfering with that...
I think it maybe the low C3 high C5 complement imbalance but this seems to be good for a few diseases like the earlier video I posted on acute covid
Others I’ve found that seem to share this imbalance are lupus,schizophrenia,aHUS,Alzheimer’s and maybe more,but they have different seemingly unrelated outcomes
Anyone tried Trypsin as suggested in the earlier video
Could lowering of C3 even in normal range be enough to cause diseases
My c3 and c4(low)are normal just got result
Others I’ve found that seem to share this imbalance are lupus,schizophrenia,aHUS,Alzheimer’s and maybe more,but they have different seemingly unrelated outcomes
Anyone tried Trypsin as suggested in the earlier video
Could lowering of C3 even in normal range be enough to cause diseases
My c3 and c4(low)are normal just got result
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Nope and he submitted to a journal that uploads the preprints once they accept to review (at least that's what he said).
The progress to accept or decline to review usually only takes a couple of days or at most a month, at least that's my knowledge. Maybe, there's some journals that take a bit longer with their decision and there's the possibilty of unlucky coincidences for example combinations of sick leaves and academic holidays, but usually this process is very quick (at least in terms of the duration of the publication process).
So if we don't hear anything in the next month or so, it's probably a decent guess that the submission (or the first few submissions) weren't successfull. I would think that Prusty would contact the journal himself around that point in time, would he not have heard back from them until then. Till then we'll have to wait and hope that the first submission is successful.
The progress to accept or decline to review usually only takes a couple of days or at most a month, at least that's my knowledge. Maybe, there's some journals that take a bit longer with their decision and there's the possibilty of unlucky coincidences for example combinations of sick leaves and academic holidays, but usually this process is very quick (at least in terms of the duration of the publication process).
So if we don't hear anything in the next month or so, it's probably a decent guess that the submission (or the first few submissions) weren't successfull. I would think that Prusty would contact the journal himself around that point in time, would he not have heard back from them until then. Till then we'll have to wait and hope that the first submission is successful.
A new MBL finding in Long-Covid brain fog patients and its connection to decreased MBL which has been previously discussed in connection to Prusty's findings "A likely association between low mannan-binding lectin level and brain fog onset in long COVID patients"
https://www.frontiersin.org/articles/10.3389/fimmu.2023.1191083/full
https://www.frontiersin.org/articles/10.3389/fimmu.2023.1191083/full
There's a better transcript available now for those still interested https://static1.squarespace.com/sta...-+Biomarker++Breakthrough,+Bhupesh+Prusty.pdf