Posted: Fri Jan 30, 2009 9:02 am
LOL! it is a little technical and it assumes the reader knows some things.
The stratton work on venous ulcers is here
http://www.nature.com/jidsp/journal/v6/ ... 0063a.html
Abstract:
CPn is present in arterial plaques always and for years has been considered an emerging pathogen in cardiac disease by the CDC.
So CPn is a good candidate for being involved with several known issues in this pathology we are talking about on this thread: endothelium is directly impacted by CPn, CPn is known to be involved with vascular plaques, etc etc. I hope they look for it if they send any removed tissue from the stricture area to pathology if such is needed in an individual case.
NO signaling and CPn and atherosclerotic plaques
from here http://circ.ahajournals.org/cgi/content ... 102/9/1039
And on the other side fromt he abxer's point of view, we've always known there must be some co factors in the CPn model too because not everyone gets better on abx, though some have great results. I personally progressed so I have something else going on in addition to any role CPn plays in MS. I hope this is "IT".
I am going to start a thread on the abx forum for exploring the possible connections between CPn and the CCVI.
The stratton work on venous ulcers is here
http://www.nature.com/jidsp/journal/v6/ ... 0063a.html
Abstract:
There is absolutely every reason to imagine CPn COULD be involved in this pathology.the genus, Chlamydophilia, as obligate intracellular pathogens, induce chronic scarring in humans. Chlamydia pneumoniae, a common cause of pneumonia, infects endothelial cells and circulating macrophages. Evidence that C. pneumoniae is an opportunistic pathogen in chronic skin ulcers and other inflammatory skin conditions analogous to its role in atherosclerosis is reviewed.
CPn is present in arterial plaques always and for years has been considered an emerging pathogen in cardiac disease by the CDC.
So CPn is a good candidate for being involved with several known issues in this pathology we are talking about on this thread: endothelium is directly impacted by CPn, CPn is known to be involved with vascular plaques, etc etc. I hope they look for it if they send any removed tissue from the stricture area to pathology if such is needed in an individual case.
NO signaling and CPn and atherosclerotic plaques
from here http://circ.ahajournals.org/cgi/content ... 102/9/1039
The fact that Zamboni has discovered, in his labs at least, he can look at a set of doppler scans and know if the person has MS, and also if they have progressive or RR disease based on scan results because people with MS have these venous drainage problems, does not mean that there are not other co factors involved. Those strictures causing the backup had to get there somehow.....Conclusions—C pneumoniae impairs arterial endothelial function, and the NO pathway is principally involved. Cyclooxygenase-dependent vasoconstricting products may also account for the infection-induced impaired relaxation. These findings further support the role of C pneumoniae infection in atherosclerosis development.
And on the other side fromt he abxer's point of view, we've always known there must be some co factors in the CPn model too because not everyone gets better on abx, though some have great results. I personally progressed so I have something else going on in addition to any role CPn plays in MS. I hope this is "IT".
I am going to start a thread on the abx forum for exploring the possible connections between CPn and the CCVI.
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