Importantly, neutrophils and monocytes from septic patients are refractory to subsequent LPS exposure and no longer produce the comparable levels of inflammatory mediators.13 This mechanism, referred to as endotoxin tolerance (also called LPS hyporesponsiveness or refractoriness), prevents overstimulation from the continuous exposure to the same and related danger signals. Although endotoxin tolerance is claimed to be a specific phenomenon, in vivo or in vitro LPS-primed cells show hyporesponsiveness to heterologous zymogen, staphylococci or streptococci as well as many other non-LPS ligands. This is known as LPS-induced cross-tolerance and has also been observed in association with cells from septic patients.14 Similarly, other TLR ligands such as PGN, lipoteichoic acid, Pam3CSK4CysSerLys4 (Pam3CSK4), LPS from Porphyromonas gingivalis and flagellin, plus cytokines such as TNF-α and IL-1β, have been shown to induce homologous tolerance in monocytes/macrophages and, interestingly, can substitute for each other and sometimes mediate cross-tolerance both in vitro and in vivo. http://www.nature.com/cmi/journal/vaop/ncurrent/full/cmi201126a.html In other words---In Pam3cys/Pam2cys it is likely they could be causeing disease instead of preventing.... What this means is our genes can swap with infectious organisms and remain hidden to just look like us...They must start treating the truth. All the hidden infections causing Our Age Of Syndromes.
And the people must push for the help we need---because they gave it to us in Pam2cys and Pam3cys used in vaccines, and because of the neglect of the truth to protect profits it is now being dissiminated in our vectors of disease.
Lyme is a Crime---Not a Bad Knee...
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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I was under the impression that we did in fact have hyperresponsiveness, overproduction of cytokines and other types of inflammatory chemicals that were inducing autoimmune markers, and sometimes cancer. But I haven't seen anyone figuring out how to accurately measure these in chronic lyme patients. I have some normal numbers in cytokine testing, but also have autoimmune markers as well as chronic lyme and other unknown germs. Is that they are not measuring the right inflammation characteristics?
And while I can see the problem with hyporesponsiveness to chronic bacterial infection, how does this mesh with what appears to be inflammation related issues that we have?
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Pinelady
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I believe thats the point..We have issues with damages caused by the spirochetes infecting the tissues..
And we have issues with the prion like proteins swapping genes with other organisms including ourselves and transversing across the neurons as recently described by those that do have the new supermicroscopes... The US is not one of the 5 that have them...
I believe it will be found to be time dependent according to the infections/and folding of the proteins to hide them in the immune system...Once they are fully dissiminated and no treatment is applied they just look like they belong but when they become stressed or attacked they do produce cytokines...
I am sure there is a few T cells that don't get fully turned off and attack...They just don't know what to attack...
So they called it autoimmune all these yrs. instead of fessing up to the truth....They gave it to us in the first place.
What's the difference in AIDS and Lyme? A virus. What's the difference in Hep. and Lyme? A virus. What's the difference in MadCow and Lyme? What ever was in a vaccine they gave to cattle that went very virulent. When they used the HepB test to detect 88% of AIDS patients someone should have slapped them all silly then for being so stupid.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady
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The superscope guys are saying our hormones are also transversing the neurons...
Could be the explaination to the flair up many women seem to see in a cycle...
Lots left to discover, but the truth is in how AIDS patients are mostly surviving today...
They are afforded all the killing meds they need and many are doing stem cells...And its working.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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I did not realize AIDS patients were doing stem cell treatment. Would have thought those would just get infected too. Where are they getting this done?
You are a lot more educated about this science than I am, but wishing I could understand it better because it sounds very important. The issue of infection/autoimmunity seems central to me.
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Pinelady
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Not in this country lou...LOL They won't give them enuf here to do the job...India, Sweden, Germany are haveing the best success..
But like everything else there are good guys and there are jerks.
This is where a friend of mine went and now taking a child there..
http://www.youtube.com/watch?v=0HZsIJJA0hY Human Embryonic Stem Cells, Dr. Geeta Shroff, India They are using lots of different stem cells now--not just embryonic..They appear to be riding in like a knight in armor but first she works to get rid of the infections. Treatment can take 3-6mths. And usually runs 15-40 grand. Best est. Which is not that bad when you consider you pay that much for a car...
http://www.ncbi.nlm.nih.gov/pubmed/21833894 Germany reports Good results with stem cells. An overall 85% 5-year-survival and 43% progression-free survival was seen, with 100-day-transplant-related-mortality (TRM) ranging between 1% (rheumatoid arthritis) and 11% (systemic lupus erythematosus and juvenile idiopathic arthritis).======This is where getting rid of the infections first could offer the best results...
And I don't know more than you--do you remember who from the IDSA cronies said that we had a ****/pee/urine disease? I can't remember...
But I know they are now saying the same thing about Cystic Fibrosis, etc. etc. LOL
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady
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THANK YOU CHINA... Furthermore, Western blots identified that the levels of the endogenous TPPP in the brains of scrapie-infected experimental hamsters were significantly reduced. http://www.ncbi.nlm.nih.gov/pubmed/21857997
PLoS One. 2011;6(8):e23079. Epub 2011 Aug 12. Molecular Interaction of TPPP with PrP Antagonized the CytoPrP-Induced Disruption of Microtubule Structures and Cytotoxicity. Zhou RM, Jing YY, Guo Y, Gao C, Zhang BY, Chen C, Shi Q, Tian C, Wang ZY, Gong HS, Han J, Xu BL, Dong XP. Source
State Key Laboratory for Infectious Disease Prevention and Control, National Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, People's Republic of China. Abstract BACKGROUND:
is a brain-specific unstructured protein with a physiological function of stabilizing cellular microtubular ultrastructures.
Whether TPPP involves in the normal functions of PrP or the pathogenesis of prion disease remains unknown.
Here, we proposed the data that TPPP formed molecular complex with PrP. We also investigated its influence on the aggregation of PrP and fibrillization of PrP106-126 in vitro, its antagonization against the disruption of microtubule structures and cytotoxicity of cytosolic PrP in cells, and its alternation in the brains of scrapie-infected experimental hamsters. METHODOLOGY/PRINCIPAL FINDINGS:
Using pull-down and immunoprecipitation assays, distinct molecular interaction between TPPP and PrP were identified and the segment of TPPP spanning residues 100-219 and the segment of PrP spanning residues 106-126 were mapped as the regions responsible for protein interaction.
Sedimentation experiments found that TPPP increased the aggregation of full-length recombinant PrP (PrP23-231) in vitro.
Transmission electron microscopy and Thioflavin T (ThT) assays showed that TPPP enhanced fibril formation of synthetic peptide PrP106-126 in vitro.
Expression of TPPP in the cultured cells did not obviously change the microtubule networks observed by a tubulin-specific immunofluorescent assay and cell growth features measured by CCK8 tests,
but significantly antagonized the disruption of microtubule structures and rescued the cytotoxicity caused by the accumulation of cytosolic PrP (CytoPrP).
Furthermore, Western blots identified that the levels of the endogenous TPPP in the brains of scrapie-infected experimental hamsters were significantly reduced. CONCLUSION/SIGNIFICANCE:
It was shown that ThT fluorescence quantum yield varies from 0.0001 in water at room temperature to 0.28 in rigid isotropic solution (T/η→0).
The deviation of the fluorescence quantum yield from unity in rigid isotropic solution suggests that fluorescence quantum yield depends not only on the ultra-fast oscillation of ThT fragments relative to each other in an excited state as was suggested earlier,
but also depends on the molecular configuration in the ground state.
This means that the fluorescence quantum yield of the dye incorporated into amyloid fibrils must depend on its conformation,
which, in turn, depends on the ThT environment.
Therefore, the fluorescence quantum yield of ThT incorporated into amyloid fibrils can differ from that in the rigid isotropic solution.
In particular, the fluorescence quantum yield of ThT incorporated into insulin fibrils was determined to be 0.43.
Consequently, the ThT fluorescence quantum yield could be used to characterize the peculiarities of the fibrillar structure, which opens some new possibilities in the ThT use for structural characterization of the amyloid fibrils. ----------------------- Thioflavin T acts as an antibiotic and as a cytokine reducer...So all this time they said they wanted to find the proteins and they used something they knew would not find it? --------------------- http://projectreporter.nih.gov/project_info_results.cfm?aid=7750609&icde=0 mtb directly regulatees memory T cells via the Toll like receptors 1 and 2. -------------------------- http://www.newswise.com/articles/umdnj-research-identifies-co-infection-that-complicates-tb-treatment They never did know what all was in adjuvants and now refuse to admit it so they don't have to treat... --------------------------- And they can't claim stupid....They knew way back when what relapsing fever was/is/did/could do....
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Pinelady
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http://www.ncbi.nlm.nih.gov/pubmed/21854463 2011 Aug 19 bioluminescent Borrelia provides a sensitive means to detect, quantify, and temporally characterize borrelial dissemination in a non-invasive, physiologically relevant environment and, more importantly, demonstrated a quantifiable infectivity defect for the bbk32 mutant.
What they would like us to believe is that the biolumen..inferes infectivity...After they have just shown us that it can be lost, but that does not mean not infected...
There is no amount of prion protein that is not infective. Of which Borrelia have 3 such proteins described as prion like.
-------------------- Suspected Lyme 07 Test neg One band migrating in IgG region unable to identify.Igenex Jan.09IFA titer 1:40 IND IgM neg pos 31 +++ 34 IND 39 IND 41 IND 83-93 + DX:Neuroborreliosis Posts: 5850 | From Kentucky | Registered: Dec 2008
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Gack. Something new to worry about. I already have an overload of worries. Now prion-like proteins. Oh no!!!
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