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Mel Thornburg, Sepsis
https://www.facebook.com/profile/1657389649/search/?q=sepsis

The thumbnail I used for this video is from Mel's Facebook, underneath she comments that it is One of Nostradaumas' depictions of destroying the serpent. Very fitting for what we are trying to do, wouldn't you agree?? ----------------------------------------------------------------------------------------------
February 23, 2016
The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3)
https://jamanetwork.com/journals/jama/fullarticle/2492881?fbclid=IwAR0HMBzVhwSkIYiahxdTFDN50OE3HkmGNklJI0gvxvZGvDMnk3n5xB1WosM

Reactivation of multiple viruses in patients with sepsis
https://pubmed.ncbi.nlm.nih.gov/24919177/

Lyme Bacteria Cyst formatiom
https://www.youtube.com/watch?app=desktop&v=lVmCa70bAxE&fbclid=IwAR1CT7C-fvmD5IEgxHdJamqf734sFGtJ5iGQN6yoYgep6sGHSHNSHVrZO90

My Horrific lyme disease blood
https://www.youtube.com/watch?v=Hbin5ZT6A5s

THE REAL CAUSE OF AIDS IMMUNE SUPPRESSION THEY GAVE US IN VACCINES!!!
WHY ALL VACCINES ARE INFECTIVE!!!
BECAUSE YOU ARE ALREADY INFECTED WITH IMMUNE SUPPRESSING STEALTH OF EPSTEIN BORRELIOSIS!
AND so called "Normal" Prion protein~Spirochetal Seed.
http://www.asianscientist.com/.../scientists-uncover-ebv.../
https://www.lymeneteurope.org/forum/viewtopic.php?f=13&t=5147&start=20&fbclid=IwAR1xxxho6mu9AwmsZvZezR1o_SSW0i4daGTPHl66dLD5iUgY0zU2FdCvrCg

Outer Membrane Vesicles from Brucella abortus promote bacterial internalization by human monocytes and modulate their innate immune response https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3506553/?fbclid=IwAR0_8N7LFEpniefed8_WnwI_oZMZgvowfCOdQE_SkB0_0gfS2QK8yEfabCQ AND YOU SAY THIS IS NOT SCIENCE? THEN WHAT IS IT? I CAN PRODUCE AN EXIT IN ALL SUFFERING THEIR SYNDROMES. IS THAT NOW NOT SCIENCE? DO YOU
CONCLUDE THE RESEARCH IS JUST LYING TO US?
The case for involvement of spiroplasma in the pathogenesis of transmissible spongiform encephalopathies.
http://www.ncbi.nlm.nih.gov/pubmed/24423635
J Neuropathol Exp Neurol. 2014 Feb;73(2):104-14. doi: 10.1097/NEN.0000000000000033.
Bastian FO.
Author information
Abstract
Spiroplasma
biofilm formation explains the role of these +++++++wall-less
bacteria+++++++++ in the pathogenesis of transmissible spongiform
encephalopathies (TSEs).
Spiroplasma embedded in the biofilm polysaccharide matrix
are
markedly resistant to physical and chemical treatment, simulating the
biologic properties of the TSE agent. Microcolonies of spiroplasma
embedded in biofilm bound to clay are the likely mechanism of lateral
transmission of scrapie in sheep and chronic wasting disease in deer via
soil ingestion. Spiroplasma in biofilm bound to the stainless steel of
surgical instruments may also cause iatrogenic transmission of
Creutzfeldt-Jakob disease. Sessile spiroplasma in biofilm attach to the
surface by curli-like fibrils, a functional amyloid that is important
for spiroplasma entering cells. Curli fibers have been shown to interact
with host proteins and initiate formation of a potentially toxic
amyloid that multiplies by self-assembly. In TSE, this mechanism may
explain how spiroplasma trigger the formation of prion amyloid.
This possibility is supported by experiments that show spiroplasma produce α-synuclein in mammalian tissue cultures.
The
data linking spiroplasma to neurodegenerative diseases provide a
rationale for developing diagnostic tests for TSE based on the presence
of spiroplasma-specific proteins or nucleic acid.
++++++++++
Research efforts should focus on this bacterium for development of
therapeutic regimens for Creutzfeldt-Jakob disease.+++++++++++++
-----------------------
http://www.ncbi.nlm.nih.gov/pubmed/23846702
Bpur,
the Lyme disease spirochete's PUR domain protein: identification as a
++++++++transcriptional modulator++++++ and characterization of nucleic
acid interactions.
Bpur, binds with high affinity to double-stranded DNA adjacent to the erp transcriptional promoter.
Bpur was found to enhance the effects of the erp repressor protein, BpaB.
+++++++++++
Bpur also bound single-stranded DNA and RNA, ++++++++++++with relative
affinities RNA > double-stranded DNA > single-stranded DNA.
--------------------
I really would like to hear your scientific explanation! I would also
like to hear Europe's explanation for slaughtering 200 Million cattle
and various assorted zoo animals and farm lots why they didn't bother to
treat the infections that cause it!
http://www.lymeneteurope.org/forum/viewtopic.php?f=13...
WHY IT WAS FROM INFECTIOUS VACCINES OF COURSE.
https://pubmed.ncbi.nlm.nih.gov/24793092/ OMVs are closed spheroid vesicles between 10 and 300 nm in diameter that are released by Gram-negative
bacteria in all growth phases [5], [6]. ^^^
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC544955/
The immunotherapy of Alzheimer's disease
http://molecularalzheimer.org/alzcyst1.html
SO WHAT YOU HAVE HERE IS FAILURE TO COMMUNICATE THE MECHANISMS, MORPHOLOGIES, AND TREATMENT FAILURES AND WHY!!!

ActionLyme.org Lyme Cryme Whistleblower's website
http://actionlyme.org/?fbclid=IwAR3kZZd-K1_Vtdt5dxjl2f7Z5bOuC-Wk5V6dwc9yz4Q2FPUOQzfOFkQopdo

Under Our Skin
https://underourskin.com/news/lyme-discoverer-willy-burgdorfer-breaks-silence-heated-controversy?fbclid=IwAR2CXHXmC6Q_JGR2fqcyi098DoZOZZ6NE02oYjuBZsOJ-_qOPRcVE5et0jw
Scientists reveal major players in severe muscle damage caused by sepsis
https://www.news-medical.net/news/20151217/Scientists-reveal-major-players-in-severe-muscle-damage-caused-by-sepsis.aspx?fbclid=IwAR1VbTYhhDGFDS-kOmjdCOVE6J1jfrBgVjw6RCXN0xrIyBynhlWJeFP6vBY

Kathleen Dickson--[REFERENCED, ALTHOUGH THAT NEVER SEEMS TO HELP, PEOPLE GET FREAKED OUT OVER REFERENCES OR SCIENTIFIC CITATIONS AND THEIR BRAINS SHUT OFF]:
Feedback from diverse sources is telling me I am failing to make the connection between Lyme and CFIDS again. It's OspA or fungal antigens that are not typically classified as "toxins" perhaps mainly because in the past it was hard to determine the structure of a lipoprotein, but now we go with FUNCTION, which is TLR2-agonist. At the same time, not everyone with CFIDS has Lyme.
Your post-sepsis syndrome (1, PSS website) could have been initiated by something else. It does not matter in the end, because we are all treated like trash, and the data says we are all dealing with reactivated herpesviruses, compounded by expanded tolerance to other infections like candida and whatever other bacteria and common viruses.
You're all, say "carriers," perhaps of Strep, various herpes, etc.
But mechanisms, no, we have this down. We know how fungal antigens turn off the immune response (2, Harding & Radolf);
gum up the normal immunity works (3, Wormser); how OspA acts like a BCL2 molecule, inhibiting NORMAL apoptosis in an infected cell (4, 101016.htm, numerous) ;
we know fungi adhere to mitochondria (5), causing fatigue, we know how EBV hijacks this same cell machinery (6) ; we know how it has been known since ancient times that fungi injected together with viruses activates the viruses (1953) (7) ;
that they put Thimerosal in vaccines for this reason - to inhibit fungi – (8); that BigPharma has reported that kids could be getting the viruses (9);
the CDC has reported that immunosuppressed kids should not get live attenuated viruses, but fully dead ones (10); and we know the CDC has flat out committed research fraud while trying to claim mycoplasma is not involved in Chronic Fatigue Syndrome by throwing out the very cells to which mycoplasma adhere and hide within, before analyzing for DNA and finding none (11);
and we have seen several mechanisms where TLR2-agonist tolerance expands to viruses and bacteria (12 Medvedev, 13 Harding, 14 newer one).
That the CDC would do that is CRUCIAL to your understanding that they are committing FRAUD on behalf of the Bigs.
1) http://www.sepsisalliance.org/sepsis/post_sepsis_syndrome/
2) http://www.jimmunol.org/cgi/content/full/167/2/910
3) http://www.ncbi.nlm.nih.gov/pubmed/10865170
4) Numerous, search for apoptosis: http://actionlyme.org/101016.htm
5) Numerous, search for mitochondria: http://www.actionlyme.org/101016.htm
6) Numerous, search for mitochondria or Epstein-Barr: http://actionlyme.org/101016.htm
7) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2136329/…
😎 http://www.nytimes.com/…/experts-say-thimerosal-ban-would-i…&
9) "Finally, there is the risk that the virus may not be fully or completely inactivated or attenuated and thus, the vaccine may actually cause disease." http://patft.uspto.gov/netacgi/nph-Parser…
10) http://www.cdc.gov/mmwr/preview/mmwrhtml/00053391.htm
11) CDC throwing out blood cells to which mycoplasma adhere so as to falsely claim no mycoplasma are associated with ME/CFS : http://jmm.sgmjournals.org/cgi/pmidlookup…
12) Medvedev http://www.jimmunol.org/content/170/1/508.long
13) Harding on bacterial-viral co-infection: "This novel mechanism, whereby TLR2 inhibits IFN-I induction by TLR7/9, may shape immune responses to microbes that express ligands for both TLR2 and TLR7/TLR9, or responses to bacteria/virus coinfection."
http://www.ncbi.nlm.nih.gov/pubmed/22227568
14) newer one on same topic as Harding’s above: http://www.nature.com/cmi/journal/v9/n4/full/cmi201211a.html

In other words in low pH and Immune Suppression they actually have activated infections--not imaginary ones!
In Immune Suppression they most likely will NOT make antibodies on criminal antibody tests to say pos.
95% of the pops have latent activated Epstein Borreliosis they rarely treat. The most highly associated Cancer ahum virus there is.
And they also have recombination of infections and junk genes they never treat already growing in their skin, guts, and brains from decades of criminal vaccines and junk gene GMO.
KD : This was one of the reports we gave the legislators aids in DC; the reason I am posting it is because of the frequency with which we see posts and questions about mycoplasma. So, that concept is becoming popular- mycoplasma in Lyme. But what people are not understanding is that Lyme and LYMErix set up the CONDITIONS (fungal antigen tolerance or TLR2 agonist tolerance, which spreads to other TLR agonists...) that allow the fatiguing mycoplasma in the blood to flourish, robbing you of oxygen. So read the criminal charge sheets on OhioactionLyme.org because we cover all this in multiple places.
The NIH agrees and has published that *** it is this fungal antigen tolerance and immunosuppression from being exposed to shed OspA-ish blebs *** that is driving the disease. This is why OspA vaccination is the same disease as Chronic Lyme. It's really an AIDS or post-sepsis syndrome.
And see more at:
http://www.actionlyme.org/EXOSOMES_BLEBS_VESICLES.htm

J Biol Chem. 1999 Nov 19;274(47):33419-25.
Toll-like receptor 2 functions as a pattern recognition receptor for diverse bacterial products.
Lien E1, Sellati TJ, Yoshimura A, Flo TH, Rawadi G, Finberg RW, Carroll JD, Espevik T, Ingalls RR, Radolf JD, Golenbock DT.
Author information
Abstract
Toll-like receptors (TLRs) 2 and 4 are signal transducers for lipopolysaccharide, the major proinflammatory constituent in the outer membrane of Gram-negative bacteria. We observed that membrane lipoproteins/lipopeptides from Borrelia burgdorferi, Treponema pallidum, and Mycoplasma fermentans activated cells heterologously expressing TLR2 but not those expressing TLR1 or TLR4. These TLR2-expressing cells were also stimulated by living motile B. burgdorferi, suggesting that TLR2 recognition of lipoproteins is relevant to natural Borrelia infection. Importantly, a TLR2 antibody inhibited bacterial lipoprotein/lipopeptide-induced tumor necrosis factor release from human peripheral blood mononuclear cells, and TLR2-null Chinese hamster macrophages were insensitive to lipoprotein/lipopeptide challenge. The data suggest a role for the native protein in cellular activation by these ligands. In addition, TLR2-dependent responses were seen using whole Mycobacterium avium and Staphylococcus aureus, demonstrating that this receptor can function as a signal transducer for a wide spectrum of bacterial products. We conclude that diverse pathogens activate cells through TLR2 and propose that this molecule is a central pattern recognition receptor in host immune responses to microbial invasion.... Outer Membrane Vesicles Derived from Escherichia coli Up-Regulate Expression of Endothelial Cell Adhesion Molecules In Vitro and In Vivo.

http://www.plosone.org/.../info%3Adoi%2F10.1371%2Fjournal...
PLoS One. 2013;8(3):e59276. doi: 10.1371/journal.pone.0059276. Epub 2013 Mar 14.
Kim JH, Yoon YJ, Lee J, Choi EJ, Yi N, Park KS, Park J, Lötvall J, Kim YK, Gho YS.
Source
Division of Molecular and Life Sciences, Pohang University of Science and Technology, Pohang, Republic of Korea.
Abstract
Escherichia coli, as one of the gut microbiota, can evoke severe inflammatory diseases including peritonitis and sepsis.
Gram-negative bacteria including E. coli
constitutively release nano-sized outer membrane vesicles (OMVs).
Although E. coli OMVs can induce the inflammatory responses without live bacteria,
the effect of E. coli OMVs in vivo on endothelial cell function has not been previously elucidated.
In this study, we show that bacteria-free OMVs
increased the expression of
endothelial intercellular adhesion molecule-1 (ICAM-1),
E-selectin and
vascular cell adhesion molecule-1,
and enhanced the leukocyte binding
on human microvascular endothelial cells in vitro.
Inhibition of NF-κB and TLR4
reduced the expression of cell adhesion molecules in vitro.
OMVs given intraperitoneally to the mice induced ICAM-1 expression and neutrophil sequestration in the lung endothelium,
and the effects were reduced in ICAM-1(-/-) and TLR4(-/-) mice.
When compared to free lipopolysaccharide,
OMVs were more potent in inducing both ICAM-1 expression
as well as leukocyte adhesion in vitro,
and ICAM-1 expression and neutrophil sequestration in the lungs in vivo.
This study shows that OMVs potently up-regulate functional cell adhesion molecules
via NF-κB- and TLR4-dependent pathways,
and that OMVs are more potent than free lipopolysaccharide.

Effect of high dose vitamin C on Epstein-Barr viral infection
https://pubmed.ncbi.nlm.nih.gov/24793092/

Pt. was totally seronegative and yet pt. is ate up in spirochetal disease of various morphological forms.
http://www.lymeneteurope.org/forum/viewtopic.php?f=5&t=5548
There is no such thing as a virus. Never was. There are legions of
morphological forms spirochetal disease they gave us for decades
conforms to and that is all
Passive immunotherapy of sporadic Alzheimer's disease offers the potential of reversing the pathologic accumulation of cerebral amyloid
beta peptide. To date the only preparation of human anti-amyloid beta
peptide antibodies that have been reported to reverse cognitive defects
in patients with sporadic Alzheimer's disease are polyclonal
anti-amyloid beta peptide antibodies contained in human IVIg. Selection
of human anti-amyloid beta peptide antibodies for clinical trial can be
tested for therapeutic effect in vivo by their treatment of
immunodeficient APP-transgenic mice.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC544955/
2004 BUT WHAT'S 11 YEARS WHEN A MEDICAL MAFIA HAVE NO EARS......EUTHANAZING YOU IS MUCH MORE FUN!!!

'Doesn't the earlobe contain a host of smorgasbord goodies like cartilage collagen & whatnots?'
Mel Thornburg
Yes Lida Mattman said they thrive on collagen/fat. Others explain thriving on Calcium. Which is why people's noses rotted off from Syphilis before they destroyed everyone's immune systems. Now you get cancers, sindumbs, and psych they refuse to treat for the cause.
MJ was clearly severely infected. His white lesions and destruction of the nose cartilage is suffering beyond belief.

The Emerging Role of Vitamin C as a Treatment for Sepsis
https://pubmed.ncbi.nlm.nih.gov/31978969/

https://www.livescience.com/47387-sepsis-diagnosis-treatment-research-nigms.html?fbclid=IwAR3pdGIX5PKj4fizHNHn8xPft9zAI5G8yOB45awQnX1mp28VmQ2UtTMMsPk

KD: These fungal toxins shed all the time by Borrelia (also called blebs or exosomes) turn off the antibody response, cause immunosuppression, inhibit apoptosis of infected cells, and help reactivate Epstein-Barr, etc, herpes. Obviously Yale lied about all this, they lied about OspA being a vaccine and they lied about the testing they used to qualify it. If Borrelia shed fungal antigens all the time, cause immunosuppresion and what the NIH calls post-sepsis syndrome with reactivated herpes viruses and other infections of all kinds, then you know the CDC is lying about the 2-tiered testing critera (Dearborn), which states that Lyme is the complete opposite - an HLA-linked hypersensitivity response. If this was designed as a bioweapon, the intention was for it to be a stealth disabler, or a disease that does not show which was the originating infection that later resulted in an "overwhelmed" immune response or turned off the immune response.
This US Govt lies their faces off about everything, but worse, they're stupid and this was all transparent and discoverable.
http://actionlyme.org/?fbclid=IwAR0fxotG1VN3hnKDEbqOgNg28ZdEzqzAeiekkj9OqLdg5vsOnaH-wzubqhs

Stealth infected parasites
https://www.lymeneteurope.org/forum/viewtopic.php?f=6&t=4840&p=36246&fbclid=IwAR0PkM3gBOasWs1dTKxdgWkrdSCPFUxbisjS7W36PbXGwCQsazFT4vKwRVM#p36246

Interestingly, the fibrillar seeds of all amyloidogenic proteins functioned as seeds.

Remarkably, knockout of PrPC suppressed the proliferation of internalized bacteria
and increased the expression of cytokines such as interleukin-1β.
http://www.lymeneteurope.org/forum/viewtopic.php?f=13...
Immune suppression 100 times we have to repeat!

https://www.lymeneteurope.org/forum/viewtopic.php?f=13&t=5147&start=10&fbclid=IwAR1vKxwyZYv6K58uM_pv0FVukI_8pMC8FUON-zcS3claO74NMUWB15Gy5GI

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