Blowing the Whistle at the FDA, Jan 2001, exposing Dearborn and how OspA causes immunosuppression rather than, "was a vaccine."
 


9 July 2017

Home


1988 Steere says Lyme is like a B cell leukemia

Assoc Blogs-n-Webs:
TruthCures.org
badlymeattitude.com/
immune2lies.com/
researchfraud.com/
may12.org
meadvocacy.org/
truthbetoldx81
lymecryme
crymedisease
theothersideofthestretcher
rjspiritualityandthe
truthaboutlymedisease
JC-LilnkedIn
KD-Linkedin.com
LD-LinkedIn
JC-academia.edu

KD-academia.edu

 


CDC "SPIDER"

Fungal Exosomes Inhibit Apoptosis

IDSA: "Vaccines serve the mfgs, not their victims"

RICO_filed_USDOJ

BlumenthalAntiTrust Lawsuit

Exosomes, Blebs

Spirochetal_Dementia


PDFs
CDC Admits Fraud, 2016
Dattwyler, 1988
Golightly, 1988
Dressler, 1994
BarbourFish, 1993
Dearborn, 1994
BarbourFishpdf.pdf
 

Pathogenic Fungi

Bush's warcrimes, Oct 2000

Trainer

170708

 



CHAPTER 10;  Biomarkers of Disease or Illness Processes discovered in Chronic Lyme victims... by the very same people who now claim that these phenomena are the result of a group internet telekinetic hoax or a self-psychogenic energy weapon.  
 

This is data the Lyme crooks (Yale/NYMC/ALDF/IDSA/Kaiser cabal) refused to turn over to the Connecticut Attorney General for a year and a half before settling out of court.



SOME of the MARKERS discovered by the Yale/UConn/NYMC/IDSA Crooks: 

GFAp in the spinal fluid of Lyme victims, shows glial cell degradation:
http://www.ncbi.nlm.nih.gov/pubmed/8740104

Robert T. Schoen, when trying to sell the Yale vaccine, LYMErix, Yale Rheumatology, Annals of Internel Medicine, Vol 132, No 8:
http://www.annals.org/content/132/8/661.full.pdf+html

"Other peripheral neuropathies and Lyme meningitis are also seen at this stage.  In late-stage disease, the central nervous system may be involved.  A new diagnostic test measuring glial fibrillary acidic protein in cerebrospinal fluid may prove to be a useful tool for measuring such involvement (20)." 



anti-gangliosides:
http://iai.asm.org/cgi/reprint/63/10/4130?view=long&pmid=7558329

anti-heat shock proteins (seen in Multiple Sclerosis):
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=9375512[uid]

anti-phospholipid (Steere and Lupus; "L2 Diagnostics"):
http://www.ncbi.nlm.nih.gov/pubmed/3408508?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/8410057?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

QEEG:
http://www.ncbi.nlm.nih.gov/pubmed/7554300

HLAs:


Quinolinic acid in the CSF (excitotoxin):
http://www.ncbi.nlm.nih.gov/pubmed/1531156

Epstein-Barr like lymphocyte changes:
 
Duray at IDSA, 1989,  and Duray at Cold Spring Harbor, 1992

SPECT (hypoperfusion or reduced blood flow to the brain):
http://www.ncbi.nlm.nih.gov/pubmed/9409364

NO in the brain:
http://www.ncbi.nlm.nih.gov/pubmed/7513330

MMPs:
http://www.ncbi.nlm.nih.gov/pubmed/9466528


dysregulated cytokines (interleukins, TNF, etc):

circulating free immune complexes (likely associated with LYMErix vascular adverse events):

histological changes (autopsy and biopsy):

EMGs (electromyography shows nerve damage):

autoeactive T cells, spinal fluid antibodies and decomplexing (Schutzer, Coyle, Sigal, Molloy, Roland Martin at the NIH),

MRI-gad (gadolinium uptake in the brain- a sign of active meningitis). 


A table was presented in the previous chapter on the IDSA Reviews.  This chapter is an expansion and an explainer regarding how suppressing these results effect (result in) illnesses that are far more serious than "Steere's bad-knees" or even real cancer outcomes.

 

The following tests were not used by Mark Klempner in his Neuroborreliosis Standard-of-Care "Study." Instead Klempner used an invalidated "Fibromyalgia Impact Questionaire."  The validation of the questionnaire showed there were two different diseases, invalidating its use for Lyme (not that it matters because check-lists are for psychiatric fairies).  To not use valid methods to detect valid signs of illness, and then to turn around in their "guidelines" for IDSA to propose that there are "no objective signs of illness in chronic Lyme" is outright criminal FRAUD.  If this research was produced on the taxpayers dime, these individuals who committed these crimes are personally accountable.

Summary of the Crook's Cold Spring Harbor Conference:
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770

COLDSPRINGHARBOR.htm   Chapter by Jorge Benach on Neurologic Lyme- not detected by the Dearborn method, as previously established in Chp 3 on what Allen Steere did in Europe to change the diagnostic standard ("ROC" is the Elephant Diagnostics Rule or is the equivalent of saying "the only kind of disease is inflammatory," when Lyme literally is a double "stealth disabler" of the neurologic type, says the Department of Energy and the Department of Defense at Brookhaven, and directly: "ticks could be used to spread diseases," says the US Military.

So, you are getting this information from top government sources.

==========================================================================

 

Monkey Histology  - Experiments with non-human primates infected with borrelia spirochetes and then autopsied.

What this adds to the biomarkers in some basis for the loss of never function as detected by EMG in Lyme victims.  We think if the monkeys suffered this nerve damage, than what Lyme victims complain of is not caused by a Viagra deficiency.

 

FROM:
"The Lyme Disease Dilemma," 2000, November, First ActionLyme website [given in full text hard copy to Yale's James Phillips (88 Noble Ave., Milford, CT), in November of 2000]:
Monkey Nerve Autopsy Data http://www.geocities.com/kmdickson0308/3-17.txt
Mainpage: http://www.geocities.com/kmdickson0308/lyme-dilemma.html

"Sensory ganglia of the dorsal root and trigeminal ganglia of animals J 831 and
K 216 had individual neurons that immunostained positive with anti-Bb 7.5kD
lipoprotein mAb (fig 16).  These neurons were swollen and were undergoing
chromatolysis.  The dorsal root ganglia of the thoracic and cervical regions
were especially affected.
  Nerve sheath fibrosis within the spinal cord was
limited to the thoracic segment in animal J 831". =
FIBROMYALGIA ??

 

1) Roberts ED, Bohm RP Jr, Lowrie RC Jr, Habicht G, Katona L, Piesman J, Philipp MT.
Pathogenesis of Lyme neuroborreliosis in the rhesus monkey: the early disseminated and chronic phases of disease in the peripheral nervous system.
.pdf file→ http://www.journals.uchicago.edu/doi/pdf/10.1086/515357  (note:  no T cells involved)


The histopathologic and immunohistochemical features of early and late neuroborreliosis of the peripheral nervous system were investigated in rhesus macaques infected with the JD1 strain of Borrelia burgdorferi. Infection was proven by culture or polymerase chain reaction analysis of skin biopsies and indirectly by Western blot analysis. Three months after infection, neuritis involving multiple nerves was the most consistent neurologic manifestation. Both macrophages and B lymphocytes but not T lymphocytes were present in the cellular infiltrates. Axonal structures surrounding infiltrates had changes consisting of demyelination and axonal phagocytosis. Some of the Schwann cells in lesions stained with anti-nitrotyrosine and anti-tumor necrosis factor-alpha antibodies. B. burgdorferi, or antigens thereof, were visualized immunohistochemically within macrophages. Forty-six months after infection, the most common changes were regenerative, whereas neuritis was infrequent. Aberrant axonal regeneration, irregularly sized myelinated fibers, and fibrosis were frequently observed. Possible mechanisms to explain the appearance and subsidence of Lyme neuritis are discussed.


2) England JD, Bohm RP Jr, Roberts ED, Philipp MT.
Lyme neuroborreliosis in the rhesus monkey.

3) Roberts ED, Bohm RP Jr, Cogswell FB, Lanners HN, Lowrie RC Jr, Povinelli L, Piesman J, Philipp MT.
Chronic lyme disease in the rhesus monkey.

 

There is plenty of data on Lyme/Borreliosis in monkeys for the American Medical Establishment to read to inoculate themselves against further nonsense by the Infectious Diseases Society of America (which has been hijacked by a cabal of medical fraudsters).  If psychiatrists as the witches and warlocks and think they can perform some incantations /divinations / hexes to come up with their ethereally-derived, preternatural causes of illness, the histology/autopsy reports are the garlic cloves MDs should wear around their necks.

 



Human Histology

/IDSA_CLINIPATH_DURAY.htm

 

I strongly recommend reading these IDSA 1989 Suppl 6 reports (Chp 9), since they tell a very different story as well as serve as a pretty significant platform for the indictments of these Lyme crime perpetrators not only as regards the shocking statements that they made in 1989 but because of the subsequent 180 degress change in their own position against the backdrop of the harassment, slander, libel, perjury, false medical board persecutions and false criminal charges show scientific fraud with intent to cause harm. 

If some other inconvenient disease comes around, people who do not suffer Lyme but get the next one had better worry because we for years before the Bush Dictatorship tried, despite our extreme illness, to be something close to real activists.  We did some protests, which are harder and harder to perform these days, without the US SS, the Storm Troopers, initiating violence upon the people for all the fun and tasering and chains and jails and so on that such brainless, evil morons enjoy.  These cop-types, these moron SWAT wannabees in the jails, these idiot "security" skinheads don't even realize that have no equivalent in the animal world.  No other species has a sub-team of punishers.  Henry Kissinger even called them "dumb, stupid animals to be used as pawn for political purposes."
 

 

Always keep in mind as we go through these markers that IDSA bases their "guidelines" on Mark Klempner ridiculous "Fibromyalgia Impact Questionaire" assessment of whether or not the standard of care for neuroborreliosis (30 days of intravenous ceftriaxone) was adequate or enough treatment.  Only 1/3 of Klempner's victims had had previous intravenous antibiotics, which did not make his study a long term or repeat treatment study. Thirty days of ceftriaxone was the standard of care at that time.  The other drug Klempner offered was 60 days of oral antibiotics but oral antibiotics are not for central nervous system infections, which is why the ceftriaxone therapy was designed by these IDSA gang members several years prior to Klempner's "long term" nonsense in the first place.

That IDSA so ferociously defends their right not to treat Lyme/Borreliosis, clearly a condition that has never arisen before in the history of medicine, should cause all parties to investigate every possible deeper reason for this craziness.  It can't be about antibiotic resistance genes in the environment since the swine lagoons and the poor hospital hygiene are orders of magnitude bigger contribution to antimicrobial resistance genes in the environment.

IDSA's craziness probably more has to do with the denial of the existence of chronic Lyme, especially latent Lyme, which appears to have been activated by OspA vaccination.  Upon closer examination (next topic), LYMErix Disease - the immune suppression outcomes of LYMErix or OspA vaccination - likely is "Chronic Lyme Disease."  In other words, these bastards injected people with Pandora's Box (New Great Imitator) and then lied about the results, and they CONTINUE to lie about Lyme, since this crime is getting huger and huger with every crooked move they make to cover up their first crimes.  The latest move of course is the production of the 2006 IDSA "guidelines."  These bogus IDSA 2006 "guidelines" follow the IDSA 2000 "guidelines" (before the release of the Klempner report), which demonstrates a pattern of prescribing less and less treatment for Lyme and further narrowing the disease definitions since Dearborn.  Soon they will say, "Borrelia burgdorferi is not a spirochete."

We are going to show that the injury to American citizens is vast and cuts across many chronic and deadly disease (ALS, MS, cancer, Lupus, HIV, "chronic fatigue syndrome" and "fibromyalgia," etc...) which were simultaneously short-changed, losing at least a decade in non-discovery, not the least of which was that a tick saliva component, SALP15, blocks the HIV virus.  This fraud has cost Uncle Sam untold billions in Social Security Disability benefits alone, when the likes of Kaiser-Permanente (et al) should have paid for the relapsing IV treatment as needed, allowing us to maintain our health and our jobs and our private insurance.

Kaiser-Permanente and this cabal, the ALDF.com and their CDC and NIH participants and insiders, and their insider biotech insider CFR-esque venture cap banker investors, defrauded Uncle Sam out of untold billions, not to mention the cost in humanity here and abroad. 

The world is going to know about it.

 

=================================================================

 

BIOMARKER-- "Epstein-Barr-like transformed cells" and the immune suppression that is probably at the crux of Lyme Disease and LYMErix Disease
 

MYSTERIOUS MUTATED CELLS, investigated further:
Mycoplasma and their link to cancer
http://www.molecular-cancer.com/content/5/1/6


Recall from Chapter 3 that OspA is a Pam3Cys lipoprotein - something found only in fungi (mycoplasma and mycobacteria) Lyme, HIV, Brucella, and E. coli and Foot and Mouth Disease to the best of our knowledge.

 

Paul Duray and his mutated lymphocytes-

at the 1992 Cold Spring Harbor crooks' conference!!
More about this below re mycoplasma

 

"On occasion, these atypical-appearing large lymphocytes have been misinterpreted in biopsy by several laboratories as cells of a malignant lymphoma or leukemia.  Bb antigens, then, may stimulate growth of immature lymphocytic suibsets in some target organs, as well as in the cerebrospinal fluid (Szyfelbein and Ross 1988).  Usual bacterial infections do not produce such lymphocytic infiltrates in tissue.  These immunoblastoid cells in Bb infections at times resemble those found in Epstein-Barr virus infections.  Does Bb reactivate latent virus infections in tissues?  Do some tick inocula harbor simultaneous infectious agents (ixodid ticks can harbor Rickettsiae, Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing multi-agent infections in some hosts?  Further studies can clarify these issues by mans of tissue-based molecular probe analysis." -  Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor Crooks' Conference, published in Steve Schutzer's Lyme Disease: Molecular and Immunologic Approaches.
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770/ref=sr_1_2?ie=UTF8&s=books&qid=1214848669&sr=1-2

 

 "These look like Epstein-Barr transformed or mutated lymphocytes... I wonder if Bb infection reactivates latent virus infections in tissues? "- Paul Duray.

I wonder if it's related to inhibition of the auto-kill kinases in latently, virally-infected cells that would otherwise undergo auto-kill when the viruses started replicating again, but don't, due to the suppression of such functions caused by these fungal lipopeptides?

I wonder if the MS-like and ALS-like outcomes are a result of the immune suppression caused by such fungal infections (as OspA)?

I wonder if due to OspA or the shed antigens, latently infected cells which would otherwise commit suicide if Epstein-Barr started replicating out of control, DON'T auto-kill themselves... and thus were Activated Latent Viral Infections?

And if these outcomes are not caused by Feminocatastrophimyalgia or antibiomania?

 

 

 

Pam3Cys fungal lipopeptides and their possible contribution to immune suppression and fatigue:

Pam3Cys (OspA/HIV's gp120 ? and gp41/mycoplasma) news, all on MedLine

 

Mycoplasmal infections changing membrane potential of erythrocytes:

Once a person is infected with Lyme, that causes immune suppression, even according to Gary Wormser, such that the tolerance is to mycoplasma-like Pam3Cys lipoproteins (we haven't investigated the other antigen type-tolerances):
http://www.ncbi.nlm.nih.gov/sit....FromResult=1471973

If you can't fight the Pam3Cys lipoproteins from Lyme because your body doesn't see them any more (you have become "TOLERIZED"), then any other old bug with similar surface antigens might not be identified by the Lyme-infected person's defense system and could spread UNDETECTED by an antibody method. I am thinking mycoplasma in the blood:
 

1) Osmotic fragility of erythrocytes was tested in weaned pigs experimentally infected with Eperythrozoon (E.) suis. Acute eperythrozoonosis of splenectomized pigs led to an increase of osmotic fragility. It is supposed that E. suis infection causes a structural change in erythrocyte membrane. Possible mechanisms of this cell membrane injury are discussed.


MEDLINE results from "mycoplasma and RBC and membrane"

 

FROM:  http://iai.asm.org/cgi/reprint/30/2/538?view=long&pmid=6777306

 

Actually we wonder if this could lead to the "chronic fatigue" business. If membrane potential is compromised, there might be a problem with oxygen transfer, which anyone with Chronic L/CFIDS/FM will tell you, is the essence of it.  There may be other markers associated with the fatigue, since as anyone with these diseases will tell you, is just like the flu- just like the flu in the TIREDNESS, the inability to move limbs, etc, with anything other than monumental effort.  It's a "toxic-sick" sensation.  Here we see the very integrity of the RBCs compromised by mycoplasma:



 

 

Mycoplasma adhering to, embedding intoerythrocytes
Click on image to view larger version.

http://iai.asm.org/cgi/content/full/76/1/71/F1

Figure 1


FIG. 1. Scanning electron micrographs of sheep (A) and chicken (B) erythrocytes after in vitro infection with a clonal derivative of M. gallisepticum strain Rlow. The arrows indicate mycoplasmas or imprints of mycoplasmas appearing to sink into the erythrocyte surface.

 

I would say mycoplasmal infections distort the shape of erythrocytes, no?  Anyone with Chronic Fibrofemzalgilyme will tell you that we have normal hemoglobin but we're so tired, how could our blood cells possibly be getting adequate oxygen to our cells??

Since we know we're not making up our symptoms, we knew there would be discovered scientifically valid explanations or at least scientifically scientific and not sooth-sayin crystal-ballific explanations.

Right.  And those are just erythrocytes.  I'm thinking IDSA is going to be somewhat regretful for having deployed the Quija-Boarders, the American Psychiatrogenic  Associashin, cuz in having laid bare the scientific incredibility of psychiatry, I'm thinking they'll wish they had maintained the option of the criminal insanity defense.

 

Remember, now:  increases in mycoplasmal infection in the blood caused by the tolerization due to chronic spirochetal blebbing in chronic Lyme victims (chronic Lyme is chronic because it chronic) is not a thing looked for in chronic fatigue patients. Psychiatrists are deployed instead.  That would be because a psychiatrist would not know an SEM from an SEX.  It would be fun to create our own Rohrshach images out of these infectious diseases graphics to see if psychiatrists have any potential at all to be scientists, or rather, to discover what is the nature of their inability to see that what they do is closer to a religion or a cult than a science.


 

2) Gary Wormser reporting the blunting of the immune response in vaccinated animals:
http://www.ncbi.nlm.nih.gov/pubmed/10865170?ordinalpos=5&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
 

"OspA interferes with the response of lymphocytes to proliferative stimuli including a blocking of cell cycle phase progression."

 

3) Barbour and "Immune System Overhwhelmed," US Patent 6,719,983-

"2.1 Methods of Treatment

"An important aspect of the invention is the recognition that Borrelia VMP-like sequences recombine at the vls site, with the result that antigenic variation is virtually limitless. Multiclonal populations therefore can exist in an infected patient so that immunological defenses are severely tested if not totally overwhelmed."

- - - - - -

"He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime. "It's using some sort of stealth-bomber-type mechanism," he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. Explains Barbour: "It's like a bacterial Star Wars defense program," in which released surface proteins might intercept incoming host antibodies keeping the spirochetes safe from immunological attack."
--
1996, The Crooks.

 

You see. Chronic Lyme is chronic because it is chronic.

 

 

OspA from Borrelia and the Mycoplasma-  affect TLR2s and not TLR4s:


THIS NOT MENTIONED BY CORIXA IN THEIR AD ABOUT THEIR "NIH BIODEFENSE CONTRACT"- 

TLR2's involvement in the immune response (below)? 
In the CORIXA NIH Biodefense Contract, they only mention TLR4.

We wonder why that is??

 

"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."   http://www.jimmunol.org/cgi/content/full/173/4/2683
 



"TLR2 may form heterodimers with TLR6 to identify diacylated lipoproteins, while TLR2 works in concert with TLR1 to recognize triacylated lipoproteins such as OspA." -- Yale's Erol Fikrig
http://www.ncbi.nlm.nih.gov/pubmed/12804162?ordinalpos=6&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

 

4) More about how OspA or LYMErix suppresses the immune response:

The Journal of Immunology, 2004, 173: 2736-2745.
Copyright © 2004 by The American Association of Immunologists

Tolerance Induced by the Lipopeptide Pam3Cys Is Due to Ablation of IL-1R-Associated Kinase-11

Maciej Siedlar*,{dagger}, Marion Frankenberger{ddagger}, Elke Benkhart*,{ddagger}, Terje Espevik§, Martina Quirling, Korbinian Brand, Marek Zembala{dagger} and Loems Ziegler-Heitbrock2,{ddagger},||

* Institute for Immunology, University of Muenchen, Muenchen, Germany; {dagger} Department of Clinical Immunology, Jagiellonian University Medical College, Kraków, Poland; {ddagger} Clinical Cooperation Group "Inflammatory Lung Diseases" (Institute for Inhalation Biology, GSF National Research Center and Asklepios Fachkliniken, München-Gauting), Gauting, Germany; § Institute of Cancer Research and Molecular Biology, Medisinsk Teknisk Senter, Trondheim, Norway; Institute of Clinical Chemistry and Pathobiochemistry, Klinikum rechts der Isar, Technische Universität, München, Germany; and || Department of Microbiology and Immunology, University of Leicester, Leicester, United Kingdom

"Although a single ligation of TLRs induces responses such as TNF production, repeated ligation will lead to a loss of response, i.e., the cells become tolerant."   http://www.jimmunol.org/cgi/content/full/173/4/2736
 

 

5)
"Signaling through TLR-2 by lipoproteins may represent a double-edged sword for host responses to chronic intracellular pathogens such as M. tuberculosis. Short-term signaling through TLR-2 activates macrophages and initiates acute inflammation that may help control initial infection. In contrast, prolonged TLR-2 signaling in macrophages results in down-regulation of certain critical immune functions, such as MHC-II Ag processing. M. tuberculosis infects, survives, and persists in macrophages. The ability of M. tuberculosis to survive acute inflammation positions the bacilli to take advantage, through secretion of lipoproteins such as LprG and LpqH, of this down-regulation of macrophage immune function."   
http://www.jimmunol.org/cgi/content/full/173/4/2660    

 

Seems like pretty bad news, don't it?

 

6) Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via Immunosuppression"
Infect Immun.
2003 July; 71(7): 3979–3987.

Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via Immunosuppression
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12819085:

Isabel Diterich,1 Carolin Rauter,1 Carsten J. Kirschning,2 and Thomas Hartung1*

Biochemical Pharmacology, Faculty of Biology, University of Konstanz, Konstanz,1 Institute of Medical Microbiology, Immunology and Hygiene, TU Munich, Munich, Germany2

 

If left untreated, infection with Borrelia burgdorferi sensu lato may lead to chronic Lyme borreliosis. It is still unknown how this pathogen manages to persist in the host in the presence of competent immune cells. It was recently reported that Borrelia suppresses the host's immune response, thus perhaps preventing the elimination of the pathogen (I. Diterich, L. Härter, D. Hassler, A. Wendel, and T. Hartung, Infect. Immun. 69:687-694, 2001). Here, we further characterize Borrelia-induced immunomodulation in order to develop a model of this anergy. We observed that the different Borrelia preparations that we tested, i.e., live, heat-inactivated, and sonicated Borrelia, could desensitize human blood monocytes, as shown by attenuated cytokine release upon restimulation with any of the different preparations. Next, we investigated whether these Borrelia-specific stimuli render monocytes tolerant, i.e. hyporesponsive, towards another Toll-like receptor 2 (TLR2) agonist, such as lipoteichoic acid from gram-positive bacteria, or towards the TLR4 agonist lipopolysaccharide. Cross-tolerance towards all tested stimuli was induced. Furthermore, using primary bone marrow cells from TLR2-deficient mice and from mice with a nonfunctional TLR4 (strain C3H/HeJ), we demonstrated that the TLR2 was required for tolerance induction by Borrelia, and using neutralizing antibodies, we identified interleukin-10 as the key mediator involved. Although peripheral blood mononuclear cells tolerized by Borrelia exhibited reduced TLR2 and TLR4 mRNA levels, the expression of the respective proteins on monocytes was not decreased, ruling out the possibility that tolerance to Borrelia is attributed to a reduced TLR2 expression. In summary, we characterized tolerance induced by B. burgdorferi, describing a model of desensitization which might mirror the immunosuppression recently attributed to the persistence of Borrelia in immunocompetent hosts.

 

 

The HIV/LYMErix/mycoplasmal Pam3Cys antigens suppress the immune system.  Of course, the crooks already knew that but did not say a word about it and instead said OspA were GREAT VACCINES!!!  having blown off all the adverse events patients and but then having to suffer the persecution of ongoing lawsuits (Gary Wormser), the poor things.

 

Yale blew off all their LYMErix systemic adverse events cases (we know for sure since SmithKline's Dennis Parenti said an a Lyme.org conference in Hartford, CT, that "there were only two adverse events to LYMErix," upon which several people got up and walked out of the conference room), which led them to not only lose a billion dollars in funding, but miss discoveries that would have had an effect on other devastating diseases like HIV (Salp15 in tick saliva blocks HIV or OspA, the LYMErix vaccine, since is the same basic molecule):
SCHOEN_INSTRUCTING_DOCS_TO_BLOW_OFF_LYMERIX_INJUREES.htm 
Because Yale blew off their vaccine-injured, they missed important discoveries about Pam3Cys.  They missed the boat on HIV, lost a billion dollars worth of funding in 9 months, and got the CT Attorney General up their butts. 
080622  Yale Lyme and HIV Flunkies Miss the Boat
"Deer tick saliva may prevent HIV" = Yale frauds miss important discovery due to Yale's lack of objective signs of intelligence.

 

Another mechanism of immune suppression associated with these antigens:
 

HIV infection alters TNF{alpha} production via TLR-dependent pathways in Alveolar Macrophages and U1 cells.
http://www.ncbi.nlm.nih.gov/pubmed/18524817?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Center for HIV/AIDS Care and Research, Boston University School of Medicine, Boston, MA; Molecular and Clinical Genetics, Royal Prince Alfred Hospital and University of Sydney, Sydney, Australia; and Pulmonary Center, Boston University School of Medicine, Boston, MA.

HIV+ persons are predisposed to pulmonary infections, even after receiving effective highly active antiretroviral therapy (HAART). The reasons for this are unclear, but may involve changes in innate immune function. HIV-1 infection of macrophages impairs effector functions, including cytokine production. We observed decreased constitutive TNFalpha concentrations, and increased sTNFRII, in bronchoalveolar lavage fluids (BALF) from HIV+ subjects, compared to healthy controls. Moreover, net proinflammatory TNFalpha activity, as measured by the TNFalpha/sTNFRII ratio, decreased as HIV-related disease progressed, as manifested by decreasing CD4 cell count and increasing HIV RNA (viral load). Since TNFalpha is an important component of the innate immune system, produced upon activation of Toll-like receptor (TLR) pathways, we hypothesized that the mechanism associated with deficient TNFalpha production in the lung involved altered TLR expression or a deficit in the TLR signaling cascade. We found decreased TLR1 and TLR4 surface expression in HIV-infected U1 monocytic cells compared to the uninfected parental U937 cell line, and decreased TLR message in alveolar macrophages (AMs) from HIV+ subjects. In addition, stimulation with TLR1/2 ligand (Pam3Cys) or TLR4 ligand (LPS) resulted in decreased intracellular phosphorylated ERK, and subsequent decreased transcription and expression of TNFalpha in U1 cells compared to U937 cells. AMs from HIV+ subjects also showed decreased TNFalpha production in response to these TLR2 and TLR4 ligands. We postulate that HIV infection alters expression of TLRs with subsequent changes in MAP kinase signaling and cytokine production that ultimately leads to deficiencies of innate immune responses that predispose HIV+ subjects to infection.


 


Another mechanism of immune suppression associated with these antigens:


    The inhibitory effect of Mycoplasma fermentans on tumour necrosis factor (TNF)-alpha-induced
apoptosis resides in the membrane lipoproteins.
http://www.ncbi.nlm.nih.gov/pubmed/16889623?ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Cell Microbiol. 2007 Jan;9(1):142-53. Epub 2006 Aug 2.Click here to read Links


    Gerlic M, Horowitz J, Farkash S, Horowitz S.

    Department of Microbiology and Immunology, Faculty of Health Sciences, Soroka
University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel,
84105.

    Mycoplasma have been shown to be involved in the alteration of several eukaryotic
cell functions, such as cytokine production, gene expression and more. We have previously
reported that infection of human myelomonocytic U937 cell line with live Mycoplasma
fermentans (M. fermentans) inhibited tumour necrosis factor (TNF-alpha)-induced
apoptosis. Mycoplasmal membrane lipoproteins are considered to be the most potent
initiators of inflammatory reactions in mycoplasmal infections. The aim of this
study was to clarify whether the inhibitory effect on TNFalpha-induced apoptosis
is exerted by M. fermentans lipoproteins (LPMf). A significant reduction in TNFalpha-induced
apoptosis was demonstrated by stimulation of U937 cells with M. fermentans total
proteins, LPMf or MALP-2 (M. fermentans synthetic lipopeptide), but not with M.
fermentans hydrophilic protein preparation (AqMf).  ***To investigate the mechanism
of M. fermentans antiapoptotic effect, the reduction of mitochondrial transmembrane
potential (delta psi m) was measured. M. fermentans total proteins LPMf and MALP-2,
but not AqMf, inhibited the reduction of delta psi m. In addition, M. fermentans
total proteins LPMf and MALP-2, but not AqMf, downregulated the formation of active
caspase-8
.***  NF-kappaB was transactivated in cells treated with M. fermentans
lipoproteins, and was essential for host cell survival, but not for the inhibition
of TNFalpha-induced apoptosis by LPMf. *** Our results suggest that the inhibitory
effect exerted by M. fermentans on TNFalpha-induced apoptosis in U937 cells is due
to the membrane lipoproteins of these bacteria.
***

 

To a casual observer, it seems strange that the Yale and the ImmuLyme teams BOTH did not investigate the mechanisms of OspA's failure- immune suppression.  But then that they did not, and that they abused the vaccine injurees in the identical way that they abuse Lyme victims, leads one to believe that they're a part of the same spin-entity, which, of course, they are.  The ALDF.com and the EUCALB are twin spin firms in association with criminal patenteering members of the CDC.

 

http://media.www.dailycollegian.com/media/storage/paper874/news/2008/02/20/News/Deer-Tick.Saliva.May.Prevent.Hiv1-3220695.shtml

Deer tick saliva may prevent HIV-1

By: Holly Seabury, Collegian Staff

Posted: 2/20/08

The attachment of the HIV-1 virus to T cells in the human body may be preventable, according to researchers at the University of Massachusetts, and it's because of an unlikely source.

According to a recent study done by a research team on campus, the use of a certain protein found in deer tick saliva could be the critical step toward curing the virus that potentially leads to AIDS, and in a number of cases, death.

The study showed that the protein may also be an effective treatment for diseases such as asthma and multiple sclerosis caused by an overactive immune system, and could also be useful in containing the immune system to prevent the rejection of transplanted organs.

The research team, including Juan Anguita, Ph.D., assistant professor of veterinary and animal sciences, published its results in this month's edition of "Biochemical and Biophysical Research Communications."

The research team also includes Ignacio Juncandella, Tonya Bates and Elias Olivera, all of veterinary and animal sciences.

"Deer ticks, which are carriers of Lyme disease, produce a protein that can interfere with the initial attachment of the HIV-1 virus, which could lead to new treatments that stop the infection process before it begins," said Anguita.

The specific protein found in deer tick saliva, Salp15, would work by stopping T cells, or white blood cells, from activating by attaching to a specific site on their surface called the CD4 receptor. The HIV-1 virus weakens the human immune system when it targets T cells from the body's strongest defense system in fighting infections, but Salp15 may prevent this step from happening, thus preventing the virus from infecting at all.

"Salp15 binds to proteins in the CD4 receptor that are furthest from the cell membrane in both mouse and human cells," said Anguita.

Anguita and Juncandella were part of a different study, with the Vermont Lung Center and the University of Vermont, that proved Salp15 slowed down the development of asthma in mice. The team produced asthma in a group of mice that also received Salp15 and compared them to a control group. The results that were published in the June 2007 issue of "The Journal of Immunology" concluded that the mice that received Salp15 had airways that were less reactive, and showed lower levels of several biochemical markers that indicated a T cell response.

Because the action of Salp15 is so specific, Anguita believes that it will be used as a treatment for HIV-1, transplant rejection and autoimmune diseases.

"HIV-1 and transplant patients are on powerful medications for life, and most of these have secondary effects like nerve damage and liver problems," he said. "This makes the development of new treatments an important area of research."

"Our current efforts are aimed at validating these results with real cells and real viruses, but before we do that, I need to secure some funding," said Anguita.

However, he added, "this is preliminary and it can be developed into something more useful, such as a vaccine."

Holly Seabury can be reached at hseabury@dailycollegian.com.

© Copyright 2008 The Daily Collegian

-----

LOOKING AT THE PATENT DATABASE (cuz that's where you find stuff the crooks don't talk about when they're slamming us):
 

http://patft.uspto.gov/netacgi/nph-Parser?Sect1=PTO1&Sect2=HITOFF&d=PALL&p=1&u=%2Fnetahtml%2FPTO%2Fsrchnum.htm&r=1&f=G&l=50&s1=6,492,113.PN.&OS=PN/6,492,113&RS=PN/6,492,113

 

2. Description of the Related Art

Chronic Fatigue Syndrome (CFS) is an illness with increasingly reported frequency in the United States and other industrialized countries (Straus, Rev. Infect. Dis. 13(Suppl. 1):S2-S7, 1991). CFS is characterized by prolonged and debilitating fatigue with multiple non-specific symptoms such as headaches, recurring sore throats, muscle and joint pains and cognitive complaints. Profound fatigue, the hallmark of the disorder, can appear suddenly or gradually and persists throughout the course of the illness. Unlike the short-term disability of an acute viral infection, for example, CFS symptoms by definition linger for at least six months and often for years (Fukuda et al., Ann. Intern. Med. 121:953-959, 1994). Physicians can evaluate patients with persistent fatigue of undetermined cause using guidelines developed by the international CFS study group (Fukuda et al., Fed. Pract. 12:12-17, 1995).

It has been well documented that individuals who suffer from fibromyalgia (FMS) exhibit many of the same symptoms found in atypical CFS (Buchwald et al., Arch. Intern. Med. 154:2049-2053, 1994; Ziem et al., Arch. Intern. Med. 154:1913, 1995) in which a patient has 6 or 7 tender points. These two illnesses are so similar that for years many medical practitioners have considered them to be the same condition.

Despite multidisciplinary investigations of CFS, its etiology remains unknown and no specific diagnostic tests or therapies for CFS exist. In about one third of cases, the sudden onset follows a respiratory, gastrointestinal, or other acute infection with flu-like symptoms, including mononucleosis (Mawle et al., Infect. Agents Dis. 2:333-341, 1994). No published data implicate a specific virus or other microbes as the cause of CFS. However, it appears that infectious agents, among other stressors, can precipitate the syndrome (National Institutes of Health Publication No. 96-484, 1996). A variety of common viruses can be reactivated in some CFS patients, including HTLV-II, Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes simplex viruses (HSV) 1 and 2, and human herpes viruses 6, 7 and 8. It is believed that virus reactivation could be occurring secondarily to some immunologic disturbance (National Institutes of Health Publication No. 96-484, 1996; Nicolson et al., Int. J. Occup. Med. Immunol. Toxicol. 5:69-78, 1996).
 

Let me think...  Hmm.  What triggering event might lead to the activation of normally, common, latent viruses that most healthy people have been exposed to, but are under control?


Mycoplasmas are bacteria which belong to the class Mollicutes. They are the smallest free-living, self-replicating bacteria known. They have no cell wall and a very limited genome of between 600 and 1,500 kilobases which makes them highly dependent on their host for survival. The mycoplasma species M. fermentans, M. hominis and M. penetrans have been isolated from individuals suffering from primary atypical pneumonia, urogenital infections, rheumatoid arthritis (RA) and AIDS-related infections (Hayes et al., Infect. Immun. 64:3419-3424, 1996; Schaeverbeke et al., Br. J. Rheumatol. 36:310-314, 1997; Montagnier et al., Clin. Infect. Dis. 17(Suppl. 1):S309-315, 1993).
 

- - -

These potential and real pathologies are never discussed openly by the crooks.  Due to their crimes and harassment it shall be all put together on one page for the whole world to see.  And since we will prove that this is the junk they mess with on Plum Island, perhaps some countries will even think of charging the US with violations to international law.

We're obviously naming names.  It might not be a good idea for any of them to leave the country given Bush's wreckage of international law in kidnapping, secret prisons, and torturing confessions out of suspects.
 

Remember, now.  These bastards tried to vaccinate everyone with this Pam3Cys shit, which clearly would have rendered thousands of people sick with all kind of infections and disease process outcomes.  It's a crime and possibly even a war crime.

==========================================================================

 

BIOMARKER- GFAp  (Schoen, Klempner),

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=8740104[uid]

Glial Fibrillary Acidic protein in the spinal fluid is a sign of gliosis or destruction of the energy-providing cells of the brain.  In other words, it's not a sign of hypochondria or whatever other DSM-IV nonsense they accuse of having instead.

Infection. 1996 Mar-Apr;24(2):125-9.

Increased cerebrospinal fluid levels of glial fibrillary acidic protein (GFAp) in Lyme neuroborreliosis.

Dept. of Infectious Diseases, Ostra University Hospital, Göteborg University, Sweden.

Glial fibrillary acidic protein (GFAp), the main protein constituent of the intermediate filaments of astrocytes, was analysed in the cerebrospinal fluid (CSF) of 20 patients with Lyme neuroborreliosis as a marker of the astroglial reaction. The mean GFAp level before antibiotic treatment in the study group was significantly elevated (592 pg/ml +/- 596 [SD]) compared to that in 24 healthy controls (121 +/- 87 [SD]) (p < 0.01). The highest CSF-GFAp levels were seen in the patients with the most severe disease, but the levels were also increased in patients with peripheral paresis, such as facial palsy with no or only minor encephalitic symptoms. This implies that the infection was not limited to radix dorsalis or the meningeal tissues, but affected the central nervous system as well. Furthermore, the astroglial reaction seemed to occur early in Lyme neuroborreliosis since CSF-GFAp levels were elevated also in patients with recent (< 3 weeks) onset of disease. After antibiotic treatment, the GFAp levels decreased. It is suggested the CSF-GFAp concentrations might be useful for monitoring CNS involvement in Lyme neuroborreliosis.

 

Robert T. Schoen, when trying to sell the Yale vaccine, LYMErix, Yale Rheumatology, Annals of Internel Medicine, Vol 132, No 8:
http://www.annals.org/content/132/8/661.full.pdf+html
 

"Other peripheral neuropathies and Lyme meningitis are also seen at this stage.  In late-stage disease, the central nervous system may be involved.  A new diagnostic test measuring glial fibrillary acidic protein in cerebrospinal fluid may prove to be a useful tool for measuring such involvement (20)." 

 

And here we see Mark Klempner discussing how serious chronic neurologic Lyme is in his 1992 MMP-130 study.

Compare this to what he said in 2003:
 

KLEMPNER:
http://www.ncbi.nlm.nih.gov/pubmed/12821733?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
 

BACKGROUND: It is controversial whether additional antibiotic treatment will improve cognitive function in patients with post-treatment chronic Lyme disease (PTCLD). OBJECTIVE: To determine whether antibiotic therapy improves cognitive function in two randomized double-blind placebo-controlled studies of patients with PTCLD. METHODS: A total of 129 patients with a physician-documented history of Lyme disease from three study sites in the northeast United States were studied. Seventy-eight were seropositive for IgG antibodies against Borrelia burgdorferi, and 51 were seronegative. Patients in each group were randomly assigned to receive IV ceftriaxone 2 g daily for 30 days followed by oral doxycycline 200 mg daily for 60 days or matching IV and oral placebos. Assessments were made at 90 and 180 days after treatment. Symptom severity was measured from the cognitive functioning, pain, and role functioning scales of the Medical Outcomes Study (MOS). Memory, attention, and executive functioning were assessed using objective tests. Mood was assessed using the Beck Depression Inventory and Minnesota Multiphasic Personality Inventory. RESULTS: There were no significant baseline differences between seropositive and seronegative groups. Both groups reported a high frequency of MOS symptoms, depression, and somatic complaints but had normal baseline neuropsychological test scores. The combined groups showed significant decreases in MOS symptoms, higher objective test scores, and improved mood between baseline and 90 days. However, there were no significant differences between those receiving antibiotics and placebo. CONCLUSION: Patients with post-treatment chronic Lyme disease who have symptoms but show no evidence of persisting Borrelia infection do not show objective evidence of cognitive impairment. Additional antibiotic therapy was not more beneficial than administering placebo.

 

They can't deny they publish this outrageous, self-ass-biting crap when they know better.  This BIOMARKERS chapter is  your "Objective Signs by the Crooks, Themselves" section.  To discount one's own real scientific handiwork is to lose a billion dollars in grants in less that 9 months, methinks, not to mention asking to have the Connecticut Attorney General drive a flag pole up their asses so the whole world can see their criminal incompetence.

 

==========================================================================

 

BIOMARKER: Quinolinic Acid in the spinal fluid (IDSA's JJ Halperin):
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=1531156[uid]

A sign that tryptophan has been hijacked for the production of reactive oxygen species by immune cells in an attempt to destroy invading pathogens.  Quin is sort of an analog of dopamine and if instead stuck in the dopamine receptor, it might not remove itself in a timely matter, resulting in the neuron being stuck on "ON," and thus auto-kill itself.  This is the definition of excitotoxin.

Neurology. 1992 Jan;42(1):43-50.

Neuroactive kynurenines in Lyme borreliosis.

Department of Neurology, SUNY, Stony Brook.

Although neurologic dysfunction occurs frequently in patients with Lyme borreliosis, it is rarely possible to demonstrate the causative organism within the neuraxis. This discordance could arise if neurologic symptoms were actually due to soluble neuromodulators produced in response to infection. Since immune stimulation is associated with the production of quinolinic acid (QUIN), an excitotoxin and N-methyl-D-aspartate (NMDA) agonist, we measured levels of CSF and serum QUIN, and lymphokines. Samples were obtained from 16 patients with CNS Borrelia burgdorferi infection, eight patients with Lyme encephalopathy (confusion without intra-CNS inflammation), and 45 controls. CSF QUIN was substantially elevated in patients with CNS Lyme and correlated strongly with CSF leukocytosis. In patients with encephalopathy, serum QUIN was elevated with corresponding increments in CSF QUIN. Lymphokine concentrations were not consistently elevated. We conclude that CSF QUIN is significantly elevated in B burgdorferi infection--dramatically in patients with CNS inflammation, less in encephalopathy. The presence of this known agonist of NMDA synaptic function--a receptor involved in learning, memory, and synaptic plasticity--may contribute to the neurologic and cognitive deficits seen in many Lyme disease patients.

 

==========================================================================

 

[Pterins]  The production of Neopterins in the spinal fluid are associated with bacterial infection.  They have been discovered in CNS-Lyme victims.

 

==========================================================================

 

Borrelia especially attack NERVE ROOTS-  

http://www.ncbi.nlm.nih.gov/pubmed/14688796?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

MEDLINE SEARCH QUERY:  "ganglia and borrelia"
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=(%22ganglia%22[MeSH+Terms]+OR+%22ganglia%22[All+Fields])+AND+(%22borrelia%22[MeSH+Terms]+OR+%22borrelia%22[All+Fields])

I suspect that Fibromyalgia is a condition of inflamed ganglia and nerve roots ("pressure points") and is more a radiculitis than hypochondria, but we are all well-aware of the fact that the Femzalgia groups cannot be penetrated since either they're all run by Pat Smithite Queens or they're run by the Managed Care crooks:

The following is a "Managed Care and their Morons" entity:
http://www.fibroandfatigue.com/

In other words, the fox is guarding the henhouse, which is why this fake clinic does not get investigated by any Narc Police for handing out fistfuls of OxyContin and related psychotropic brain-candy.

 

==========================================================================

 

BIOMARKERS, AUTOANTIBODIES, NON-ARTHRITIC:

 

Antibodies to Heat Shock Proteins  (discovered by and discussed by all the crooks)
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=9375512[uid]

They say such a cross-reacting antibody to human heat shock proteins comes from cross-reacting regions from anti-flagellar antibodies.

 

Anti-cardiolipin antibodies (Lupus-like, by Steere and Benach),
http://www.ncbi.nlm.nih.gov/pubmed/3408508?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
http://www.ncbi.nlm.nih.gov/pubmed/8410057?ordinalpos=1&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

Antigangliosides (Benach)-   See the graphic, next.
http://iai.asm.org/cgi/reprint/63/10/4130?view=long&pmid=7558329


Jorge Benach demonstrating the cross-reacting antibodies caused by Borreliosis attacking the nodes of Ranvier, potentially affecting nerve conduction.
http://iai.asm.org/cgi/reprint/63/10/4130?view=long&pmid=7558329

Infect Immun. 1995 Oct;63(10):4130-7.

Experimental immunization with Borrelia burgdorferi induces development of antibodies to gangliosides.

Department of Neurology, Hospital de Galdacano, Vizcaya, Spain.

Patients with neuroborreliosis produce antibodies, mostly of the immunoglobulin M (IgM) class, to gangliosides, particularly to those with Gal(beta 1-3)GalNac terminal sequences. Lewis rats were immunized with a nonpathogenic strain of Borrelia burgdorferi and with a chloroform-methanol extract (nonprotein) of this organism (CM) to determine whether antibodies to B. burgdorferi also recognized gangliosides. Rats were also immunized with asialo-GM1 to determine whether the elicited antibodies recognized antigens in B. burgdorferi. Rats immunized with B. burgdorferi produced low levels of IgM antibodies that cross-reacted with asialo-GM1 and GM1. Rats immunized with CM had marked IgM reactivity to asialo-GM1 and GM1. Immunization with asialo-GM1 resulted in antibodies that cross-reacted with B. burgdorferi antigens. Although antibodies to B. burgdorferi were of both the IgM and IgG classes, those to CM and to asialo-GM1 and GM1 were predominantly in the IgM fraction. Reactivity of the IgM antibodies decreased after adsorption with the heterologous and the homologous antigens, indicating bidirectional cross-reactivity between CM, asialo-GM1, and GM1 and that immunization with one produces antibodies to the other. There was no in vivo deposition of Ig in peripheral nerves, nor was there nerve pathology as a result of immunizations, but IgM antibodies to asialo-GM1 and CM recognized homologous antigens in the nodes of Ranvier of peripheral nerves from nonimmunized rats. This immunization model suggests that antibodies to gangliosides in Lyme disease have a microbial origin and are potentially relevant in pathogenesis.

 

Are these IgM antibodies ever looked for routinely by the IDSA Catastrophizer Club?

 

I find it hard to believe that all of us'n internet culters and our monkey co-conspirators knew ahead of time that we should be generating that specific antibody - one of course not detected in Lyme Western blotting or any other common diagnostic test for Lyme at the present time because that would be too much like not working for BigInsurance - yet that is their assertion as regards the source of our complaints.

Benach of course, wrote a letter to the editor of the New York Times where he stated that indeed we chronic Lymers are crazy and that "Steere has the science on his side," when Steere says we're just crazy and don't have a real disease.

We think this is utterly hilarious, because why waste your reputation over a nutcase fairy-ass puke like Allen Steere?
 

http://query.nytimes.com/gst/fullpage.html?res=9F05EFDE173CF933A05756C0A9669C8B63

May 30, 2000

A Lyme Battle Rages

To the Editor:

The May 23 article depicts the sad state of affairs regarding the ''bitter medical debate over Lyme disease.'' Who would have thought back in the late 70's when Dr. Allen Steere described the clinical syndrome that we know today as Lyme disease that he would be the subject of complaints by patients who do not agree with his diagnoses.

Increasingly, groups of patients (who may or may not have Lyme disease) are attempting to impose their will on governmental agencies charged with health care and research, and thus to subvert the scientific process. The ''bitter debate over Lyme disease'' is not that at all; it is a debate between science and ignorance, with science on the side of Dr. Steere.

DR. JORGE L. BENACH
Stony Brook, N.Y.

The writer is the director of the Center for Infectious Disease and a professor at SU

 

Oh. 

Maybe someone forgot to tell Benach how science was actually performed.  He can read Chapters 1 and 3 of Cryme Disease.  Either that or he can change the FDA's rules for the validation of an analytical method to make it all like Steere's "ROC" Elephant Rule Diagnostics, although I think Homelame Stupidity would at that point step in.

Oh, NOW what am I saying?
 

 

==========================================================================

 

BIOMARKER; Matrix-Metalloproteinases (MMPs) (Klempner); 

Matrix-metalloproteinases are tissue degrading enzymes found (elsewhere, normally; females as regards wasted fertility cycles and effected by estrogen) in the spinal fluid of neuroborreliosis patients to the tune of 78% when speaking about the specific Klempner one, MMP-130.  Neuroborreliosis is the other word for that non-disease prevented by the placebo vaccine, LYMErix.

See all Related Articles...

Estrogen effects MMPs which means all wimmiz is cultic scary witches, naturally, and so there is no prejudice in saying wimminz is bad to be having fake complaints of chronic illness and should be charged with Munchausen's and Munchausen's by proxy.

This is well-understood in "courts" where judges say things like:
"I always thought Ireland was a pretty tough nut to crack."

Irish people = Bad
Wimminz = Bad
Blacks = Bad

Next?

 

Says Lenny Sigal:

http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=9125553:

Infect Immun. 1997 May;65(5):1722-8.

Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903, USA.

Although Borrelia burgdorferi is found at the site of many manifestations of Lyme disease, local infection may not explain all features of the disease. Previous work has demonstrated that the organism's flagellin cross-reacts with a component of human peripheral nerve axon, heat shock protein 60. The cross-reacting epitope is identified by a single anti-B. burgdorferi flagellin monoclonal antibody, H9724. We now report that the spontaneous and peptide growth factor-stimulated in vitro neuritogenesis of SK-N-SH neuroblastoma cells and other neural tumor cell lines is suppressed by H9724. In contrast, changes induced by exposure of these cells to optimal and suboptimal concentrations of cyclic AMP, phorbol ester, or retinoic acid are not affected by H9724. H9724 does not decrease cell viability or the ability of the cells to anchor to the culture plate or extracellular matrix and does not block nerve growth factor binding to the cells. These findings are compatible with the premise that antiaxonal antibodies formed during the immune response to B. burgdorferi flagellin might modify axonal function in vivo and play a role in the pathogenesis of neurologic features of Lyme disease. A humoral immune response predicated on molecular mimicry could explain persistent or ongoing neurologic dysfunction occurring after elimination of the organism by appropriate antibiotic therapy.

 

Oh, see, we thot we was catastrophizin duh feminozalgia simpoms speshully cuz Yale be saying ifn weez habs band 41 it don' mean nuttin:

 

Arthritis Rheum. 2000 Nov;43(11):2493-500.

The role of catastrophizing in the pain and depression of women with fibromyalgia syndrome.

Department of Medicine, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick 08903, USA.

OBJECTIVE: Although 2 recent studies have found associations between catastrophizing and poor medical outcomes in patients with fibromyalgia syndrome (FMS), neither assessed these findings in comparison with a similar group of patients with chronic pain. Our study examined the complex relationships between depression, catastrophizing, and the multidimensional aspects of pain in women with FMS and compared these relationships with those in women with rheumatoid arthritis (RA). METHODS: Sixty-four FMS patients and 30 RA patients completed the Coping Strategies Questionnaire (CSQ), the Beck Depression Inventory II (BDI-II), and the McGill Pain Questionnaire. RESULTS: Compared with subjects with RA, FMS subjects scored significantly higher on the catastrophizing subscale of the CSQ. FMS patients also earned higher scores on overall depression and on the cognitive subscale of the BDI-II. Furthermore, the relationship between catastrophizing and depression was significant in the FMS group only. Regression analyses revealed that in FMS, catastrophizing as a measure of coping predicted patients' perception of pain better than demographic variables such as age, duration of illness, and education. CONCLUSION: Cognitive factors, such as catastrophizing and depressive self-statements, have a more pronounced role in the self-reported pain of patients with FMS than in patients with RA. Clinically, this indicates that treating pain and depression in FMS by adding cognitive therapy and coping skills components to a comprehensive treatment program may improve the outcomes obtained with pharmacologic interventions.

 

Ya, see.  It's not the other way around or anything.  It's not like these woman have been abused for years, never having any scientifically valid tests run on them, the likes of which their abusers (Kaiser-deployed Lyme criminals deploying psychiatric imaginators), as shown in this chapter, know all about and know how to run because they themselves developed these scientifically valid methods to run such scientifically valid tests for real disease processes.  Such tests have been developed with a range of "NORMAL" in mind, against which to compare the results of the sick people (that being the entire point of medical laboratory testing).

Allow me to propose a hypothesis that needs to be tested:
How about if we start out by believing these women about their complaints?

Oh, what am I saying?  My premise was invalid.  I started out with "women" in the premise.

Women are penis ports, as demonstrated by the behavior of the DCF and the "herd of porkers" at the US universities' "Schools of Social Work." 

Penis ports also belong to the domain of psychiatry.  The Yale Centre for the Study of Erections has determined that women have an open-ended Twilight Zone (see the Glossary) which allows for all sorts of demons to enter.

 

==========================================================================

 

BIOMARKER: Quantitative Electro-Encephalogram QEEG (Sigal),
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=7554300[uid]

Lenny Sqeegal!!!  I'll have to add that to the Connecticutisms.

Dr. Sqeegal finds that people with Lymechondria or Catastrophizitis have abnormalities in brain electroencephalograms, which proves hypochondria is a real disease, like Femzalgia.  Femzalgia is treated with a Pfizer drug that's actually a psychotropic, and thus, is also a treatment for Femzalgia, Lymechondria or Catastrophizitis.  The other, probably more expensive and time-consuming Pfizer drug for Femzalgia is Viagra, to be prescribed for the Femzalgia sufferer's husband.  Lots of expensive drugs are good, as long as they're not antibiotics, because those are for use by pig farmers and the hotdogs and so on and so forth.  Sooner or later, after years and years of these kinds of treatments, we wonder if everyone in range of pharmaceutical water will be too antidepressed to bother with the Viagra-related activities, which will in the end have repercussions as regards the pediatric market of such pig farmer mystery meat..

 

QEEG and evoked potentials in central nervous system Lyme disease.

Clin Electroencephalogr. 1995 Jul;26(3):137-45.

Department of Psychiatry, New York University School of Medicine, N.Y., USA.

Quantitative EEG, flash visual evoked potentials, auditory evoked potentials to common and rare tones, and median nerve somatosensory evoked potentials were obtained from 12 patients with active CNS Lyme disease and from 11 patients previously treated for active CNS Lyme disease. Abnormal QEEG and/or EPs were found in 75% of the active Lyme disease patients and in 54% of the post CNS Lyme disease patients. Three different types of neurophysiological abnormality were observed in these patients including QEEG slowing, possible signs of cortical hyperexcitability, and focal patterns indicating disturbed interhemispheric relationships. In patients tested before and after treatment QEEG and EP normalization was associated with clinical improvement.

 

==========================================================================

 

BIOMARKER; Brain Single Photon Emission Computerized Tomogram (SPECT) (All, Steere),

Here, Allen Steere admits that brain perfusion imaging demonstrates relief upon intravenous antimicrobial therapy, but there was no real (real means "not the Steere kind") follow up on those patients.  Brian Fallon at Columbia University had a few thousand patients who had received previous intravenous ceftriaxone treatment (unlike Mark Klempner, as only 1/3 of his victims had had IV ceftriaxone prior to being enrolled in his "study") from which to select relapsed patients who, upon real re-treatment by Brian Fallon (14 weeks of intravenous ceftriaxone) improved, but then relapsed again, since Lyme is really relapsing fever:

http://www.ncbi.nlm.nih.gov/pubmed/9409364?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

Neurology. 1997 Dec;49(6):1661-70.

Reversible cerebral hypoperfusion in Lyme encephalopathy.

Logigian EL, Johnson KA, Kijewski MF, Kaplan RF, Becker JA, Jones KJ, Garada BM, Holman BL, Steere AC.

Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Cambridge, MA, USA.

Lyme encephalopathy (LE) presents with subtle neuropsychiatric symptoms months to years after onset of infection with Borrelia burgdorferi. Brain magnetic resonance images are usually normal. We asked whether quantitative single photon emission computed tomography (SPECT) is a useful method to diagnose LE, to measure the response to antibiotic therapy, and to determine its neuroanatomic basis. In 13 patients with objective evidence of LE, SPECT demonstrated reduced cerebral perfusion (mean perfusion defect index [PDI] = 255), particularly in frontal subcortical and cortical regions. Six months after treatment with 1 month of intravenous ceftriaxone, perfusion significantly improved in all 13 patients (mean PDI = 188). In nine patients with neuropsychiatric symptoms following Lyme disease, but without objective abnormalities (e.g., possible LE), perfusion was similar to that of the treated LE group (mean PDI = 198); six possible LE patients (67%) had already received ceftriaxone prior to our evaluation. Perfusion was significantly lower in patients with LE and possible LE than in 26 normal subjects (mean PDI = 136), but 4 normal subjects (15%) had low perfusion in the LE range. We conclude that LE patients have hypoperfusion of frontal subcortical and cortical structures that is partially reversed after ceftriaxone therapy. However, SPECT cannot be used alone to diagnose LE or determine the presence of active CNS infection.

 

"SPECT cannot be used alone to diagnose LE-" 

We agree, but it also helps to NOT DIAGNOSE HYPOCHONDRIA.  Besides, when we get done here, the only kind of hypochondria that will be scientifically diagnosable will be scientifically diagnosable with an exorcism.  Because to assert otherwise, to assert that American Medicine knows absolutely 100% of everything there is to know about health and non-health processes, and about all of human genetics, down to the last person on earth, would be to deny you are reading this chapter right now.

That's my main point about psychiatrists being 100% delusional to think they can guess the source of illness signs, or to assert, perversely and reversely, that medical changes, medical signs determined scientifically to be out of range, are caused by "crazy." 

Where's the recorded, observed, scientifically controlled experiment where it has been proven that people can induce their own out-of-range, compromised SPECT scans and the like.  If it is possible, I think we will find such people among the psychics or the out-of-body-projectors, and the like.  Prove THAT happens first.

No human has the right to judge the will of another, permanently, for all time, as if they have the ability to predict the future; as if to assert that anyone can know the will of another, and is able to predict all future behaviors of another person.  Such is not only asserting that psychiatrists are all God, but it's commonly known as "discrimination."

 

 

Department of Neurology, University of Rochester Medical Center, Rochester, NY 14642, USA. elogigian@mail.neurology.rochester.edu

The efficacy of intravenous ceftriaxone, 2 g per day for 30 days, was evaluated in a case series of 18 consecutive patients who met strict criteria for Lyme encephalopathy. Months to years after classic manifestations of Lyme disease, the 18 patients presented with memory difficulty, minor depression, somnolence, or headache. Sixteen (89%) had abnormal memory scores; 16 (89%) had cerebrospinal fluid (CSF) abnormalities, and all 7 patients tested had frontotemporal perfusion defects on single photon emission computed tomographic (SPECT) imaging. Six months after treatment, memory scores in the 15 patients who completed the study according to protocol were significantly improved (P<.01). In the 10 patients who had follow-up CSF analyses, total protein levels were significantly lower (P<.05). In the 7 patients who had SPECT imaging, posttreatment perfusion was significantly better (P<.01). Twelve to 24 months after treatment, all 18 patients rated themselves as back to normal or improved. We conclude that Lyme encephalopathy can be treated successfully with ceftriaxone.

 

Back to normal or improved.  I think all of us are improved with ceftriaxone, but we still relapse, although it is not as bad as untreated Lyme/Chronic Fatigue Syndrome with the constant, everyday fever for years on end (like myself).

This shows is that Allen Steere is aware that Lyme is a brain disease but he signs on to "guidelines" that basically say such a kind of Lyme is due to hypochondria.  We NEVER hear IDSA say Lyme patients have a delirium or that it's a brain disease when speaking to the public or the press.  WE NEVER hear them denounce the Dearborn diagnostic method as regards this more common type of Lyme.  In fact, they are moving more and more in the direction of fantasy-land, arbitrarily shortening and shortening further their first arbitrarily-defined, and then fraudulently-defined (Klempner), treatment protocols.

 

==========================================================================

 

BIOMARKER: Nitrous Oxide (Steere) possibly damaging the brain:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=7513330[uid]

 

Who could have guessed that Allen Steere and brains were ever in the same room together?

 

J Infect Dis. 1994 May;169(5):1014-22.

Borrelia burgdorferi and Escherichia coli lipopolysaccharides induce nitric oxide and interleukin-6 production in cultured rat brain cells.

Division of Endocrinology, New England Medical Center Hospitals, Boston, MA 02111.

Borrelia burgdorferi, the spirochetal agent of Lyme disease, infects the central nervous system (CNS), but the factors that mediate inflammation and neurologic dysfunction are not known. Sonicated B. burgdorferi stimulated in a concentration-dependent manner the production of nitric oxide (NO) in glial-enriched primary cultures of neonatal rat brain cells via induction of NO synthase activity. Lipopolysaccharide (LPS) of Escherichia coli also stimulated nitrite accumulation in a concentration-dependent manner. Stimulation of NO production by B. burgdorferi sonicate and E. coli LPS was associated with increased levels of mRNA coding for the cytokine-inducible form of NO synthase. B. burgdorferi sonicate also stimulated release of interleukin-6, with a concentration-response relationship similar to that for its stimulation of nitrite production, as did E. coli LPS. A competitive antagonist of E. coli LPS, Rhodopseudomonas sphaeroides lipid A, inhibited LPS-induced stimulation of NO synthase activity but markedly potentiated that of B. burgdorferi, indicating that the initial triggering mechanism of B. burgdorferi is distinct from that of E. coli LPS. Induction of NO synthase by bacterial agents within the brain may represent a common pathway of CNS inflammation and neurotoxicity.

 

Superioxide Digestion of OspA-type molecules (from E. coli)  (1990)

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1131368&blobtype=pdf

 

OspA could be bad when used as a vaccine. 

 

==========================================================================

 

BIOMARKER; Gadolium contrast MRI for active meningitis (monkey studies),
http://www.neurology.org/cgi/content/abstract/45/1/165

 

Only the monkeys are allowed to be sick and have these tests for ongoing meningitis.  Humans are catastrophizing.

 

NEUROLOGY 1995;45:165-172
© 1995 American Academy of Neurology

 

Inoculation of nonhuman primates with the N40 strain of Borrelia burgdorferi leads to a model of lyme neuroborreliosis faithful to the human disease

A. R. Pachner, MD, E. Delaney, T. O'Neill, DVM, PhD and E. Major, PhD

Article abstract-We injected rhesus macaques with a highly infective strain of Borrelia burgdorferi to assess whether experimentally inoculated nonhuman primates (NHPs) could serve as models of human Lyme neuroborreliosis (LNB). The animals developed biopsy-confirmed erythema migrans in the area of the inoculations. ELISA testing of sera revealed strong antibody reactivity to B burgdorferi antigens, and Western blotting showed that 16-, 22-, 31-, 34-, and 41-kd proteins of the spirochete were major antigens recognized by antibody. Culture and polymerase chain reaction (PCR) testing of serial CSF specimens revealed that chronic infection of the CNS occurred in all NHPs injected. CSF pleocytosis occurred concurrently with CNS infection. Brain MRI revealed intense meningeal inflammation in one NHP as manifested by gadolinium uptake by the dura at the base of the temporal lobes. All animals had measurable antibody in the CSF after invasion. These studies are the first to demonstrate that experimental LNB in NHPs is a reliable model faithful to the human disease, with spirochetal invasion of the subarachnoid space. This also is the first report of CSF samples positive by culture in experimental LNB. Inflammation in the CNS as manifested by CSF pleocytosis and MRI findings was also correlated with the presence of spirochetal DNA detected by PCR. These data support the hypothesis that the pathogenesis of LNB is associated with direct spirochetal invasion, and provide evidence that CNS involvement is more common than heretofore thought.

NEUROLOGY 1995;45: 165-172

 

==========================================================================

 

BIOMARKERS: Dysregulated Cytokines (Pachner, Sigal)

 

Femzalgia, sleep disorders and the interleukens - only discussed at secret Cold Spring Harbor conferences (to be scanned).  Well, we know Mr. Watson of Watson and Crick, who ended up there at Cold Spring Harbor (think PNAC's "race specific bioweapons") does not think much of black people.  We might conclude that Cold Spring Harbor Labs would also be a He-Man-Wimmin-Haters Club??

http://entertainment.timesonline.co.uk/tol/arts_and_entertainment/books/article2630748.ece

Well, we concluded correctly.  Watson was to have his pet female human to add to the collection of specimens there.  Later he added a pet black female human.

Feminists are a constant source of trouble for him. I remember him turning to me the day the headline “Abort babies with gay genes, says Nobel winner” appeared in a British broadsheet 10 years ago. Eyes wild and voice uncharacteristically strained, he asked: “What should I do about the press?” He refers to the incident again at lunch. “It was a hypothetical thing,” he explains. “If you could detect it pre-natally, could a woman abort a child who was homosexual? I said they should have the right to, because most women want to have grandchildren, period. We can’t do it, but it’s common sense. Anyways,” he says, shaking his head wearily, “it was a bad day when that headline hit. I was just arguing for the freedom of women to try and have the children they want, not what is right or wrong.”

It's interesting that Watson can't tell that his own brilliance is the key to autism in his own son.  The same thing happened to Albert Einstein and his son:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=11897815

'Reversed duplication (and over-expression) of a no-autokill molecule (BCL8), resulting in the abrogation of normal synaptic pruning.  We autistic people have large heads and large brains. My father had it, I have it and my nephew has it, while my sister has Neurofibromatosis and two of her kids have Neurofibromatosis.  The nephew with autism has both.  The nephew's teachers say his IQ is so high, they can't assess it (his score is higher than the tests go).

My father was as design engineer for AVCO and a fine artist, connoting high visual-spatial performance:
http://patft.uspto.gov/netacgi/nph-Parser.............4,431,050

Sons of very intelligent men are weaker creatures than their daughters.  This we know from the differences between high functioning autistic females and males.  Just in general, as is common knowledge just from empirical observation, males are more genetically, cognitively, and morally inferior or fragile than females.

As we can see, my IQ is "very superior" in the visual spatial domain, which is what high-functioning autism is.  Watson has some reading to do, I would say.  The reading should include the contribution of selfishness, deception and self-aggrandizing behavior, as discussed in later chapters.  I have observed that lawyers and psychiatrists score low in visual-spatial abilities. 

That is, I hypothesize that: "The performance IQs of lawyers and psychiatrists are lower because they spent their lives lying and manipulating others." 

What else explains both lawyers and psychiatrists as parasites of the already-injured?

They're both parasites, they both lie as easily as normal people breathe, and they're both no good at all at science.  I hypothesize that "they auto-cognitively-remediate into the left, lying hemisphere of their brain, through childhood development."  If this is found not to be so, and lawyers and psychiatrists are just born that way, I wonder if we could detect lawyers and psychiatrists early enough in their development such that their mothers could abort them?

No mother wants a demonic offspring. 

 

As regards intelligence, in general, it is an abomination if given to those who don't have the will to use it for the betterment of mankind, and in this instance, something as serious as Borreliosis, having intelligence is only a good thing if used to expose the truth about such awful crimes as "Lyme/LYMErix Disease." If intelligence is used to  not participate in exposing these crimes, or is neglect, that's nearly as criminal as the original commission of the crime.

One does not have to be especially smart to understand this crime because you can see it with your own eyeballs: USDOJ_COMPLAINT_RICO.htm.  What's been lacking is the will, the desire, on the part of everyone involved to DO something about it.

There we see the Grand Canyon or the Marianis Trench, so huge is the Mount Everest of Neglect (cowardice, selfishness).

Will or intent is independent of talent.  No one in Lymeland has an excuse for not participating at the highest level.  Whoever can read this website, can build one of their own like it. 

 

==========================================================================

 

BIOMARKER;  The biomarker here is the Oligoclonal Bands in the spinal fluid of Lyme-That-Appears-Identical, Clinically, to Multiple Sclerosis

Autoreactive Neurologic T Cells, MS Haplotypes


NINDS' Roland Martin, Klempner

We think this is a non-issue, however, but we can't rule out the effect of OspA or Lyme Disease or LYMErix-Disease induced increases in mycoplasmal infections and their association to badly mutated T cells and leukemia (mycoplasma are associated with the production of cancer).  It's just unfortunate all around that such greedy evil mental midgets got their filthy paws on this disease.  Consider what we missed in the past 30 years with this "controversy."

 

Roland Martin went home to Germany after not exactly discovering that autoimmune T cells are the result of Lyme infection:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=17060473

Studies of Lyme arthritis and chronic neuroborreliosis suggest that spirochete-specific T cells cross-reacting with self-antigens may be at least partly responsible for autoimmune mechanisms possibly leading to chronic disease manifestations (8, 12, 25).

Cross-recognition of self-antigens by B. burgdorferi-specific CD4+ T cells has been implicated in the pathogenesis of chronic manifestations of the disease. Patients with treatment-resistant Lyme arthritis, but not other forms of arthritis, expressing the rheumatoid arthritis-associated MHC allele HLA-DRB1*0401 generated clonal responses to both the immunodominant borrelial outer surface protein A and the human leukocyte function-associated antigen 1, which was tested as a candidate autoantigen (8). In a patient with chronic NB expressing the MS-associated HLA-DRB1*1501 allele, we previously showed that a single TCC preferentially recognizes different borrelial peptides but also responds to human autoantigenic mimics (12). Our data clearly indicate that degenerate antigen recognition that includes pathogen-derived and self-epitopes is not restricted to chronic and treatment-resistant manifestations of the disease. Molecular mimicry alone is thus not sufficient to induce chronic Lyme disease, and other genetic, environmental, and infectious factors must be involved. Probably the best risk-conferring candidate is the HLA haplotype, since both of the aforementioned studies were performed with patients who expressed HLA class II alleles associated with autoimmunity in the affected organ compartment. However, studies investigating the association between HLA haplotypes and chronic Lyme disease have up until now been lacking, and a clear association between certain HLA alleles and organ involvement other than the joints, e.g., the brain and/or spinal cord, has not yet been documented.

 

Apparently, Roland Martin did not hear about the secret Mark Klempner haplotype (HLA-DQB1*0602):
http://www.youtube.com/watch?v=yPn_T9qy4C0&mode=related&search=

Or maybe he did, and that's the reason he went home to Germany.

 

SPLAINER-  Trying to find out how MS T-cell autoimmunity happens:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18155234

"Nevertheless, some T cells are still able to escape negative selection in the thymus. Self-reactive TCRs have been extensively studied in experimental autoimmune encephalomyelitis (EAE), a widely used animal model for multiple sclerosis. EAE is induced in B10.PL mice by immunization with myelin basic protein (MBP). Disease in these mice is mediated exclusively by CD4+ T cells specific for MBPAc1-11.11 MBPAc1-11-specific T cells escape clonal deletion in the thymus due to poor binding of the MBPAc1-11 peptide to I-Au.11-13 In addition, recent structural studies have suggested that self-reactive TCRs in the periphery escape negative selection by interacting with pMHC complexes in an atypical orientation, which may not generate a sufficiently strong interaction to induce negative selection.14 However, no structural studies have been reported for MHC class II TCRs that undergo negative selection as a comparison. T cells that are normally negatively-selected can be obtained by immunization of MBP-deficient (MBP-/-) B10.PL mice with MBP. Using this approach, we identified a distinct, highly immunogenic region within MBP121-151.13 T cells responding to this region undergo extensive thymic tolerance and are not readily detected in wild-type B10.PL mice.15 Two core epitopes identified within this region are presented by I-Au: MBP125-135 (GGRASDYKSAH) and MBP136-146 (KGFKGAYDAQG).4 Surprisingly, many T cells isolated from MBP-/- mice degenerately respond to both I-Au/MBP125-135 (pMHC125) and I-Au/MBP136-146 (pMHC136). Anchor and TCR contact positions for the peptides were defined by measuring both MHC binding complex half-life (τ1/2) and T cell responses to a series of peptide mutations.4 The major TCR contacts (rather than MHC anchor residues) in each peptide required for recognition by degenerate TCRs are chemically distinct, thus providing an ideal system for investigating degenerate TCR recognition of pMHCs.

 

TABLE 2. Origin, sequence, potency, and function of stimulatory peptides for CSF TCC X8a

TABLE 2.

I think it is interesting work, but I bet on there being activation of other latent viral infections due to the immune suppression outcomes in chronic Lyme infections.  You know, the secret, TLR2-tolerization (no antibodies)-, Corixa-NIH Biodefense-Contractin-, Paul Duray-esque "Epstein-Barr transformed"-, Plum Island stuff.

If we're betting on genetics, I'm betting on fungi and the HLA-DQB1*0602/HLA-DRB1*1501 pair as more related to certain Northern Europeans being intolerant to fighting off fungal antigens and susceptible to the immune suppression-related outcomes of activation of latent viruses. 

They say there is no Multiple Sclerosis down at the equator.  Would that be because the children are exposed to all sorts of fungi and therefore have become tolerant before that Thymus-hardening phenomenon?

http://www.ncbi.nlm.nih.gov/sites/MEDLNE:  Multiple Sclerosis and Equator:


"Multiple sclerosis is unevenly distributed throughout the world. Its prevalence depends on latitude: it decreases in each hemisphere from pole to equator. France is situated in a high prevalence zone, with 40 cases for 100,000 inhabitants. The prevalence of multiple sclerosis is modulated by risk factors unrelated to latitude; genetic susceptibility factors (HLA, Gm), as well as environmental, occupational, nutritional and infectious (notably viral) factors have been identified, but no conclusion can be drawn concerning their role in the aetiology and pathogenesis of the disease. Among the hypotheses that could put an end to this deadlock, the heterogeneity of multiple sclerosis must seriously be considered, and it might serve as a basis for further epidemiological studies benefiting from recent technological developments such as molecular genetics and magnetic resonance imaging."

 

OSPA_AND_EPSTEINBARR.htm

The inhibitory effect of Mycoplasma fermentans on tumour necrosis factor (TNF)-alpha-induced apoptosis resides in the membrane lipoproteins.

Mycoplasma have been shown to be involved in the alteration of several eukaryotic cell functions, such as cytokine production, gene expression and more. We have previously reported that infection of human myelomonocytic U937 cell line with live Mycoplasma fermentans (M. fermentans) inhibited tumour necrosis factor (TNF-alpha)-induced apoptosis. Mycoplasmal membrane lipoproteins [Pam3Cys- that infamous HIV antigen, discussed in Chapter 3, Steere in Europe and in the Plum Island Chapter] are considered to be the most potent initiators of inflammatory reactions in mycoplasmal infections. The aim of this study was to clarify whether the inhibitory effect on TNFalpha-induced apoptosis is exerted by M. fermentans lipoproteins (LPMf). A significant reduction in TNFalpha-induced apoptosis was demonstrated by stimulation of U937 cells with M. fermentans total proteins, LPMf or MALP-2 (M. fermentans synthetic lipopeptide), but not with M. fermentans hydrophilic protein preparation (AqMf). To investigate the mechanism of M. fermentans antiapoptotic effect, the reduction of mitochondrial transmembrane potential (delta psi m) was measured. M. fermentans total proteins LPMf and MALP-2, but not AqMf, inhibited the reduction of delta psi m. In addition, M. fermentans total proteins LPMf and MALP-2, but not AqMf, downregulated the formation of active caspase-8. NF-kappaB was transactivated in cells treated with M. fermentans lipoproteins, and was essential for host cell survival, but not for the inhibition of TNFalpha-induced apoptosis by LPMf. Our results suggest that the inhibitory effect exerted by M. fermentans on TNFalpha-induced apoptosis in U937 cells is due to the membrane lipoproteins of these bacteria.

http://www.ncbi.nlm.nih.gov/pubmed/16889623?ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

Idea!!

Tell the truth for a change.  You might actually help people with all sorts of other diseases !!

 

==========================================================================

 

BIOMARKER:  Circulating Immune Complexes (stroke, vasculitis, UConn's Louis Reik)
http://www.ncbi.nlm.nih.gov/sites/entrez?MEDLINE  "circulating immune complexes and Lyme"

 

The always-never-discussed strokes associated with both Lyme Disease and LYMErix.

"always-never-discussed" =  alnever.  I'll have to add that to the Connecticutisms and define it as the crooks' "Negative Data Rule."

 

What were those Lyme-like exclusion criteria again, Dr. Schoen?

Huh?

Did you say, "chronic Lyme disease" ?

Oh.

 

So, how many heart attacks, now, and new cases of breast cancer, Dr. Schoen??

We don't know what "injuries" Schoen is talking about in this Phase IV trial but if I were to wager, I would say vascular injury ("requiring surgery" - I'm thinking by-pass surgery), especially in light of the blot-smudging or the conglobulation or mismicellation of OspA in the actual vaccine vial.  In other words, I think the blot-smudging is a function of OspA not being free in the vial, due to its tendency to stick to itself.  If OspA is conglobulating, we think that would result in stroke, in much the same way circulating immune complexes can cause stroke.

Perhaps even moreso.

The Blot-Smudging report by Lenny Sqeegal and RICO Persing:

 

The RICO-Schoen and RICO-Persing original, 1996, OspA Blot-Smudging report:
http://jcm.asm.org/cgi/reprint/35/1/233?view=long&pmid=8968914

The RICO Monopoly Patent on testing and LYMErix 
The Dave Persing, Mayo Clinic FRAUD Patent-6,045,804 
Note the date on the patent.  May, 1996.

"The present invention provides a method useful to detect a B. burgdorferi infection in a
 subject. The method provided by the invention is particularly useful to discriminate B.
 burgdorferi infection from OspA vaccination, although it is sufficiently sensitive and
 specific to use in any general Lyme disease screening or diagnostic application. Thus, the
 method of the invention is particularly appropriate for large scale screening or
 diagnostic applications where only part of the subject population has been vaccinated
 or where the vaccination status of the population is unknown. "

 

 (Or, "appropriate for a monopoly on vaccines and testing to go to Imugen and Yale's L2
 Diagnostics," ya mean?)

 

Anyways, who knows.  No matter what comes out of this particular crook, Robert Schoen, it's a lie.  We wonder why Schoen even bothered with this Phase IV trial knowing he still had no way to tell whether or not LYMErix prevented Lyme, since he had been all along keeping it rather a secret that he could not read his Western Blots in OspA-vaccinated people in the Phase III trial.  The Phase III trial report said they used the Steere/Dearborn method to assess this "vaccine's" outcome:

As seen in Chapter 4 on "What I told the FDA morons"

The 1998 Vaccines Reports (ImmuLyme and LYMErix):

LYMErix results (76% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/209  (Note that the criteria for a positive test or vaccine failure was the Dearborn interpretation of "Lyme Disease" and that later we learned that none of these criminals could even read their Western Blots in LYMErix vaccinated people.)

ImmuLyme results (92% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/216  (New England Journal, again.  NEJM never looked at the diagnostic standard to assess whether or not this was a scientifically valid report, yet that would be the whole point of "peer review.")

From the LYMErix trial:
http://content.nejm.org/cgi/content-nw/full/339/4/209/T1

----------------------------

CONCLUSION:

Amazing things have happened to the participants of the Lyme Wars.  Steere was apparently abducted by space aliens and threatened to retract his previous observations or else because “chronic Lyme disease” became the most magical phenomenon observed in modern times.  Second only to the collapse of the World Trade Center Building 7 on 9/11/01 which was clearly due Thermate Paranoia, as I call it.

Keep in mind that the neurologic signs of pathological processes are not identified with the Dearborn/CDC's diagnostic standard for "Lyme Disease."  That is, this damage will be ongoing for months to years before a person finds the right MD who is competent to diagnosing Borreliosis or Relapsing Fever.

All of the above biomarkers of disease or illness processes are reports by people in the Steere camp, or were referenced by the Steere camp - those who now say the disease is not real.

 

Note the libel:

Robert T. Schoen, Yale Rheumatology, Annals of Internel Medicine, Vol 132, No 8:

"Other peripheral neuropathies and Lyme meningitis are also seen at this stage.  In late-stage disease, the central nervous system may be involved.  A new diagnostic test measuring glial fibrillary acidic protein in cerebrospinal fluid may prove to be a useful tool for measuring such involvement (20)." 

 

Robert T. Schoen, Yale Rheumatology, Prevention Magazine:

 “While it's especially important at this time of year to be aware of the warning signs of the disease – a skin rash around the site of a tick bite, headache, fever, fatigue and muscle or joint pain – Lyme paranoia, as I call it, is not warranted.”-- The previous text was excerpted from Prevention magazine, published by Rodale Press. Lyme fear prevails more than disease. , The Washington Times, 04-18-1999

 

 

 

 

 

CHAPTER 11, KLEMPNER ("a bogus article")
 

http://www.ourladyswarriors.org/prayer/michael.htm

Saint Michael the Archangel,
defend us in battle.
Be our protection against the wickedness and snares of the devil.
May God rebuke him, we humbly pray;
and do Thou, O Prince of the Heavenly Host -
by the Divine Power of God -
cast into hell, satan and all the evil spirits,
who roam throughout the world seeking the ruin of souls.

Amen.

 

See the BIOMARKERS_AUTOPLAY.htm movie page for the complete movie (It's Benach, not Benache)  This movie shows the RICO Scam, as regards leaving OspA and B out of the diagnostic standard in order to acquire a monopoly on blood testing and all the patentable goodies in the blood.  This data is the essential be the template for the criminal homicide and racketeering indictment.  Yale's Robert Schoen reports that they could not read their Western Blots in LYMErix-vaccinated people, so they lied to the FDA about the safety and efficacy of LYMErix.  This is a "fraud on the government."
 

 

Lyme crooks have asserted that we have "Lyme internet cult" "group-telekinesis," yet they are the authors of the scientifically valid biomarkers of real illness.  We assert that if we had magical powers we would not be using it on ourselves in order to be further tortured by these pukes.  Think about it.  We'd be puttin our potions on them!!
 

Okay, so according to Mark Klempner, Lyme is cured by "the placebo effect of antibiotics," and "Lyme is Fibromyalgia," but "Fibromyalgia is due to 'catastrophizing'":
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=11083273[uid]

Got that? If you have Chronic Lyme, you're catastrophizing whichin dem wimminz do.

 

In this purple box are the keys to the New Great Imitator outcomes and the Crime of Lyme and LYMErix- they are the same thing.  The bacterial star wars or the shed Osps cause immune suppression outcomes which are the New Great Imitator outcomes, which are the LYMErix adverse events deliberately not reported to the FDA by Yale's Robert Schoen et al...

Try to keep the images you see in this chapter in your head because what you will see 100% refutes anything IDSA has to say about "Lyme disease" and LYMErix.  In the next chapter on Mark Klempner (which should really be a chapter on Anthony Fauci, too), Klempner's world of discovery where he says that people with Steere's disease do not suffer the overall illness signs of chronic Lyme (interesting point, since only Steere's kind of Lyme were considered Lyme in what Klempner alleged were "Two-controlled trials of the standard of care for chronic Lyme" ...), and that there is no genetic relationship to the adverse neurological outcomes - outcomes over which the National Institute of Neurological Disorders and Stroke recruited the German scientist Roland Martin (Chp 20) - really make it look like Lyme and LYMErix caused the same New Great Imitator outcomes due to the ablation of antigen processing or the cessation of the production of antibodies to Borrelial antigens (not restricted to haplotypes, now; a third of all people are at risk for these chronic Lyme outcomes), and the inhibition of normal immune responses such as apoptosis of infected cells.

Anthony Fauci, while he publicly agrees with the Lyme criminals that "Lyme is only an inflammatory disease," meanwhile has a couple of patents for immune system treatment of people who have damaged or turned off immune systems, such as from chronic Lyme being chronic or LYMErix vaccination, shedding or injecting these Pam3Cys surface antigens as you see below in these graphics:

Yer gonna really flip out when you understand what these assholes are saying as opposed to what they know.

"Borrelia burgdorferi-Induced Tolerance as a Model of Persistence via Immunosuppression" - 
"In summary, we characterized tolerance induced by B. burgdorferi, describing a model of desensitization
which might mirror the immunosuppression recently attributed to the persistence of
Borrelia in immunocompetent hosts." 
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=12819085

 

 

 

 

 

 

 

 

"On occasion, these atypical-appearing large lymphocytes have been misinterpreted in biopsy by several laboratories as cells of a malignant lymphoma or leukemia.  Bb antigens, then, may stimulate growth of immature lymphocytic suibsets in some target organs, as well as in the cerebrospinal fluid (Szyfelbein and Ross 1988).  Usual bacterial infections do not produce such lymphocytic infiltrates in tissue.  These immunoblastoid cells in Bb infections at times resemble those found in Epstein-Barr virus infections.  Does Bb reactivate latent virus infections in tissues?  Do some tick inocula harbor simultaneous infectious agents (ixodid ticks can harbor Rickettsiae, Babesia microti, and Ehrlichia bacteria, in addition to Bb), producing multi-agent infections in some hosts?  Further studies can clarify these issues by mans of tissue-based molecular probe analysis." -  Paul Duray, NCI, NIH, Ft. Detrick, at the 1992 Cold Spring Harbor Crooks' Conference, published in Steve Schutzer's



Lyme Disease: Molecular and Immunologic Approaches.
http://www.amazon.com/Lyme-Disease-Immunologic-Approaches-Communications/dp/0879693770/ref=sr_1_2?ie=UTF8&s=books&qid=1214848669&sr=1-2


Mixed Lyme and Epstein-Barr (Czech Republic):
http://www.ncbi.nlm.nih.gov/pubmed/12630667?ordinalpos=12&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

Many researchers believe that the secret to B. burgdorferi's infectivity and inflammatory capacity lies in the interaction of its surface proteins with the host's immunological system. Yale researcher Stephen Barthold, a veterinarian and professor of comparative medicine who developed the first mouse model of Lyme disease, studies the expression of B. burgdorferi surface proteins throughout various stages of the spirochete's life cycle. He finds that during the early stages of infection, B. burgdorferi avoids immune detection by decreasing its expression of surface proteins or cloaking its expressed surface proteins under a layer of slime. "It's using some sort of stealth-bomber-type mechanism," he says. Or, using another diversionary tactic called blebbing, the spirochete can pinch off bits of its membrane in order to release its surface proteins. Explains Barbour: "It's like a bacterial Star Wars defense program," in which released surface proteins might intercept incoming host antibodies, keeping the spirochete safe from immunological attack.
http://www.actionlyme.org/BARBOURS_STEALTH_BOMBERS.htm

 

The next graphic is from Dave Nelson at URI, when he demonstrates that spirochetes encapsulate but then revert to the intact spirochete form when exposed to whole blood cells, since that's their favorite food:

 

Mycoplasma/mycobacterial lipoproteins (vaccines) screwing up the immune response:
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Link&db=pubmed&dbFrom=PubMed&from_uid=15294983

AND:
http://www.ncbi.nlm.nih.gov/pubmed/16889623?ordinalpos=8&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum

 

: Cell Microbiol. 2007 Jan;9(1):142-53. Epub 2006 Aug 2. Links

 

The inhibitory effect of Mycoplasma fermentans on tumour necrosis factor (TNF)-alpha-induced apoptosis resides in the membrane lipoproteins.

Department of Microbiology and Immunology, Faculty of Health Sciences, Soroka University Medical Center, Ben-Gurion University of the Negev, Beer-Sheva, Israel, 84105.

Mycoplasma have been shown to be involved in the alteration of several eukaryotic cell functions, such as cytokine production, gene expression and more. We have previously reported that infection of human myelomonocytic U937 cell line with live Mycoplasma fermentans (M. fermentans) inhibited tumour necrosis factor (TNF-alpha)-induced apoptosis. Mycoplasmal membrane lipoproteins are considered to be the most potent initiators of inflammatory reactions in mycoplasmal infections. The aim of this study was to clarify whether the inhibitory effect on TNFalpha-induced apoptosis is exerted by M. fermentans lipoproteins (LPMf). A significant reduction in TNFalpha-induced apoptosis was demonstrated by stimulation of U937 cells with M. fermentans total proteins, LPMf or MALP-2 (M. fermentans synthetic lipopeptide), but not with M. fermentans hydrophilic protein preparation (AqMf). To investigate the mechanism of M. fermentans antiapoptotic effect, the reduction of mitochondrial transmembrane potential (delta psi m) was measured. M. fermentans total proteins LPMf and MALP-2, but not AqMf, inhibited the reduction of delta psi m. In addition, M. fermentans total proteins LPMf and MALP-2, but not AqMf, downregulated the formation of active caspase-8. NF-kappaB was transactivated in cells treated with M. fermentans lipoproteins, and was essential for host cell survival, but not for the inhibition of TNFalpha-induced apoptosis by LPMf. Our results suggest that the inhibitory effect exerted by M. fermentans on TNFalpha-induced apoptosis in U937 cells is due to the membrane lipoproteins of these bacteria.

 

So, we are showing you the essential data which shows that by deliberately blowing off Lyme and LYMErix victims, these criminals inhibited important discovery in many areas.  Recall from Chapter 3 that ospA is the same kind of fungal antigens as those found in HIV, mycoplasma, and E. coli.

 

 

 

ETHICS LECTURE:

In my own case of Chronic Lyme, I have quite abundant evidence of relapsing brain relapsing fever, that it comes from Lyme (positive Lyme tests, positive EMGs, relapsing-remitting brain SPECT scans with IV treatment, OspA antigen in my spinal fluid, activated latent viral infections all kinds, and positive congenital Lyme tests for my children; it isn't possible for me to be more positive for Lyme Borreliosis until I am autopsied), and that these records were given to Yale's James Phillips in the summer of 2000.  Phillips then proceeded to commit malpractice, give me further brain damage, and then he lied about it under oath. Because it is obvious that James Phillips committed perjury in addition to being medically incompetent, all "cases" in Connecticut for which James Phillips served as a "forensic expert" have to be thrown out and retried.

No matter how you look at it, there is no excuse for James Phillips not looking at mine and my kids' medical records showing what Lyme IS and that I gave it to my children.  There is NO EXCUSE for saying all of this is MY FAULT and that I could cure the entire world of all their ills if I would become a slut, like the internationally infamous Connecticut "Department of Children and Families" former Commissioner, Kristine Ragaglia.  In fact, DCF's Chief drunken slut lost her children to her ex-husband because of all her slutty, drunken behavior. 

Perhaps Ragaglia would endeavor to demonstrate to all the Junior-DCF-Whores-in-Training at America's universities' "Schools of Social Work," that the porking recommended by psychiatry is not always a winning strategy. 

From Malachi Martin's book Hostage to the Devil in an exorcism case where an atheist psychiatrist ("Dr. Hammond") who was given a pseudonym as this book is not fiction but a recording of events) was a participant, the following exchange occurred between the possessing demons, the psychiatrist, and the exorcist (Gerald):

"Richard/Rita’s sudden scream split their eardrums. “We go, Priest. We go.” It was a million turbulent voices as one, full of eternal ache and pain. “We go in hate. And no one will change our hate. And we will wait for you. When you come to die, we’ll be there. We go. But”-Gerald heard the sharp injection of hate hissing through the sorrow-“we take him.” Richard/Rita’s hands suddenly swept up in a wide arc toward Dr. Hammond. It was a quick but clumsy movement.


Hammond jumped backward. And Richard/Rita fell off the couch to the floor as the assistants jumped forward and held him down.

'"We already have his soul. We claim him. He is ours. And you cannot do anything about that. We already have him. He is ours. We needn’t fight for him.'


Richard/Rita was wheezing like someone being asphyxiated, eyes bulging, neck muscles standing out, his long hair falling back, his chest heaving, as he half-rose in his effort.
“You can’t get him back. He is ours. He does our work. He doesn’t need a box. He puts everybody else into it.”


All calm was gone from Dr. Hammond
[the psychiatrist]; his face was a picture of black fear....

From Hostage to the Devil, a conversation with Satan about Freudian psychiatrists encouraging slutty, porking behavior.  Right now all duh DCF stupid porkers are trained by psychiatry to "GO FOR IT!!, GET ALL YOU CAN OUT OF SEX!!"

 

In later chapters I will give a thorough explanation of why psychiatrists are so evil and unintelligent. A student of them becomes aware through much study that psychiatrists are actually very, very confused people who struggle with their own sanity their whole lives.  There is abundant independent evidence that a high percentage of them are of extremely evil which I will discuss and be confident that no one will win a libel suit against me.  It will all be true and I will be naming names.  This information will be beneficial to the community so that these perpetrators of fraud, malpractice and perjury can be avoided. 

 

NEW WORLD ORDER CORRUPTICOURTS:
 

I don't expect these revelations to cause too much of a shake up in Corrupticut, because no amount of evidence of the outrageous, unconstitutional, criminal behavior being performed in the name of the State, in the name of the people, and on the taxpayers dime - especially in the self-alleged courts - ever effects any changes.  Connecticut is the lead, the first, New World Order state and the judges have no qualms about revealing this openly in the self-alleged courts.  One judge said attorneys have no First Amendment rights. Another judge was caught driving between court districts to illegally place documents in other cases. One judge made numerous phone calls to judges in Massachusetts to get them all to file complaints about an attorney defending cases in Connecticut to get rid of this winning, annoying attorney.  One judge openly calls Hispanics, "El Stupido," and illegally denies them a public defender.  One judge actually barred note-taking by reporters in a trial.  Many of the judges in the probate courts (CT is known as the worst probate court system in the nation) are not even lawyers.  Many of the newly approved judges on the bench in Connecticut have had no trial experience whatsoever, and it is even true, that some of the people who win judgships have never set foot in a Connecticut court to file a single motion, ever.  They don't know what goes on in a courtroom. These new judges have no idea what kind of railroading tricks the prosecutors pull.  These totally inexperienced people don't know the law to know whether or not one particular piece of evidence is admissible and have to rely on the crooked prosecutors. 


That's what innocent people are up against here- anything goes.  This NWO system is meant to terrorize the citizenry.  The very known-to-be-crazy "judges" are actually advanced in the court system.  They're promoted.  Complaints about them in CT Legislative Judicial Committee Hearings or the "Judicial Review Board" are retaliated against with false criminal charges, or are ignored, and are literally shredded soon after received by this "Complaint Department:"   The only thing missing is the actual burning of the accused at the stake.  We have openly recommended that the crematoriums should be adjacent to the self-alleged court houses, because your life is over, once you're in BigBrother's crosshairs.  But it is more beneficial to the moron union members to keep people alive for decades in the prisons, because "prison guard" is a position for white racist morons- people better suited to driving garbage collection vehicles or laying railroad ties.


Connecticut really ought to have its own Comedy Central cartoon, sitcom or Daily Show.


What irks me the most is that these "judges" (and numerous other people involved in the State, who work for the State, who work-for-Yale-for-the-State), in view of their very abundant examples of outrageous behavior, that they perform these outrageous behaviors, that they would even think of pulling these antics, that the "elected representatives" have been made aware of the insane behaviors on the part of the judges but don't care in the least, can only mean that they - the judges, especially - fully believe that this kind of sneaky, low-life behavior is common to all the people and acceptable to all the people, yet to believe that such is so, is prejudice against all the people.  If this the best this state can come up with, everyone better be very, very scared.

 

As mentioned in the introduction, there is a never ending swarm of demonic nutcases emerging from the hell hole known as Corrupticut that residents and especially Lyme victims have to exhaust themselves further dodging.  We wonder where these Statees get the energy to be so perpetually vicious.  Corrupticut is a unique earthly phenomenon.

 

END ETHICS LECTURE, CHP 10