How many people peport that Arthur Weinstein is a liar???

ON THIS PAGE:

How many people say Arthur Weinstein is a liar (besides Ray Dattwyler at the 1994 FDA Vaccine Committee Meeting?), that he most certainly had conflicts of interest (is a liar and a murderer as regards his participation in the ImmuLyme OspA trial), and that "Lyme Disease" and OspA vaccination are not inflammatory diseases but diseases of immunosuppression and immune dysregulation?

◄ "Seronegative Lyme victims are the sickest" - Ray Dattwyler at the
1994 FDA Vaccine Committee Meeting.

But is this chargeable as a scientific fraud and racketeering crime?

Let's just look at one person's role in this...

Arthur Weinstein was the guy in charge of the CDC's 1994 Dearborn "Work Group" to approve the bogus Steere/Dressler method to diagnose Lyme, despite the fact that NONE OF THE INVITED LABS AGREED WITH THEM!!

http://www.cdc.gov/mmwr/preview/mmwrhtml/00038469.htm (◄Dearborn standard)

Dearborn, Michigan is where it was decided that one has to have "Late Lyme Arthritis in a knee" in order to have a "case" of "Early Lyme," and this guy Weinstein was apparently the final "decider" despite none of the labs agreeing with Steere's proposal to change the diagnostic standard.

How many people say Arthur Weinstein is a liar (besides Ray Dattwyler at the 1994 FDA Vaccine Committee Meeting?), that he most certainly had conflicts of interest (is a liar and a murderer as regards his participation in the ImmuLyme OspA trial), and that "Lyme Disease" and OspA vaccination are not inflammatory diseases but diseases of immunosuppression and immune dysregulation?

(twice)
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=8308100
Serodiagnosis in Early Lyme Disease:
"Steere's Dearborn proposal for a case definition sucks and only detects 9/59 cases by IgG alone
so it shouldn't be used for any vaccine trials."

3) Justin Radolf
http://www.jimmunol.org/cgi/content/full/167/2/910
Synthetic analogs of lipopeptides from Treponema pallidumalso inhibited Ag processing. Despite the ability
of MTB 19-kDalipoprotein to activate microbicidal and innate immune functionsearly in infection, TLR 2-dependent
inhibition of MHC-II expressionand Ag processing by MTB 19-kDa lipoprotein during later phasesof macrophage
infection may prevent presentation of MTB Agsand decrease recognition by T cells.

5) John Dunn at Brookhaven says Lyme is a stealth pathogen that results in non-knee diseases
http://www.actionlyme.org/JohnDunn_Brookhaven.htm
"It's the perfect stealth bacteria," says one frustrated physician. He's talking about Borrelia burgdorferi, the bacterium that causes Lyme disease. This illness, which is often mistaken for diseases ranging from multiple sclerosis to Lupus, can inflict excruciating headaches and muscle pain, affect the brain and nervous system, attack major organs, and inflame joints.

IGENEX says of the Dearborn Standard: http://igenex.com/labtest.htm
"It is difficult for each laboratory to perform clinical studies and establish its own ranges for normal and disease populations. For this reason, the CDC assembled a group of academic scientists with the assistance of the FDA and the Association of State and Territorial Public Health Laboratory Directors (ASTPHLD) to reach a consensus on certain criteria for the Western blot. After several meetings they arrived at the CDC/ASPHLD consensus criteria presented in Table 2 (7,36). These criteria were based in large part on the work of Dressler et al (37), using well-defined patients with active Lyme arthritis or neuroborreliosis. Interestingly, in their publication none of the three CDC/ASPHLD recommended strains of B. burgdorferi (B31, 297 and 2591) were used. Rather, they used G39/40 with a 10% acrylamide gel, although a gel with less than 11% of acrylamide does not have enough resolution nor definition of all the important antigens of B. burgdorferi.

"The criteria for a positive Western blot to B. burgdorferi developed by the CDC/ASPHLD are very conservative and require 5 of 10 antibody bands for IgG positivity; the original recommendations do not even recognize equivocal or borderline results if less than five bands are detected. Their cut-off assumes that all Lyme patients have similar immune systems. They ignore the diversity of the immune response seen in other diseases. Their studies were problematic in that they primarily focused on patients with early (usually within four months of an EM) Lyme disease. They drew blood in most patients every two weeks during this four-month period and any positive event (five out of ten bands) was counted as a positive patient, even if they were negative at a different time of the study. In addition, the criteria include antibodies to 41 kDa, a common antigen of most flagella-bearing organisms, and exclude two of the most important and specific antigens, 31 kDa (Osp A) and 34 kDa (Osp B), which appear later in the response. A review by Hilton et al (38) in a group of 50 patients with confirmed Lyme disease showed that they would have missed 4 patients by excluding 31 kDa (Osp A) and 34 kDa (Osp B). The author's own laboratory would have missed 2 of 18 proficiency samples by excluding antibodies to these two antigens."

17) David Volkman
http://www.mlasg.com/files/VolkmanIDSA.pdf
"In our original report (7) we described a group of 17 patients who all suffered from either
neurological or arthritic signs frequently attributed to chronic borrelia infection. These
individuals lived in areas endemic for Lyme disease, all had had a pathognomonic
erythema migrans (EM) rash, all had a course of antibiotics (tetracycline, erythromycin,
or an abbreviated course of another antibiotic) early in their illness, all had T cell
blastogenic responses consistent with exposure to borrelia, and curiously, all lacked
detectable antibodies against borrelia. Although early antibiotic treatment abrogated
antibody responses, it did not eradicate infection. When retreated, most of these chronic
patients markedly improved within a month of completing a course of intravenous
ceftriaxone, consistent with their problems being due to persistent, ongoing occult
infection;

"Immature B cells can also be seen in the spinal fluid. These cells can
appear quite atypical - not unlike those of transformed or neoplastic
lymphocytes."

(twice)
http://www.actionlyme.org/Duray.htm

"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 subsets 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 deliver
simultaneous infectious agents (ixodid ticks and harbor Rickettsiae, Babesia microti,
and Ehrlichia bacteria, in addition to Bb), producing multi-agent infections?"

So, unlike what Weinstein claims, this ▲ is not: "all Lyme patients test Steere-HLA-
hypersensitivity-related-inflammation-positive, and if they don't, they're don't have
illness, but have 'crazy.'"

And, obviously, improve SENSITIVITY, since in actuality and contrary to
what Weinstein claims, SENSITIVITY is an FDA criterion also called LIMIT
OF QUANTITATION or LIMIT OF DETECTION, and refers to the method
validation requirement that one shows that one's method detects which lowest
concentration of the analyte in question, which is the complete opposite of
Weinstein's fraudulent article where he falsely claims that "the more antibodies,
the more valid the Steere Method."

Weinstein's Bogus Article on the "Validation" of the Dearborn/Steere
proposal:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=8053960[uid]
Western blot band intensity analysis. Application to the diagnosis of Lyme arthritis.
CONCLUSION. Band intensity analysis increases the objectivity and accuracy of Western blot
interpretation for the diagnosis of Lyme arthritis.

So that ▲is a bogus article and a criminal charge because that's not how
validations work. "Objectivity" is not a requirement. That's why we have
very sensitive analytical instrumentation in a real-life chemistry lab and
method validations require reporting of instrumentation and calibrations of
the instrumentation, to show that performance of the actual instruments is
also valid and reliable.

That, in my lifetime, is the most ridiculous scientific report ever published.
It is the dumbest scientific report I have ever seen.
That it was published in a Rheumatology journal in addition to Malawista's
report where he says the brain is a complicating variable which should therefore
be thrown out, tells you a lot about Rheumatology.

(Fibromyalgia patients should be made aware of their scientific caliber.)

22) Coyle and Schutzer
Sequestration of antibody to Borrelia burgdorferi in immune complexes in seronegative Lyme disease.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=1967770[uid
"To find out whether apparent seronegativity in patients strongly suspected of having Lyme disease can be due
to sequestration of antibodies in immune complexes, such complexes were isolated and tested for antibody to Borrelia
burgdorferi. In a blinded analysis the antibody was detected in all 10 seronegative Lyme disease patients with erythema
chronicum migrans (ECM),..."

Again, this ▲ is where a person could be seronegative - but isn't, but if Weinstein
got ahold of them, they would be declared "not sick but insane."

"Although a single ligation of TLRs induces responses such asTNF production, repeated ligation [vaccination with OspA
or being subject to Osp-blebbing, which is a chronic condition of infection, since as Alan Barbour says, these spirochetes shed
these antigens, which is an immune evasion mechanism in addition to part of what Relapsing Fever spirochetes DO] will lead to
a loss of response,i.e., the cells become tolerant. Tolerance to self and alsoto nonself is a general phenomenon preventing or
diminishinginflammatory responses of the immune system, and involves eitherdeletion of responder cells, down-regulation of the
respectivereceptors, blockade of signal transduction, or induction ofsuppressive cytokines."
http://www.actionlyme.org/BARBOURS_STEALTH_BOMBERS.htm

Tolerance of immune cells will occur when leukocytes down-regulate their response after a primary encounter with antigen
or other ligands. Tolerance can act via deletion, receptor down-regulation, blockade of signal transduction or via the action
of suppressive cytokines. Monocytes and dendritic cells (DCs) belong to the innate immune system but they are instrumental in
instructing the cells of the adaptive immune system via antigen presentation and cytokine production. One of the main cytokines
produced by these cells is tumor necrosis factor (TNF), a cytokine that acts at various levels in order to promote immune response
and inflammation.

TNF is produced upon activation of monocytes and DCs by microbial products like lipopolysaccharide (LPS) of Pam₃Cys, which
act by binding to toll like receptors (TLRs). When cells are exposed to these compounds repeatedly, then the TNF production is
decreased, i.e. the cells have become tolerant. The molecular mechanism of tolerance to date has been studied only in monocytes
and macrophages. For LPS stimulation it was shown early on that the CD14 co-receptor was not down but rather up-regulated in
tolerant cells [1]. Also, signal transduction still occurred with mobilisation of p50/p65 of NF-κB, but there was at the same time an
increase in NF-κB p50-homodimers which bind to the promoter and displace the p50/p65 heterodimer. Since p50 cannot transactivate
this will lead to blockade of TNF gene expression [1,2]. In addition to this p50-homodimer mechanism, blockade in LPS tolerant
monocytes can also occur through interruption of the signalling cascade at the level of IRAK-1 in that this adaptor protein is proteolytically
degraded [3,4]. For monocytes tolerant to the TLR-ligand Pam₃Cys this mechanism also applied and there was a strong and complete
ablation of IRAK-1 [5].

OspA Pam3Cys vaccination causes the same immunosuppression as the
chronic blebbing of chronic Lyme. Therefore, Weinstein is scientifically
wrong that "Lyme only produces chronic inflammation in a knee, and that
if people state otherwise, they're crazy."

Clearly all these science and all these proofs prove that it is Weinstein
who is crazy. That's what happens to liars. They go crazy. They get
stuck in their own vortex of lies and falsehoods and insane justifications
from which they almost never emerge, partly from all the guilt from all the
harm they know they've caused with their previous evil, lying and selfish
deeds.

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 TNFα-induced apoptosis is exerted by M. fermentans lipoproteins (LPMf). A significant reduction in TNFα-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 (ΔΨm) was measured. M. fermentans total proteins LPMf and MALP-2, but not AqMf, inhibited the reduction of ΔΨm. In addition, M. fermentans total proteins LPMf and MALP-2, but not AqMf, downregulated the formation of active caspase-8. NF-κB was transactivated in cells treated with M. fermentans lipoproteins, and was essential for host cell survival, but not for the inhibition of TNFα-induced apoptosis by LPMf. Our results suggest that the inhibitory effect exerted by M. fermentans on TNFα-induced apoptosis in U937 cells is due to the membrane lipoproteins of these bacteria.

28) NYU Disagrees with Weinstein (Sep, 2009) (OspA causes immunosuppression)http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=19629181
"To specifically address the role of TLR2 signaling in mediating this inhibition, we
stimulated macrophages with the specific TLR2/1 ligand ***Pam3CSK4 and
assayed responses to IFN-ã. Pam3CSK4 stimulation prior to IFN-ã
inhibited transcription of the unrelated IFN-ã-inducible genes, CIITA
and CXCL11. Surface expression of MHC class II and secretion of CXCL11
were greatly reduced as well,*** indicating that the reduction in
transcripts had downstream effects."

That means after a time, antibodies will not be produced, if the MHC molecules
are down-regulated.

That means Weinstein is wrong.

Schroder and Schumann:
"With the exception of Mycoplasma-caused pneumonia, clinically important pathogens carrying lipoproteins represent causes of slow, cyclic or chronic infectious diseases, e.g., Lyme disease or tuberculosis. Even mycoplasm pneumonia, although frequent in children, is often afebrile and self-limitingin contrast to pneumonia caused by other pathogens (61). Ourdata suggest that recognition of these slow-acting microorganismsmay also be accomplished by LBP. Synthetic lipopeptides havebeen the basis for broad vaccine development lately for a widevariety of diseases including HIV, malaria, CMV, and HSV (reviewedin Ref. 16). Understanding of the molecular mechanisms of hostrecognition of lipopeptides and lipoproteins in more detailmay further help to further improve these innovative strategies.^"