04/26/2013 04:54:09
Cryme Trainer (moved)
Non-HLA-linked Diseases
Hurricane Sandy and Mold-Related
illnesses (like LYMErix and Lyme Disease, and CFIDS/FM).
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References for psychotropics-induced brain damage
Older data on the incurability of Relapsing Fever
1986, McSweegan trashes Navy for $$$ for ALDF.com
1988, Dattwyler & about immune-suppressing, seronegative Lyme
1990, CDC: "Diagnose Lyme as if it was Relapsing Fever."
Allen Steere "NeuroLyme won't test positive," 1990.
1992, CDC officer Allen Steere falsifies testing in Europe
1992, CDC patents with SmithKline show 2 kinds of Lyme
Compare the 2 kinds of Lyme in the RICO complaint
1994, CDC's Dearborn Booklet .pdf
CDC's invitation to participate in Dearborn .pdf
Evidence Lyme criminals knew LYMErix produced the same "multisystem disease" as "Chronic Lyme"
LYMErix Damage Coverup
(short)
1998, CIA Oilmen & Israelis plan to overthrow Saddam for the oil.
Bush/Gore Oil/War-(Oct,2000)
Bush's own explainer (Oct
2000) re:
Iraq Oil
CHAPTER 5, the RNA and RNA Primers Shell Game
See also, CENTRAL_LYME_RICO_PATENTS.htm for how Alan Barbour and Gary Wormser tricked Ed Masters out of Lone Stari, a cow Relapsing Fever organism (using the wrong DNA. The wrong DNA is the OspA gene, because flagelin defines the species and there are plenty of RF spirochetes that do not have the synthetic Pam3Cys in it.
PART I; We propose that there are four reports which show that these Lyme 180s knew they could not assess (unreadable results) whether or not LYMErix or OspA vaccinations prevented "Lyme Disease" with Western Blotting, and that therefore they simply lied to the FDA, to the public, and to the journals that published their ImmuLyme and LYMErix results.LYMERIX RESULTS (76% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/209
IMMULYME RESULTS (92% "safe and effective"):
http://content.nejm.org/cgi/content/abstract/339/4/216 (New England Journal, again. They never looked at the standard to assess whether or not this was a scientifically valid report, as was the case with the Klempner - no DNA primers listed in the method - report yikes these Mass Medical Society people are scary stupid and just plain dangerous.)Here are those 4 reports:
1) SCHOEN and PERSING, with JOHN ANDERSON,1996:
http://jcm.asm.org/cgi/reprint/35/1/233?view=long&pmid=8968914
2) SCHOEN AND PERSING IN THEIR 1996 RICO METHOD PATENT:
The Dave Persing, Mayo Clinic FRAUD Patent-6,045,804
3) PERSING WITH SIGAL EXPLAINING THAT THE WESTERN BLOTS WERE UNREADABLE, 2000:
http://www.journals.uchicago.edu/doi/pdf/10.1086/313920
4) Yale's ROBERT SCHOEN in the 1998 Munchausen's Book, instructing MDs to blow off LYMErix systemically injured people.We can't imagine what their explanation will be when asked under oath what was the meaning of all of this. They could have used a recombinant, specific, FDA-valid flagellin method (CHAPTER 1) which they had already validated and to some extent worked up (Magnarelli and Fikrig in 1992), or they could have used the correct DNA and RNA primers to assess spinal fluid and blood products from persons who claimed to feel ill subsequent to LYMErix vaccination, particularly those people who had "already had Lyme before," since those were the people who bubbled to the surface in Southeastern Corrupticut Lyme Support Groupland, as mentioned in the previous chapter (and to the FDA Vaccine Committee).
PART II - THE PRIMERS SHELL GAME -- The 180s have never used the correct gene primers to detect Borrelia DNA or RNA in patient treatment or vaccine outcomes with the exceptions of then Wormser tick-bite treatment efficacy report, below, and the Steere-Nocton knee-persistence report seen in Chapter 11, where they both proved with these methods that treatment fails. Yet, they all know which are the correct primers to use.
They should be using species specific RNA intragenic spacer genes, such as 16S or 23S RNA, since there are more copies of them, than, say, the flagellin gene. The 180s always use the variable DNA encoded on the plasmids (like OspA) in order to find "NO LYME," when appropriate to their spin protocol. This plasmid DNA changes, since these are the sources of the varying proteins seen on the surface of the spirochete, which make them relapsing fever organisms that execute "antigenic variation." Antigenic Variation is the mechanism that causes the relapse or growth of a new population of organism that don't make the surface proteins against which any vaccine or antibodies would do any good. It's SIMPLE.
The following reports show that these criminals know which are the correct primers to have been using all along to detect Borreliosis either after treatment or for vaccines assessments:1) Yale (Schoen and Persing are the authors of this report) and all the Lyme 180s know how to detect any kind of borreliosis and they have known since the early 1990s: Use Borreliae-specific RNA or DNA primers encoded on the chromosome (and don't use any varying plasmid DNA). This happens to be the same RICO report that went with the RICO patent.
The RICO report was reported after the RICO patent was applied for, by the way, yet they are basically the same report:.
In this report (above and linked in full text below) - and this is the RICO report associated with the RICO patent - Yale demonstrates that they know how to diagnose any kind of Lyme or borreliosis anywhere in the USA by using Borrelia burgdorferi-specific 23S RNA primers. These primers have never been used to assess treatment (antibiotics) outcomes in humans (except Gary Wormser on tick bite, and Steere-Nocton with knees, as mentioned).
Yale demonstrates that they know how to diagnose any kind of Lyme or borreliosis anywhere in the USA by using 23S RNA primers.
from:
http://jcm.asm.org/cgi/reprint/35/1/233?view=long&pmid=8968914
2) The 1992 Wormser report where he uses the correct RNA primers to assess erythema migrans rashes (this is the only report where they use the correct primers to assess any kind of treatment outcome, and in this case, this is where they found that 2/9 people who were treated with antibiotics for tick bite still had spirochetal RNA in their skin samples at follow up skin puncture biopsy):
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=1452688
The associated full text .pdf file (use this link for your website):
http://jcm.asm.org/cgi/reprint/30/12/3082?view=long&pmid=1452688
shows exactly what Gary Wormser did and why:
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3) Wormser in 1999 using the correct primers to look for all sorts of borrelia- primers not used to assess any recent human treatment outcomes.
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=9986813
J Clin Microbiol. 1999 Mar;37(3):565-9.
Genetic diversity of Borrelia burgdorferi in lyme disease patients as determined by culture versus direct PCR with clinical specimens.Departments of Biochemistry and Molecular Biology, New York Medical College, Valhalla, New York 10595, USA.
Two hundred seventeen isolates of Borrelia burgdorferi originally cultured from skin biopsy samples or blood of early Lyme disease patients were genetically characterized by PCR-restriction fragment length polymorphism (RFLP) typing of the 16S-23S ribosomal DNA intergenic spacer. Three major RFLP types were observed. Of the cultured isolates, 63 of 217 (29.0%) were type 1, 85 of 217 (39.2%) were type 2, and 58 of 217 (26.7%) were type 3; mixtures of two RFLP types were obtained in 6.0% (13 of 217) of the cultures. Comparison of typing of B. burgdorferi performed directly on 51 patient skin specimens with typing of cultures originally isolated from the same tissue revealed that a much larger proportion of direct tissue samples had mixtures of RFLP types (43.1% by direct typing versus 5.9% by culture [P < 0.001). In addition, identical RFLP types were observed in only 35.5% (11 of 31) of the paired samples. RFLP type 3 organisms were recovered from blood at a significantly lower rate than were either type 1 or type 2 strains. These studies demonstrate that the genetic diversity of B. burgdorferi patient isolates as determined by cultivation differs from that assessed by PCR performed directly on patient tissue.
PMID: 9986813 [PubMed - indexed for MEDLINE]
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4) Yale's Durland Fish, in 2001, using the correct primers whenever he wants to find spirochetes in ticks. These primers have never been used to assess human treatment outcomes (except for Wormser on tick bite in 1992 and Nocton-Steere on knees in 1994).
http://mic.sgmjournals.org/cgi/content/full/147/6/1425?view=long&pmid=11390674
Microbiology (2001), 147, 1425-1436.
© 2001 Society for General Microbiology
Visualization of Borrelia burgdorferi sensu lato by fluorescence in situ hybridization (FISH) on whole-body sections of Ixodes ricinus ticks and gerbil skin biopsies
Bettina Hammer1 ,Annette Moter1 ,Olaf Kahl2 ,Gerd Alberti3 andUlf B. Göbel1
Institut für Mikrobiologie und Hygiene, Universitätsklinikum Charité, Humboldt-Universität zu Berlin, Dorotheenstraße 96, D-10117 Berlin, Germany1
Institut für Biologie, Angewandte Zoologie/Ökologie der Tiere, Freie Universität Berlin, Haderslebener Straße 9, D-12163 Berlin, Germany2
Zoologisches Institut und Museum, Ernst-Moritz-Arndt-Universität, J.-S.-Bachstraße 11/12, D-17487 Greifswald, Germany3Author for correspondence: Bettina Hammer. Tel: +49 30 450 524074. Fax: +49 30 450 524902. e-mail: bettina.hammer@charite.de
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5) Dattwyler and Luft using the correct DNA primers- ones encoded on the chromosome and not on any varying DNA plasmids (non-varying, species-specific, heat shock protein DNA):
http://iai.asm.org/cgi/reprint/60/9/3704?view=long&pmid=1379988
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6) 1992, Yves Lobet of SmithKline, Belgium, using the correct (non-varying DNA) primers to assess for spirochetes in ticks. Never used in human treatment vaccines outcomes:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=1356932
Evaluation of genetic divergence among Borrelia burgdorferi isolates by use of OspA, fla, HSP60, and HSP70 gene probes.
German Cancer Research Center, Heidelberg.
In order to assess the genetic variation of immunologically relevant structures among isolates of the Lyme disease spirochete, Borrelia burgdorferi, three chromosomal genes encoding flagellin (fla) and the heat shock proteins HSP60 and HSP70, as well as the plasmid gene encoding outer surface protein A (OspA), from 55 different European and North American strains obtained from ticks and mammal hosts have been investigated by restriction fragment length polymorphisms (RFLPs). RFLPs of fla and the HSP60 and HSP70 genes revealed two distinct banding patterns (A and B) for each of the three genes and allowed the definition of four genomic groups [AAA, BBB, BBA, and B(A/B)A] for the three chromosomal genes. On the other hand, RFLPs of the OspA gene revealed six distinct banding patterns (types I to VI) making up six independent genomic groups for the plasmid-encoded gene. Furthermore, we have sequenced the chromosomal HSP60 gene from B. burgdorferi ZS7 and the plasmid-encoded OspA gene from two strains, ZQ1 and 19857. Alignment of the deduced HSP60 amino acid sequence from B. burgdorferi ZS7 (genomic group AAA) to a previously published HSP60 sequence derived from strain ACA-1, which according to the proposed classification is in a different genomic group (BBA), revealed a sequence identity of > 99%. Similar alignments of the OspA sequence of strain ZQ1 to those of other isolates that were published previously revealed sequence identities of between 70 and 94% among strains of distinct OspA genomic groups. These data indicate the existence of a restricted number of species-specific subgroups and clearly show that genotypic variation is much more pronounced for the OspA gene than for fla and the HSP60 and HSP70 genes. A phylogenetic tree constructed on the basis of distance matrix analyses of 12 OspA sequences supports the proposed classification of genomic groups of B. burgdorferi.
PMID: 1356932 [PubMed - indexed for MEDLINE]
They wanted to make "Lyme Disease" all about OspA and they even pulled the wool over the eyes of Edwin Masters and basically stole his "Southern Lyme Disease" or "Master's Disease" from him and renamed it Borrelia barbouri.
There is no test available for B. barbouri, but the way, as if that would surprise you. Barbour owns barbouri and no one is allowed to have it. Sound familiar?
To this day we are not sure Edwin Masters understands the Shell Game. All MDs should take a close look at the NIH NLM Taxonomy database and look at the references the taxonomizers use for determination of relatedness between these Borreliae spirochetes:
http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=138
Click on Borrelia, the main heading name:
http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=138&lvl=3&lin=f&keep=1&srchmode=1&unlockComments and References:
- Skerman VBD et al. (1980)
- Skerman, V.B.D., McGowan, V., and Sneath, P.H.A. (editors). "Approved lists of bacterial names." Int. J. Syst. Bacteriol. (1980) 30:225-420. [No PubMed record available.]
Borrelia (Euzeby link)
Fukunaga M et al. (1996b)
- Fukunaga, M., Okada, K., Nakao, M., Konishi, T., and Sato, Y. "Phylogenetic analysis of Borrelia species based on flagellin gene sequences and its application for molecular typing of Lyme disease borreliae." Int. J. Syst. Bacteriol. (1996) 46:898-905.
- Ras, N.M., Lascola, B., Postic, D., Cutler, S.J., Rodhain, F., Baranton, G., Raoult, D. "Phylogenesis of relapsing fever Borrelia spp." Int. J. Syst. Bacteriol. (1996) 46:859-865.
They are organized by differences in flagellin. Then, the point is to look for all Borreliae in a sick person by using all recombinant specific flagellins or species-specific RNA spacer genes from ALL American Relapsing Fever species in America, and likewise for Europe and everywhere else - because those genes don't undergo antigen variation. This was all already determined in the early 1990s.
The 180s never mention this, and worse, Mark Klempner never reported which DNA primers he used in his fake long term treatment study. Worse still, the 180s all know these Borreliae are not "clonal," if all the plasmids undergo antigenic variation, that all the spirochetes "host adapt," and that one can "select for mutants" (are all Relapsing Fever organisms) simply by vaccinating or exposing the bugs to antibodies.
Here are those proofs:
1992, CDC "officer" Alan Barbour, discussing "selecting mutants:"
BARBOUR_MUTANTS_1992.htm
1995, Yale's Erol Fikrig and Richard Flavell, on how LYMErix vaccination failed but would also "select mutants":
http://iai.asm.org/cgi/reprint/63/5/1658?view=long&pmid=77298702001, CDC Officer Alan Barbour on "Antigenic Variation in Vector-Borne Pathogens:"
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=10998374%5Buid%5D
We like this report very much because it exposes the fact that due to antigenic variation, not only can there never be vaccine for them, the Steere diagnostic method is bogus. How can they say that "due to antigenic variations vaccines would do no good," but also claim that we have to have 5 of 10 of the Dressler/Steere bands in order to have a case of Lyme Disease? If you can't make a vaccine out of Relapsing Fever relapsing antigens, then it is also true that all we can do is test for these Relapsing FEver infections with antigens that DON'T CHANGE, like flagellin.
1990, Andrew Pachner on Borrelial plasmids in the brain:
PACHNER_BRAINS_1990.htm"The plasmid content of N40Br was different from that of the infecting strain implying either a highly selective process during infection or DNA rearrangement in the organism in vivo. "
Recall that the 180s claim that there is no such thing as Lyme as a brain disease. Mark Klempner published in 2003 that there was no such thing as brain signs in "post-treatment chronic Lyme disease."
To which we respond, "That's fine, Mark, because there is no such entity as 'Lyme Disease,' or Steere's 'receiver operating characteristics,' or an autoimmune, hypersensitivity knee disease that requires the meningitis drug ceftriaxone (as Steere proposes and practices), or even a vaccine for this non-disease. We assert that it was your 'neuroborreliosis' patients who had the matrix-metalloproteinases or nerve and brain degrading enzymes in their spinal fluid, and as you mentioned in that same report, the destruction of glial cells (energy providing cells for the brain). We agree, Mark. There are no disease signs for Steere's imaginary disease. Why should there be?"
Cognitive function in post-treatment Lyme disease: do additional antibiotics help?
University of Connecticut School of Medicine, Farmington, USA. kaplan@psychiatry.uchc.edu
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.
We have no idea who these patients are, who still test positive to the imaginary Steere/Dearborn method after treatment. If they are knee patients, we don't expect them to have cognitive signs, as was asserted by Vijay Sikand (East Lyme, CT) at the 1998 FDA Vaccine Meeting. Sikand said these seropositive patients were "immune competent," implying they made enough antibodies to manage the disease and prevent its spread (into neurologic, protected areas).
Brian Fallon at Columbia University found 0.5% of all of the patients that he screened for his Chronic Neurologic Lyme study were still Steere/Dearborn positive after previous ceftriaxone, intravenous, meningitis treatment.
Mark Klempner in 2001, found only 78 Steere/Dearborn positive patients out of 1800 (4% accuracy for the Steere/Dearborn method), but a 2/3 of his victims had not had previous intravenous ceftriaxone treatment, which was supposedly the stipulation for his long term re-treatment "study." In the Klempner study, these patients were offered the standard of care - 30 days of intravenous ceftriaxone for this permanent central nervous system disease - Relapsing Fever. At that time, 1997, 30 days of ceftriaxone was the standard of care (arbitrarily devised), so we have no idea what was the point of proposing a 4.7 million dollar study to assess the standard of care, since we knew it was inadequate or not enough treatment, leading to such studies of more or longer treatment. The Klempner study was yet another hoax.
We say: It is not up to the patients to determine which drugs should be used for central nervous system bacterial infection. That was why the Infectious Diseases Society of America was using intravenous ceftriaxone even at the time of the 1989 IDSA Reviews, where Dattwyler, Luft, Sigal and Steere all said "treatment fails in more than half the cases," and "we don't know the ceftriaxone treatment endpoint."
So, now it's a non-disease.
Fine.
In the 8 months from September 2007 to May 2008, over billion dollars worth of grants were given out and this clique got none of it. It's clear that some people in control of the money - the NIH, the Howard Hughes Foundation, and even a new Rockefeller Foundation neurosciences venture cap group - have had enough of this nonsense. The Czech Republic basically finished them off by saying:
Biological aspects of Lyme disease spirochetes: Unique bacteria of the Borrelia burgdorferi species group.
Department of Immunology, Faculty of Medicine, Hnevotinska 3, Palacky University, Olomouc, 775 15, Czech Republic. majkl.krupka@centrum.cz.
Background: Borrelia burgdorferi sensu lato is a group of at least twelve closely related species some of which are responsible for Lyme disease, the most frequent zoonosis in Europe and the USA. Many of the biological features of Borrelia are unique in prokaryotes and very interesting not only from the medical viewpoint but also from the view of molecular biology. Methods: Relevant recent articles were searched using PubMed and Google search tools. Results and Conclusion: This is a review of the biological, genetic and physiological features of the spirochete species group, Borrelia burgdorferi sensu lato. In spite of a lot of recent articles focused on B. burgdorferi sensu lato, many features of Borrelia biology remain obscure. It is one of the main reasons for persisting problems with prevention, diagnosis and therapy of Lyme disease. The aim of the review is to summarize ongoing current knowledge into a lucid and comprehensible form.
TRANSLATION: "US Lyme research is incomprehensible and stupid. Back to the drawing board. And where we'll start is the taxonomy database. We're talking about Borreliae or Relapsing Fever and no more of this 'LYME DISEASE' nonsense."
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.CHAPTER 6, RICO PATENTS (tell a different story from the public one)
http://www.ourladyswarriors.org/prayer/michael.htm
Amen.
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.======================================================
