01 Oct 2017
Home
File List, RICO
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
CrymeDiseaseNorway
crymedisease
theothersideofthestretcher
rjspiritualityandtuth
LymeTruthSite
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
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*,,
Marion Frankenberger,
Elke Benkhart*,,
Terje Espevik,
Martina Quirling¶, Korbinian Brand¶,
Marek Zembala
and Loems Ziegler-Heitbrock2,,||
* Institute for Immunology, University of
Muenchen, Muenchen, Germany;
Department of Clinical Immunology, Jagiellonian University Medical
College, Kraków, Poland;
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.
Copyright
© 2003, American Society for Microbiology
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
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
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
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
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
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
|