Mort Zuckerman
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 Posted: Thu Nov 13, 2008 7:43 pm Post subject: Simon Wessely>s foolishness makes other real scientists FURI |
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Subject: Simon Wessely>s Foolishness makes other real scientists
FURIOUS
Date: Nov 13, 2008 2:41 PM
From Malcolm Hooper Ph.D.,B.Pharm.,C.Chem.,MRIC
Emeritus Professor of Medicinal Chemistry
School of Sciences
Fleming Building
Wharncliffe Street
University of Sunderland
SUNDERLAND SR2 3SD
Phone 0191 515 2501
FAX 0191 515 3405
Public Relations Office 0191 515 2691
Chief Scientific Adviser to the Gulf Veterans' Association
web site http://osiris.sunderland.ac.uk/autism
26 January 2006
Dear Sir,
I attended the lecture on Gulf War Syndrome by Professor Simon Wessely
on Jan 25th
at 6.00 pm.
I write to express my extreme disquiet about the proceedings
surrounding the lecture
which led to many, including myself being totally misled about whether
the lecture
would be cancelled or not. Repeatedly, I phoned 3 times, I was told
categorically
by your office staff that the lecture had been cancelled and had been
withdrawn
from the College web site. Several others were similarly informed,
including one
member of the House of Lords.
When Professor Wessely was contacted directly he gave a clear
assurance that the
lecture would proceed to one person, but indicated to me that he “had
not yet decided”
about whether he would proceed with the lecture. The whole thing
became a farce
with disturbing overtones of deception and obfuscation. Wittingly or
unwittingly
your staff were drawn into all this. These activities reflect very
badly on the
College and particularly since no apology for all the confusion was
offered to those
attending the lecture. The College prides itself on providing public
lectures in
honour of its Founder. To be faced with such dissimulation is not in
accord with
the ethos behind the lectures and besmirches the honour of Sir Thomas
Gresham.
I have written elsewhere about the contents of the lecture and will
forward a copy
to you. To do this important subject justice it is important that you
invite a response
from someone who can present a more up to date and hopeful picture of
the truth
about Gulf War Syndrome that comprehensively covers the peer reviewed
literature
particularly that which shows the extent of sickness among veterans
and the failure
of Government to care for all the sick veterans.
I would be willing to give such a lecture if invited.
Yours sincerely
Malcolm Hooper
============================================http://web.archive.org/web/20060220171303/www.meactionuk.org.uk/Gresham_college_letter_By_Malcolm_Hooper.html
http://web.archive.org/web/20060814224225/www.illnessdenied.org.uk/report.html
http://web.archive.org/web/20060813122150/http://www.illnessdenied.org.uk/
See, Simon Wessely abused and harassed Lyme/CFIDS victims
as well as Gulf War Illness victims:
http://www.actionlyme.org/ROCKET_SCIENCE.htm
Lisa Masterson was involved in that Simon Quack-Quack
Wessely protest.
Soon thereafter, she was bagged and thrown in a mental
hospital.
They use the same techniques, here in the USA:
http://www.actionlyme.org/STEERE_FAIRY_UNSTALKED.htm
It>s quite like the Israelicons and Karl Rove: 'Be the
first to point the finger at what you yourself are doing
in order to cause a distraction.
Additionally, King>s College is probably upset about IDSA
being thrown out of the UK, since clearly IDSA (it>s really
the ALDF.com) works with SmithKline, which is based in Great
Britain. SmithKline gets away with all kinds of bad drugs
and insane crap in America.
Right now SmithKline has absorbed Corixa, who got a
"NIH Biodefense Contract"
http://www.actionlyme.org/EMBASSIES_CORIXA_TLR_13_JULY_06.htm
"None other than Simon Wessely."
===========
Unfortunately for them (Corixa, the ALDF Lyme crooks, and the entire,
global healthcare arena), they were completely wrong about how innate
defenses actually work:
http://www.actionlyme.org/PAM3CYS_IMMUNE_SUPPRESSION.htm
"Prior exposure to LPS both in vitro and in vivo can lead to
desensitization
of immune cells to subsequent challenge with LPS, a phenomenon that
has been referred
to as "endotoxin tolerance."
"Pretreatment of macrophages with a pure TLR4 agonist (protein-free
Escherichia
coli (Ec) LPS) or with TLR2 agonists (Porphyromonas gingivalis LPS or
synthetic
lipoprotein Pam3Cys) led to suppression of TNF-alpha secretion, IL-1R-
associated
kinase-1, and IkappaB kinase (IKK) kinase activities, c-jun N-terminal
kinase, and
extracellular signal-regulated kinase phosphorylation, and to
suppression of NF-kappaB
DNA binding and transactivation upon challenge with the same agonist
(TLR4 or TLR2
"homotolerance," respectively).
"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."
"After performing the PCR for Mycoplasma sp. the following results
were obtained:
among the patients with ALS, 10 were found to be positive (50%) and 10
were negative
(50%), whereas in the control subjects we found six positives (10.91%)
and 49 negatives
(89.09%); these results were statistically significant (p = 0.001). On
calculating
the estimated risk, an odds ratio of 8167 (CI 95%: 2.4-27.6) was
obtained. This
indicates that the risk of suffering from ALS, if the PCR test for
Mycoplasma sp.
is positive, is 8:1. CONCLUSIONS: There is a strong link between
suffering from
a chronic infection due to Mycoplasma and developing ALS.
Intracellular pathogenic
agents such as Mycoplasma can play a role in the genesis of
neurodegenerative diseases.
http://www.ncbi.nlm.nih.gov/pubmed/16138281
"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 how important it is to get psychiatrists out of the way
of real science:
http://www.actionlyme.org/PAM3CYS_IMMUNE_SUPPRESSION.htm
◄"On occasion, these atypical-appearing large lymphocytes have been
misinterpreted
in biopsy by several laboratories as cells of a malignant lymphoma or
leukemia.
Bb antigens, then, may stimulate growth of immature lymphocytic
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
EPSTEIN-BARR AND MULTIPLE SCLEROSIS:
Lancet Neurol. 2008 Sep;7(9):852-8.Click here to read Links
B cells and multiple sclerosis.
Franciotta D, Salvetti M, Lolli F, Serafini B, Aloisi F.
http://www.ncbi.nlm.nih.gov/pubmed/18703007?ordinalpos=3&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
Clonal expansion of B cells and the production of oligoclonal IgG in
the brain and
cerebrospinal fluid (CSF) of patients with multiple sclerosis (MS)
have long been
interpreted as circumstantial evidence of the immune-mediated
pathogenesis of the
disease and suggest a possible infectious cause. Extensive work on
intrathecally
produced antibodies has not yet clarified whether they are
pathogenetically relevant.
Irrespective of antibody specificity, however, the processes of
antibody synthesis
in the CNS of patients with MS are becoming increasingly clear.
Likewise, targeting
B cells might be therapeutically relevant in MS and other autoimmune
diseases that
are deemed to be driven predominantly by T cells. Accumulating
evidence indicates
that in MS, similar to rheumatoid arthritis, B cells aggregate into
lymphoid-like
structures in the target organ. The process of aggregation is mediated
through the
expression of lymphoid-homing chemokines. In the brain of a patient
with MS, ectopic
B-cell follicles preferentially adjoin the pial membrane within the
subarachnoid
space. *** Recent findings indicate that substantial numbers of B
cells that are
infected with Epstein-Barr virus (EBV) accumulate in these
intrameningeal follicles
and in white matter lesions and are probably the target of a cytotoxic
immune response.****
These findings, which await confirmation, could be an explanation for
the continuous
B-cell and T-cell activation in MS, but leave open concerns about the
possible pathogenicity
of autoantibodies. Going beyond the antimyelin-antibody dogma, the
above data warrant
further work on various B-cell-related mechanisms, including
investigation of B-cell
effector and regulatory functions, definition of the consistency of
CNS colonisation
by Epstein-Barr virus-infected B cells, and understanding of the
mechanisms that
underlie the formation and persistence of tertiary lymphoid tissues in
patients
with MS and other chronic autoimmune diseases (ectopic follicle
syndromes). This
work will stimulate new and unconventional ways of reasoning about MS
pathogenesis.
From the 1989 IDSA Reviews Special Supplement on Lyme and Spirochetal
Diseases,
article by Paul Duray:
"Immature B cells can also be seen in the spinal fluid. These cells
can appear
quite atypical- not unlike those of transformed or neoplastic
lymphocytes."
- - - -
"Recent findings indicate that substantial numbers of B cells that are
infected
with Epstein-Barr virus (EBV) accumulate in these intrameningeal
follicles and in
white matter lesions and are probably the target of a cytotoxic immune
response."
Get it?
MS is probably not an autoimmune disease, but we might
have found that out in the mid-1990s, had not Yale, Inc
decided to LIE about the outcomes of LYMErix and about
Lyme, in general.
We don>t need "Unabomber-" saying psychiatric idiots in the
way of this.
Kathleen M. Dickson
http://www.actionlyme.org
http://www.relapsingfever.org |
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