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 |
| |
141120-- This
chapter will probably be re-written
(originally written Nov, 2007) or
included in another chapter
when I reduce it all for the
New "Khan Academy" of Lyme Cryme.
Much of the same data is
included in other reports - see the
homepage. KMDickson
The
German scientist Roland Martin,
former head of the NINDS-Multiple
Sclerosis Division because he found Lyme
to be a cause of MS, quit his job at
the NIH went back home to Germany once he
found that the TLR2 agonist OspA was
actually the cause of the MS
presentation of Lyme.
Meanwhile,
in his lab at the NIH were all foreign
students (see the bottom of this page)
because... they wanted the
DISINFORMATION of "auto-immune T cells
as the cause of MS" to spread out around
the world, once these students when home
to their native countries.
Martin
quit when he found out he had been used
and that, in fact, the LYMErix vaccine,
OspA, was immunosuppressive (caused
seronegative disease) and was
responsible for the chronic illness:
Borrelia burgdorferi Induces TLR1 and TLR2 in human microglia and peripheral blood monocytes but differentially regulates HLA-class II expression.
Borrelia burgdorferi lipoprotein-mediated TLR2 stimulation causes the down-regulation of TLR5 [manages flagellin] in human monocytes.
CHAPTER 18;
Corrupticut Unions and Politicians
*
Martin R on autoimmune T cells in the CSF of
Borreliosis victims (full text scanned in)
Connecticut,
everyone will learn, is an extraordinary place. It's a locale where
the viciousness of WWII and Cold War clandestine warfare is nearly 100%
common; everyday life and everyday thinking. The citizens of this
state have the world's worst case of Keeping Up With the Joneses. If a
case study were the goal, anthropologists would find that it is a literal
fact that "a human rights activist is insane," according to the vast
majority of Connecticut residents. Although bartering and finagling
and skimming and cheating, and the drugs, alcohol, hatred and paranoia are
of course frowned-upon publicly, no anthropologists point out that these
happen to be The Great White Way, in contrast to the sorts of social
faux-pas that Blacks are customarily accused. What we have here is the
likes of a Jew calling a German a Jew for his behavior. The Great
Whites are only great in their hypocrisy.
So bizarre is this
state, that I had to listen to a lecture by a staff member of State
Representative James Amann's (D- Milford) whose name also happens to be
Kathleen. Amann's Kathleen tells me she is a chemist and that she
knows all about the testing for "Lyme
Disease." That surprises me because she would not be a chemist
working for James Amann if that were true. Amann's Kathleen tells me
she knows more about Lyme disease than I do because her mother had it and
that her mother got better from it. Usually people are criticized when
making general exclamations about medical conditions on the basis of a
relative's brief experience with it. In fact, the likes of Amann's
"chemist" are the very scary tards the Lyme criminals warn us about.
Amann's full time
job is to be a fund-raiser for the Multiple Sclerosis Society of America.
He gets a percent of the money he raises. Thus, he is so good at
selling himself and his retarded bullshit, he not only became a politician,
he became the Connecticut State Speaker of the House. The unions elect
the democrats because republicans have generally, in the past, been against
big government and unionized screw-driver-turners. The republicans in
Connecticut keep a low profile except for when they want to create the
emergencies of "bad parents and criminals" in order to defraud Uncle Sam
over how much "bad" goes on in this state, in order to not raise CT State
income taxes. It's a simple formulary where anyone who is not rich or
a State employee union member is fodder for this human hamburger processor.
The mere people have the same function they did in Machu Picchu. The
mere people are the materiél and maintenance of slaughter needed to
keep the political gods and the union gods happy so it will rain dollars
from China.
The National
Institute of Neurological Disorder and Stroke's MS Chief, Roland Martin,
having been unable to prove that the Multiple Sclerosis version of Lyme
Disease/Relapsing Fever (undetectable with the current Dearborn CDC diagnostic
method) is due to autoimmune T cells returned to his home country, Germany.
One can go to the CRISP database and enter Martin, Roland and search for all
his grants. http://crisp.cit.nih.gov/crisp/crisp_query.generate_screen
Grant Number |
PI Name |
Project Title |
1Z01NS002204-28 |
MARTIN, ROLAND |
Immunologic Mechanisms In Experimental
Autoimmune Diseas |
1Z01NS002204-29 |
MARTIN, ROLAND |
Immunologic Mechanisms In Experimental
Autoimmune Diseas |
1Z01NS002205-23 |
MARTIN, ROLAND |
INTERACTIONS BETWEEN THE HUMAN IMMUNE
SYSTEM AND ANTIGENS IN THE NERVOUS SYSTEM |
1Z01NS002205-24 |
MARTIN, ROLAND |
INTERACTIONS BETWEEN THE HUMAN IMMUNE
SYSTEM AND ANTIGENS IN THE NERVOUS SYSTEM |
1Z01NS002205-25 |
MARTIN, ROLAND |
INTERACTIONS BETWEEN THE HUMAN IMMUNE
SYSTEM AND ANTIGENS IN THE NERVOUS SYSTEM |
1Z01NS002205-26 |
MARTIN, ROLAND |
Interactions Between The Human Immune
System And Antigen |
1Z01NS002205-27 |
MARTIN, ROLAND |
Interactions Between The Human Immune
System And Antigen |
1Z01NS002205-28 |
MARTIN, ROLAND |
Interactions Between The Human Immune
System And Antigen |
1Z01NS002205-29 |
MARTIN, ROLAND |
Interactions Between The Human Immune
System And Antigen |
Grant
Number: |
1Z01NS002205-29 |
Project
Title: |
Interactions
Between The Human Immune System And Antigen |
PI
Information: |
Name |
Email |
Title |
|
MARTIN, ROLAND |
|
|
Abstract:
This project examines the immunological
mechanisms which involved in the pathogenesis of autoimmune- and infectious
diseases of the central nervous system such as multiple sclerosis (MS) and
chronic Lyme disease. We characterize the fine specificity, function and
phenotype of T lymphocytes in the above diseases. These experiments allow
a better understanding of the foreign antigens that may trigger autoimmune
responses in MS and also of their function with respect to cytokine
secretion and chemokine receptor expression. Based on this knowledge the
project attempts to develop both specific immunomodulatory treatments such
as altered peptide ligands (APL) or therapies that influence immune
recognition in MS in a broader way. Examples of the latter are the humanized
antibody against the interleukin-2 receptor alpha chain (Zenapax) or the
phosphodiesterase type IV inhibitor Rolipram. The trial with the APL peptide
has been concluded, and the data published. The clinical trials with Zenapax
and Rolipram are both supported through bench-to-bedside proposals.
Treatment of relapsing-remitting MS patients failing interferon-beta with
Zenapax has been well tolerated and successful, i.e. the primary outcome has
been met. Clinicial testing of Rolipram has been stopped due to lack of
efficacy and necessary changes of trial design. Mechanistic studies along
the experimental trials are ongoing and have e.g. delineated that Zenapax
acts primarily via expansion of immunoregulatory NK cells. These studies
will help us to understand better the complex mechanism of action of these
compounds and eventually also the disease pathogenesis itself. All the
clinical projects are being pursued in close collaboration with the
Neurological Disease Section Section/Office of the Chief under Henry F.
McFarland, M.D. Another important project, which is currently being pursued
at NIB, NINDS, NIH, addresses the question which foreign antigens, e.g.
viruses or bacteria, may trigger the initiation or exacerbations of disease
via a mechanism referred to as molecular mimicry. This concept refers to
cross-recognition between autoantigens, e.g. derived from the myelin sheath,
and antigens derived from foreign agents. For this purpose, we currently
employ a novel methodology called combinatorial peptide libraries in the
positional scanning format (ps-SCL) together with bioinformatic approaches
to identify the entire spectrum of stimulatory ligands for autoreactive T
cell clones derived from MS patients. In brief, we test T cell clones
with ps-SCL, which represent highly complex mixtures of trillions of
peptides, and deduce stimulatory peptide sequences from these assays before
we screen the databases of all known protein sequences for potential
stimulatory peptides. We are currently in the process of developing this
methodology further and anticipate that the combination of ps-SCL and
biometric data analysis will lead to advances in the identification of
target antigens for autoimmune diseases, but also for tumor-specific
lymphocytes or T cells that are involved in infectious disease. As an
example for the latter, our data for organ-infiltrating T cells in chronic
nervous system Lyme disease already suggest that the immune response in the
chronic stage of the disease is directed against tissue autoantigens and
that this process is thus very similar to an autoimmune disease.
Currently, we also develop molecular biology strategies, i.e. the expression
of cDNA clones from MS brain in a special eukaryotic expression system, for
the identification of novel proteins that are expressed in MS brains and
serve as targets for the autoimmune response. New projects include: The
migration and differentiation of neural stem cells into glial/neural cells.
Integration of immunological studies, MRI, clinical examination, expression
profiling and proteomics for the stratification of MS subtypes.
Public Health Relevance:
This Public Health Relevance is not available [because to admit that Lyme
causes MS is not politically correct].
Thesaurus Terms: Lyme disease, autoantigen, human therapy evaluation, immunopathology,
monoclonal antibody, multiple sclerosis, nervous system disorder
chemotherapy, neuroimmunomodulation, phosphodiesterase inhibitor T cell
receptor, T lymphocyte, bacterial protein, chemokine receptor, clinical
trial, cytokine receptor, method development, natural killer cell, nerve
stem cell, pathologic process, receptor expression, virus protein
combinatorial chemistry, human subject, magnetic resonance imaging, patient
oriented research, peptide library
Institution: |
|
Fiscal Year: |
2004 |
Department: |
|
Project Start: |
|
Project End: |
|
ICD: |
NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS
AND STROKE |
IRG: |
NIB |
Now, let's
take another look at what we know from the Steere/Dearborn method to
diagnose Lyme. The data, the files, the journal report (Dressler/Steere) is in the public domain because it was entered as
evidence to the FDA's LYMErix vaccine meeting January 31, 2001,
by myself
and not James Amann's chemist. The differences in the Western Blotting
between Steere's HLA and Roland Martin and Mark Klempner's HLAs look like this:
Recall from
Chp 3 that I got this data from Germany:
http://alpha1.mpk.med.uni-muenchen.de/bak/nrz-borrelia/miq-lyme/Frame-MiQ-microbiological53.html
From the Dressler/Steere report, when reported the result of his field test
("Prospective study") of his
proposed method:
Steere here redefines Lyme according to
his own criteria because he intended all along to state that Lyme was
only a hypersensitivity reaction in a knee. This,
Dressler/Steere
in Germany with the bogus high passage strains and making up validation
criteria like "receiver operating characteristic," is research fraud or
a medical hoax. This is a "bogus article" as explained previously
in Chapter 3.The people who have
Neuroborreliosis AND the inflammatory kind of Lyme are
rare even today. We only know a handful of such people who have
had neurologic Lyme for years in addition to the arthritis signs.
Half the people with
Neuroborreliosis have detectable "proteins" or invasion with
inflammatory lymphocytes, according to Andrew Pachner in 1989.
Cerebrospinal fluid analysis (looking for cells), and EMG are not "clinical" criteria. In 1989 it was known by IDSA that
Lyme meningitis was mistakenly missed because it is an ASEPTIC
meningitis (low or no cells in the CSF):
IDSA_GREATIMITATOR.htm
Steere in 1991, when he published about
seronegative Lyme using the Dattwyler/Volkman seronegative Lyme T-cell
proliferation assay, reported that 4/9 of his Borrelia lab workers had
been exposed to Borrelia (we assume this was due to inhalation of
spheroplasts, as discussed by the US Army manual on infectious diseases
in Haiti).
Steere reported here in Dressler/Steere
that either 17 or 35 out of 237
patients who all thought they had Lyme as diagnosed by other labs to
had Steere's idea of Lyme. Remember, Steere and Imugen were
at that time using high passage G39/40 and FRG in their Imugen Lab, when
both strains are illegal. One because it is German and the other
because it as high passage. It's tough to tell exactly what he
did, as Steere's reports tend to be intentionally illogically garbled
and impossible to follow.
If you read and re-read carefully, the
full text of this Dressler report, the Antigens in Europe report, and
Steere's original standard ("look for changing and expanding IgM by
sequential Western Blot"), you will see that they wanted to contain
(keep small) the number of cases of Lyme Disease because they originally
thought Lyme originated in the United States in the Plum Island area.
Steere went to Germany as well as
Russia to "instruct" the researchers there as to what they were to
perceive as regards testing for Lyme. He screwed-up-and-lied to
Russia and he screwed-up-and-lied to Germany. If Lyme is not an
accidental release from Plum Island there would have been no need for
the Lie-Trips to Europe.
It was all spin and scientific garbage.
You can see with your own eyeballs that
Steere's kind of Lyme is a hypersensitivity response.
"Receiver operating characteristic"
means "the more antibodies, the better," when, well, we would hope
Steere would never be put in charge of detecting plutonium for UNSCOM.
If Allen Steere was in charge of AIDS,
it still would not be a recognized disease.
A real student of this will look very,
very closely at what Allen Steere did and what Gary Wormser and his gang
are trying to do at the present time. It is a do-over of the first
crime. They insist Lyme is only a bad knee, when we know it is a
very serious relapsing fever type of spirochete because it
is not in the blood most of the time like the other relapsing fevers-
which can be detected readily by blood smear during the relapse.
Roland Martin in latest report (2006)
basically reported the same finding as his first (1988) report which had the result of Martin coming to the United States:
*
Martin R on autoimmune T cells in the CSF of
Borreliosis victims (full text scanned in)
Infection and Immunity, January
2007, p. 243-251, Vol. 75, No. 1 0019-9567/07/$08.00+0 doi:10.1128/IAI.01110-06 Copyright © 2007,
American Society for Microbiology. All
Rights Reserved.
Cerebrospinal Fluid-Infiltrating
CD4+ T Cells Recognize Borrelia burgdorferi Lysine-Enriched
Protein Domains and Central Nervous System Autoantigens in Early Lyme
EncephalitisJan D.
Lünemann,1,5 Harald Gelderblom,1,6 Mireia
Sospedra,1,2 Jacqueline A. Quandt,1 Clemencia
Pinilla,3 Adriana Marques,4 and Roland Martin1,2*
Neuroimmunology Branch, Cellular
Immunology Section, National Institute of Neurological Disorders and
Stroke, National Institutes of Health, Bethesda, Maryland 20892,1
Institute for Neuroimmunology and Clinical MS Research (INiMS), Center
for Molecular Neurobiology Hamburg (ZMNH), University Clinic Eppendorf,
Falkenried 94, 20251 Hamburg, Germany,2 Mixture Science and
Torrey Pines Institute for Molecular Studies, San Diego, California
92121,3 Laboratory of Clinical Infectious Diseases, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health, Bethesda, Maryland 20892,4 Laboratory of Viral
Immunobiology, The Rockefeller University, New York, New York 10021,5
Department of Neurology and Psychiatry, Charité Medical Center, Humboldt
University, 10098 Berlin, Germany6
Received 14 July
2006/ Returned for modification 15 September 2006/ Accepted 10 October
2006
Neurological manifestations of Lyme
disease are usually accompanied by inflammatory changes in
the cerebrospinal fluid (CSF) and the recruitment of
activated T cells into the CSF compartment. In order to
characterize the phenotype and identify target antigens of
CSF-infiltrating T cells in early neuroborreliosis with central nervous system (CNS) involvement, we combined T-cell cloning, functional testing of T-cell responses with positional scanning synthetic combinatorial peptide libraries, and biometric data analysis. We demonstrate that CD4+ gamma
interferon-producing T cells specifically responding to
Borrelia burgdorferi lysate were present in the CSF of a
patient with acute Lyme encephalitis. Some T-cell clones
recognized previously uncharacterized B. burgdorferi epitopes
which show a specific enrichment for lysine, such as the heat
shock-induced chaperone HSP90. Degenerate T-cell recognition
that included T-cell responses to borrelia-specific and
CNS-specific autoantigens derived from the myelin protein 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase) could be demonstrated for one representative clone. Our results show that spirochetal antigen-specific and Th1-polarized CD4+
lymphocytes infiltrate the CSF during monophasic CNS symptoms
of Lyme disease and demonstrate that cross-recognition of CNS
antigens by B. burgdorferi-specific T cells is not restricted
to chronic and treatment-resistant manifestations.
We say, okay. What do we know from
the MS-Lyme experiment?
Basically that Lyme can be mistaken for
Multiple Sclerosis since there is really no way to tell them apart based on
the clinical and the lab data, combined. There is no diagnostic class
of badly cloned T cells, such that you could run a comparative T-cell check
on an MS person or a Lyme person. Everyone does their own personal T
cell (and B) warping based on their particular antigen-varying spirochetes and their
genetic background. Remember from the RICO patents chapter, CDC
officer Alan Barbour said that Lyme infected people could have just
overwhelmed immune systems from this non-clonality, the variety of original
spirochetes, and the infinite variations in the blebs.
Our immune systems have gone haywire.
And everyone is different.
And if you ask a Lyme specialist, they will
tell you too: Everyone is different with their daily and hourly and
typical Lyme complaints. It really is relentless torture. One
minute you're almost fine and you can get the laundry done (since this chore
only takes 30 seconds at time), and the next minute you have a splitting
migraine on one side of your head. Then later in the day you'll have
sharp pains here and there and you're dead tired. The headache is literally
blinding in that your eyes won't focus or even work together (one goes one
way and the other goes another), and all you can think about is SHUT
OFF THE LIGHTS AND THE NOISE!! and
LET ME CRAWL INTO A CAVE and EVERYONE SHUT
UP!!!
'Just like the flu. Every little
noise bothers you and you would kill for sleep, since that's the only escape
from it.
Sunlight is like metal cylinders stabbing
into your eye sockets and your thoughts turn to ghosts, since that's what
you've become. You hide from the sunlight. You walk around the
windows because you can't bear to get any near your head. It is
something no one can understand unless they've tried it or have very
recently had a very bad flu. You're saying to yourself (foolishlessly;
as a result of your previous American establishment brainwarping) "Maybe I should call a doctor?!!"
Then you remember.
There is no one to call.
Maybe by 5 o'clock PM you feel almost normal (for everyday Lyme) again but
by 7 you're ready to collapse.... That's Lyme Disease- an all day long
all year long all life long variety show that would make Job look like the
Princess and her Pea.
As we Lymies always say, If you don't
believe us, by all means, try it.
Bill Chinook (Bruce Springsteen's E- Street Band, living in Maine) killed
himself last summer (2007) and it wasn't because he was looking for sex or
attention. He did it because he could not stand the misery of this
disease any more. Say what you will, but take the risk of eternal
damnation for not being sympathetic, since "CARE" is what the
"is" is about life itself. You have already seen enough
evidence that this disease causes nearly limitless misery.
You can see with your own eyeballs that the
testing for it is a criminal matter and that the persistence past treatment
matter was already a known and a given in 1975- says the representative of
US Military Medical in Bethesda.
MS Laboratory positive in Lyme:
Oligoclonal bands in the CSF
and T-weighted images (ischemia or mini-strokes) on brain MRI:
Martin R on oligoclonal bands in the CSF
(formerly a marker of Multiple Sclerosis) of Borreliosis victims
See also
the BIOMARKERS, BRAIN PERMANENT, and the
FUNGAL VACCINES
chapters because this MS data, the
OspA-induced-immune-suppression-and-activation-of-viral-infections outcomes,
the strange common failure method of other fungal vaccines (Tuberculosis and
Lyme), and the mycoplasma-and-fatigue and mycoplasma-and-cancer data, all appear to be related to the chronicity. In other words, if
not for the "Barbour's Stealth Bombers" or the Barbour "Bacterial Star Wars"
or what I simply call the flak aspect of the chronic shedding of surface
antigens- something relapsing fever spirochetes do anyway - in combination
with the OspA types of shed antigen, seem to be the key combo to produce a
wicked bioweapon.
1) Chronic lies about what's a positive
test 2) Denial of the potential diagnostic value of anti-flagellar antibodies 3) CDC's lies even to CT AG Richard Blumenthal 4) Stealth, microscopic tick 5) Deployment of very abusive tactics against victims and their treaters (McSweegan
and Fish) 6) The Wreckage of OspA vaccination and the deliberate non-reporting of
systemic adverse events (LYMErix causes a Lyme-like illness because chronic
Lyme and LYMErix Disease® are the same thing: all the immune suppression
outcomes of chronic Lyme including the bad, bad, irresponsible T cells in the spinal fluid and not only the knee...) 7) Deployment of the psychiatric morons, who still won't admit they're being
used by the Bigs and the "government" against the very sick Gulf War I
veterans (Humanity and the Periodicy of Social Delusions: Let's see,
the Jews and the Goyem, the Inquisition, Martin Luther, witch hunts, the
Divine Rights of Kings, Psychiatry, McCarthyism, The War on Terror,
Political-US-Attorneys, Polish-Iranian ICBM interceptors...) 8) The suppression of immune-suppression facts; the denial that this is
anything BUT an inflammatory disease 9) Ferocious attacks on mothers with children with
Congenital Lyme.
The flat-out denial of Congenital Lyme
and the latest distortion of facts,
10) Lyme came from Europe.
Bologna. It's all relapsing fever and
this OspA one just happened to be OspA-in-a-hard-bodied-tick
10 miles from
where they do such experiments. It's nearest relatives are B.
hermsii and B. anserina (African bird spirochetes), based on
differences in flagellar DNA (Picken, 1992). The rest of the characteristic of all tick
borne spirochetes is that after the linear chromosome and the wave length
code, it's almost all a matter of the plasmid DNA.
Metabolically, we can discover few
differences between them. If a borrelia is going to take to a tick two
factors must be present. Enough mutants have to be present to generate
the right surface antigens to adhere to whatever they need inside a tick,
and then more of them acquire bacteriophage-vectored DNA from other
organisms. Since Lyme came from the Plum Island area and mycoplasma
and E.coli share the same general OspA, we guess that the OspA
antigen was some DNA shared by these organisms who happen to share the same
phage. Whether or not this was deliberate or an accident, no one with
Lyme really cares. Think about it. Once you are terribly sick
from this disease, all you can think about it how you can get better and the
utter absurdity of the denial by the Lyme crooks of the existence of their
very own reports describing how very sick we are.
Then as the years go by and you get 100%
better but then relapse and discover it's all been a hoax. Your blood
boils and you try to reach back into your genetic past for a fragment of
endowment or a debt to repay or famous solider or a saint in your
lineage or the one with your name or the saint of your day - any and all of
the good people of the past who you represent today - that gives you the "We
Are" to tear these evil IDSA/ALDF/Yale lying Lyme bastards apart and throw
them into the inferno.
That they would harm so many people and
take pleasure in witnessing the double torture of their victims?
Who would be such a coward as to not to
fight them? To me, not to fight these evil pitbulls of "medicine" once I found out
what they did is unimaginable. It would be like standing by and doing
nothing while some grizzly old crazy drunk kidnaps a baby out of a shopping
cart and beats it with a baseball bat. That's how I see the people who
do nothing to help us. We're sick and we're innocent. Tick bites
are not a character flaw.
Why am
I writing this?
Why am I telling this story?? Who in a million years
imagines this sort of thing will be dumped in their laps? What kid
wishes to be a corporate cop? What kid dreams about one day punking
the latter day NAZIs? Or that fate would land them on nearly the same
town on the southeastern Connecticut coast where there was no support group
for this strange-but-not-new disease that bears the town's name, in 1993, 18
years after the disease was discovered by the famous mother
(and not father or MD), Mrs. Polly Murray.
NO SUPPORT GROUP IN THE COUNTY OF LYME in
1993 ???
What was I saying about Corrupticut?
===========ROLAND MARTIN'S FORMER WEBPAGE AT THE
NIH ============
Roland Martin, M.D.,
Investigator
Dr. Martin received his
medical training at the University of Würzburg, Germany, and prepared his
M.D. dissertation with Jörg Draeger at the University of Hamburg, Germany.
Following a post-doctoral fellowship with Hans-Wolfgang Kreth, Institute
for Virology and Immunobiology, Würzburg, and a neurology residency with
Hans-Georg Mertens, Department of Neurology, Würzburg, he received
additional post-doctoral training with Henry McFarland, Neuroimmunology
Branch, NINDS, studying cellular immunity in multiple sclerosis (MS). Dr.
Martin joined the faculty at the Department of Neurology, Tübingen,
Germany, with Johannes Dichgans, and conducted research in
neuroimmunology. Dr. Martin continued his research at the Neuroimmunology
Branch of the NIH and the Department of Neurology, University of Maryland
at Baltimore with Kenneth Johnson. In 1997 he moved to the NINDS where he
is the Acting Chief of the Cellular Immunology Section, Neuroimmunology
Branch. He has received the Heinrich Pette Award of the German
Neurological Association and a Heisenberg Professorship of the Deutsche
Forschungsgemeinschaft. Dr. Martin's laboratory investigates the cellular
immune system in multiple sclerosis and chronic Lyme disease and, together
with Henry McFarland, develops novel treatment modalities for
MS.
|
|
Staff:
- Bibiana Bielekova,
M.D., Staff Clinician bielekob@ninds.nih.gov
- Gregg Blevins,
M.D., Clinical Fellow blevinsg@ninds.nih.gov
- Erik Cabral, B.S.,
Student, (301) 496-0518
- Ricardo
Cassiani-Ingoni, Ph.D., Postdoctoral Fellow
cassanir@ninds.nih.gov
- Azita Kashani,
B.S., Research Assistant, (301) 496-0518
- Dr. Paolo A.
Muraro, M.D., Ph.D., Senior Research Fellow
murarop@ninds.nih.gov
- Elisabetta Prat,
M.D. prate@ninds.nih.gov
- Susan Scrivner,
M.S., Research Assistant scrivners@ninds.nih.gov
- Mireia Sospedra,
Ph.D., Postdoctoral Fellow sospedrm@ninds.nih.gov
- Xiang Wang, M.S.,
Senior Research Assistant, (301) 402-4488
wangxi@ninds.nih.gov
Research
Interests:
We are
interested in a better understanding of how the cellular immune system in
multiple sclerosis (MS) patients reacts to autoantigens of the central
nervous system. Our research includes studies on the molecular mechanisms
of T cell recognition, i.e. how T lymphocytes recognize antigens in the
context of MS-associated HLA-DR antigens, in particular HLA-DR15 Dw2.
These experiments address the functional and phenotypic repertoire of T
cells responding to various myelin antigens including myelin basic protein
(MBP), 2’3’-cyclic nucleotide-3’ phosphodiesterase (CNPase),
proteolipidprotein (PLP), myelin oligodendroglia glycoprotein (MOG), and
myelin oligodendroglia basic protein (MOBP), but also which foreign agents
may trigger autoreactive T cells via molecular mimicry. Through
collaborations, we develop novel methods to study molecular mimicry. Along
studies of the immunologic pathomechanisms of MS, we try to design new
immunotherapeuties based on the concepts evolving from the above work. It
is our final goal to develop these new therapeutic strategies until they
are applicable in MS patients and test them in phase I/II trials.
Candidate therapies which are currently being studied are altered peptide
ligands based on MBP peptide (83-99) as a highly specific
immunomodulation, phosphodiesterase type IV inhibitors to block
Th1-cytokines, and the administration of a humanized monoclonal antibody
against the IL-2 receptor a-chain expressed on activated T cells. In
treatment trials as well as in longitudinal studies of disease activity in
MS patients immunologic disease markers (measured by ELISA, quantitative
PCR, cDNA microarrays, T cell frequencies and specificity) are correlated
with the clinical course and disease activity as assessed by MRI. These
experiments shall not only help us to evaluate the efficacy of novel
treatments, but also try to prove the pathogenetic concepts derived from
animal studies.
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Selected Recent
Publications:
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Kondo, T.,
Cortese, I., Markovic-Plese, S., Wandinger, K.-P., Carter, C., Brown, M.,
Leitman, S., Martin, R. (2001) Dendritic cells signal T cells in
the absence of exogenous antigen., Nat. Immunol. 2, 932-938.
-
Kondo, T.,
Cortese, I., Markovic-Plese, S., Wandinger, K.-P., Carter, C., Brown, M.,
Leitman, S., Martin, R. (2001) Dendritic cells signal T cells in
the absence of exogenous antigen., Nat. Immunol. 2, 932-938.
-
Bielekova,
B., Goodwin, B., Richert, N., Kondo, T., Eaton, J., Afshar, G., Antel, J.
Frank, J.A., McFarland, H.F., Martin, R. (2000) Encephalitogenic
potential of myelin basic protein peptide (83-99) in multiple sclerosis –
Results of a phase II clinical trial with an altered peptide ligand. , Nature
Medicine 6, 1167-1175.
-
Hemmer, B.*,
Gran, B.*, Zhao, Y., Marques, A., Pinilla, C., Pascal, J., Tzou, A., Kondo,
T., Cortese, I., Bielekova, B., Straus, S., McFarland, H.F., Houghten, R.,
Simon, R., Martin, R. (1999) Identification of candidate epitopes
and molecular mimics in chronic Lyme disease. , Nature Medicine 5, 1375-1382.
-
Hemmer, B.,
Fleckenstein, B, Vergelli, M., Jung, G., McFarland, H.F., Martin, R.,
Wiesmüller, K.-H. (1997) Identification of high potency microbial
and self ligands for a human autoreactive class II restricted T cell clone.,
J. Exp. Med. 185, 1651-1659 .
All Selected
Publications
Contact
Information:
Dr. Roland Martin
Cellular Immunology Section Neuroimmunology
Branch, NINDS Building 10, Room 5B16 10 Center Drive, MSC
1400 Bethesda, MD 20892-1400
Telephone: (301) 402-4488 (office), (301)
402-4488 (laboratory), (301) 402-0373 (fax) Email:
martinr@ninds.nih.gov
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CHAPTER 23,
THE DISTRICT OF
CORRUPTICUT USDOJ, PORNOGRAPHY, AND BANTAM LAKE
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