A DCF Whores' Boyfriend Reports
Mort Zuckerman
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Subject: A DCF Whores' Boyfriend Reports
Date: Aug 12, 2008 1:59 PM
http://www.topix.net/forum/source/hartford-courant/T4TG2IEQJ5I95VRU3/p4#lastPost
No One Knows
Wallingford, CT
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#77
6 min ago
Nino Brown wrote:
<quoted text>First of all moron , what makes you think I live in
West
Hartford ??? the IPO address that the post was routed on ???? you are
more ignorant
then one could describe .... second half-wit ... I have had 7 years of
dealing with
DCF mostly defending myself against stupid allegations made by
mentally ill children
and schools .... I am no fan of DCF .... but the abuses of the system
YOU describe
are in the minority .... few and far between .... do cases like you
mention happen
... YES THEY DO .... they happened to me BUT the MAJORITY of the DCF
workers are
trying very hard to do the RIGHT thing ..... and doing it against
incredible odds
....the bureaucrats make things difficult for them to do an already
difficult job
... I'm willing to bet that for every kid that the system fails ....
there are
10 kids where it is a success ..... nobady wants to talk about the
GOOD things DCF
does ....and Riverview ... the staff does a wonderful job considering
what they
must put up with (not unlike a correction officer) MAYBE if the
PARENTS acted responsibly
in bringing up their kids ..., maybe ACTED like parents ..... these
kids would'nt
be in the system in the first place ..... put the blame where it
belongs .... THE
BREAKDOWN OF THE FAMILY AND FAMILY VALUES AND MORALS
=============================
"NO. The abuses of the system are not rare. They are actually very
common.
"My girlfriend is a DCF social worker and even she knows it is all
corrupt.
She tells me she can't take it there anymore and wants to find another
job.
She just needs to find one that pays well enough. Her main complaints
are supervisors
making her do things that are not correct. I always tell her that by
being an employee
- she is just as guilty.
"You are wrong."
========================
I'll just keep reporting this stuff to the "proper authorities"
so that when the day comes, the USA will have no foreign allies
because all will see that the "authorities" have no problem
with these outrageous human rights abuses.
LOL.
We who have been through it, know the Corrupticut legislators
have already heard all of this before and either don't care or
don't want to see an end to their own gravy train.
To Wit:
James Amann and Multiple Sclerosis:
http://www.actionlyme.org/MARTIN_NINDS_MS_CHRONIC_LYME.htm
CHAPTER 22, THE CORRUPTICUT UNIONS, THE DEMS, AND JAMES AMANN
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.
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.
Steere found either 17 or 35 out of 237 patients who all thought
they had Lyme
as diagnosed by other labs to also have 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.)
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 screweed
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 Encephalitis{triangledown}
Jan 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 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 ============
Cellular Immunology Section
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
biel...@ninds.nih.gov
* Gregg Blevins, M.D., Clinical Fellow blev...@ninds.nih.gov
* Erik Cabral, B.S., Student, (301) 496-0518
* Ricardo Cassiani-Ingoni, Ph.D., Postdoctoral Fellow
cass...@ninds.nih.gov
* Azita Kashani, B.S., Research Assistant, (301) 496-0518
* Dr. Paolo A. Muraro, M.D., Ph.D., Senior Research Fellow
mur...@ninds.nih.gov
* Elisabetta Prat, M.D. pr...@ninds.nih.gov
* Susan Scrivner, M.S., Research Assistant
scri...@ninds.nih.gov
* Mireia Sospedra, Ph.D., Postdoctoral Fellow
sosp...@ninds.nih.gov
* Xiang Wang, M.S., Senior Research Assistant, (301) 402-4488
wan...@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.
Selected Recent Publications:
*
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: mar...@ninds.nih.gov
Last updated Friday, September 13, 2002
Comments or questions? Send email to intraw...@ninds.nih.gov
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