Subject: Hilarious Justin Radolf News
Date: Dec 18, 2009 11:31 AM
ARTICLE BELOW
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"Oy! We think we know about how come
some people aren't tolerized enough
to Pam3Cys and end up with Steere's
Bad Knees! That horrible deadly disease
where 'patients generally feel well except
for their arthritis symptoms, or else
is DSM-IV Munchery.'
"Jus *Nevermind* allin our's previouser splainers
on the mechanisms of the downregulation of HLA (RADOLF!),
the inhibition of antibody production (seronegative,
worser Lyme http://www.actionlyme.org/ARTHURWEINSTEIN.htm
and the inhibition of the autokill kinases (and
resultant New Great Imitators:
http://www.actionlyme.org/Pam3Cys_Version15.htm
SAYS WE-DON'T-KNOW Radolf:
"***compromising the induction of tolerance in macrophages and
engendering more severe and persistent inflammatory responses to B.
burgdorferi.***"
The reverse. Now this set of crooks
is acting like it's a worser thing
to get BAD KNEE than it is to get ALS,
http://www.actionlyme.org/ALSLYME47.htm
MS, and cancer from the Pam3Cys immunosuppression
Diseases set, Chronic Lyme:
http://www.actionlyme.org/CHP_9_IDSA_REVIEWS.htm
http://www.actionlyme.org/Pam3Cys_Version15.htm
Yo, J-man:
http://www.journals.uchicago.edu/doi/pdf/10.1086/432733
"Patients generally feel well aside from their arthritis
symptoms."
Yikes.
Now they're *ALL* pulling the same insane
crap. If they didn't know Lyme was Relapsing
Fever, now they don't know Lyme could be
Borreliosis...
http://www.actionlyme.org/RICOCHRON.htm
LymeCrookLand is a never ending series of skits
performed for the AMA-and-duh-CT-Medical-Board
Swooners, Sniffers and Inhalers of Jim Jones'
KoolAid, AKA, Allen Steere Downwind of a Boston
Baked-Bean Dinner.
Justin, come on. Are ya that much of
a cowardly dick?
You know, you could always contact Pfizer
and see if they have something for shrunken
testicles to go with their Primacy of the
Weiners "drug."
Kathleen M. Dickson
http://www.actionlyme.org
http://www.relapsingfever.org
===============================
http://www.ncbi.nlm.nih.gov/pubmed?term=20011115[uid]&cmd=DetailsSearch&log$=details
CD14 Signaling Restrains Chronic Inflammation through Induction of p38-
MAPK/SOCS-Dependent Tolerance.
Sahay B, Patsey RL, Eggers CH, Salazar JC, Radolf JD, Sellati TJ.
Center for Immunology and Microbial Disease, Albany Medical College,
Albany, New York, United States of America.
Current thinking emphasizes the primacy of CD14 in facilitating
recognition of microbes by certain TLRs to initiate pro-inflammatory
signaling events and the importance of p38-MAPK in augmenting such
responses. Herein, this paradigm is challenged by demonstrating that
recognition of live Borrelia burgdorferi not only triggers an
inflammatory response in the absence of CD14, but one that is, in
part, a consequence of altered PI3K/AKT/p38-MAPK signaling and
impaired negative regulation of TLR2. CD14 deficiency results in
increased localization of PI3K to lipid rafts, hyperphosphorylation of
AKT, and reduced activation of p38. Such aberrant signaling leads to
decreased negative regulation by SOCS1, SOCS3, and CIS, thereby
***compromising the induction of tolerance in macrophages and
engendering more severe and persistent inflammatory responses to B.
burgdorferi.*** Importantly, these altered signaling events and the
higher cytokine production observed can be mimicked through shRNA and
pharmacological inhibition of p38 activity in CD14-expressing
macrophages. Perturbation of this CD14/p38-MAPK-dependent immune
regulation may underlie development of infectious chronic inflammatory
syndromes.
PMID: 20011115 [PubMed - in process]
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci