Discussion:
Anti-Inflammatory LYMErix/HIV vaccines good for heart attack patients
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Mort Zuckerman
2010-02-22 06:20:49 UTC
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Subject: Anti-Inflammatory LYMErix/HIV vaccines good for heart attack
patients

Date: Feb 22, 2010 1:19 AM

Pam3Cys = the Lyme, Tuberculosis, & HIV vaccines
http://www.actionlyme.org

Good thing Yale was honest
about LYMErix, because not
only does LYMErix not produce
antibodies when used as an
HIV vaccine and not only is
Pam3Cys/LYMErix so predictably
an agent to inhibit apoptosis
and CNS damage, it could be
used to limit heart damage.

(DUMMB-da-dumb-dumb...)

=========
http://www.ncbi.nlm.nih.gov/pubmed?term=20081527[uid]&cmd=DetailsSearch&log$=details

t Care Med. 2010 Mar;38(3):903-909.
Preconditioning by toll-like receptor 2 agonist Pam3CSK4 reduces CXCL1-
dependent leukocyte recruitment in murine myocardial ischemia/
reperfusion injury.

Mersmann J, Berkels R, Zacharowski P, Tran N, Koch A, Iekushi K,
Dimmeler S, Granja TF, Boehm O, Claycomb WC, Zacharowski K.

From the Clinic of Anesthesiology (JM, NT, AK, TFG, KZ), Intensive
Care Medicine, and Pain Management, JW Goethe University, Frankfurt,
Germany; the Department of Anesthesiology (JM, RB, PZ, IB, University
Hospital Düsseldorf, Düsseldorf Germany; the Institute of
Cardiovascular Regeneration (KI, SD), Center for Molecular Medicine,
JW Goethe University, Frankfurt, Germany; the Department of
Anesthesiology and Intensive Care (OB), University Hospital Bonn,
Bonn, Germany; and the Department of Biochemistry and Molecular
Biology (WCC), Louisiana State University Health Sciences Center, New
Orleans, LA.

OBJECTIVE:: To test whether preconditioning with a toll-like receptor
(TLR) 2 agonist protects against myocardial ischemia and reperfusion
by interfering with chemokine CXCL1 release from cardiomyocytes.
DESIGN:: C3H mice were challenged with vehicle or synthetic TLR2
agonist Pam3Cys-Ser-Lys4 (Pam3CSK4; 1 mg/kg) 24 hrs before myocardial
ischemia (20 mins) and reperfusion (2 hrs or 24 hrs). Infarct size,
troponin T release, and leukocyte recruitment were quantified. In
murine cardiomyocytes (HL-1), we studied the expression/activation
profile of TLR2 in response to stimulation with Pam3CSK4 (0.01-1 mg/
mL). Furthermore, we studied the chemokine ligand 1 (CXCL1) response
to Pam3CSK4 and ischemia/reperfusion in vivo and in vitro. SETTING::
University hospital research laboratory. SUBJECTS:: Anesthetized male
mice and murine cardiomyocytes. MEASUREMENTS AND MAIN RESULTS::
Preconditioning by Pam3CSK4 reduced infarct size and troponin T
release. This was accompanied by a decreased recruitment of leukocytes
into the ischemic area and an improved cardiac function. In HL-1
cells, TLR2 activation amplified the expression of the receptor in a
time-dependent manner and led to CXCL1 release in a concentration-
dependent manner. Preconditioning by Pam3CSK4 impaired CXCL1 release
in response to a second inflammatory stimulus in vivo and in vitro.
CONCLUSIONS:: Preconditioning by TLR2 agonist Pam3CSK4 reduces
myocardial infarct size after myocardial ischemia/reperfusion. One of
the mechanisms involved is a diminished chemokine release from
cardiomyocytes, which subsequently limits leukocyte infiltration.

PMID: 20081527 [PubMed - as supplied by publisher]

LinkOut - more resources

"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci
Lipanj
2010-03-02 22:34:00 UTC
Permalink
You said it K. dumb da dumb dumb - I'd say money money get more
money....I was just going thru some old lyme newsltrs and it said
some people after getting their 2nd booster lyme vaccine shot got
cardiac arrest. One was a truck driver.....they are all nuts and
money hungrey - act like a great new discovery - also another shitty
project to keep them in business. Just like the lady from Bethlehem
Pa at the class action lawsuit hearing whose husband was serverly
injured from the vaccine....She said to them WOULD YOU GIVE IT TO YOUR
LOVED ONES---and that other Dr. ??? Alan Steere decendant of the
middle east ---said he wouldn't get it as he doesn't live in an
endemic area ---ho ho Mass. not an endemic area......I wasn't like
this before as crude in expressing myself but --what choice do I
have....I understand completely how you feel K.....you too have went
thru HELL on the earth.....take care.
RESULTS::
Preconditioning by Pam3CSK4 reduced infarct size and troponin T
release. This was accompanied by a decreased recruitment of
leukocytes
into the ischemic area and an improved cardiac function. In HL-1
cells, TLR2 activation amplified the expression of the receptor in a
time-dependent manner and led to CXCL1 release in a concentration-
dependent manner. Preconditioning by Pam3CSK4 impaired CXCL1 release
in response to a second inflammatory stimulus in vivo and in vitro.
CONCLUSIONS:: Preconditioning by TLR2 agonist Pam3CSK4 reduces
myocardial infarct size after myocardial ischemia/reperfusion. One of
the mechanisms involved is a diminished chemokine release from
cardiomyocytes, which subsequently limits leukocyte infiltration.


PMID: 20081527 [PubMed - as supplied by publisher]
Post by Mort Zuckerman
Subject: Anti-Inflammatory LYMErix/HIV vaccines good for heart attack
patients
Date: Feb 22, 2010 1:19 AM
Pam3Cys = the Lyme, Tuberculosis, & HIV vaccineshttp://www.actionlyme.org
Good thing Yale was honest
about LYMErix, because not
only does LYMErix not produce
antibodies when used as an
HIV vaccine and not only is
Pam3Cys/LYMErix so predictably
an agent to inhibit apoptosis
and CNS damage, it could be
used to limit heart damage.
(DUMMB-da-dumb-dumb...)
=========http://www.ncbi.nlm.nih.gov/pubmed?term=20081527[uid]&cmd=DetailsSearch&log$=details
t Care Med. 2010 Mar;38(3):903-909.
Preconditioning by toll-like receptor 2 agonist Pam3CSK4 reduces CXCL1-
dependent leukocyte recruitment in murine myocardial ischemia/
reperfusion injury.
Mersmann J, Berkels R, Zacharowski P, Tran N, Koch A, Iekushi K,
Dimmeler S, Granja TF, Boehm O, Claycomb WC, Zacharowski K.
From the Clinic of Anesthesiology (JM, NT, AK, TFG, KZ), Intensive
Care Medicine, and Pain Management, JW Goethe University, Frankfurt,
Germany; the Department of Anesthesiology (JM, RB, PZ, IB, University
Hospital D�sseldorf, D�sseldorf Germany; the Institute of
Cardiovascular Regeneration (KI, SD), Center for Molecular Medicine,
JW Goethe University, Frankfurt, Germany; the Department of
Anesthesiology and Intensive Care (OB), University Hospital Bonn,
Bonn, Germany; and the Department of Biochemistry and Molecular
Biology (WCC), Louisiana State University Health Sciences Center, New
Orleans, LA.
OBJECTIVE:: To test whether preconditioning with a toll-like receptor
(TLR) 2 agonist protects against myocardial ischemia and reperfusion
by interfering with chemokine CXCL1 release from cardiomyocytes.
DESIGN:: C3H mice were challenged with vehicle or synthetic TLR2
agonist Pam3Cys-Ser-Lys4 (Pam3CSK4; 1 mg/kg) 24 hrs before myocardial
ischemia (20 mins) and reperfusion (2 hrs or 24 hrs). Infarct size,
troponin T release, and leukocyte recruitment were quantified. In
murine cardiomyocytes (HL-1), we studied the expression/activation
profile of TLR2 in response to stimulation with Pam3CSK4 (0.01-1 mg/
mL). Furthermore, we studied the chemokine ligand 1 (CXCL1) response
University hospital research laboratory. SUBJECTS:: Anesthetized male
Preconditioning by Pam3CSK4 reduced infarct size and troponin T
release. This was accompanied by a decreased recruitment of leukocytes
into the ischemic area and an improved cardiac function. In HL-1
cells, TLR2 activation amplified the expression of the receptor in a
time-dependent manner and led to CXCL1 release in a concentration-
dependent manner. Preconditioning by Pam3CSK4 impaired CXCL1 release
in response to a second inflammatory stimulus in vivo and in vitro.
CONCLUSIONS:: Preconditioning by TLR2 agonist Pam3CSK4 reduces
myocardial infarct size after myocardial ischemia/reperfusion. One of
the mechanisms involved is a diminished chemokine release from
cardiomyocytes, which subsequently limits leukocyte infiltration.
PMID: 20081527 [PubMed - as supplied by publisher]
LinkOut - more resources
"[Real] scientists are *fiercely* independent. �That's the good
news."-- NIH's Top Fool, Anthony Fauci
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