How LYMErix Disease causes brain damage in babies (new)
Mort Zuckerman
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Subject: How LYMErix Disease causes brain damage in babies (new)
Date: May 12, 2010 9:54 AM
ARTICLE BELOW [TLR2 Agonism (OspA) in neonates]
=================================
Mice, anyway. Human children we
know from Allen Steere, Yale's lab:
"The death of the newborn was probably due to respiratory failure as a
consequence of perinatal brain damage."-- Yale Department of
Pathology.
http://www.actionlyme.org/Congenital_Brain_Infection_of_Newborn_Resulting_in_Death.htm
http://www.actionlyme.org/Schoen.htm
http://www.actionlyme.org/MOMS_CAN_GIVE_LYME_TO_BABIES.htm
investigations, and SmithKline's "vaccine"
(and many others:
http://www.docguide.com/news/content.nsf/news/852576140048867C8525771F006B7B44
)
At the 2001 FDA Hearing on LYMErix, SmithKline
Yale admitted that something like 13 out
of 30 women lost their babies in the trial:
http://www.fda.gov/ohrms/dockets/ac/01/transcripts/3680t2.rtf
http://www.fda.gov/ohrms/dockets/ac/01/slides/3680s2.htm
Now we know the mechanisms by which
children suffer brain damage and
so many women spontaneously abort
with Lyme-and-LYMErix:
http://www.ncbi.nlm.nih.gov/pubmed/20456021
TLR2 Activation Inhibits Embryonic Neural Progenitor Cell
Proliferation.
Okun E, Griffioen KJ, Gen-Son T, Lee JH, Roberts NJ, Mughal MR,
Hutchison E, Cheng A, Arumugam TV, Lathia JD, van Praag H, Mattson MP.
Laboratory of Neurosciences, National Institute on Aging Intramural
Research Program, Baltimore, Maryland 21224, U.S.A.
Abstract
Abstract Toll-like receptors (TLRs) play essential roles in innate
immunity, and increasing evidence indicates that these receptors are
expressed in neurons, astrocytes and microglia in the brain, where
they mediate responses to infection, stress and injury. To address the
possibility that TLR2 heterodimer activation could affect progenitor
cells in the developing brain, we analyzed the expression of TLR2
throughout the mouse cortical development, and assessed the role of
TLR2 heterodimer activation in neural progenitor cell (NPC)
proliferation. TLR2 mRNA and protein was expressed in the cortex in
embryonic and early postnatal stages of development, and in cultured
cortical NPC. While NPC from TLR2-deficient and wild type embryos had
the same proliferative capacity, TLR2 activation by the synthetic
bacterial lipopeptides Pam(3)CSK(4) and FSL1, or low molecular weight
hyaluronan, an endogenous ligand for TLR2, inhibited neurosphere
formation in vitro. Intracerebral in utero administration of TLR2
ligands resulted in ventricular dysgenesis characterized by increased
ventricle size, reduced proliferative area around the ventricles,
increased cell density, an increase in PH3 (+) cells and a decrease in
BrdU(+) cells in the sub-ventricular zone. Our findings indicate that
loss of TLR2 does not result in defects in cerebral development.
However, TLR2 is expressed and functional in the developing
telencephalon from early embryonic stages and infectious agent-related
activation of TLR2 inhibits NPC proliferation. TLR2-mediated
inhibition of NPC proliferation may therefore be a mechanism by which
infection, ischemia and inflammation adversely affect brain
development.
PMID: 20456021 [PubMed - as supplied by publisher]
=====================
KMDickson
http://www.relapsingfever.org
http://www.actionlyme.org
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci
Dan Sullivan
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> Subject: How LYMErix Disease causes brain damage in babies (new)
>
> Date: May 12, 2010 9:54 AM
>
> ARTICLE BELOW [TLR2 Agonism (OspA) in neonates]
> =================================
>
> Mice, anyway. Human children we
> know from Allen Steere, Yale's lab:
> "The death of the newborn was probably due to respiratory failure as a
> consequence of perinatal brain damage."-- Yale Department of
> investigations, and SmithKline's "vaccine"
> )
>
> At the 2001 FDA Hearing on LYMErix, SmithKline
> Yale admitted that something like 13 out