The mechanism of Yale's described fetal brain injury in LYMErix/Lyme Disease
Mort Zuckerman
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Subject: The mechanism of Yale's described fetal brain injury in
LYMErix/Lyme Disease
Date: Jun 9, 2010 1:13 PM
ARTICLE BELOW
=============================
http://www.actionlyme.org/Pam3Cys_Version15.htm
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed&uid=15905502
Yale Department of Pathology:
http://www.actionlyme.org/Congenital_Brain_Infection_of_Newborn_Resulting_in_Death.htm
"The death of the newborn was probably due
to respiratory failure as a consequence of
perinatal brain damage."
It appears that LYMErix - the thing
that caused 4/13 pregnancy losses
during Yale's OspA/Pam3Cys vaccine
trial - is likely to be the reason.
The following report says the TLR2
agonist LYMErix or OspA (Pam3Cys)
inhibits brain maturation in the fetus.
What implications this might have
re other vaccines/adjuvants (autism)
will never be answered as long as
Yale and UConn remain so terrified
of criminal charges over what they
did with their LYMErix vaccine and
the testing schema falsified to
sell this vaccine... and as long as
the likes of ILADS.org and their
"lawyers" *also* suffer microencephaly.
KMDickson
http://www.actionlyme.org
-----------
http://www.ncbi.nlm.nih.gov/pubmed/20456021
J Neurochem. 2010 Apr 29. [Epub ahead of print]
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, USA.
Abstract
J. Neurochem. (2010) 10.1111/j.1471-4159.2010.06778.x 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 mouse
cortical development, and assessed the role of TLR2 heterodimer
activation in neuronal 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 phospho-histone 3 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]
"[Real] scientists are *fiercely* independent. That's the good
news."-- NIH's Top Fool, Anthony Fauci
Richard
"Mort Zuckerman" <morp...@yahoo.com> wrote in message
news:d27f56da-0951-48e7-8c0f-...but no one gave a rat's arse.