Lithium *promotes* BCL2 related apoptosis inhibition. (CORRECTION)
kathleen
kshe...@calea.org, fit...@gmail.com, patrick.f...@usdoj.gov,
model...@sbcglobal.net, jdr...@nejm.org, let...@courant.com,
Jgerb...@cdc.gov, len...@courant.com,
steven....@po.state.ct.us, con...@po.state.ct.us, executive-
edi...@nytimes.com, managin...@nytimes.com, news-
ti...@nytimes.com, the-...@nytimes.com, biz...@nytimes.com,
for...@nytimes.com, me...@nytimes.com, nati...@nytimes.com,
spo...@nytimes.com, dv...@cdc.gov, brigidc...@optonline.net,
tr...@hotmail.com, ubi...@courant.com, ma...@concentric.net,
camp...@courant.com, jhorn...@fff.org, thomas...@usdoj.gov,
edi...@commondreams.org, kur...@washpost.com, georg...@washpost.com,
hor...@courant.com, commissi...@po.state.ct.us,
cohen...@aol.com, FalN...@aol.com, brans...@comcast.net,
vts...@comcast.net, mcne...@aol.com, o...@po.state.ct.us, dand@davila-
dilzer.com, scott....@po.state.ct.us, govern...@po.state.ct.us,
attorney...@po.state.ct.us, randall...@usdoj.gov
Cc: fra...@ucia.gov, dr-ahma...@president.ir,
eugener...@washpost.com, hor...@courant.com,
bmi...@newstimes.com, tr...@hotmail.com, rast...@aol.com,
billc...@gmail.com, thomas...@usdoj.gov, amcg...@rms-law.com,
rjmu...@aol.com, paulcrai...@yahoo.com,
sidney_b...@yahoo.com, criminal...@usdoj.gov,
karla.d...@usdoj.gov, christophe...@usdoj.gov
Subject: Lithium *promotes* BCL2 related apoptosis inhibition.
Date: Jul 11, 2007 2:45 AM
Correction: Lithium PROMOTES the production of BCL2 related
neuroprotection.
I said the opposite in the previous report on Autism.
Sorry. Terrible mistake. You can't screw people up when presenting
scientific
data. (We have enough people at Yale and New York Medical College
presenting such
screwed up science for us already.)
I will therefore provide the BCL2 class molecules protections
mechanisms references.
BCL2 means B cell Lymphoma.
Too much BCL2 promotes the condition where a cell under some sort of
toxic attack
(like latent viruses start dividing again, such as Epstein Barr,
cytomegalovirus,
the Herpes, etc...). There are conditions, like stroke, where we wish
the cells
would not die, so that the victim has a greater potential to recover
neurological
functioning.
Lithium promotes the neuroprotective effects of BCL2.
I will cite some references about these mechanisms below.
In the case of high functioning autism and neurofibromatosis, the
little that is
known is that there appears to be a reversed-duplication of a BCL2
class molecule
(BCL8) in the same region of a chromosome where a known typically
chromosome 17-
bearing NF1 gene is transposed to chromosome 15 and gets reverse
duplicated with
the BCL2 gene.
Here is that report:
J Med Genet. 2002 Mar;39(3):170-7.Click here to read Links
Organisation of the pericentromeric region of chromosome 15: at
least four partial
gene copies are amplified in patients with a proximal duplication of
15q.
Fantes JA, Mewborn SK, Lese CM, Hedrick J, Brown RL, Dyomin V,
Chaganti RS,
Christian SL, Ledbetter DH.
Department of Human Genetics, University of Chicago, Chicago, IL
60637, USA.
Clinical cytogenetic laboratories frequently identify an apparent
duplication
of proximal 15q that does not involve probes within the PWS/AS
critical region and
is not associated with any consistent phenotype. Previous mapping data
placed several
pseudogenes, NF1, IgH D/V, and GABRA5 in the pericentromeric region of
proximal
15q. Recent studies have shown that these pseudogene sequences have
increased copy
numbers in subjects with apparent duplications of proximal 15q. To
determine the
extent of variation in a control population, we analysed NF1 and IgH D
pseudogene
copy number in interphase nuclei from 20 cytogenetically normal
subjects by FISH.
Both loci are polymorphic in controls, ranging from 1-4 signals for
NF1 and 1-3
signals for IgH D. Eight subjects with apparent duplications, examined
by the same
method, showed significantly increased NF1 copy number (5-10 signals).
IgH D copy
number was also increased in 6/8 of these patients (4-9 signals). We
identified
a fourth pseudogene, BCL8A, which maps to the pericentromeric region
and is coamplified
along with the NF1 sequences. Interphase FISH ordering experiments
show that IgH
D lies closest to the centromere, while BCL8A is the most distal locus
in this pseudogene
array; the total size of the amplicon is estimated at approximately 1
Mb. The duplicated
chromosome was inherited from either sex parent, indicating no parent
of origin
effect, and no consistent phenotype was present. FISH analysis with
one or more
of these probes is therefore useful in discriminating polymorphic
amplification
of proximal pseudogene sequences from clinically significant
duplications of 15q.
PMID: 11897815 [PubMed - indexed for MEDLINE]
==================
When a gene is overrepresented, it is often overexpressed (meaning you
get the physical
or physiological result or the phenotype or you can see it).
These mechanisms are not completely understood.
1) Autism: large heads, lack of normal synaptic pruning.
2) Expression of the neurofibromas, by LACK OF INHIBITION of the
growth of them
because of too much BLC2, or dysregulated BCL2 expression over time.
'Hypothetically. 'Based on what we know so far.
=====================
Lithium BCL2 related data:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=DetailsSearch&Term=(%22lithium%22%5BMeSH+Terms%5D+OR+lithium%5BText+Word%5D)+AND+(%22bcl-2+genes%22%5BText+Word%5D+OR+%22genes,+bcl-2%22%5BMeSH+Terms%5D+OR+BCL2%5BText+Word%5D)
Go there, and look at all the articles ***and the related articles.***
=======================
CONVERSELY, Yale studies the mechanisms of cell death; the caspases
and their downstream
milieu:
And this is very, very important because Yale wants to capitalize on
patenting the
mechanisms of caspase inhibition (to produce an expensive
pharmaceutical or two,
for which they will get the royalties), without revealing the fact
that programmed
cell death (apoptosis) can be inhibited by the non-patentable lithium
and the like.
This is not to mention the domain of specific pharmaceutical
targeting. (The best
example of targeting is Viagra. Pfizer meant to target blood vessel
dilation in
the heart.)
AND THIRDLY, Yale has a team of researchers studying the mechanisms of
neuroprotection
via promoting brain and nerve growth factors:
- - - - -
You can see how frustrating it is when we are stonewalled by the Yale
Psychiatric
Department and their sex-obsessed bullshit, perjury, lies, waste;
their lies and
perjury about Lyme being a brain disease; their whoring for BigPharma
and the so-called
courts...
They could be helping people instead. (<---I realize I am talking
about both
Yale and America, so delete this last statement. Helping others is
not what we
do.)
Again, please accept my apologies for confusing anyone.
Kathleen M. Dickson
ActionLyme.org