Is This The Cause of ALL Ai conditions Part II
randall
Same as yesterday.
Dan Littman is the HERO or Angel for a Psor Cure.
I just looked... Only TEN hits for littman on our group for Dan.
His
http://www.med.nyu.edu/microbiology/faculty/littman/index.html
Here is his work:
And the most recent news links for DAN LITTMAN and all the scientists
who worked
on this.
http://www.news-medical.net/news/20091019/Discovery-may-yield-better-understanding-of-protective-gut-dwelling-bacteria.aspx
Discovery may yield better understanding of protective gut-dwelling
bacteria
Medical researchers have long suspected that obscure bacteria living
within the intestinal tract may help keep the human immune system in
balance. An international collaboration co-led by scientists at NYU
Langone Medical Center has now identified a bizarre-looking microbial
species that can single-handedly spur the production of specialized
immune cells in mice.
This remarkable activation of the immune response could point to a
similar phenomenon in humans, helping researchers understand how gut-
dwelling bacteria protect us from pathogenic bacteria, such as
virulent strains of E. coli. The study, published in the Oct. 30,
2009, issue of Cell, also supports the idea that specific bacteria may
act like neighborhood watchdogs at key locations within the small
intestine, where they sense the local microbial community and sound
the alarm if something seems amiss.
In mice, at least, the newly identified neighborhood watchdog looks
like something out of Disney's "The Shaggy D.A." Distinguished by long
hair-like filaments, "These bacteria are the most astounding things
I've ever seen," says Dan Littman, MD, PhD, the Helen L. and Martin S.
Kimmel Professor of Molecular Immunology and a Howard Hughes Medical
Institute Investigator.
Co-led by Dr. Littman's lab, the collaboration with researchers in
Japan, California, and Massachusetts zeroed in on a little-known
microbe named segmented filamentous bacterium, or SFB. In mice raised
under germ-free conditions, the scientists found that adding SFB was
sufficient to trigger the appearance of specialized T helper cells
known as Th17 cells. These immune specialists, in turn, can send
signals that tell epithelial cells lining the small intestine to
increase their output of molecules targeting selected microbes.
For the study's mice, the infection-fighting response was enough to
ward off the pathogen Citrobacter rodentium, considered a good model
for the type of disease-causing E. coli found in contaminated foods
like spinach or ground beef. Without SFB to protect them, mice
infected with Citrobacter rodentium became ill before recovering.
In the same way, commensal microbes-beneficial bacteria-could decrease
our susceptibility to various pathogenic invaders. "So you can
immediately see some practical application of this, if one can mimic
the presence of these commensal bacteria to strengthen resistance to
pathogenic microbes," Dr. Littman says.
Thanks to rapid progress in the field of genomics, he expects the
entire DNA sequence of the SFB species to be completed within a few
months. Armed with the sequence, researchers could focus on specific
proteins. "For example, can we identify a protein that, when we inject
it into an epithelial cell, sets off in motion the whole pathway to
make Th17 cells?" he says. "By knowing how to do this, you may be able
to give people a peptide or a compound that induces Th17 cells by
mimicking the bacterial product, and in that way either protect or
ameliorate the effect of the infection."
Too much Th17 cell activation, however, can lead to harmful
inflammation, Dr. Littman says. Excessive induction by specific
microbes in the gut, then, could contribute to autoimmune diseases
such as rheumatoid arthritis, psoriasis, Crohn's disease, and possibly
even multiple sclerosis.
Source: NYU Langone Medical Center / New York University School of
Medicine
-------------
This is still odd as the previous story doesn't mention the French
Input?
OK, there is another hit on google news that may explain that
connection to this
HUGE discovery.
This is a NOBEL prize in medicine FUR SURE, just as important as Barry
Marshall for
the h. pylori-- ulcer inspired prize-- IMO.
--------------
http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=22602
Friendly Bacteria
(Ivanhoe Newswire) -- New studies offer insight into the constant
dialogue between intestinal microbes and the human immune system,
pointing to a major role for a class of microbes known as segmented
filamentous bacteria (SFB) in shaping the human immune response.
"It's the first example of a commensal bacteria that can induce
accumulation in the gut of a highly specific branch of the immune
system," Dan Littman of the Howard Hughes Medical Institute and the
New York University School of Medicine, who led the study reported in
Cell, was quoted as saying. "We're headed into an exciting new area,
and we hope more pieces of how the microbial-host interaction
contributes to health will begin to fall into place."
"Our study provides the surprising result that among the hundreds of
bacterial species composing the gut microbiota -- only a very small
number, the prototype of which is SFB -- can efficiently stimulate the
post-natal physiologic maturation of the immune barrier," Valérie
Gaboriau-Routhiau of INSERM in France, who led the Immunity report,
was quoted as saying. Most notably, the studies show that the SFBs
stimulate particular types of helper T cells, known as Th17 cells.
The findings by Littman's group were an accidental discovery.
Researchers were studying T cells in the intestine and were getting
some inconsistencies that could be traced to differences in the gut
floras of mice in the presence or absence of SFB.
They found that introduction of SFB, but not other bacteria,
stimulated the production of Th17 cells in mice that were otherwise
deficient. The bacteria also set in motion a pro-inflammatory gene
program. The SFB-induced immune response protected the mice from
becoming ill with an intestinal pathogen, suggesting that the SFBs
played a role in setting up the intestine's immunity barrier.
Gaboriau-Routhiau found in similar studies of mice that colonization
of the gut induced a broad spectrum of pro-inflammatory and T cell
responses, including the emergence of Th17 cells. That function
appeared limited to a restricted number of bacteria, her team
reported, the prototype of which is the SFB.
"For us, it was first a surprise to observe so little redundancy in
the role of commensal bacteria on stimulating immune responses,"
Gaboriau-Routhiau said. "One striking feature of SFB, which makes it
very different from the vast majority of the members of the
microbiota, is its capacity to adhere to epithelial cells notably in
the ileum, a property normally more the prerogative of pathogens." The
ileum is the final section of the small intestine and has many folds,
giving it a very large surface area.
The studies also suggest how such bacteria might go from beneficial
inhabitants, helping to fend off nasty bugs, to ones that may tip the
balance of the immune system toward the development of inflammatory
autoimmune disease, such as Crohn's disease, psoriasis and even
arthritis, according to the researchers. Indeed, the Th17 cells
observed in the new studies have been noted in recent years because of
their importance in autoimmune diseases, Littman explained.
"Th17 cells make cytokines that can be highly protective in the case
of infection," he said. "At the same time, in the wrong context or in
the wrong amount [they can lead to disease]. You need to have the
right balance."
Given the bacterial diversity within our guts, the studies show how
much there is to learn about this important aspect of the immune
system. While probiotic products on the market today do not have the
benefit of such a thorough understanding, said Littman, there is
little doubt that down the road we may be able to manipulate our
immune system in beneficial ways with microbes.
SOURCE: Cell and Immunity, October 16, 2009
------
The French Connection was posted in this group yesterday as their
Abstract was
on pubmed by Friday (Today is monday)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/3b4e1e54f340dee8
------------------------
Other's who have worked on this tirelessly should be able to further
their former work based on this huge revelation.
Of course I've called the Gi tract and area where the small
and large intestine the hot zone for a long time and the
most likely area for a CURE.
http://en.wikipedia.org/wiki/Ileum
No more biologicals or tar or UVB's or anything.
Just a simple gut bug adjustment and I know
the wit kit produces that magic anyway. LOL
------
Some how SFB must tie in with Psors1 and Runx genes elucidated by
Anne Bowcock
---
The genetics of psoriasis and autoimmunity.
__Bowcock__ AM.
Department of Genetics, Washington University School of Medicine, St.
Louis, Missouri 63110, USA. bowcock @genetics.wustl.edu
Psoriasis is an inflammatory/autoimmune disease and, as with many
autoimmune diseases, is associated with alleles from the major
histocompatibility complex (MHC). With psoriasis and autoimmune
disease, the penetrance of the MHC-associated alleles is never 100%,
even for monozygotic twins. This may be because development requires
additional environmental and/or genetic modifiers or requires specific
T-cell receptor arrangements. Families segregating single or
multilocus susceptibility alleles other than the MHC have also been
reported. Overlapping genetic locations of loci for different
autoimmune diseases have been known for several years and are starting
to reveal common genes or genetic variants. These include genes
normally involved in preventing spontaneous T-cell activation or
proliferation, immune synapse formation, or cytokine production via
pathways such as those mediated by NFkappaB and those involved in
thymic selection. Autoimmunity may also involve dysregulation of genes
or pathways regulated by the RUNX family of transcription factors.
RUNX is involved in hematopoietic cell development, development of T
cells in the thymus, chromatin remodeling, and gene silencing. Hence,
its effect on cells of the immune system may be due to variable
changes in gene expression and could account for variable body surface
involvement and waxing and waning of disease.
PMID: 16124855
=======================
Perspectives on RUNX genes: An update.
Cohen Jr MM.
Department of Pediatrics, Faculty of Medicine, Dalhousie University,
Halifax, Nova Scotia, Canada.
This perspective on RUNX genes discusses their basic biological
features, including their DNA-binding alpha subunit, their non-DNA
binding beta subunit, and their Runt domain. The evolution of Runx
genes begins with one most like Runx3 in invertebrates, progresses to
four genes in Drosophila, and to three in vertebrates. Runx genes have
two promoters and various numbers of exons and isoforms. All three
genes with expressions in the same biological tissues act either
synergistically or at different time periods. Runx genes have
downstream target genes. Furthermore, Runx genes are mediated by
TGFbeta or BMP pathways. They also have cohesin-dependent regulation.
Runx1 binds the CD4 silencer and represses transcription in immature
double negative thymocytes. Runx1 also activates CD8 as the double
negative population progresses to double positive thymocytes. Runx3
establishes epigenetic silencing in CD4 - CD8+ cytotoxic T-cells by
binding the CD4 silencer core sequence. Runx1 may also be involved in
CD4 silencing in CD8+ T-cells. RUNX1 mutations cause familial
thrombocytopenia with a propensity for developing acute myelogenous
leukemia; two functional consequences of these mutations include
haploinsufficiency and a dominant negative effect. The latter tends to
be associated with a higher frequency of leukemia. RUNX2 mutations
cause cleidocranial dysplasia; most are of the missense type and
commonly occur in the Runt domain. RUNX3 is a tumor suppressor gene
with hemizygous deletion of one allele and hypermethylation of the
other, resulting in gastric adenocarcinoma.
PMID: 19830829
Oh well.. Time for me to go have FUN...
randall... still all jazzed uP.. :)
JRStern
Probably not.
Probably no single cause at all, but whatever comes even close to a
root cause is going to involve some human genetics, or I'll be pretty
surprised.
J.
randall
JRSTERN,
How can you doubt me?
Do you wish to suPPort BIG PHARMA with LOW DOSE nonsense
some HOW? LOL
OR,
Is it because i'm a huge psor FLAKE? :(
And YOU don't believe ONE of your OWN?
I've been one for longer then YOU. LOL
Give me a BREAK. ;~/
It's PSOR ME for over a freaking lifetime of SEVERE psor vile.
A virtual prisioner of the most henious insidious and stupid disease,
and we've been screwed by BIG PIG PHARMA all along the same
way the ulcer people were.
Why wouldn't i be first to put the puzzle to-gether?
Give me a FREAKING break.... you KNOW i'm REAL..
I'm NOT that stupid fat OPRAH crooning vote for Obama....
because he's NOT BUSH. LOL
And that does sound RASCIST to me? How about you?
Furthermore, i live'd in the mild pasi range due to this very
freaking crap and i've used xyz (wit kit et al) against it to prove
the empirical TRUTH.
And waited for nearly half a century for the exact truth.... h'mmm!
Why haven't you come on board?
Don't you WANT to be CLEAR?
OR do you want those behind wipe pharma's to do
you right? LOL
The GosPel of Galactose (sweet whey) is the HOLY truth..
And now you doubt my DDx?
http://en.wikipedia.org/wiki/Differential_diagnosis
I'm surprised. LOL
And after ALL this time. <w>
Anyway I'm glad for your GENETIC propensity towards CAUSATION.
http://en.wikipedia.org/wiki/Causality
But the SFB cow is NOW out of the BARN.
So who are you? You want to be CLEAR or NOT?
I'll start your trial tomorrow... chicken or just BS'ing perhaps?
But what does one do if there isn't A, B or C... GENEs? Like with
psoriasis and a whole
bunch of arse-wiPes running around pushing TNF bio ill logicals to the
unknowing psor folks?
If WE or you wish to point to nature (DNA) or mother nurture (SFB -
segmented filamentous bacteria - bugs in the gut or NOT for
instance) i loaded that FIRST
post to answer YOUR question, perhaPs?
So?
BAcK to Bowcock:
JR your ONLY half right as to genetics SO FAR, but still no concurence
even with
monozygotic twins [exact genes].
READ Anne Bowcock again:
www.ncbi.nlm.nih.gov/pubmed/16124855
[...]
With psoriasis and autoimmune disease, the penetrance of the MHC-
associated alleles is never 100%, even for monozygotic twins. This may
be because development requires additional environmental and/or
genetic modifiers or requires specific T-cell receptor arrangements.
Families segregating single or multilocus susceptibility alleles other
than the MHC have also been reported. Overlapping genetic locations of
loci for different autoimmune diseases have been known for several
years and are starting to reveal common genes or genetic variants.
<sniP>
What does it mean?
If your twin with ____identical genes___ doesn't onset with psoriasis,
then THAT ALONE
almost 100% guarantee's a nurture WRENCH in the monkey works of NATURE
(which is mostly corrupted by nurture anyway). LOL
http://en.wikipedia.org/wiki/Twin#Monozygotic_twins
from
http://en.wikipedia.org/wiki/Twin
Are you on board?
Need some more?
Reread the most recent runx genetic abstract which I also included.
www.ncbi.nlm.nih.gov/pubmed/19830829
Try DNA-binding alpha subunit? Or?
http://en.wikipedia.org/wiki/RUNX1
RUNX1 is an eukaryotic gene and the protein encoded by this gene is a
transcription factor associated with M2 AML, a type of leukemia. It
belongs to the Runt-related transcription factor (RUNX) family of
genes which are also called core binding factor-a (CBFa). RUNX
proteins form a heterodimeric complex with CBFß which confers
increased ____DNA binding____ and stability to the complex.
<snip>
http://en.wikipedia.org/wiki/RUNX2
interacts with c-jun and c-fos [AP-1 components]
[possible areas to look at: CRYSTAL STRUCTURE OF RUNX-1/AML1/CBFALPHA
RUNT DOMAIN
go to http://www.rcsb.org/pdb/explore.do?structureId=1HJC ]
So?
C-jun takes us back to AP-1 & c-jun:
http://en.wikipedia.org/wiki/C-jun
http://en.wikipedia.org/wiki/AP-1_(transcription_factor)
AP-1 + psoria* [on pubmed-- 36 important HITs btw]
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=ap-1+psoria*&log$=activity
http://en.wikipedia.org/wiki/RUNX3
[...]
This gene encodes a member of the runt domain-containing family of
transcription factors. A heterodimer of this protein and a beta
subunit forms a complex that binds to the core DNA sequence 5'-
PYGPYGGT-3' found in a number of enhancers and promoters,
[...]
Runx3 null mouse gastric mucosa exhibits hyperplasia due to stimulated
proliferation and suppressed apoptosis in epithelial cells, and the
cells are resistant to ______TGF-beta_____ stimulation.[4]
to: Tle1 :
http://en.wikipedia.org/wiki/TLE1
-----------
But the big connect is TGF-beta.
I hope you didn't miss that. LOL
Anyway...
www.ncbi.nlm.nih.gov/pubmed/19830829
[...]
Furthermore, Runx genes are mediated by TGFbeta or BMP pathways
[notes: http://en.wikipedia.org/wiki/Tgf-beta
Transforming growth factor beta (TGF-ß) controls proliferation,
cellular differentiation, and other functions in most cells. It plays
a role in immunity, cancer, heart disease, diabetes, and Marfan
syndrome. TGF-beta acts as an antiproliferative factor in normal
epithelial cells and at early stages of oncogenesis.[1]
<sniP> ]
ARE WE CLeAR YET? LOL
Check pubmed if NOT:
TGF-beta + psoria* -- 104 hits on pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=tgf-beta+psoria*&log$=activity
----
The most recent::
A Role for TGFbeta Signaling in the Pathogenesis of Psoriasis.
Han G, Williams CA, Salter K, Garl PJ, Li AG, Wang XJ.
Department of Pathology, University of Colorado Denver, Aurora,
Colorado, USA.
Deregulation of transforming growth factor-beta (TGFbeta) signaling
has been reported in human psoriasis. Our recent study using a keratin
5 promoter (K5.TGFbeta1(wt)) showed that transgenic mice expressing
wild-type TGFbeta1 in the epidermis developed severe skin
inflammation. Additional experimental data further support a direct
role for TGFbeta1 overexpression in skin inflammation. First, we
temporally induced TGFbeta1 expression in keratinocytes in our gene-
switch TGFbeta1(wt) transgenic mice and found inflammation severity
correlated with TGFbeta1(wt) transgene expression. Second, deletion of
T cells in K5.TGFbeta1(wt) mice significantly delayed skin
inflammation and associated epidermal hyperplasia/hyperkeratosis.
Third, therapeutic approaches effective for human psoriasis, that is,
Etanercept and Rosiglitazone, are effective in alleviating the
symptoms observed in K5.TGFbeta1(wt) mice. Future studies will analyze
specific mechanisms and identify key factors in TGFbeta1-induced skin
inflammation. Our mouse models will provide a useful tool for
understanding the molecular mechanisms of inflammatory skin disorders
in which TGFbeta1 is overexpressed.Journal of Investigative
Dermatology advance online publication, 27 August 2009; doi:10.1038/
jid.2009.252.
PMID: 19710682
---------------------
Your GENETICAL psoriatical theory of why they HAVEN'T found any
SPECIFIC PSOR gene is
noted. LOL
They do have nine good ones and another few hundred here and there to
keep
playing with.
But why now?
Without SFB to explain this GUT FLORA model, they might NEVER HAVE
BEEN found otherwise?
YET, I haven't understood the rest of:
the most recent runx abstract.
www.ncbi.nlm.nih.gov/pubmed/19830829
goes WAY over my PAY grade... or until
i take the time to completely understand it.
But why bother?
Why not test for exactly the details of the abstract in question?
Which is easy.
Will only take three or four weeks after i gather the lacti loving
bugs and run the trial. LOL
Don't you love it?
Science works or creates a bigger or another question.
And i stand by the importance of SFB for Ai, this being a nobel prize,
discovery.
And WILL see... how that goes.
Why NOT?
If they gave obama a nobel they should give one
to those folks who prove autoimmune is not genetical but driven
by SFB.
randall... don't you think? Or shall we prove it?
JRStern
wrote:
>Anyway I'm glad for your GENETIC propensity towards CAUSATION.
Quite.
>If WE or you wish to point to nature (DNA) or mother nurture (SFB -
>segmented filamentous bacteria - bugs in the gut or NOT for
>instance) i loaded that FIRST
>post to answer YOUR question, perhaPs?
It'd be lovely if it were that simple, or even that simple on top of a
genetic predisposition, and I'm glad you've had some degree of
success, but I've done pretty much the equivalent and it doesn't do a
thing for me. If it ever occurs that whole bunches of people get
cured by changing intestinal flora alone, I'll send you one of those
huge floral boquets like they put around the Kentucky Derby winners.
>www.ncbi.nlm.nih.gov/pubmed/16124855
>
>[...]
>With psoriasis and autoimmune disease, the penetrance of the MHC-
>associated alleles is never 100%, even for monozygotic twins. This may
>be because development requires additional environmental and/or
>genetic modifiers or requires specific T-cell receptor arrangements.
>Families segregating single or multilocus susceptibility alleles other
>than the MHC have also been reported. Overlapping genetic locations of
>loci for different autoimmune diseases have been known for several
>years and are starting to reveal common genes or genetic variants.
><sniP>
>
>What does it mean?
>
>If your twin with ____identical genes___ doesn't onset with psoriasis,
>then THAT ALONE
>almost 100% guarantee's a nurture WRENCH in the monkey works of NATURE
>(which is mostly corrupted by nurture anyway). LOL
Does anything here say that, cases of identical twins were only one
gets psoriasis?
The MHC-difference is ... curious. I wonder if it's even true.
Certainly that part of the genome is built for individual variation,
and who knows maybe it varies after conception, that would be kinky.
But that's just one of our two or three or five different immune
systems, and not necessarily causal to psoriasis. Is it? I'm pretty
fuzzy on that level of detail.
(btw, on a mostly unrelated note, REALLY interesting article on New
Scientist the other day on the origin of life:
http://www.newscientist.com/article/mg20427306.200-was-our-oldest-ancestor-a-protonpowered-rock.html?full=true&print=true
Was our oldest ancestor a proton-powered rock?
)
J.
randall
> On Tue, 20 Oct 2009 20:34:58 -0700 (PDT), randall <ranhu...@aol.com>
> wrote:
>
> >Anyway I'm glad for your GENETIC propensity towards CAUSATION.
>
> Quite.
>
> >If WE or you wish to point to nature (DNA) or mother nurture (SFB -
> >segmented filamentous bacteria - bugs in the gut or NOT for
> >instance) i loaded that FIRST
> >post to answer YOUR question, perhaPs?
>
> It'd be lovely if it were that simple,
So was h. pylori. Do you agree or not?
> or even that simple on top of a
> genetic predisposition, and I'm glad you've had some degree of
> success,
You have not idea about my success or you'd agee with me.
:)
Right?
> but I've done pretty much the equivalent and it doesn't do a
> thing for me.
And you failure was WHAT?
I've failed a thousand times. Big DEAL.
Anyone can do that..
> If it ever occurs that whole bunches of people get
> cured by changing intestinal flora alone, I'll send you one of those
> huge floral boquets like they put around the Kentucky Derby winners.
I'll let you know after I make a few million. LOL
Maybe I won't bother as i'm sure you'lll read about it. LOL
> Scientist the other day on the origin of life:http://www.newscientist.com/article/mg20427306.200-was-our-oldest-anc...
> Was our oldest ancestor a proton-powered rock?
> )
>
> J.- Hide quoted text -
>
> - Show quoted text -
Love to know exactly what hasn't worked for your. ...
Then again maybe NOT.
randall... why does it have to be this hard?
JRStern
wrote:
>> It'd be lovely if it were that simple,
>
>So was h. pylori. Do you agree or not?
Sure. It was in all the papers.
Now find the bacteria for rheumatoid arthritis, or atheroschlerosis.
>You have not idea about my success or you'd agee with me.
You haven't posted about it a couple of hundred times?
J.
randall
> On Tue, 20 Oct 2009 21:48:57 -0700 (PDT), randall <ranhu...@aol.com>
> wrote:
>
> >> It'd be lovely if it were that simple,
>
> >So was h. pylori. Do you agree or not?
>
> Sure. It was in all the papers.
So it's our turn to be in all the papers.
WE just need Dr. Littman to eat some segmented filamentous bacterium
(SFB)
and SEE if his Th17 levels go beyond the ability of his Treg's to stop
the
inflammation. But whose to say his excess Th17 doesn't stay sub
clinical until
he drops dead at 69?
Whats that A word?
Oh yes asymptomatic....
Littman did say something about these bugs are the most astounding
things he's
seen.
And Th17 doesn't JUST mean psoriasis.
We're talking all of the conditions with excess Th17 versus Treg's.
From those articles:
**Too much Th17 cell activation, however, can lead to harmful
inflammation, Dr. Littman says. Excessive induction by specific
microbes in the gut, then, could contribute to autoimmune diseases
such as rheumatoid arthritis, psoriasis, Crohn's disease, and
possibly
even multiple sclerosis.**
If they can hook up exact genes with a causation it would seem
simpler to run their trials knowing that h. pylori or SFB is in
that equation. LOL
With simple deduction and the scientific method it can
be eliminated
So as usual we wait for more SFB studies and then we see.
Or you do the wit kit and grow a kilo of good flora and it
might crowd out the crap in your ileum.
What's wrong with doing that pray tell? <G>
What is it with GUT valves anyway? Unlike the heart valve
situation this one involves alkaline on one side and hopefully
slightly acidic due to lacti loving flora on the other side.
http://en.wikipedia.org/wiki/Ileocecal_valve
It's no wonder if the colon is full of putrefactive bacteria and not
enough lacti bugs that something could go wrong for all the folks
who have Ai conditions with to much Th17 and not enough treg's. <w>
Let us check the cecum in our group.
It brings back those appendix hits and your:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_thread/thread/1adb0106f005d826/c6503e36ff0b7991?hl=en&lnk=gst&q=cecum#c6503e36ff0b7991
We do get 11 hits for cecum in oUR GROUP:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=cecum
And this one ::
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/4436e52545944714
Manfred posted a link that said:
Here:
http://www.wjgnet.com/1007-9327/14/2029.asp
[...]
In another study with healthy adults and with patients with
Crohn’s disease, L. rhamnosus GG decreased the production of IL-2,
IL-10 and IL-4 from PBMCs sorted as naïve and memory T cells[33]. It
seems that L. rhamnosus GG has a role in modulating the cytokine
responses and may possess an anti-inflammatory potential in healthy
individuals
<sniP>
Then:
http://www.nytimes.com/2008/06/17/health/research/17appe.html?ref=science
Helpful Bacteria May Hide in Appendix
By NICHOLAS BAKALAR
Published: June 17, 2008
Everyone is born with one, but no one knows what it’s for. The human
appendix is a small dead-end tube connected to the cecum, or
ascending
colon, one section of the large intestine.
<sniP>
>
> Now find the bacteria for rheumatoid arthritis, or atheroschlerosis.
Good GOD man give me time to digest one thing at a time. LOL
But here are some PAD people with asymptomatic... you read it:
http://www.reuters.com/article/pressRelease/idUS141972+21-Oct-2009+PRN20091021
>
> >You have not idea about my success or you'd agee with me.
>
> You haven't posted about it a couple of hundred times?
WELL without looking at each post like the one by DEB, there
are over 80 hits for randall HOT ZONE (the Gi tract)
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=randall+hot+zone
And must be at least a few hundred for Gi tract:
I take that back 667 hits for randall + Gi + track
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=randall+Gi+tract
So i go back and forth with it.Or up and down or clear and plaque-ish.
My trials are never ending. But certainly i'm more apt to knock down
the flare du jour (red spots), while in the past i'd simply watch as
it took
territory and held it forever.
I"M the MASTER of my PSOR.
Now I claim back ankles, knees and other area's AT WILL.
Could i do it without sweet whey and resveratrol and fish oil?
That will be a trial as well, once I clear my pasi to 0%.
Do I need to brag about it?
I thought i'd over done that?
But maybe YOU all need MOrE?
randall... psorLESS in GAZA...
>
> J.
zzznot
news:7k8q1sF...@mid.individual.net...
> x-no-archive: yes
>
> I want to go on record as not having a dog in this fight; I think you're
> both all wet. ;-)
Call me surfer dude, cowabunga!
Unknown of course is what effect all this turmeric, or randall's bugs,
may have on the endocrine system that you like to talk about.
Blind men and the elephant, and all that.
J.
randall
> x-no-archive: yes
>
> zzznot wrote:
> > Call me surfer dude, cowabunga!
>
I'm even more shocked to think i was in love with a left wing
nut. LOL
How can i love your mind when your another obama mime?
LOL
>
>
>
> > Unknown of course is what effect all this turmeric, or randall's bugs,
> > may have on the endocrine system that you like to talk about.
>
> > Blind men and the elephant, and all that.
>
> \Speak for yourself, it's not unknown, just unknown to those who don't look:
Kooky kooky lend me your comb.
LOOKs like more left wing ding a ling to me. LOL
http://www.youtube.com/watch?v=PYCuslbXC6c
**Kookie, kookie, Stop combing your hair and kiss me.** <w>
>
> http://www.ncbi.nlm.nih.gov/sites/entrez?term=curcumin%20%20%20%20%20...
>
> Brain Res. 2006 Nov 29;1122(1):56-64. Epub 2006 Oct 3. Links
> Curcumin reverses the effects of chronic stress on behavior, the HPA
> axis, BDNF expression and phosphorylation of CREB.
>
> Xu Y, Ku B, Tie L, Yao H, Jiang W, Ma X, Li X.
> Department of Pharmacology, School of Basic Medical Science, Peking
> University, 38 Xueyuan Road, Beijing, 100083, PR China.
> Curcuma longa is a major constituent of the traditional Chinese medicine
> Xiaoyao-san, which has been used to effectively manage stress and
> depression-related disorders in China.
BFD (Big F**king DEAL) so is hydrangea (aka- halofuginone) and what
good
is another bioiogical?
> Curcumin is the active component
> of curcuma longa, and its antidepressant effects were described in our
> prior studies in mouse models of behavioral despair. We hypothesized
> that curcumin may also alleviate stress-induced depressive-like
> behaviors and hypothalamic-pituitary-adrenal (HPA) axis dysfunction.
> Thus in present study we assessed whether curcumin treatment (2.5, 5 and
> 10 mg/kg, p.o.) affects behavior in a chronic unpredictable stress model
> of depression in rats and examined what its molecular targets may be. We
> found that subjecting animals to the chronic stress protocol for 20days
> resulted in performance deficits in the shuttle-box task and several
> physiological effects, such as an abnormal adrenal gland weight to body
> weight (AG/B) ratio and increased thickness of the adrenal cortex as
> well as elevated serum corticosterone levels and reduced glucocorticoid
> receptor (GR) mRNA expression. These changes were reversed by chronic
> curcumin administration (5 or 10 mg/kg, p.o.). In addition, we also
> found that the chronic stress procedure induced a down-regulation of
> brain-derived neurotrophic factor (BDNF) protein levels and reduced the
> ratio of phosphorylated cAMP response element-binding protein (pCREB) to
> CREB levels (pCREB/CREB) in the hippocampus and frontal cortex of
> stressed rats. Furthermore, these stress-induced decreases in BDNF and
> pCREB/CREB were also blocked by chronic curcumin administration (5 or 10
> mg/kg, p.o.). These results provide compelling evidence that the
> behavioral effects of curcumin in chronically stressed animals, and by
> extension humans, may be related to their modulating effects on the HPA
> axis and neurotrophin factor expressions.
> PMID: 17022948 [PubMed - indexed for MEDLINE
>
> Susan
LOOKs like pure unadulterated nonsense to me.
What i'd expect from a left wing LOON> LOL
OH crap, but you said you ******** her.
WeLL yeah...
But that was before..
OK, before what...
Before i acted like an ASS.
Ok, we get you... your a phony.
Well, well, but a CLEAR one.
randalll....still loves that libby pooh whatz her name. LOL
zzznot
Regarding which, am I to conclude from your post
that you approve of using curcumin because it does
seem to address the endocrine system?
Which is just what I was suggesting, you know.
J.
"Susan" <su...@nothanks.org> wrote in message
news:7k9ohiF...@mid.individual.net...
> x-no-archive: yes
>
> zzznot wrote:
>
>> Call me surfer dude, cowabunga!
>
> I'm too shocked at finding out you're a right wingnut!
>
>>
>> Unknown of course is what effect all this turmeric, or randall's bugs,
>> may have on the endocrine system that you like to talk about.
>>
>> Blind men and the elephant, and all that.
>>
>
> \Speak for yourself, it's not unknown, just unknown to those who don't
> look:
>
> http://www.ncbi.nlm.nih.gov/sites/entrez?term=curcumin%20%20%20%20%20HPA%20axis&db=pubmed
>
> Brain Res. 2006 Nov 29;1122(1):56-64. Epub 2006 Oct 3. Links
> Curcumin reverses the effects of chronic stress on behavior, the HPA axis,
> BDNF expression and phosphorylation of CREB.
>
> Xu Y, Ku B, Tie L, Yao H, Jiang W, Ma X, Li X.
> Department of Pharmacology, School of Basic Medical Science, Peking
> University, 38 Xueyuan Road, Beijing, 100083, PR China.
> Curcuma longa is a major constituent of the traditional Chinese medicine
> Xiaoyao-san, which has been used to effectively manage stress and
> depression-related disorders in China. Curcumin is the active component of
randall
> I still respect your medical knowledge.
>
> Regarding which, am I to conclude from your post
> that you approve of using curcumin because it does
> seem to address the endocrine system?
>
> Which is just what I was suggesting, you know.
>
> J.
>
> "Susan" <su...@nothanks.org> wrote in message
>
> news:7k9ohiF...@mid.individual.net...
>
>
>
> > x-no-archive: yes
>
> > zzznot wrote:
>
> >> Call me surfer dude, cowabunga!
>
> > I'm too shocked at finding out you're a right wingnut!
>
> >> Unknown of course is what effect all this turmeric, or randall's bugs,
> >> may have on the endocrine system that you like to talk about.
>
> >> Blind men and the elephant, and all that.
>
> > \Speak for yourself, it's not unknown, just unknown to those who don't
> > look:
>
>
> - Show quoted text -
jr,
What?
are you a pussy?
What rat's ass do you give if she think's otherwise?
This is psoriasis and your SKIN doesn't care what your political
affiliation is. LOL
And furthermore that has NOTHING to do with it.
If Susan is a psor person and I am, then so what?
I like her and if she doesn't LIKE me because
i'm not a poltical person she approves of, then so what?
Doesn't bother me and never will.
I will take the oportunity to have a laugh.
What else is there?
randall... are we that vain besides being PSOR?
zzznot
... no, the Dodgers,
... no, ... hoo boy
J.
JRStern
>x-no-archive: yes
>
>zzznot wrote:
>> I still respect your medical knowledge.
>>
>> Regarding which, am I to conclude from your post
>> that you approve of using curcumin because it does
>> seem to address the endocrine system?
>>
>> Which is just what I was suggesting, you know.
>>
>
>You seem to be ascribing beliefs and attitudes to me that I don't hold.
>
>I approve of ANYTHING someone does to help him/herself that does more
>good than harm. That's pretty much my only rule.
>
>Susan
Well and good.
Geez, it's hard just to make conversation these days, everybody thinks
you're making an argument, not just clarifying what each side said,
expanding and revising, and like that.
J.
randall
>
> - Show quoted text -
Jr & Susan,
I guess the Yankees are losing now. LOL
Let's see.
It's 4 to O in the seventh inning in favor of the dodgers.
I can live with or without that.
Jeter is up now... LOOK out..?
Seeing that my football team has a new stadium
to sneak off to in LA i'm saying the SOUTH of
California needs to leave this state and become part of
Arizona.
We'll become CALzonians.
It those monkey rear ends in sacramento want to
give our water to a smelt and not us, it's time to leave
this state of stupidly.
OK, where was i?
OH, bases are full. Jeter is on first.
And a pop out and they didn't score on it. I bet
Jr is pissing NOW. LOL
And Susan as well. LOL
Anyway back to Psoriasis.
Maybe JRSTern is right on.
As these psoriasin abstracts today raise interesting questions.
www.ncbi.nlm.nih.gov/pubmed/19707901
Psoriasin (S100A7), an antimicrobial peptide, is increased in human
middle ear cholesteatoma.
Kim KH, Cho JG, Song JJ, Woo JS, Lee HM, Jung HH, Hwang SJ, Chae S.
Department of Otolaryngology, Pundang Jesaeng Hospital, Daejin Medical
Center, Seongnam.
Conclusion. Increased psoriasin in cholesteatoma epithelium may play a
role in epithelial inflammatory response and differentiation.
Objectives. Cholesteatoma is characterized by excessive keratinocyte
differentiation leading to inflammation, granulation tissue, and
osteolytic activity. Moreover, psoriasin may act as an antimicrobial
peptide, stimulate granulocytes, and control keratinocyte
differentiation. The purpose of this study was to investigate the
differential expression patterns and the localization of psoriasin in
cholesteatoma and in normal external auditory canal skin. Materials
and methods. Expression levels of psoriasin mRNA were evaluated by
real-time PCR and Western blotting. Cholesteatoma-affected and normal
external auditory canal skin samples were immunostained with
monoclonal antibody to psoriasin. Localization of immunoreactivity to
psoriasin antibody was then compared. Results. By real-time PCR,
expression levels of psoriasin mRNA in cholesteatoma were
significantly higher than in normal external auditory canal skin, and
this was confirmed by Western blotting. Immunohistochemical staining
revealed that psoriasin protein is mainly expressed in the granular
layer and in the upper parts of the spinous layer in cholesteatoma
epithelium, but that it is expressed in the superficial layer of
normal external auditory canal skin.
PMID: 19707901
www.ncbi.nlm.nih.gov/pubmed/19844956
Structural and functional characterization of a triple mutant form of
S100A7 defective for Jab1 binding.
<sniP>
www.ncbi.nlm.nih.gov/pubmed/19810752
Identification and Characterization of Binding Sites on S100A7, a
Participant in Cancer and Inflammation Pathways.
<sniP>
But the one for psoriasis is S100A4 not S100A7.
www.ncbi.nlm.nih.gov/pubmed/19641515
So? Punt.
While psoriatics may have a lower cancer incidence, I don't know the
exact demographics, I suppose it's possible.
Does psoriasis protect against CANCER due to Th1 (T helper 1 cells)
SKEW or
is psoriasin S100A4 or 7 working behind the scenes?
Does S100A7 with a Th2 skew a CANCER death sentence or treatable?
But it would be nice to think that excess IFN and TNF keeps the
CANCER away, making psoriasis compensatory for worse health outcomes.
=====================
Back to SFB.
Let's look at psoriasis & SFB in regards to IFN.
Does SBF cause the excess IFN?
www.ncbi.nlm.nih.gov/pubmed/19327545
Intestinal Bifidobacterium association in germ-free T cell receptor
transgenic mice down-regulates dietary antigen-specific immune
responses of the small intestine but enhances those of the large
intestine.
Tsuda M, Hosono A, Yanagibashi T, Hachimura S, Hirayama K, Umesaki Y,
Itoh K, Takahashi K, Kaminogawa S.
Department of Food Science and Technology, College of Bioresource
Sciences, Nihon University, 1866 Kameino, Fujisawa-shi, Kanagawa
252-8510, Japan.
Bifidobacterium is a dominant bacterial species among commensals in
the human intestine and is thought to have probiotic immunomodulatory
effects. In this study, we investigated the effect of the association
with Bifidobacterium pseudocatenulatum JCM 7041 (Bp) on dietary
ovalbumin (OVA)-specific immune responses using germ-free OVA-specific
T cell receptor transgenic mice (OVA23-3 mice). We established germ-
free OVA23-3 mice, and then associated with Bp (BIF group) or without
(CONT group) and additionally associated with segmented filamentous
bacteria (SFB) and clostridia in both groups. BIF and CONT mice were
fed an egg-white diet containing OVA for 1 week. Cytokine production
in response to OVA by cells of Peyer's patches (PPs) and lamina
propria (LP) from the small and large intestine was measured.
Interferon (IFN)-gamma and interleukin (IL)-6 production by PP cells
from BIF group mice was lower than that of the CONT group. The
proportion of PP cells expressing CD4+CD62L(low), an activated/memory
T cell phenotype, was higher in BIF group mice than the CONT group.
Furthermore, LP cells from the small intestine in Bp-associated mice
showed a tendency to produce slightly lower IFN-gamma and IL-6, while
the cells from large intestine produced markedly higher IFN-gamma,
IL-5 and IL-6 than those in the CONT group. The pattern of cytokine
production by PP in BIF animals was similar to those isolated from
conventional mice. These results suggest that intestinal association
with Bp might down-regulate excessive immune responses to dietary
antigens of the small intestine but enhance those of the large
intestine.
PMID: 19327545
So LACTi loving bugs lowers IFN levels.
And the higher your IFN (due to sFB?) the worse your psoriasis
severity.
keywords: psoria* + interferon 622 hits on pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+interferon&log$=activity
The most recent:
www.ncbi.nlm.nih.gov/pubmed/19843085
Serum cytokines and growth factor levels in Japanese patients with
psoriasis.
Takahashi H, Tsuji H, Hashimoto Y, Ishida-Yamamoto A, Iizuka H.
Department of Dermatology, Asahikawa Medical College,
Midorigaokahigashi, Asahikawa, Japan.
Summary Background. Although the precise pathomechanism of psoriasis
is still unknown, various cytokines and growth factors derived from T
cells, dendritic cells or keratinocytes, are critically involved in
this disease. There have been several studies determining the serum
levels of cytokines in patients with psoriasis, but with conflicting
results. The levels of various cytokines and growth factors were
measured in the sera of patients with psoriasis and compared with
those of healthy controls. The correlation with disease severity was
also determined. Methods. Sera were collected from 122 patients with
psoriasis and 78 healthy controls for ELISA analysis to evaluate the
levels of cytokines and growth factors. The severity of psoriasis was
determined by the Psoriasis Area and Severity Index (PASI). Results.
Serum levels of tumour necrosis factor (TNF)-alpha, interferon (IFN)-
gamma, interleukin (IL)-2, IL-6, IL-7, IL-8, IL-12, IL-17, IL-18 and
vascular endothelial growth factor (VEGF) were significantly increased
in patients with psoriasis compared with those of healthy controls.
The serum levels of IL-2, soluble intercellular adhesion molecule-1,
epidermal growth factor, hepatocyte growth factor and amphiregulin
were not significantly different from those of healthy controls.
Increased serum levels of TNF-alpha, IFN-gamma, IL-12, IL-17, IL-18
and VEGF correlated with PASI. Furthermore, these cytokine levels were
decreased after psoriasis treatment. In contrast, serum levels of
IL-10 were decreased in psoriasis and negatively correlated with PASI.
Discussion. Serum levels of TNF-alpha, IFN-gamma, IL2, IL-6, IL-7,
IL-8, IL-12, IL-17, IL-18 and VEGF were positively correlated and that
of IL-10 was negatively correlated with PASI in Japanese patients with
psoriasis. These parameters might be useful for determining the
disease activity of psoriasis.
PMID: 19843085
Classic psoriasis profile, high TNF & IFN and LOW IL-10
Another recent IFN abstract:
www.ncbi.nlm.nih.gov/pubmed/19842576
Serum interferon-gamma is a psoriasis severity and prognostic marker.
Abdallah MA, Abdel-Hamid MF, Kotb AM, Mabrouk EA.
Department of Dermatology and Venereology, Faculty of Medicine, Ain
Shams University, Cairo, Egypt. marwa_a...@hotmail.com
The aim of this study was to measure serum interferon-gamma (IFN-
gamma) levels in participants with different types and severities of
psoriasis. The study was conducted on 21 participants with psoriasis.
Participants were divided into 3 groups according to disease severity:
erythrodermic, severe plaque, and mild to moderate plaque psoriasis.
Fifteen participants received different treatment modalities for 16
weeks and were followed for an additional 12 weeks. The enzyme-linked
immunosorbent assay technique was used to measure serum IFN-gamma
levels in participants before treatment and compared with matched
controls and participants receiving treatment. Significant differences
were detected between participants and controls in mean serum IFN-
gamma levels before treatment (P<.05). There was a positive
correlation between serum IFN-gamma levels and psoriasis area and
severity index (PASI) scores, and between serum IFN-gamm levels and
clinical type of psoriasis, with the highest serum IFN-gamma levels in
the erythrodermic psoriasis group and the lowest in the mild to
moderate plaque psoriasis group. Irrespective of the type of
treatment, 13 of 15 participants who showed improvement in disease
condition with a significant decrease in PASI scores also had a
significant decrease in serum IFN-gamma levels (P < .05). Moreover,
participants with serum IFN-gamma levels that did not dramatically
decrease had a shorter remission period compared with those who showed
a significant decrease in serum IFN-gamma levels. The substantial
elevation and variation in serum IFN-gamma levels according to disease
severity suggest that IFN-gamma has a role in determining disease
severity and therapy evaluation, which encourages further research on
anti-IFN-gamma biologic therapy in the treatment of psoriasis.
PMID: 19842576
You get the idea.
Christ the yankees just got two more runs. It's now a 4-3 ballgame.
The yankees are within ONE...
Very exciting. I"m loving it.
And either Susan or Jr will be happy.
So it's a wash. LOL
OK, back to my PROTOCOLs,
I crave kimchi and NOW I KNOW exactly why.
It's freaking loaded with L. Plantarum. The very lacti loving bug that
beats the crap out of SFB (segmented filamentous bacterium).
The link was in my psor post a few days back:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/3b4e1e54f340dee8
[...]
*****SFB in the ileum of immunocompromised mice, which was abolished
upon administration of L. plantarum, an effect not described to date.
PMID: 18081591*******
Thusly:: the KimChi link with L. plantarum and NOW eradication of
SFB
in the ileum of Autoimmune folks.
http://www3.interscience.wiley.com/journal/121573886/abstract?CRETRY=1&SRETRY=0
[...]
Keywords
kimchi lactic acid bacteria • immunopotentiating activity • nitric
oxide • tumor necrosis factor- • interleukin-6
Abstract
The present study investigated immunopotentiating activities of lactic
acid bacteria isolated from kimchi (KLAB) in vitro. A RAW264.7
macrophage cell line was stimulated with four strains of KLAB and two
strains of bifidobacteria, and then the production of nitric oxide
(NO) and cytokines - tumor necrosis factor- (TNF-) and interleukin-6
(IL-6) - was determined. Lactobacillus plantarum, a lactic acid
bacteria involved in the latent fermentation of kimchi, was the most
effective for the generation of NO, TNF-, and IL-6 in macrophage. All
strains generated NO, while for the TNF- and IL-6, only L. plantarum
had significant activity. Our results indicate that L. plantarum plays
an important role in the immunopotentiating activity of kimchi.
<snip>
--------------------
One of my most recent trials involves increased iodine from sea kelp.
Seems to help energy levels. Which may be a real boon to hiv/aids
patients. :)
The iodine link is below these two links I found the supplement on.
Found these on a site that has iodine supplements I was looking at:::
http://www.braintuner.com/transtechlinks.htm
http://www.braintuner.com/ttlinks_2.htm
Take some iodine:
http://www.tpcsdirect.com/
IOSOL iodine and iodide is water-soluble non-toxic dietary food
supplement
[this is off their page II above]
You might need a ND naturopath for this, i'm not sure.
--------------
Found this interesting as well. [did read these]
But NOT this one YET:
http://www.mgwater.com/bicarb.shtml
Take a potassium bicarbonate dietary supplement to buffer your diet.
http://www.life-enhancement.com/article_template.asp?ID=2089
http://www.life-enhancement.com/article_template.asp?ID=2164
http://www.life-enhancement.com/article_template.asp?id=2099
The vitamin C bi carb thingy: [for cancer]
http://www.vitamincfoundation.org/forum/viewtopic.php?f=3&t=6248
[...]
Re: Potassium Bicarbonate
I use potassium bicarbonate every day, reacting it with ascorbic acid
to make potassium ascorbate. The stoichiometric ratio of potassium
bicarbonate to ascorbic acid is 0.57. For example, it would take 57
milligrams of potassium bicarbonate to react with 100 milligrams of
ascorbic acid. Care must be taken not to overdose on potassium, which
can easily happen with any soluble potassium salt. Potassium
bicarbonate (KHCO3) is 39% potassium by mass. The FDA limit on the
amount of potassium in a single dose of any supplement is 99
milligrams.
I make potassium ascorbate in a tapered shot glass by placing 110 mg
potassium bicarbonate powder into the glass, adding 400 mg of ascorbic
acid on top of that, then adding a teaspoon of warm water. When the
fizzing subsides, I have a 50/50 mixture of potassium ascorbate and
ascorbic acid. Twice as much ascorbic acid as the stoichiometric
amount is used, to ensure that all of the potassium bicarbonate is
reacted. Then I add a few ounces of water, stir, and the mixture
dissolves completely.
The late Gianfranco Pantellini, a professor of chemistry in Italy,
conducted a clinical trial, in collaboration with medical doctors, in
which potassium ascorbate was administered to patients terminally ill
with cancer. The results were dramatically positive, such that a few
of them were able to return to normal life. To my knowledge, no
clinical trial of potassium ascorbate for the treatment of cancer was
ever done in the USA. My own hypothesis to explain the efficacy of
potassium ascorbate is that the potassium attached to the ascorbate
facilitates its entry into cells. Here is a link to a thread on
potassium ascorbate in this forum.
<sniP>
How to use bicarbonate for PSORIASIS
http://talkpsoriasis.org/showthread.php?t=25458
-----------
BiCarb plus maple syrup for Psoriasis
http://www.godlikeproductions.com/forum1/message601580/pg1
-------------
But the role that IFN plays is another story and in my book points at
SFB more then ever.
When, OH when will JRstern and Susan go the sweet whey route?
Never perhaps?
I can't control them or their lives. But i'll pray and love them
because i do.
randall.. OH my... it's ALL tied up NOW.... so exciting...
randall
>
> - Show quoted text -
JR,
What freaking **expanding or revising** have you ever done with
an abstract or FACT?
You've been doing your curry, curcumin trial forever now.
You relate 100% from an empirical position.
And it's most likely due to the fact that your
trials last five or more years. LOL
You should take Susan at face value and try
estrogen. LOL
HPA-axis + estrogen: 144 hits [pubmed]
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=hpa-axis+estrogen&log$=activity
You and the Dodgers both. I see the Yankees scored
six runs and now lead by two runs, toP of
the seventh.
Ouch..
You are in LA.... maybe some selenium will help?
Selenium - a mineral anti-oxidant. Research suggests relationship
between low selenium levels and increased risk of various types of
cancer . Daily supplement recommendations are anywhere from 55
microgram per day to 200 microgram, depending upon the authority.
Selenium is also known to reduce infectious viral activity in Hiv/Aids
as well as other viruses. The richest food source of selenium is found
in Brazil Nuts, where two Brazil nuts can supply an average of 53
micrograms selenium. Nuts in the shell are more potent than pre-
shelled nuts.
See article for more information:
http://ods.od.nih.gov/factsheets/selenium.asp
<W>
And susan has been on top of this next one.
Niacinamide - a form of vitamin B3 - exciting and ground-breaking
research at the University of California, Irvine, has demonstrated a
complete reversal of alzheimers in MICE. Specially bred laboratory
mice with the same clinical brain condition of human alzheimers, were
given 2,000 to 3,000mg. of Niacinamide daily for only four months.
(Important - this is NOT regular Niacin, which is different from
Niacinamide). They experienced a complete reversal of memory loss and
performed as well as normal mice on a series of tests. Niacinamide
also improved the memory of non-affected mice. While mice are not
human, these same effects may be possible in human alzheimers
patients. These studies are now under way with the same research team.
They will be giving 1,500mg. niacinamide two times per day with a test
group and a placebo group. Niacinamide is very inexpensive with few
minor side effects in some individuals (mild nausea) and these dosages
are very low with no toxicity. Some medical authorities recommend
1,000 milligram capsules taken three times daily. One should look for
formulas without additives, colorants, preservatives, etc. Medical
reference: JNeurosci 08;28:11500-11510 (journal of neuroscience).
Wow... if this is true. Many folks could be helped and we'd save a ton
of money when
that obama health care BILL comes around.
You do support our prez i hoPe?
I'm going to GO all out to support healthcare and from a capitalist
point of view.
Otherwise it won't be successful....
Until the prez works for FREE i still thing i should make a buck.
So?
Most likely i'm gonna take his example and say GOODbye SOON.
Thank GOD for democrats to set us STRAIGHT.
Randall...well... whatever. LOL
randall
>
> > Regarding which, am I to conclude from your post
> > that you approve of using curcumin because it does
> > seem to address the endocrine system?
>
> > Which is just what I was suggesting, you know.
>
>
> I approve of ANYTHING someone does to help him/herself that does more
> good than harm. That's pretty much my only rule.
>
> Susan
Dearest Susan,
Your the brightest light in my MIND and psor SKIN. :)
And now the nyy and LAA game is tied at 6 each.
Wow, this is a GAME.
I love it.
Anyway.... the angels just scored and now lead by ONE.
7 to 6 in bottom of the 7th.
I ONLY want to DO GOOD. LOL
Oh the 7th inning is OVER and 7-6 favor of dodgers.
randall.. your hpa-axis admirer.
randall
> > I guess the Yankees are losing now. LOL
>
> > Let's see.
>
> > It's 4 to O in the seventh inning in favor of the dodgers.
>
> > I can live with or without that.
>
>
> Susan
7- 6 top of the 9th....
Dodgers might get this one.
randall...
randall
> > Oh the 7th inning is OVER and 7-6 favor of dodgers.
>
>
> Susan
Susan,
Thank YOU, i just realized that. LOL
Them are Angels and not dodger dogs.
They just walked the tie-ing run with 2 outs.
Could be over in a minute or less.
randall
randall
> > Wow... if this is true. Many folks could be helped and we'd save a ton
> > of money when
> > that obama health care BILL comes around.
>
>
> And the only way to save money for real is to cut the high glycemic load
> responsible for most dementia.
I posted something on bicarb to ward off the sugar blues today.
Where is that?
[...]
http://www.mgwater.com/bicarb.shtml
http://www.vitamincfoundation.org/forum/viewtopic.php?f=3&t=6248
<sniP>
http://talkpsoriasis.org/showthread.php?t=25458
-----------
<sniP>
=======================
>
>
>
> > You do support our prez i hoPe?
>
> Yes, but I'm very disappointed in his drinking the Daschle/Mayo Clinic
> Kool Aid; we can't control costs as long as pharma is writing the
> consensus guidelines that are called "best practices." They're only
> best for drug and sugar pusher profits.
>
> I support our president, but not uncritically. I'm also disappointed
> that we got Geithner and Summers back in charge of the economy and
> regulation.
>
> Susan
I have to get behind the prez in true american
fashion.
I want to cure autoimmune as my small part . <w>
And If i can i WILL...
The game is over. What is it now?
The yankee's are 3-2 in this series?
Let's see:
Four minutes ago::
http://fromthedugout.freedomblogging.com/2009/10/22/angels-rally-to-stay-alive-7-6/39285/
Angels rally to stay alive, 7-6
October 22nd, 2009, 8:31 pm · Post a Comment · posted by BILL
PLUNKETT, OCREGISTER.COM
ANAHEIM
It’s merely a flesh wound.
Like the Black Knight in Monty Python’s ‘Holy Grail,’ the Angels shook
off the Yankees’ near-fatal blows with more conviction than
circumstances warrant but lived to fight another day with a 7-6
victory in Game 5 of the American League Championship Series Thursday
night at Angel Stadium.
The win forces a Game 6 at Yankee Stadium Saturday night (start time
4:57 p.m. PDT).
But it took a three-run rally in the bottom of the seventh inning to
shake off a six-run blow by the Yankees in the top of the inning.
Angels starter John Lackey cruised into the seventh inning with a 4-0
lead only to run into the kind of moment that would have been debated
for months to come.
The second-guessing began even as Scioscia was approaching the
pitcher’s mound to replace Lackey. TV cameras clearly caught Lackey
saying, “This is mine, Sosh. This is mine. Are you (kidding) me? This
is mine.”
Lackey’s swan song began with a one-out double by Melky Cabrera. When
home-plate umpire Fieldin Culbreth called his low-and-inside fastball
on full count to Jorge Posada a ball, Lackey reacted angrily.
The call seemed to stick with Lackey who walked Derek Jeter on four
pitches to load the bases. When Johnny Damon flew out and Cabrera
scampered back to third base, Lackey used the opportunity to discuss
the call some more with Culbreth as the pitcher backed up home plate.
Lackey had thrown only 104 pitches but Scioscia had seen enough and
came out to get Lackey, much to Lackey’s consternation.
Scioscia brought in left-hander Darren Oliver to face switch-hitter
Mark Teixeira. It was a matchup that had recent history on the Angels’
side – Oliver had not given up a run in his first six innings this
post-season while Teixeira was 3 for 21 without an RBI in this series.
But Teixeira ripped Oliver’s first pitch, a curveball, to the wall in
left-center field for a three-run double. After an intentional walk to
Rodriguez, Yankees DH Hideki Matsui singled to center, scoring
Teixeira with the tying run.
Scioscia brought in right-hander Kevin Jepsen to face left-handed
hitting Robinson Cano and Cano tripled to center field, driving in
Rodriguez and Matsui with the go-ahead runs.
But the Angels had an answer in the bottom of the inning.
Held in check by Yankees starter A.J. Burnett after scoring four times
in the first inning, the Angels started their rally from the bottom up
– No. 8 hitter Jeff Mathis singled (his club-record sixth consecutive
post-season at-bat with a hit) and Burnett walked No. 9 hitter Erick
Aybar before giving way to the bullpen.
Chone Figgins bunted both runners over and Mathis scored on Bobby
Abreu’s ground out to first, cutting the Yankees’ lead in half.
With two outs, Yankees reliever Phil Hughes walked Torii Hunter and
gave up an RBI single to Vladimir Guerrero that tied the game. Kendry
Morales followed with a ground-ball single through the right side of
the infield, driving in Hunter with the go-ahead run.
Oliver and Jepsen having cracked in the seventh inning, Scioscia
turned to Jered Weaver in the eighth and the right-hander retired the
Yankees in order, striking out two.
But in the ninth he went with closer Brian Fuentes who retired Damon
and Teixeira quickly – then intentionally walked Rodriguez, putting
the tying run on base with two outs.
When Fuentes also walked Hideki Matsui, the tying run moved into
scoring postion. When he hit Robinson Cano with an 0-and-1 curveball,
the bases were loaded with the tying run at third and the go-ahead run
in scoring position.
Fuentes got ahead of Nick Swisher, 0-and-2, but Swisher worked the
count full before getting him to pop out to shortstop.
<sniP>
randall... that was FUN... :)
JRStern
wrote:
>What freaking **expanding or revising** have you ever done with
>an abstract or FACT?
I am a fount of facts about myself, that none of the biochem articles
shines a light on. Call me Dr. Empiricus.
>You've been doing your curry, curcumin trial forever now.
With some success, and many variations, but that's not a trial,
exactly, more like survival.
>You relate 100% from an empirical position.
It's a dirty job.
But come on, I try to be informed by what I read, in your posts and
Susan's and whatever else crosses my sight line, including other
empirical reports, but most of them are a long way from being
immediately applicable, outside of a biochem lab. And I'm sure 80% or
more of them are as Sturgeon's Law suggests, it applies even to
refereed science, you know.
>You and the Dodgers both. I see the Yankees scored
>six runs and now lead by two runs, toP of
>the seventh.
Dodgers are blue and holding their breath until April now, these are
Angels.
>You are in LA.... maybe some selenium will help?
>
>Selenium - a mineral anti-oxidant. Research suggests relationship
>between low selenium levels and increased risk of various types of
>cancer . Daily supplement recommendations are anywhere from 55
>microgram per day to 200 microgram, depending upon the authority.
>Selenium is also known to reduce infectious viral activity in Hiv/Aids
>as well as other viruses. The richest food source of selenium is found
>in Brazil Nuts, where two Brazil nuts can supply an average of 53
>micrograms selenium. Nuts in the shell are more potent than pre-
>shelled nuts.
I take the supplement, brazil nuts are tasty but full of radium.
J.
randall
> On Thu, 22 Oct 2009 19:41:58 -0700 (PDT), randall <ranhu...@aol.com>
J,
You are the keePer of symmetry in this group, fur sure. :)
But,
OK so radium is BAD now? Like the Sun and UVB's?
What if you put curry in your kimchi?
You do eat kimchi don't you?
Why not?
What i posted yesterday might be BIG.
L. Plantarum in kimchi kills SFB DEAD, dead, deadski. LOL
Please recall now that SFB is segmented filamentous bacteria
that reside in the ileum.
Thusly SFB is BAD GUT FLORA... how do they symetricate
the psoriatic so WELL... time will tell.. i hope. <G>
I wonder how much kimchi plantarum makes it to your ileum?
I'll go buy a quart and chow down for a week. :)
Otherwise it's yin/yang time again. LOL
How much radium btw are in them nutz from Brazil?
I did post that nut link for the hiv/aids connections and i've
always taken selenium as a supplement.
OK,
Congrats on the angels hanging on for another gAME.
Yet,
Maybe the radium and uvb has a DNA link?
What is that word for a poison in a small dose that
creates some sort of beneficial response? Can't recall for now.
Look at this next story for DNA and P.
http://health.usnews.com/articles/health/healthday/2009/10/22/some-parts-of-human-genome-get-lost.html
Some Parts of Human Genome Get Lost
Technology allows scientists to spot non-essential DNA base pairs
THURSDAY, Oct. 22 (HealthDay News) -- Researchers have created their
first map of parts of the human genome
that are considered disposable.
Scientists estimate that at least 2.7 million base pairs of the human
genome, which reside in 58 distinct regions of DNA, are non-essential
and can disappear without hurting people's health.
The new report builds on previous findings by using microarray
technology to find DNA in 600 young and healthy Dutch subjects. Nearly
all of the study participants
carried so-called complete DNA losses. On average, the number was
50,000 base pairs.
"The results of this study have provided insight into the 'non-
essential' parts of the human genome, which will aid in expanding our
current understanding of genetic variation among humans," study co-
author Terry Vrijenhoek, a medical geneticist from Radboud University
Nijmegen in the Netherlands, said in a news release from the American
Society of Human Genetics.
"Clearly, while the large majority of our genes are essential, the
current research results suggest that hardly any one of us possesses a
complete genome," Vrijenhoek added.
The researchers noted that most people can do just fine without the
DNA base pairs, even though some of the genes seem to play a role in
disease -- like ______________psoriasis_____________ -- and food
digestion.
It also appears that evolution protects the most important genes by
making sure they're not in areas where base pairs are often lost, the
study authors explained.
The findings were to be released this week at the American Society of
Human Genetics annual meeting, in Honolulu.
[randall note: what is it with DNA and psoriasis? LOL]
What is that r word for response?
Still can't recall.
==============
Do you worship the SUN?
If your going to become a UVB junky to lower your psors, then consider
this.
http://www.lef.org/newsletter/2009/1023_Protective-Effect-Found-for-Ginkgo-Against-Radiation-Damage.htm
Protective effect found for ginkgo against radiation damage
A report published in the October 11, 2009 issue of the International
Journal of Low Radiation added evidence to a protective effect for
Ginkgo biloba against radiation damage. Ginkgo biloba is a tree
species whose leaves have been used for centuries in Chinese medicine.
Ginkgo leaf extract contains antioxidant compounds called ginkgolides
and bilobalides which help scavenge free radicals that attack nearly
all components of the cell, including DNA.
In their article, Chang-Mo Kang of the Korea Institute of Radiological
and Medical Sciences in Taegu and colleagues describe their use of an
assay for radiation-induced programmed cell death (apoptosis) to
evaluate the protective effect of ginkgo extract against radiation
exposure that occurs during accidents or occupational overexposure. In
one experiment, white blood cells from human donors aged 18 to 50 were
treated with one of four concentrations of ginkgo extract or a 9
percent saline solution before being exposed to gamma rays.
The researchers found a significant dose-dependent reduction in
apoptotic cells among those treated with ginkgo. While radiation-
induced apoptosis occurred in nearly one third of irradiated cells not
treated with ginkgo, the number declined to 5 percent or less in cells
treated with the herb.
In another experiment, mice were treated with ginkgo extract or saline
before and after receiving whole body ionizing radiation. Mice that
did not undergo radiation served as controls. Examination of the
animals' spleens found that treatment with ginkgo maintained organ
size comparable with that of animals that did not receive radiation,
while spleens in irradiated animals that did not receive ginkgo were
significantly smaller.
In their discussion of the findings, the authors note that cell-
damaging free radicals and reactive oxygen species can be generated in
excess under numerous conditions, including exposure to environmental
chemicals, specific drugs, and during normal aging.
"These results indicate that the radioprotective effects of ginkgo
extracts administered prior to radiation are due to the OH radical
scavenging activity," the authors write. "Therefore, ginkgo extract
should be useful for the protection of radiosensitive organs against
free radicals.
===========
While ginkgo may be good, resveratrol is Golden.
The secrets of sirtuins and YOU versus aging.
This is an amazing article.
http://www.life-enhancement.com/article_template.asp?id=2056
I haven't tried their supplement.
But I LOVE the longevinex product and fully endorse it.
Go to
In the news off reuters:
http://www.reuters.com/article/pressRelease/idUS86075+21-Oct-2009+PRN20091021
=============
This was put up yesterday and i'm still amazed a day later.
Susan has been on to Niacinamide effects, but most of her posts are
gone. :(
So maybe it was nicotinamide. LOL
177 hits for nicotinamide on our group:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=nicotinamide
So let's google: Niacinamide susan - for our group - 5 hits:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=Niacinamide+susan
Oh well... angels/dodgers and nicotinamide/niacinamide what do i
know?
Nothing apprayently..
But, but, but
The one from yesterday really astounded for good reason.
See:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/c9e5a8b9b542940b
[...]
Niacinamide - a form of vitamin B3 - exciting and ground-breaking
research at the University of California, Irvine, has demonstrated a
complete reversal of alzheimers in MICE. Specially bred laboratory
mice with the same clinical brain condition of human alzheimers, were
given 2,000 to 3,000mg. of Niacinamide daily for only four months.
(Important - this is NOT regular Niacin, which is different from
Niacinamide). They experienced a complete reversal of memory loss and
performed as well as normal mice on a series of tests. Niacinamide
also improved the memory of non-affected mice. While mice are not
human, these same effects may be possible in human alzheimers
patients. These studies are now under way with the same research
team.
They will be giving 1,500mg. niacinamide two times per day with a
test
group and a placebo group. Niacinamide is very inexpensive with few
minor side effects in some individuals (mild nausea) and these
dosages
are very low with no toxicity. Some medical authorities recommend
1,000 milligram capsules taken three times daily. One should look for
formulas without additives, colorants, preservatives, etc. Medical
reference: JNeurosci 08;28:11500-11510 (journal of neuroscience).
<snip>
From VRp.com today:: mORE in the sAME vein:
www.vrp.com
Four Ways to Keep Your Brain “Young” for Good
Health News
By VRP Staff
In the war against aging, you choose your battles. For some, a wrinkle-
free face takes first priority—while for others, a svelte figure, more
energy or a healthy heart wins out every time. But whatever concern
tops your own personal list, one thing is certain: A youthful body is
of little use if you don’t have a healthy brain to coordinate and
control it… a fact that anyone familiar with the tragic effects of
Alzheimer’s disease can attest to.
The good news is that, while a slippery slope of “senior moments” used
to seem inevitable, scientists now know that your brain cells can
regenerate themselves, given the right conditions—offering an antidote
not only to age-related memory loss, but also to a whole host of other
neurodegenerative conditions. And the solution may be as simple as the
right combination of nutrients.
Among these nutrients, acetyl carnitine may be the most important.
Laboratory studies show that this nutrient increases the natural
replenishing effects of nerve growth factor (NGF) on your brain cells—
helping to boost neurite outgrowth (the branches that form your
brain’s communication network) a full 100 times greater than NGF alone.
1 In human trials, this effect has translated to improvements in
disorders ranging from mild cognitive impairment and early Alzheimer’s
disease to chronic fatigue syndrome, multiple sclerosis, diabetic
neuropathy and depression.2-6
When taken in combination with acetyl carnitine arginate—which mimics
NGF in your brain—acetyl carnitine’s effects are even more powerful.7
Together, these compounds synergistically boost the production of key
neurotransmitters, such as GABA and glutamate, while protecting
neurons from toxic proteins like beta amyloid— strongly implicated in
the cognitive declines associated with aging and development of
Alzheimer’s disease.8-9
Uridine is another essential compound for brain function. It’s a
nutraceutical “building block” of cytidine, an important carrier of
choline, which is necessary for memory-related neural signaling. In
vitro experiments reveal that human brain cells exposed to uridine
experience increased neurite outgrowth and regeneration.10-12 Similar
results have been seen with oral supplementation of uridine in aged
rats.13
Finally, there’s Gotu kola—an Indian plant with a long history of use
in Ayurvedic medicine preparations for senility, epilepsy and other
conditions. It was only recently that scientists identified two of the
unique compounds responsible for Gotu kola’s traditional reputation as
a brain tonic: asiaticosides and asiatic acid. Extracts of the herb
containing a higher percentage of these active constituents have been
shown to repair damaged neurons in cell culture studies and foster
improved brain functioning in animal studies.14
You can find exactly this type of Gotu kola extract—standardized to 20
percent asiaticosides—along with all three of the neuron-stimulating
compounds described above in a single memory-preserving formula called
Neuron Growth Factors (NGF™) from Vitamin Research Products.
[randall note: uridine is in those sugar packets for aids/hiv patients
to bolster RNA and in baby forumula's for the same reason?]
==========================
I guess i wait for more info on SFB and the gut as i've already
exhausted anything I felt was relevant.
But the gut itself and immunity will never leave my radium...
I mean radar. SFB is segmented filamentous bacterium.
Here's gut immune du jour:::
http://www.signaling-gateway.org/update/updates/200910/nrmicro2229.html
Innate immunity: Help from 'friendly' bacteria
Gut microbiota stimulate Toll-like receptors on dendritic cells (DCs),
which signal through MYD88 to mediate DC activation and induce
immunity to the parasite Toxoplasma gondii.
Commensal gut bacteria have many beneficial effects for the host,
including competition with pathogens and induction of the development
of gut-associated lymphoid tissues. Now, Benson et al. add another
function to this list by showing that the gut microbiota acts as an
adjuvant to induce immunity to Toxoplasma gondii.
In mice T. gondii is sensed by Toll-like receptor 11 (TLR11) on
dendritic cells (DCs), which secrete interleukin-12 (IL-12) to
activate CD4+ T helper 1 (TH1) cells; these then produce interferon-
(IFN) to kill the parasite. However, TLR11 is a pseudogene in humans,
so a different mechanism must operate. To investigate this, the
authors infected wild-type mice and Tlr11-/- mice with T. gondii. When
the mice were infected orally (which mimics natural infection in
humans) the production of IL-12 by DCs was reduced but not abolished
in Tlr11-/- mice; by contrast, IL-12 secretion following
intraperitoneal infection required TLR11. Furthermore, CD4+ T cells
from Tlr11-/- mice could still produce IFN when the mice were infected
orally but not following intraperitoneal infection. These findings
indicate that the mucosal immune system can initiate immune responses
to T. gondii in the absence of TLR11.
Based on these findings, the authors speculated that either DCs
directly detect T. gondii in a TLR11-independent manner or the gut
microbiota indirectly stimulates DCs to activate TH1 cell-mediated
immune responses. DCs isolated from the intestine of Tlr11-/- mice
could not detect the parasite in vitro, indicating that TLR11 is
required for this process. However, depletion of the gut microbiota in
Tlr11-/- mice abolished the production of IL-12p40 (a component of
IL-12) by DCs and subsequent immune responses to the parasite.
Therefore, commensal gut bacteria must indirectly stimulate immune
responses against the parasite in the absence of TLR11. This TLR11-
independent activation of immune responses was found to result in
reduced immunopathology compared with TLR11-dependent stimulation,
with wild-type mice showing marked immune-mediated damage in the small
intestine and significantly higher mortality than Tlr11-/- mice.
So how do commensal gut bacteria trigger adaptive immune responses
against T. gondii? Oral infection of mice lacking TLR9 or both TLR2
and TLR4 (which are used by DCs to sense bacteria) resulted in a
marked decrease in IFN production by CD4+T cells. These TLRs signal
through myeloid differentiation primary response protein 88 (MYD88),
lack of which (in Myd88-/- mice) abolished IL-12p40 production
following oral or intraperitoneal infection with T. gondii. Together,
these observations suggest that commensal bacteria stimulate TLR2 and
TLR4, or TLR9, of DCs, which signal through MYD88 to mediate DC
activation and the induction of TH1 cell-mediated immunity against T.
gondii. Further studies will be required to determine how DCs
differentiate between commensal and pathogenic bacteria, and how
commensal bacteria induce parasite-specific T cell responses without
triggering an antibacterial immune response.
Rachel David
References
1.Benson, A., Pifer, R., Behrendt, C., Hooper, L. V. & Yarovinsky, F.
Gut commensal bacteria direct a protective immune response against
Toxoplasma gondii. Cell Host Microbe 6, 187–196 (2009)
---
www.ncbi.nlm.nih.gov/pubmed/19683684
Gut commensal bacteria direct a protective immune response against
Toxoplasma gondii.
Benson A, Pifer R, Behrendt CL, Hooper LV, Yarovinsky F.
Department of Immunology, University of Texas Southwestern Medical
Center at Dallas, Dallas, TX 75390, USA.
Toxoplasma gondii is a universally distributed pathogen that infects
over one billion people worldwide. Host resistance to this protozoan
parasite depends on a Th1 immune response with potent production of
the cytokines interleukin-12 and interferon gamma. Although Toll-like
receptor 11 (TLR11) plays a major role in controlling Th1 immunity to
this pathogen in mice, this innate immune receptor is nonfunctional in
humans, and the mechanisms of TLR11-independent sensing of T. gondii
remain elusive. Here, we show that oral infection by T. gondii
triggers a TLR11-independent but MyD88-dependent Th1 response that is
impaired in TLR2xTLR4 double knockout and TLR9 single knockout mice.
These mucosal innate and adaptive immune responses to T. gondii rely
on the indirect stimulation of dendritic cells by normal gut
microflora. Thus, our results reveal that gut commensal bacteria can
serve as molecular adjuvants during parasitic infection, providing
indirect immunostimulation that protects against T. gondii in the
absence of TLR11.
PMID: 19683684
=======================================
New abstracts:
What's this stuff?
www.ncbi.nlm.nih.gov/pubmed/19846872
Apurinic/Apyrimidinic Endonuclease 1 Is a Key Modulator of
Keratinocyte Inflammatory Responses.
Lee HM, Yuk JM, Shin DM, Yang CS, Kim KK, Choi DK, Liang ZL, Kim JM,
Jeon BH, Kim CD, Lee JH, Jo EK.
*Department of Microbiology.
Apurinic/apyrimidinic endonuclease 1/redox factor-1 (APE1) functions
in both DNA repair and redox signaling, making it an attractive
emerging therapeutic target. However, the role of APE1 in cutaneous
inflammatory responses is largely unknown. In this study, we report
that APE1 is a key upstream regulator in TLR2-dependent keratinocyte
inflammatory responses. We found that nuclear expression of APE1 in
epidermal layers was markedly up-regulated in psoriatic skin. APE1 was
essential for the transcriptional activation and nuclear translocation
of hypoxia-inducible factor-1alpha and NF-kappaB, both of which are
crucial for inflammatory signaling in keratinocytes. Moreover, APE1
played a crucial role in the expression of TLR2-mediated inflammatory
mediators, including TNF-alpha, CXCL8, and LL-37, in HaCaT cells and
human primary keratinocytes. Silencing of APE1 attenuated cyclin D1/
cyclin-dependent kinase 4 expression and phosphorylation of ERK1/2 and
Akt, thereby affecting keratinocyte proliferation. Importantly, TLR2-
induced generation of reactive oxygen species contributed to the
nuclear translocation and expression of APE1, suggesting an
autoregulatory circuit in which the subcellular localization of APE1
is associated with the production of APE1 per se through reactive
oxygen species-dependent signaling. Taken together, these findings
establish a role for APE1 as a master regulator of TLR2-dependent
inflammatory responses in human keratinocytes.
PMID: 19846872
With all that radium from brazil nuts and UVB's from the SUN you might
need a little APE1 to protect your DNA?
Wow... i want APE1 right NOW and HOW, brown cat...
How do i go ape with this ape1?
Wiki?
Right..
http://en.wikipedia.org/wiki/APEX1
DNA-(apurinic or apyrimidinic site) lyase is an enzyme that in humans
is encoded by the APEX1 gene.
Apurinic/apyrimidinic (AP) sites (also called "abasic sites") occur
frequently in DNA molecules by spontaneous hydrolysis, by DNA damaging
agents or by DNA glycosylases that remove specific abnormal bases. AP
sites are pre-mutagenic lesions that can prevent normal DNA
replication. All cells, from simple prokaryotes to humans, have
evolved systems to identify and repair such sites. Class II AP
endonucleases cleave the phosphodiester backbone 5' to the AP site,
thereby initiating a process known as base excision repair (BER). The
APEX gene (alternatively named APE1, HAP1, APEN) encodes the major AP
endonuclease in human cells. Splice variants have been found for this
gene; all encode the same protein.[1]
Interactions
APEX1 has been shown to interact with MUTYH,[2] Flap structure-
specific endonuclease 1[3] and XRCC1.[4]
<snip>
This ape thing really fits that DNA and hole article that mentions
psoriasis.
But how?
And is it symmetrical.
randall... I just want to KNOW the TRUTH. Is it in US or OUT THERE?
JRStern
wrote:
>OK so radium is BAD now? Like the Sun and UVB's?
Bad enough you don't want to make them a habit.
I suppose not so bad you can't have a few a year.
>What if you put curry in your kimchi?
>
>You do eat kimchi don't you?
>
>Why not?
>
>What i posted yesterday might be BIG.
>
>L. Plantarum in kimchi kills SFB DEAD, dead, deadski. LOL
>
>Please recall now that SFB is segmented filamentous bacteria
>that reside in the ileum.
>
>Thusly SFB is BAD GUT FLORA... how do they symetricate
>the psoriatic so WELL... time will tell.. i hope. <G>
Well I've eaten kimchi and didn't clear immediately.
And, what antibiotics might kill SFB?
--
And while I loves my turmeric, I can't eat curry, gives me cardiac
arythmias - apparently harmless, but uncomfortable. God only knows
exactly what ingredient combination it takes to trigger that effect it
me. The red chili flavor used in some Szechuan dishes does the same
for me. I used to eat both in mass quantities, until I finally
figured out the relationship - that I've never seen described anywhere
else, btw.
Just goes to show ... whatever it goes to show.
J.
randall
> On Fri, 23 Oct 2009 11:12:59 -0700 (PDT), randall <ranhu...@aol.com>
J,
Only goes to show you need BAD flora.
Either do the wit kit or figure out how to incorporate
L. plantarum that will make it to YOUR ileum
Other then that, sucking up some resveratrol may help.
But why not go to the source.
I'll keep you appraised on my next trial.
Or maybe not. LOL
randall