Vitiligo & HSP70i --> Evetsm ->15 Years AGO --QKRAA or QRAA with HSP70 -- Salty MEAT & Paleodiet Questions -->Iodine? --Sodium & Potassium PUMP --Mapk (Consequence)- Orange not RED? TCM meds! - Susan and JXR hpa-axis?

[randall]

hi


How does ONE be a Total GOON?

i don't know tar baby, how?

Sorry id squid...you are a GOON. LOL

Albeit part of ME i still LOVE you... and most sentient life forms.

In their PLACE and not being a DISGRACE.

STILL,

Don't we all add up to ... nothing barely in a black hole?

&

except for the BLACK smoke who KNOWs? LoL

So recently and autoimmune and elicits questions of an Ai nature.

-------------

Vitiligo, an autoimmune condition, treated with modified heat shock
protein.

Will this suffice for NOT being cancer (Th2 skew) with the goofus?

OK so?

When did we last do heat shock proteins?

YOU don't KNOW?

Maybe... we didn't do them enough?

This one goes back nearly 15 years in this VERY GROUP.

Will nit wit pick a booger or suck it uP? LoL


http://www.sciencedaily.com/releases/2013/02/130227150908.htm
Modified Protein Could Become First Effective Treatment for Vitiligo
Skin Disorder

Feb. 27, 2013 — Loyola University Chicago Stritch School of Medicine
researchers have developed a genetically modified protein that
dramatically reverses the skin disorder vitiligo in mice, and has
similar effects on immune responses in human skin tissue samples.

The modified protein is potentially the first effective treatment for
vitiligo, which causes unsightly white patches on the face, hands and
other parts of the body. Loyola University Chicago has submitted a
patent application for the protein, and researchers are seeking
regulatory approval and funding for a clinical trial in humans.

I. Caroline Le Poole, PhD, and colleagues describe the modified
protein in the journal Science Translational Medicine. Le Poole is a
professor in Loyola's Oncology Institute and in the departments of
Pathology and Microbiology and Immunology.

About 1 million Americans have vitiligo, and the condition affects
about 1 in 200 people worldwide. Vitiligo is most noticeable in people
of color, but also can be distressing to Caucasians. Vitiligo is an
autoimmune disease, in which the immune system goes into overdrive and
kills pigment cells, which give skin its color.

Previous studies have found that a protein called HSP70i plays a vital
role in the autoimmune response that causes vitiligo. (HSP70i stands
for inducible heat shock protein 70.)

HSP70i consists of 641 building blocks called amino acids. Le Poole
and colleagues genetically modified one of these amino acids to create
a mutant HSP70i. This mutant protein supplants normal HSP70i, thereby
reversing vitiligo's autoimmune response.

Resarchers Jeffrey A. Mosenson and Andrew Zloza gave mutant HSP70i to
mice that developed vitiligo, and the results were striking. Mouse fur
-- affected by vitiligo -- had the coloring of a salt-and-pepper
beard. But when the mice were vaccinated with mutant HSP70i, the fur
turned black.

"The mice look normal," Le Poole said.

Some of the effects seen in mice also were seen in human skin
specimens.

There are no long-term effective treatments for vitiligo. Steroid
creams sometimes return some color to affected skin. But this
treatment also thins the skin, and can cause streaks or lines. Bright
lights, similar to tanning booths, also can return color, but can
cause sunburns and other side effects, including vitiligo. Skin grafts
transfer skin from unaffected areas to the white patches, but can be
painful and expensive. None of the existing treatments effectively
prevent vitiligo from progressing.

Le Poole and colleagues wrote that mutant HSP70i "may offer potent
treatment opportunities for vitiligo."

The study was supported by a NIH/National Institute of Arthritis and
Musculoskeletal and Skin Diseases grant to Le Poole.

Authors of the study are Jeffrey A. Mosenson, Andrew Zloza, John D.
Nieland, Elizabeth Garrett-Mayer, Jonathan M. Eby, Erica J. Huelsmann,
Previn Kumar, Cecele Denman, Andrew T. Lacek, Federick J. Kohlhapp,
Ahmad Alamiri, Tasha Hughes, Steven D. Bines, Howard L. Kaufman,
Andreas Overbeck, Shikhar Mehrotra, Claudia Hernandez, Michael I.
Nishimura, Jose A. Guevara-Patiño and I. Caroline Le Poole.

Work on this study was performed primarily in the laboratories of
Guevara-Patino and Le Poole at Loyola University Chicago Stritch
School of Medicine. Other institutions involved in the study are Rush
University Medical Center, Aarhus University in Denmark, Medical
University of South Carolina, Illinois Math and Science Academy,
University of Chicago, University of Illinois at Chicago and Lumiderm
in Madrid, Spain.


Journal Reference:
J. A. Mosenson, A. Zloza, J. D. Nieland, E. Garrett-Mayer, J. M. Eby,
E. J. Huelsmann, P. Kumar, C. J. Denman, A. T. Lacek, F. J. Kohlhapp,
A. Alamiri, T. Hughes, S. D. Bines, H. L. Kaufman, A. Overbeck, S.
Mehrotra, C. Hernandez, M. I. Nishimura, J. A. Guevara-Patino, I. C.
Le Poole. Mutant HSP70 Reverses Autoimmune Depigmentation in Vitiligo.
Science Translational Medicine, 2013; 5 (174): 174ra28 DOI: 10.1126/
scitranslmed.3005127


http://stm.sciencemag.org/content/5/174/174ra28
VITILIGO
http://www.ncbi.nlm.nih.gov/pubmed/23447019
Mutant HSP70 Reverses Autoimmune Depigmentation in Vitiligo

<authors: above>

ABSTRACT
Vitiligo is an autoimmune disease characterized by destruction of
melanocytes, leaving 0.5% of the population with progressive
depigmentation. Current treatments offer limited efficacy. We report
that modified inducible heat shock protein 70 (HSP70i) prevents T cell–
mediated depigmentation. HSP70i is the molecular link between stress
and the resultant immune response. We previously showed that HSP70i
induces an inflammatory dendritic cell (DC) phenotype and is necessary
for depigmentation in vitiligo mouse models. Here, we observed a
similar DC inflammatory phenotype in vitiligo patients. In a mouse
model of depigmentation, DNA vaccination with a melanocyte antigen and
the carboxyl terminus of HSP70i was sufficient to drive autoimmunity.
Mutational analysis of the HSP70i substrate-binding domain established
the peptide QPGVLIQVYEG as invaluable for DC activation, and mutant
HSP70i could not induce depigmentation. Moreover, mutant HSP70iQ435A
bound human DCs and reduced their activation, as well as induced a
shift from inflammatory to tolerogenic DCs in mice. HSP70iQ435A-
encoding DNA applied months before spontaneous depigmentation
prevented vitiligo in mice expressing a transgenic, melanocyte-
reactive T cell receptor. Furthermore, use of HSP70iQ435A
therapeutically in a different, rapidly depigmenting model after loss
of differentiated melanocytes resulted in 76% recovery of
pigmentation. Treatment also prevented relevant T cells from
populating mouse skin. In addition, ex vivo treatment of human skin
averted the disease-related shift from quiescent to effector T cell
phenotype. Thus, HSP70iQ435A DNA delivery may offer potent treatment
opportunities for vitiligo.

PMID: 23447019
<snip>

We've GOT 45 hits for HSP70 (no -- i -- on our p ng hsp70's- btw) - p
ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=hsp70&start=0&hl=en&


hit #2 of 45:
Evetsm back in 1998 has a nice one:
1998/06/24
Subject: Re: Is this the cause of P ? (was : A little key ?)
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_thread/thread/6bb12e42fccd7c8a/0d179d4d46a470a6?hl=en&lnk=gst&q=hsp70#0d179d4d46a470a6

And nine of 45 (HSP70 hits) belong to : evetsm - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=hsp70+evetsm&start=0&hl=en&


And since he has 2,580 total hits:
i will search those: (still only nine hits.. LOL)
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=evetsm&qt_g=Search+this+group


This one being most recent is quite nice:

https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_thread/thread/ae96e5fd90f0c964/a9ec21eae8c2d681?hl=en&q=#a9ec21eae8c2d681

And post #2 in this thread is SUSAN (only because she spelled ARCHICE
wrong. LOL)

Wow.. Steve or zc94 and jxr and what more can you want?
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_thread/thread/ae96e5fd90f0c964/a9ec21eae8c2d681?hl=en&q=#
or
https://groups.google.com/groups/profile?hl=en&enc_user=WoKVSBEAAACXjMITmTgDQ9PbOeJZF_N9kdEasx1kiYTQavV7mdW13Q

[...] The MHC not only presents foreign peptides, but it also
presents
peptides derived from the proteins of genes comprising the MHC
itself.
The susceptiblity genes for autism are: DRB1*0404, DRB1*401 and
DRB1*0101 (2). In a particular portion of these genes (the third
hypervariable region [HVR-3]), there is a common amino acid sequence
shared by all three genes. This amino acid sequence is either QKRAA
(glutamine-lysine-arginine-arginine-alanine-alanine) or QRRAA.
Thus,
either the QKRAA amino acid motif or the QRRAA amino acid motif can
be
presented to circulating T-lymphocytes. This particular shared
epitope increases the susceptibility to a number of autoimmune
diseases, including rheumatoid arthritis (3).

The QKRAA or QRRAA amino acid motif also occurs quite frequently
in pathogens which reside in the human gastro-intestinal tract
including Escherichia coli, Proteus mirabilis, lactobacillus lactis,
Brucella
ovis and many other anaerobic gut bacteria (3). The QKRAA or
QRRAA
sequences are found specifically in a particular type of protein
contained in gut bacteria, called DnaJ proteins. DnaJ proteins
normally have a bacterial partner/ligand protein called heat shock
proteins (HSP70). It is the QKRAA or QRRAA amino acid sequence of
DnaJ which allows it to bind HSP70.

When the MHC presents endogenously derived DRB1 alleles which
contain the QKRAA or QRRAA amino acid motif, then circulating HSP70
proteins (which normally bind DnaJ proteins) can bind the body's own
MHC presented QKRAA or QRRAA sequences. Circulating CD4+ T-
lymphocytes
recognize this HSP70/QRRAA sequence as foreign and mount an immune
response on all cells presenting this (HSP70) amino acid motif.

We believe that myelin basic protein contains an amino acid
sequence that is homologous to an A.A. sequence found in HSP70, and
it
is this three way mimicry between DRB1 peptides, bacterial peptides
and
self peptides which causes self tolerance to be broken.

So, how does a paleodiet have anything to do with this
process?
Paleodiets are characterized by their lack of cereal grains, legumes,
dairy products, and yeast containing foods. Both cereal grains and
legumes contain glycoproteins called lectins which bind intestinal
epithelial cells and change the permeability characteristics of these
intestinal cells (4,5). Not only do these lectins cause an increase
of the translocation of gut bacteria to the peripheracy, they cause
an
increased overgrowth of gut bacteria as well as a change in the gut
flora (4,5). Further, cereal and legume derived lectins (WGA, PHA
respectively) cause increased expression of intracellular adhesion
molecules (ICAM) in lymphocytes (6) which allow bacterial/immune
complexes to move from gut to the affected tissue. Additionally,
cereal and legume lectins increase lymphocytic expression of common
inflammatory cytokines such as tumor necrosis factor alpha (TNFa),
interleukin 1 (IL-1) and IL-6 which are known promoters of autoimmune
disease.

The cell walls of cereals and legumes contain a storage protein,
GRP 180, which also can act as a ligand to self presented MHC
peptides
(7). Further, peptides contained in dairy proteins (bovine serum
albumins - BSA, among many) also may contain peptide sequences which
can interact with endogenously presented peptides (8). Cereal,
legume,
dairy and yeast free diets potentially have therapeutic benefit in
many
autoimmune related disorders via their ability to reduce gut
permeability and decrease the exogenous antigenic load both from
pathogenic bacteria and from potentially self mimicking dietary
peptides.
<snip of evetsm's post of what he reposted>

And found it by keywording:
:: Reed Warren's mhc hsp70 paleodiet QKRAA QRRAA transloction gut
bacteria :: google search

3 hits: (our evetsm group and these two)

Autism and paleodiets - Direct-MS
www.direct-ms.org/pdf/EvolutionPaleolithic/AutismPaleodiets.pdf

or not using a pdf:
http://www.beyondveg.com/cordain-l/grains-leg/grains-legumes-1b.shtml

OK what of Qrraa or:

49 hits: QKRAA - pubmed
http://www.ncbi.nlm.nih.gov/pubmed/?term=QKRAA

50 hits: QRAA -pubmed
http://www.ncbi.nlm.nih.gov/pubmed/?term=QRRAA

And both of them on PMC brings 61 hits
http://www.ncbi.nlm.nih.gov/pmc/?term=QRRAA%20QKraa

Hit #1 of 61 says its chimeric :

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3188444/
Acquisition of the Rheumatoid Arthritis HLA Shared Epitope Through
Microchimerism
Zhen Yan, Tessa Aydelotte, VK Gadi, Katherine A. Guthrie, J. Lee
Nelson
Arthritis Rheum. Author manuscript; available in PMC 2012 March 1.
Published in final edited form as: Arthritis Rheum. 2011 March; 63(3):
640–644. doi: 10.1002/art.30160
PMCID: PMC3188444

But WHAT if...

I want salt on my MEAT.. LOL

Oh wait.. that makes psor or autoimmune people FLARE?

EXCESS in ONE side of the potassium/sodium pumP?

Is that this equation?

To much salt and to little postassium?

see
http://en.wikipedia.org/wiki/Na%2B/K%2B-ATPase
Na+/K+-ATPase (Sodium-potassium adenosine triphosphatase, also known
as Na+/K+ pump, sodium-potassium pump, or sodium pump) is an
antiporter enzyme (EC 3.6.3.9) (an electrogenic transmembrane ATPase)
located in the plasma membrane of all animal cells.

[...] 3 to 2 how do you DO?
Sodium-potassium pumps
Active transport is responsible for cells containing relatively high
concentrations of potassium ions but low concentrations of sodium
ions. The mechanism responsible for this is the sodium-potassium pump,
which moves these two ions in opposite directions across the plasma
membrane. This was investigated by following the passage of
radioactively labeled ions across the plasma membrane of certain
cells. It was found that the concentrations of sodium and potassium
ions on the two sides of the membrane are interdependent, suggesting
that the same carrier transports both ions. It is now known that the
carrier is an ATP-ase and that it pumps three sodium ions out of the
cell for every two potassium ions pumped in.

[...] Function
The Na+/K+-ATPase helps maintain resting potential, avail transport,
and regulate cellular volume.[1] It also functions as signal
transducer/integrator to regulate MAPK pathway, ROS, as well as
intracellular calcium. In most animal cells, the Na+/K+-ATPase is
responsible for about 1/5 of the cell's energy expenditure.[citation
needed] For neurons, the Na+/K+-ATPase can be responsible for up to
2/3 of the cell's energy expenditure.[2]
<snip>

So mapk again? LOL
No spin...
217 hits for : mapk - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=mapk&start=0&hl=en&

http://en.wikipedia.org/wiki/MAPK/ERK_pathway


If we can only take ALL the folks who went paleo WISE and had an
autoimmune condition and then
had them subtract the SALT in their diets and add in some iodine from
seaweed?


Am i on fire? LOL

OK the opposite polarity of Th1 (autoimmune) is Th2 (cancer).

That isn't important for guys with WET psoriasis apparently.. LOL

What should we look at?

The apple in the garden of eden or an orange?

I'm going away from the RED thing bob.

Try ORANGE.

For more energy i FOUND Citrus aurantium (bitter orange). pmid:
22991491

http://www.ncbi.nlm.nih.gov/pubmed/22991491
A review of the human clinical studies involving Citrus aurantium
(bitter orange) extract and its primary protoalkaloid p-synephrine.
PMID: 22991491
PMCID: PMC3444973
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22991491/

And might be more key for cancer like habenero peppers?

http://www.nutraingredients-usa.com/Research/Bitter-orange-synephrine-safety-gets-new-review-support

BESIDES FAT we need to LOOK at sugars!

If you ONLY ate FAT like an eskimo (Inuit) all day long, you don't get
heart attacks.

<or so we thought till thousand year old mummies came up with artery
disease- LOL:>

39 hits: inuit - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=inuit&start=0&

#3 of 39 looks familiar:
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/68a70761c7cf63d2/7e79aa1a772c6e41?lnk=gst&q=inuit#7e79aa1a772c6e41


And six of these 39 have: oogruk
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=inuit+oogruk&start=0&

And its in ALL of their cook books in MOST of the recipes.

So hit #1 of 6 is the same as hit #3 of 39 ... it's ME... LOL
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/68a70761c7cf63d2/7e79aa1a772c6e41?lnk=gst&q=inuit+oogruk#7e79aa1a772c6e41

so..

WeLL think abou it and if it's a DIET deal? Inuit don't get it btw
and eat FAT all day LONG.

So what do we DO randall tar baby? Have a heart attack?

no... LOL


Does plaque on your skin stop or slow plaque in your Heart?

I hear you... LOL

Let's see it!

I'm whiPPPing it OUT..

keyword : 76 results for ____glycosylation____ - p ng:
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=glycosylation+&start=0&


Hit #1 of 76 from Mar. 19, 1999 (by evetsm)

https://groups.google.com/group/alt.support.skin-diseases.psoriasis/browse_frm/thread/da6f6bce2843387a/8baffdd667e75101?lnk=gst&q=glycosylation+#8baffdd667e75101

[...] Not at all. Hyperglycemia causes cell glycosylation which
causes
inflammation. Check this for yourself. Here are two of many,many
studies.
This study clearly says that first you get hyperglycemia and
glycosylation(adhering of sugars to proteins) and then you get
inflammation
and glucose damage. This is unequivocal. (check glycosylation through
a
normal web search if you are really unconvinced). This makes sense
because a
Type 2 diabetic is born glucose intolerant and gets diabetic
complictions as
they get older and not the other way around. (Before you yell that
these have
nothing to do with psoriasis, remember we are trying to establish here
that
hyperglycemia causes inflammation and not the other way around.)

and evetsm has two abstacts without pmid's...

!st a look at plaque in the area you DON'T want it... like a widow
maker area:

http://upload.wikimedia.org/wikipedia/commons/3/39/PTCA_stent_NIH.gif


And those pmids: PMID: 9322186 and PMID: 8606261

http://www.ncbi.nlm.nih.gov/pubmed?term=9322186
J Am Coll Nutr. 1997 Oct;16(5):397-403.
Effects of glucose/insulin perturbations on aging and chronic
disorders of aging: the evidence.

Preuss HG.

Source
Department of Medicine, Georgetown University Medical Center,
Washington, DC, USA.

Abstract
Among changes associated with aging is a decline in glucose tolerance.
The reported causes are increased insulin resistance from receptor and/
or post receptor disturbances and diminished pancreatic islet B-cell
sensitivity to glucose. Many recent reports indicate that insulin
resistance with hyperinsulinemia and/or hyperglycemia contribute to or
even causes many chronic disorders associated with aging, i.e.,
chronic metabolic perturbations including noninsulin-dependent
diabetes mellitus, obesity, hypertension, lipid abnormalities, and
atherosclerosis. How could such disturbances in glucose/insulin
metabolism lead to many chronic disorders associated with aging? In
aging, similar to diabetes, the elevation in circulating glucose and
other reducing sugars secondary to age-induced insulin resistance can
react nonenzymatically with proteins and nucleic acids to form
products that affect function and diminish tissue elasticity. Also,
perturbations in glucose/insulin metabolism are associated with
enhanced lipid peroxidation secondary to greater free radical
formation. Free radicals of oxygen are important known causes of
tissue damage and have been associated with many aspects of aging
including inflammatory diseases, cataracts, diabetes, and
cardiovascular diseases. Augmented free radical formation and lipid
peroxidation are not uncommon in diabetes mellitus, commonly
associated with "premature aging". Ingestion of sugars, fats, and
sodium have been linked to decreased insulin sensitivity, while
caloric restriction, exercise, ingestion of chromium, vanadium,
soluble fibers, magnesium, and certain antioxidants are associated
with greater insulin sensitivity. Thus, manipulation of diet by
influencing the glucose/insulin system may favorably affect lifespan
and reduce the incidence of chronic disorders associated with aging.

PMID: 9322186

and

http://www.ncbi.nlm.nih.gov/pubmed/8606261
J Am Coll Cardiol. 1996 Mar 1;27(3):528-35.
Potential mechanisms promoting restenosis in diabetic patients.

Aronson D, Bloomgarden Z, Rayfield EJ.

Source
Department of Medicine, Mount Sinai Medical Center, New York, NY
10029, USA.

Abstract
Diabetes is associated with greater restenosis rates after successful
balloon angioplasty. The metabolic alterations that occur as a result
of hyperglycemia or hyperinsulinemia can accelerate many of the
pathophysiologic processes that lead to restenosis. Diabetes results
in endothelial dysfunction and accelerated platelet deposition, which
increase the propensity to thrombosis. Several growth factors known to
promote the restenosis process are overexpressed in the presence of
hyperglycemia. Advanced glycosylation promotes inflammatory cell
recruitment and smooth muscle cell proliferation. Many of the
potential mechanisms promoting restenosis in diabetic patients can be
ameliorated by improved metabolic control.

PMID: 8606261

http://en.wikipedia.org/wiki/Restenosis
Restenosis literally means the recurrence of stenosis, a narrowing of
a blood vessel, leading to restricted blood flow. Restenosis usually
pertains to an artery or other large blood vessel that has become
narrowed, received treatment to clear the blockage and subsequently
become renarrowed. This is usually restenosis of an artery, or other
blood vessel, or possibly a vessel within an organ.


*****************

And could sugars cause cancer via "Cross-glycosylation" of proteins
like p53?


http://www.ncbi.nlm.nih.gov/pubmed/23258847
Glycobiology. 2012 Dec 19.
"Cross-glycosylation" of proteins in Bacteriodales species.

Posch G, Pabst M, Neumann L, Coyne MJ, Altmann F, Messner P, Comstock
LE, Schäffer C.

Source
Department of NanoBiotechnology, NanoGlycobiology unit, Universität
für Bodenkultur Wien, Muthgasse 11, 1190 Vienna, Austria.

Abstract
While it is now evident that the two Bacteroidales species Bacteroides
fragilis and Tannerella forsythia both have general O-glycosylation
systems and share a common glycosylation sequon, the ability of these
organisms to glycosylate a protein native to the other organism has
not yet been demonstrated. Here, we report on the glycosylation of
heterologous proteins between these two organisms. Using genetic tools
previously developed for Bacteroides species, two B. fragilis model
glycoproteins were expressed in the fastidious anaerobe T. forsythia
and the attachment of the known T. forsythia O-glycan to these
proteins was demonstrated by liquid chromatography electrospray
ionization tandem mass spectrometry (LC-ESI-MS/MS). Likewise, two
predominant T. forsythia glycoproteins were expressed in B. fragilis
and glycosylation with the B. fragilis O-glycan was confirmed.
Purification of these proteins from B. fragilis allowed for the
preliminary characterization of the previously uncharacterized B.
fragilis protein O-glycan. Based on mass spectrometric data, we show
that the B. fragilis protein O-glycan is an oligosaccharide composed
of nine sugar units. Compositional and structural similarities with
the T. forsythia O-glycan suggest commonalities in their biosynthesis.
These data demonstrate the feasibility of exploiting these organisms
for the design of novel glycoproteins.

PMID: 23258847

ONLY 71 hits: glycosylation p53 -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=glycosylation%20p53

0 hits of 71 with: fragilis
http://www.ncbi.nlm.nih.gov/pubmed?term=glycosylation%20p53%20fragilis

YET and this indicts YKW we've got 54 hits: cancer fragilis -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=cancer%20B.%20fragilis


And 71 for the above.

And is it simply panx-1 then?

#2 of 71

http://www.ncbi.nlm.nih.gov/pubmed/22982782
Am J Physiol Heart Circ Physiol. 2012 Nov 15;303(10):H1208-18. doi:
10.1152/ajpheart.00251.2012. Epub 2012 Sep 14.
Cardiomyocyte ATP release through pannexin 1 aids in early fibroblast
activation.

Dolmatova E, Spagnol G, Boassa D, Baum JR, Keith K, Ambrosi C,
Kontaridis MI, Sorgen PL, Sosinsky GE, Duffy HS.

Source
Beth Israel Deaconess Medical Center, Harvard Medical School, Boston,
MA, USA.

Abstract
Fibrosis following myocardial infarction is associated with increases
in arrhythmias and sudden cardiac death. Initial steps in the
development of fibrosis are not clear; however, it is likely that
cardiac fibroblasts play an important role. In immune cells, ATP
release from pannexin 1 (Panx1) channels acts as a paracrine signal
initiating activation of innate immunity. ATP has been shown in
noncardiac systems to initiate fibroblast activation. Therefore, we
propose that ATP release through Panx1 channels and subsequent
fibroblast activation in the heart drives the development of fibrosis
in the heart following myocardial infarction. We identified for the
first time that Panx1 is localized within sarcolemmal membranes of
canine cardiac myocytes where it directly interacts with the
postsynaptic density 95/Drosophila disk large/zonula occludens-1-
containing scaffolding protein synapse-associated protein 97 via its
carboxyl terminal domain (amino acids 300-357). Induced ischemia
rapidly increased glycosylation of Panx1, resulting in increased
trafficking to the plasma membrane as well as increased interaction
with synapse-associated protein 97. Cellular stress enhanced ATP
release from myocyte Panx1 channels, which, in turn, causes fibroblast
transformation to the activated myofibroblast phenotype via activation
of the MAPK and p53 pathways, both of which are involved in the
development of cardiac fibrosis. ATP release through Panx1 channels in
cardiac myocytes during ischemia may be an early paracrine event
leading to profibrotic responses to ischemic cardiac injury.

PMID: 22982782
PMCID: PMC3517637
[Available on 2013/11/15]

and we've only had one maybe 2 hits for : pannexin - p ng
https://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?q=pannexin&start=0&


))))))))))))))))))))(((((((((((((((((((((((((((

And the skin cancer caveat with this citrus... as i'm not an orange
juice sorta person.

Citrus aurantium

http://www.ncbi.nlm.nih.gov/pubmed/17881138
Med Hypotheses. 2008;70(4):855-9. Epub 2007 Sep 18.
The increase in melanoma: are dietary furocoumarins responsible?

Sayre RM, Dowdy JC.

Source
Division of Dermatology, Department of Medicine, University of
Tennessee Health Science Center, Memphis, TN 38104, United States.
RP...@aol.com

Abstract
According to most cancer registries the incidence of cutaneous
melanoma (CM) has been increasing for several decades. Unlike other
skin cancers, CM does not clearly correlate with exposure to
ultraviolet radiation. The strongest etiological evidence for CM in
man is genetic predisposition, evidenced by very high risks in primary
relatives of melanoma patients, and photochemotherapy with 8-methoxy
psoralen in combination with ultraviolet-A radiation (PUVA) to treat
psoriasis and vitiligo. Retrospective studies of PUVA patients show
significantly increased incidence of CM. Psoralens, and other
furocoumarins, are phototoxic and photocarcinogenic, intercalate DNA
and photochemically induce mutations. Furocoumarins are botanical
phytoalexins found to varying extents in a variety of vegetables and
fruits, notably citrus fruits. The levels of furocoumarins present in
our diets, while normally well below that causing evident acute
phototoxicity, do cause pharmacologically relevant drug interactions.
For the past approximately 50 years CM has increased at similar rates
as the increased availability and consumption of citrus products.
Recently in a large study of nurses, only orange juice drinking,
indicative of dietary preference for citrus, was positively associated
with significantly increased risk of developing CM. We hypothesize
that the increases in cutaneous melanoma incidence may be in part
related to concomitant increases in dietary photocarcinogenic
furocoumarins.
Comment in
Can dietary furocoumarins really be responsible for the increase in
melanoma? [Med Hypotheses. 2008]

PMID: 17881138


What a GLOOM... made you READ.. LoL


I luv it. :)


and it's all so special NOW.. ;~?

So be a WET BRAIN? LOL

brain or skin i'll exxxplain?


http://hamsnetwork.org/wetbrain/

[...]
Introduction

Wet brain is a form of brain damage. Wet brain is also called Wernicke-
Korsakoff syndrome, Korsakoff's psychosis, Wernicke's encephalopathy,
and beri beri. The symptoms of wet brain may sometimes improve with
therapy but it is often permanent and irreversible.

Wet brain is caused by a deficiency of thiamine which is also known as
vitamin B1. Chronic, heavy alcohol consumption can lead to a thiamine
deficiency which can then lead to wet brain. This is because alcohol
interferes with the absorption of thiamine. Wet brain can also occur
in people who have never consumed alcohol. A diet of nothing but
polished rice can cause wet brain because of the lack of thiamine in
the diet. Wet brain can also be brought on by periods of vomiting
which last for several days such as might result from severe morning
sickness or bulimia.

Wet brain is not caused by alcohol killing brain cells. A study by
Jensen and Pakkenberg suggests that chronic heavy drinking does not
result in the loss of gray matter--the thinking part of the brain--
although it can result in the loss of white matter. The exact nature
of the impact of chronic heavy drinking on cognitive abilities in well
nourished individuals remains something of a matter of dispute. For
more information on this topic please visit our page Myths and Facts
about Alcohol and Brain Damage.
http://hamsnetwork.org/brain_damage

Wet brain is not a case of gradual brain damage occurring over time--
wet brain has a sudden onset and is often brought on by an sudden
large dose of glucose in an individual suffering from a severe
thiamine deficiency. It is generally agreed that wet brain occurs in
two stages. The first stage of wet brain is Wernicke's encephalopathy
which results from a severe thiamine deficiency and which may be
precipitated by a sudden influx of glucose. If Wernicke's
encephalopathy is immediately treated with thiamine injections it can
be completely reversed and the patient can return to normal. If the
Wernicke's encephalopathy goes untreated then it will progress to the
second stage of wet brain which is known as Korsakoff's psychosis.
Korsakoff's psychosis is not reversible although it can be improved
somewhat through treatment.
<snip.. see top link for more critical B vitamin info>


randall... it ONLY get's BETTER and BETTER... except for Susan and hpa-
axis. LOL

[Bohgosity BumaskiL]

Vitiligo. Pirated article. No relevance shown beyond autoimmunity,
which may be an artifact of allergy.

Major Histocompatibility Complex (MHC) article snippet.
No relevance shown. Extremely difficult genetics material to comprehend.

Paleodiet. Question asked. Not answered. Frustrating. Switches into
plain English from acronym-infested MHC-related document, then back.
Very strange.

Monologue begins with conclusion that salt causes inflammation,
which it doesn't.

Wikipedia basics article about ion pumps. What for?

> That isn't important for guys with WET psoriasis apparently.. LOL

I hav no clue what joke is about.

Article about bitter orange, which iz probably a better choice than
coffee for stimulants, but otherwise just not connected at all to
psoriasis.

Eskimo heart disease evasion from eating fish ignores stroke
problems that statistically, psoriasis sufferers face. Randall is
still in the wrong ball park for psoriasis.

Diabetes links. I know of about one person in this newsgroup with
diabetes. It iz NOT related to psoriasis. Bat being used to beat
relevance out of this newsgroup. Diabetes and heart disease. Yet
more shit.

Microbiology article displays no relevance. Randall does not try to
explain it. More about heart disease not related to P.

Speculative document about melanoma and a phytochemical that we are
probably not eating enough of. My head is full of irritation at this
point, because Randall is not making points or links, and he does
not seem to accept that cancer and psoriasis are in most respects
opposite problems. Strangely enough, he writes about P and cancer
being opposite problems. Why write about them both?

Article from wikipedia about thiamine deficiency. WHO THE FUCK GIVES
A SHIT IN A GROUP ABOUT PSORIASIS!

You've outdone yourself, Randall. You've copied nothing but
irrelvance into a USENET post.

[randall]

On Mar 12, 7:33 pm, Bohgosity BumaskiL

you are a m o r o n.. LOL


btw.. did not bother to READ this either... LOL

so how do i know this>>?

easy..

read your last two years of nonsense. LOL

[Julie Bove]

Hmmm... Interesting! I had what I assumed was vitiligo when I was younger.
Like an older child to young adult. But now it's gone. I used to try to
tan. Not that one can get much of a tan here. We don't get much sun here.
But... I had a couple of spots on my right front thigh that went totally
white. They just would not tan! But now? The spots are gone. *shrug*
"randall" <ranh...@aol.com> wrote in message
news:24458140-2094-4c8b...@f5g2000pbs.googlegroups.com...

Nishimura, Jose A. Guevara-Pati�o and I. Caroline Le Poole.

LE, Sch�ffer C.

Source
Department of NanoBiotechnology, NanoGlycobiology unit, Universit�t
f�r Bodenkultur Wien, Muthgasse 11, 1190 Vienna, Austria.

[randall]

On Mar 20, 4:47 am, "Julie Bove" <julieb...@frontier.com> wrote:
> Hmmm...  Interesting!  I had what I assumed was vitiligo when I was younger.
> Like an older child to young adult. But now it's gone.  I used to try to
> tan.  Not that one can get much of a tan here.  We don't get much sun here.
> But...  I had a couple of spots on my right front thigh that went totally
> white.  They just would not tan!  But now?  The spots are gone.  *shrug*"

Julie,

But you don't have psoriasis 24/7 either?

Right?

While most psoriatic's live with it all the time and progress in
severity
and thus treatments, you're lucky it simply went away one day.

I wish mine would simply go away for whatever reason.

But i wouldn't trade it for excess TREG;s or a Th2 skew immune profile
that leads to CANCER.

And what if a hair trigger on Th1 immunity prevents that for the MOST
part?

Maybe you're in that middle zone of T helper cells and
we need to study why in terms of plasticity and polarity of immunity?

You may SAVE us all?

Our skin that is..

randall.. Th1 or Th2 or Th neutral depends on gut flora and
enterotypes imo. & genes