Psoriasis support

Author

P News

randall

2006-09-16, 9:29 pm

Hi,

P News from around the World.

First stoP. NY times

http://www.nytimes.com/2006/09/17/jobs/17boss.html

The Boss

The Professor in the Back Lot

WHEN I was less than a year old, my family moved from Detroit to Canoga
Park, Calif., in the San Fernando Valley. It was a brand-new suburb,
but growing quickly. I recall almost Spielbergian moments riding my
bike to the edge of our neighborhood, reaching a big orange grove.

[randall note: spiel what again? This psoriatic is triPPing. 2001
time!]

My dad started as a chemical engineer, then became a patent attorney
and eventually a civil rights lawyer. My mother had an associate degree
in studio arts but in midlife went to night law school and became one
of L.A.'s first female deputy district attorneys. At the dinner
table, occasionally I would see open files with evidence photos that
came right out of a James Ellroy novel, at least temporarily killing my
appetite.

I grew up with disfiguring _____psoriasis____, semidisabled with the
attendant tendonitis. I also skipped some grades, so was usually the
youngest in the class. All of this has given me a great gift: to
empathize with the outsider and the underdog. That's where my heart
always goes; you see it in many of the films I've produced or
written, like "The Ice Storm" or "Brokeback Mountain."

Growing up, I had no interaction with the film business, though I went
to Hollywood High, which people think of as the belly of the film
industry beast. But back then Hollywood was the epicenter of teenage
runaways, drug culture, misfits and street people. I was the
straightest, dullest nerd you could imagine. Now, at Focus Features
staff meetings, I often look around the room and marvel at how I'm
surrounded by all these incredibly smart, successful and talented
people, almost all of whom also were - and sometimes still are -
misfits and outcasts.

I went to Hollywood High mainly for the legendary theater program run
by J. D. Melton. On one hand, he was the caricature of every drama
teacher, shouting, "You idiots!" in rehearsals. But we also knew he
was incredibly devoted to us.

After bouncing around several colleges, I got my bachelor's in
English at U.C. Berkeley in 1982. In grad school there, my academic
interests shifted from Milton to the history of cinema. One of my first
teaching jobs was as an assistant for Prof. Carol Clover's Ingmar
Bergman class. Incredibly, this summer Ang Lee and I were invited to
visit Bergman on his little island in the Baltic Sea. He's 89 and has
been my hero since I was a kid. He touched our faces as if we were
small children, which, I suppose, we were. As Ang said, "You can
dream of winning an Oscar, but you could never dream of this."

In 1987, I moved to New York to write my Ph.D. dissertation and work
for a few months in film. The independent film scene was just taking
off and I got sucked in. It took me until 2003 to finish my
dissertation.

I was 28 and would serve coffee to the crew one day and the next call
them to staff up for an art film I was producing. The experience of
simultaneously being the lowest person on the totem pole and a producer
has made me think about the filmmaking process from the point of view
of everyone I work with.

Helping run Focus Features can be overwhelming. At the same time I am
an associate professor at Columbia University, teaching film history,
theory and aesthetics. I find that my academic life provides a space to
explore and imagine outside the day-to-day pressures of the business.

Ang and I are working together on our 10th film in Hong Kong. I first
met him in 1990, and over the years we have come to see more
similarities between our upbringings than differences. After all, Jews
and Chinese both love to eat and both have guilt about family.

To prep for "Crouching Tiger, Hidden Dragon," which came out in
2000, I started reading a lot on Buddhism. Ang said, "Please don't.
If you read too much of that stuff, you will stop making movies."

My wife, the novelist Nancy Kricorian, is active in Codepink, a
women's peace group. We try not to drag our kids, who are 14 and 10,
to too many events. That said, they came with us this spring to the
Mother's Day vigil in front of the White House.

Background:: James Schamus
http://graphics10.nytimes.com/image...oss.bio.190.jpg

Hey! This psoriatic hac come out of the closet.

http://closet.velvet.jp/images/sad/suicide.jpg

I shall be respectful! within limits, lol

-----------

BUT,

What the freak is disfiguring psoriasis?

It all looks like craP. So? Does it make some of us look like
LON Chaney?

http://theatreorgans.com/southerncr...on%20Chaney.jpg

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

There is NO counting for P genes? As you can see? LOL

Let's role the genetic dice NOW and see what's up with psoriasis and
abstracts this week.

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Psoriasis vulgaris in Chinese individuals is associated with PSORS1C3
and CDSN genes.

* Chang YT,
* Chou CT,
* Shiao YM,
* Lin MW,
* Yu CW,
* Chen CC,
* Huang CH,
* Lee DD,
* Liu HN,
* Wang WJ,
* Tsai SF.

Department of Dermatology, National Yang-Ming University, Taipei,
Taiwan.

Background Besides the HLA-Cw*0602 allele, the psoriasis susceptibility
1 candidate 3 (PSORS1C3) and corneodesmosin (CDSN) genes are two
probable psoriasis susceptibility genes in the PSORS1 locus. The -79C,
-26C and +246A alleles of the PSORS1C3 gene, the CDSN*971T allele,
CDSN*TTC (619T-1236T-1243C) and CDSN*5 (619T-1240G-1243C) are strongly
associated with psoriasis in the caucasian population. Until now, no
haplotype study of the PSORS1C3 and CDSN genes has been documented in
Chinese patients with psoriasis vulgaris. Objectives We aimed to
determine whether genetic polymorphisms of the PSORS1C3 and CDSN genes
were associated with an increased risk of psoriasis vulgaris in Chinese
patients in Taiwan. Methods We investigated the PSORS1C3 and CDSN genes
for disease association by direct sequencing in 178 patients with
psoriasis vulgaris and 203 control subjects. Genotyping for
HLA-Cw*0602, alpha-helix coiled-coil rod homologue (HCR) gene and
single nucleotide polymorphism (SNP) n.9 was also carried out using a
sequence-based typing method. Results The PSORS1C3*582A allele, an SNP
in the 3'-untranslated region of the PSORS1C3 gene, was a major
psoriasis vulgaris susceptibility allele in the Chinese population, and
the association was much stronger in patients with early-onset
psoriasis vulgaris (22.3% vs. 6.9%, odds ratio = 3.87, P(c)
=0.0000072). The frequencies of CDSN*TTC and CDSN*971T were also
significantly increased in patients with early-onset psoriasis
vulgaris. Moreover, PSORS1C3*582A, SNP n.9*C, Cw*0602 and HCR*WWCC were
in near complete linkage disequilibrium (LD) with each other; in
contrast, the LD with the CDSN gene was not so strong. SNP
n.9*C-Cw*0602-PSORS1C3*582A-HCR*WWCC was a major susceptibility
haplotype in patients with early-onset psoriasis vulgaris (P < 10(-7))
and this risk haplotype also carried CDSN*TTC and CDSN*971T.
Conclusions The PSORS1C3 and CDSN genes are important psoriasis
susceptibility genes in Chinese patients with psoriasis vulgaris.

PMID: 16965413

This isn't a biggie. What it means to me is some of us are probably
prone
to some LPS glitch that creates the situation for early onset.

But don't ask me to go there now!

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

To bad this next one doesn't have an abstract to go along with the
sentiments.

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Dose-dependent reduction in psoriasis severity as evidence of
immunosuppressive activity of an oral jak3 inhibitor in humans.

[No authors listed]

PMID: 16974290

[ randall note: Oral meds, bring them on!]

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

Is this that green lip mussel stuff?

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Identification of avarol derivatives as potential antipsoriatic drugs
using an in vitro model for keratinocyte growth and differentiation.

* Amigo M,
* Schalkwijk J,
* Olthuis D,
* De Rosa S,
* Paya M,
* Terencio MC,
* Lamme E.

Departamento de Farmacologia, Facultad de Farmacia, Universidad de
Valencia, Av., Vicente Andres Estelles s/n, 46100, Burjasot, Valencia,
Spain.

Avarol, a marine sesquiterpenoid hydroquinone, and 14 avarol
derivatives have shown interesting anti-inflammatory properties in
previous studies. In this study, avarol and derivatives were evaluated
in high-throughput keratinocyte culture models using cytokeratin 10 and
SKALP/Elafin expression as markers for respectively normal and
psoriatic differentiation. Avarol and five of its derivatives (5, 10,
13, 14 and 15) were selected for further study. Only 10, 13, 14 and 15
were able to inhibit keratinocyte cell growth. Changes in expression
levels of 22 genes were assessed by quantitative real time PCR (qPCR).
>From these genes, TNFalpha mRNA levels showed the strongest changes.
For compound 13, 15 and dithranol (used as a model antipsoriatic drug),
a dose-dependent downregulation of TNFalpha mRNA was found. The changes
in TNFalpha mRNA were confirmed at the protein level for compound 13.
Additionally, this compound was able to reduce also IL-8 and COX-2 mRNA
levels and this effect was correlated with a reduction in COX-2 protein
expression. The mechanism of action of this compound involves at least
the inhibition of NF-kappaB-DNA binding activity. In conclusion, our
high-throughput screening models in combination with quantitative
assessment of changes in gene expression profiles identified the avarol
derivative 13, a benzylamine derivative of avarol at the 4' position of
benzoquinone ring, as an interesting anti-psoriatic drug candidate that
inhibits keratinocyte cell growth and TNFalpha and COX-2 expression.

PMID: 16973179

Avarol? Isn't that the green liPPed mussel stuff? Checking the group,
http://groups.google.com/group/alt....riasis&q=avarol

And pubmed,
http://www.ncbi.nlm.nih.gov/entrez/...&term=%20avarol

Is it a sponge or a mussel? I'll eat the latter! LOL

------

Here's a psoriatic crucifixon. They only forgot alcoholism in the
lineUP.

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Metabolic disorders in patients with psoriasis and psoriatic arthritis.

* Mallbris L,
* Ritchlin CT,
* Stahle M.

Department of Medicine, Dermatology Unit,Karolinska Institutet, 171 76,
Stockholm, Sweden. lotus.mallbris@ki.se.

Psoriasis is one of the common complex disorders in Western world,
affecting 2% to 3% of the population. Recent studies indicate that
psoriasis is associated with an increased risk of comorbidity and
mortality compared to the general population. It appears that patients
with psoriasis have a higher prevalence of metabolic disorders such as
diabetes, hypertension, obesity, and hyperlipidemia, as well as a
higher frequency of cigarette smoking. These concomitant diseases can
complicate the treatment of psoriasis. Even though the etiology of
these associations is elusive, physicians should be aware of them and
take active steps to reduce the risk profiles of patients with
psoriasis and psoriatic arthritis, in order to lessen mortality and
comorbidity.
PMID: 16973109

-----------

Nice MICE with psoriasis! What a model they serve?

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Animal Models of Psoriasis andPsoriatic Arthritis: An Update.

* Conrad C,
* Nestle FO.

Department of Dermatology, university Hospital Zurich,8091 Zurich,
Switzerland. curdin.conrad@usz.ch.

Psoriasis is a chronic inflammatory skin disorder characterized by
accelerated growth and altered differentiation of keratinocytes and
angiogenesis with marked ectasia of blood vessels. It develops through
interactions between the skin and immune system mediated by T cells,
dendritic cells, and inflammatory cytokines. The understanding of the
cellular and molecular alterations underlying the disease has advanced,
yet the majority of factors leading to the initiation and maintenance
of disease remain elusive. Researchers have attempted to reproduce
psoriasis in genetically modified and xenotransplantation mouse models
to gain insight into its pathogenesis, and they are beginning to use
these models to test new therapeutic agents and define mechanisms of
action. Every mouse model has strengths and weaknesses, with room for
improvement. Still, these models will accelerate knowledge of psoriasis
pathogenesis and aid in the development of new therapeutics.
PMID: 16973107

--------
http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Abatacept: A review of a new biologic agent for refractory rheumatoid
arthritis for dermatologists.

* Scheinfeld N.

Department of Dermatology, St Luke's Roosevelt Hospital Center, New
York, NY, USA.

Abatacept is a newly approved treatment for rheumatoid arthritis
refractory to other agents. Abatacept is a fusion protein of the
cytotoxic T-lymphocyte antigen (CTLA) molecule and immunoglobulin (Ig)
G1 that blocks CD28. Specifically, abatacept blocks the CD80 and CD86
ligands on the surface of antigen-presenting cells that must interface
with the T-cell's CD28 receptor to activate T cells. Abatacept seems to
be more immunosuppressive than tumor necrosis factor alpha blockers.
The combination of abatacept and a tumor necrosis factor alpha blocking
agent does not seem more effective than either agent alone. Because
abatacept has the ability to suppress T-cell function, it has the
potential to be a treatment for psoriasis and other autoimmune
conditions involving pathologic processes driven by T cells.
PMID: 16971318

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

Did you like to play with fire growing uP?

Good news for radiation (uvr) freaks. YOU won't get cancer or maybe you
will?

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Abstract No. 3 Is there a skin cancer risk with narrowband ultraviolet
B phototherapy? Preliminary data from the second phase of the Dundee
follow-up study.

* Hearn RM,
* Dawe RS,
* Kerr A,
* Rahim K,
* Ibbotson SH,
* Ferguson J.

Department of Dermatology, Ninewells Hospital and Medical School,
Dundee DD1 9SY, U.K.

We do not know whether narrowband ultraviolet B (NB-UVB, TL-01)
phototherapy carries any increased risk of skin cancers. Follow-up of
126 patients treated with NB-UVB in Germany (Weischer M, Blum A,
Eberhard F et al. No evidence for increased skin cancer risk in
psoriasis patients treated with broadband or narrowband UVB
phototherapy: a first retrospective study. Acta Derm Venereol (Stockh)
2004; 84: 370-4) did not detect any increased skin cancer risk. Our
follow-up study (with linkage to Scottish Cancer Registry data complete
to 1998) showed greater than expected (compared with age- and
sex-matched Scottish population) numbers of basal cell carcinomas
(BCCs) in those treated with NB-UVB (Man I, Crombie IK, Dawe RS et al.
The photocarcinogenic risk of narrowband UVB (TL-01) phototherapy:
early follow-up data. Br J Dermatol 2005; 152: 755-7). Whether the
modestly increased standardized incidence rate (SIR) of 213 (95%
confidence interval, CI 102-391) was due to treatment or factors such
as ascertainment bias was not clear. Analysis of data from the next
phase of this follow-up study, with linkage to the Scottish Cancer
Registry complete to December 2002, is ongoing. The summary
phototherapy records of 4050 patients treated with NB-UVB between 1985
and 2002 were examined. The median duration of follow-up was 5.8 years
(up to 16.7) from end of first NB-UVB course. We now have 26 633
person-years of follow-up data. The most frequent primary diagnoses
were: psoriasis (55%), atopic dermatitis (15.4%), polymorphic light
eruption (7.7%) and chronic urticaria (3.9%). Indirect standardization,
adjusting for age and sex, was used to compare numbers of skin tumours
identified with numbers expected in the general Scottish population. We
did not find significantly more melanomas [SIR 164 (95% CI 60-357), P =
0.16] nor squamous cell carcinomas [SIR 173 (95% CI 79-329), P = 0.08]
than expected. More BCCs than expected were registered in patients who
had received NB-UVB and psoralen plus ultraviolet A [SIR 184 (95% CI
128-255), P = 0.0007] and who had received only NB-UVB [SIR 211 (95% CI
135-314), P = 0.0007, n = 3082]. So far, these findings are reassuring.
A possible explanation for the excess BCCs is a causative association
between NB-UVB exposure and BCC development. Alternatively, more BCCs
may have been registered in our treated patients because of careful
surveillance leading to more BCCs being detected earlier and treated
with modalities leading to a histopathological diagnosis (and,
therefore, registration). However, only with more prolonged follow-up
of patients who have received high cumulative numbers of treatments
might a definite skin cancer risk become detectable. Therefore, we
should remain cautious as we cannot dismiss the possibility that NB-UVB
is carcinogenic in humans.

PMID: 16965459

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

randall.. have a haPPy abstractual day and eat those sponges! I should
grow some.

randall

2006-09-20, 2:25 am

Hi,

P News

A resource i've found helpful is expanding.

>From wikipedia to wikibooks,
http://www.nature.com/news/2006/060.../060911-13.html
or

http://en.wikipedia.org/wiki/Wikibooks

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

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Problems encountered during anti-tumour necrosis factor therapy.

* Desai SB,
* Furst DE.

Department of Rheumatology, university of California, Los Angeles, CA,
USA.

Worldwide, over 400 000 patients have been treated with tumour necrosis
factor (TNF)-alpha antagonists for indications that include rheumatoid
arthritis, juvenile rheumatoid arthritis, inflammatory bowel disease,
psoriatic arthritis and ankylosing spondylitis. Since their approval,
concerns regarding safety have been raised. There is a risk of
re-activation of granulomatous diseases, especially tuberculosis, and
measures should be taken for detection and treatment of latent
tuberculosis infections. Preliminary data suggest that anti-TNF therapy
may be safe in chronic hepatitis C. However, TNF-alpha antagonists have
resulted in re-activation of chronic hepatitis B if not given
concurrently with antiviral therapy. Solid tumours do not appear to be
increased with anti-TNF therapy. Variable rates of increased lymphoma
risk have been described with anti-TNF therapy compared with the
general population, although no increased risk was found compared with
a rheumatoid arthritis population. Large phase II and III trials with
TNF-alpha antagonists in advanced heart failure have shown trends
towards a worse prognosis, and should therefore be avoided in this
population. Both etanercept and infliximab are associated with the
formation of autoantibodies, and these autoantibodies are rarely
associated with any specific clinical syndrome. Rare cases of aplastic
anaemia, pancytopenia, vasculitis and demyelination have been described
with anti-TNF therapy. This chapter will discuss the safety profile and
adverse events of the three commercially available TNF-alpha
antagonists: etanercept, infliximab and adalimumab. The data presented
in this review have been collected from published data, individual case
reports or series, package inserts, the Food and Drug Administration
postmarketing adverse events surveillance system, and abstracts from
the American college of Rheumatology and European Congress of
Rheumatology meetings for 2005.

PMID: 16979537

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

Possible sinus gene to look at.
http://news.biocompare.com/newsstory.asp?id=151199

[...]

An earlier study published by the same team in the March-April issue of
the American Journal of Rhinology also showed that sinus tissue from
people with chronic sinusitis that resisted treatment had 30 times
lower than normal activity of a so-called toll-like receptor gene,
TLR9.

Inside the nose, researchers say, toll-like receptor proteins (TLRs)
detect invading bacteria and other pathogens in the air by attaching to
their trace byproducts. Once a threat is identified, the receptors
stimulate the epithelial cells to produce antibiotic proteins, such as
HBD2 and MBL, to fight the invading organisms. This innate response
helps prevent airborne bacteria or fungi from settling in the nose and
sinus cavities, causing infection.

"Colonization with microorganisms is a common problem in patients with
chronic sinusitis and polyps, but the reasons for this are incompletely
understood," says Andrew Lane, M.D., an associate professor at The
Johns Hopkins university School of Medicine and director of its
rhinology and sinus surgery center. "Now we are uncovering new clues as
to what might be wrong and perhaps, ultimately, how it might be
treated.

"The nose's first line of defense is the epithelium, and when the local
innate immune function is curtailed, infections can get a head start,
which might serve to worsen the sinus inflammation.

"The potential is there to manipulate these chemical receptors and
proteins to see if this makes patients more responsive to conventional
therapy," says Lane.

The study, led by Lane, was believed to be the first to determine
levels of each TLR - there are 10 - by directly measuring messenger RNA
expression in sinusitis patients and those more fortunate to not have
it. Scientists have known for more than a year that TLRs were present
in both the healthy and sinusitis-wracked nose, but not which receptors
or proteins were more important than others in the condition's chronic
form. That study involved 30 men and women, mostly from the Baltimore
region, who had surgery for chronic sinusitis at Hopkins. (Another 10
had no sinus problem and served as study controls.)
<sniP>
_______________________________________________

http://news.biocompare.com/newsstory.asp?id=151263

[...]

In the study, scientists focused on blood cells from two French
children with a deficiency for UNC-93B, an endoplasmic reticulum
protein involved in the recognition of pathogens. When infected with
herpes simplex virus-1, the UNC-93B-deficient cells were unable to
produce natural interferons alpha, beta, and gamma (IFNs -?/? and -?).
Interferons are produced by the immune system to fight infections and
tumors.

This deficiency resulted in high rates of herpes simplex virus-1
proliferation and cell death. Assuming these findings extend to
neurons, they provide a plausible mechanism for herpes simplex
encephalitis.

"We and our colleagues have identified recessive UNC-93B deficiency as
a genetic etiology of herpes simplex encephalitis in otherwise healthy
patients," said Professor Bruce Beutler, M.D., one of three Scripps
Research scientists who contributed to the study. "The discovery of
this genetic cause for herpes simplex encephalitis not only broadens
our understanding of these types of immunodeficiencies, but also has
important therapeutic implications-some of these patients could benefit
from recombinant interferon alpha (IFN-?) treatment, just as patients
with low levels of naturally occurring interferon gamma (IFN-?) benefit
from a similar life-saving approach."

Herpes simplex virus-1 is a common virus that infects about 80 percent
of young adults worldwide. Herpes simplex encephalitis, a viral
infection of the brain that affects otherwise healthy patients, affects
an extremely small percentage of those infected with herpes simplex
virus-1: the number of annual cases is two per million people,
according to the university of Maryland Medical Center.

Nonetheless, herpes simplex encephalitis, which was first described in
1941, is the most common type of sporadic viral encephalitis in
developed countries, accounting for about 10 to 20 percent of all viral
encephalitis cases, according to the university of Maryland Medical
Center. Before the advent of anti-viral drugs vidarabine in 1973 and
acyclovir in 1981, mortality rates reached up to 70 percent. While the
introduction of anti-viral treatment has been a boon to patients, brain
damage still poses a substantial risk.

"In contrast to most current thinking, we suspected that herpes simplex
encephalitis susceptibility could be inherited as a monogenic trait
resulting in the specific impairment of immunity to herpes simplex
virus-1," Beutler said. "Here we have defined a genetic lesion that is
permissive for an infection: a trait that most would regard as
quintessentially environmental in cause. It is likely that other
mutations will also be found to permit herpes simplex virus
encephalitis, and likely that other infectious diseases will ultimately
be traced to mutations that affect UNC-93B."

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

http://www.medicalnewstoday.com/med...d=51711&nfid=nl

New Study Demonstrates Dietary Supplement Lutein Increases Skin
Hydration, Elasticity And Lipid Levels

Main Category: Dermatology News
Article Date: 13 Sep 2006 - 0:00am (PDT)

Highlights from a new clinical study presented today at the "Beyond
Beauty Paris" conference in France provide compelling evidence that
lutein, a dietary nutrient available as a supplement and long-known for
its effectiveness in promoting eye health, also provides specific skin
health benefits. These include increasing the hydration, elasticity and
superficial lipids of the skin, while decreasing the oxidation - a
process that causes degradation - of those beneficial skin lipids.

Topline results of the study, presented by Dr. Pierfrancesco Morganti,
professor of applied cosmetic dermatology at the university of Naples,
on behalf of the research team, indicated that lutein and its
associated molecule zeaxanthin, when taken daily as a 10 mg oral lutein
supplement, increased skin hydration by 38 percent, skin elasticity by
8 percent and the level of superficial lipids present in the skin by 33
percent after adjustments for placebo. Results also showed that lutein
decreased oxidation of those beneficial lipids by 55 percent after
adjustment for placebo.

The study further demonstrated that the combination of oral and topical
administration of lutein/zeaxanthin provided even more powerful
improvements, increasing skin hydration by 60 percent, skin elasticity
by 20 percent and the amount of superficial lipids present in the skin
by 50 percent after adjustment for placebo, all while decreasing the
oxidation of those beneficial lipids by 64 percent.

Lutein, a nutrient naturally found in dark green leafy vegetables like
spinach, kale and collard greens, as well as broccoli, corn and egg
yolks, is present in tissues in the eye, blood serum, skin, cervix,
brain and breast. It is not produced by the human body and thus must be
ingested daily through food or taken as a supplement.

The study, entitled "Clinical Evidence for Lutein and Zeaxanthin in
Skin Health, Part 1: Comparison of Placebo, Oral, Topical and Combined
Oral/Topical Xanthophyll Treatments," was conducted in Italy on female
subjects, age 25-50, over a 12-week period. The test product utilized
in the study contained FloraGLO(R) Lutein, manufactured by Kemin
Health, L.C., of Des Moines Iowa. It was administered daily at 10 mg
(oral supplementation) and 50 ppm (topical formulation) to subjects in
the study's different test groups.

"This is the first study to determine the impact of lutein/zeaxanthin
alone on the human skin," said Richard L. ("Dick") Roberts, Ph.D.,
senior manager of scientific affairs for Kemin Health, the leading
manufacturer of lutein. "It provides strong new evidence of lutein's
positive role in promoting skin health and appearance by increasing
hydration, elasticity and lipid content."

"This research underscores the importance of thinking about skin health
and beauty from the 'inside out,'" said Bruce Katz, M.D., a
dermatologist and director of the JUVA Skin & Laser Center in New York,
who is working with Kemin to educate consumers on the role of nutrition
as part of a total skin health and beauty regimen. "The benefits of
taking lutein daily will be of great interest to people who are looking
for new ways to improve the hydration and elasticity of their skin and
help reduce the appearance of premature aging."

The new study adds to an existing body of research that suggests
lutein, when taken on a daily basis, may help bolster the skin's
natural antioxidant defense system, helping to protect skin from
potentially damaging effects of sun and artificial light exposure.

About Kemin

A nutritional ingredient manufacturer, Kemin is committed to improving
the nutrition of the world with functional products that deliver
maximum efficacy through superior chemistry. FloraGLO(R) Lutein is the
world's leading patented, purified lutein. Products with FloraGLO(R)
Lutein contain the same lutein naturally found in dark green leafy
vegetables as well as eggs. Studies indicate daily lutein intake of 6
mg to 10 mg may be beneficial.

A Kemin-affiliated company, Kemin Health is ISO 9001:2000 certified and
headquartered in Des Moines, Iowa, USA. Kemin has manufacturing
facilities in Iowa, Texas, Belgium, India, Singapore, China and
Thailand. To learn more visit http://www.luteininfo.com or
http://www.kemin.com.

Kemin Health
http://www.luteininfo.com
http://www.kemin.com/

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

http://www.life-enhancement.com/art...ate.asp?ID=1745

C-Reactive Protein May Induce Leptin Resistance

The hormone leptin, secreted by adipocytes (fat cells), has numerous
effects, including, among others, immune system regulation, regulation
of the reproductive system, and acting as a nutrient signal in the
hypothalamus that helps regulate food intake. In normal-weight
individuals, increases in leptin signaling decrease food intake. In
leptin-deficient animals and humans, treatment with leptin has a
profound normalizing effect upon food intake and weight. Obese humans,
however, have increased levels of leptin rather than leptin deficiency,
and leptin treatment has proven ineffective in decreasing food intake
and, hence, body weight. This ?leptin resistance? has been
extensively studied to determine how obesity decreases the effects of
leptin signaling.

Authors of a very recent paper1 propose that leptin resistance may be
?partially attributed to interactions between leptin and plasma
circulating factors.? They suggest that such factors might bind
leptin to affect its transport or otherwise inhibit its effects. They
note that ?elevation of the protein suppressor of cytokine
signaling-3 (SOCS-3), which is induced by leptin, might diminish the
actions of leptin in the central nervous system.?

They now identify C-reactive protein (CRP), a marker of inflammation
found in the bloodstream and a risk factor for cardiovascular disease,
as a blood-borne substance that not only ?binds to plasma leptin but
also impairs leptin signaling and attenuates its: physiological effects
in vivo.? Moreover, they report, ?leptin directly stimulates
expression of CRP in human primary hepatocytes [liver cells] in
vitro.? In their experiments, the researchers found that the
concentration of human CRP and rat CRP required to block one of
leptin?s effects (phosphorylation of STAT3) were within the ranges
observed in rat and human plasma. They also found that human CRP
inhibited human leptin signaling in the leptin-triggered JAK-STAT and
PI3K pathways in rat primary hypothalamic neurons. In the ob/ob
(genetically obese) mouse studies, human leptin produced the expected
reduction in food intake and body weight. However, when coadministered
with human CRP, the result was a partially attenuated effect of leptin
(at low CRP dose) or a completely blocked leptin effect (at high CRP
dose). CRP alone had no effect on food intake or body weight.

Chronically elevated CRP (a state of chronic inflammation) has also
been found to be positively correlated with adiposity (as well as with
leptin levels).1 The authors suggest that, because human CRP forms a
doughnut-shaped pentameric structure, its binding to leptin may
interfere with leptin?s passing through the blood-brain barrier to
reach the medial hypothalamus, one of the features of leptin
resistance.

For obese individuals, then, reduction of CRP is an important target.
This is also very important for those at risk of heart attack. A recent
paper2 suggests that the damage due to a heart attack can be reduced by
quickly suppressing CRP levels with a CRP inhibitor. As a commentary on
the paper notes,3 ?CRP levels increase dramatically in patients with
myocardial infarction, beginning 6 hours after the onset of ischemia
and peaking at approximately 50 hours. CRP values after acute
myocardial infarction predict outcome, including death and heart
failure.?

VITAMINS It has been reported elsewhere4 that, ?in a post hoc
analysis of a randomized, double-blind, placebo-controlled study,
multivitamin use was associated with lower C-reactive protein
levels.? The multivitamin used was an ordinary, commercially
available, 24-ingredient vitamin and mineral formulation. ?After the
intervention, the prevalence of a C-reactive protein level >3.0 mg/L
decreased to 14% in the multivitamin group but increased to 32% in the
placebo group (P<0.05 for difference at 6 months).? Niacin also
reduces C-reactive protein levels.9

FIBER Another study5 reported that, in an examination of the
association between dietary fiber and serum CRP using data from the
National Health and Nutrition Examination Survey 1999?2000, it was
found that ?fiber intake is independently associated with serum CRP
concentration and support the recommendations of a diet with a high
fiber content.?

ARGININE A further study6 reported, after analyzing the Third National
Health Nutrition and Examination Survey 1988?1994, that ?the
likelihood of having a high level of CRP (>3.0 mg/L), from the lowest
to the highest level of arginine intake, were 34.8%, 31.0%, 27.7%, and
18.4%, respectively. In the adjusted regression, subjects in the
highest level (90th percentile) of arginine intake were 30% less likely
to have a CRP above 3.0 mg/L than were subjects with a median arginine
intake (odds ratio = 0.70, 95% confidence interval = 0.56 to 0.88).?

HORMONE REPLACEMENT It has been reported that female hormone
replacement with Premarin? conjugated horse estrogens increases
levels of CRP.7 It is not clear, however, whether other types of
hormone replacement (such as bioidentical human estrogen replacement)
would have the same effect. Moreover, it appears that beginning hormone
replacement shortly after menopause results in cardioprotective
effects, while hormone replacement begun many years after menopause may
not be protective or may actually be detrimental.

OTHER Life Extension magazine (March 2001) suggests that C-reactive
protein may be suppressed by taking aspirin, vitamin E, DHEA, nettle
leaf, and fish oils. Sleep loss has also been reported to increase CRP
levels.8 Statins, weight loss, and exercise reduce CRP levels.9

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

randall

randall

2006-09-20, 9:32 pm

Hi,

Yesterday I was scrambling to find psoriasis abstracts and articles.
The article
on lutein was a reach.

Today seemingly was a repeat till I looked at the new abstracts for
psoriasis.

A veritable blockbuster of abstracts popped up. These mice models
(psoriaform) are really paying off big time.

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Lessons learned from psoriatic plaques concerning mechanisms of tissue
repair, remodeling, and inflammation.

* Nickoloff BJ,
* Bonish BK,
* Marble DJ,
* Schriedel KA,
* Dipietro LA,
* Gordon KB,
* Lingen MW.

1Department of Pathology, Cardinal Bernardin Cancer Center, Loyola
University Medical Center, Maywood, Illinois, USA.

Following injury, skin establishes a balance between too little
inflammation increasing risk of infection, and excessive inflammation
contributing to delayed wound healing and scarring. Mounting evidence
indicates both initiation and termination of inflammation involve
active mechanisms. Not only does inflammation itself seem to be a
paradox because inflammatory responses are both essential and
potentially detrimental, but one chronic inflammatory skin disease
(e.g. psoriasis) presents additional paradoxes. While plaques share
several factors with wound healing, two understudied and puzzling
aspects include why do not inflamed plaques more frequently transform?;
and why do not plaques result in scarring? To get at these questions,
we review responses involved in wound repair. Oral mucosa was probed
because, like fetal skin, wound repair is characterized by its
rapidity, low inflammation, and scarless resolution. Active roles for
macrophages as both initiators and terminators of inflammation are
highlighted. Therapeutic implications are discussed regarding psoriasis
and pyoderma gangrenosum. Based on biochemical and immunohistochemical
considerations linking psoriatic plaques to hard palate, a novel
metaplastic model is presented. We hypothesize saliva and chronic
trauma contribute to a constitutive epithelial program where
keratinocyte proliferation is more intense prior to differentiation,
accompanied by keratin 16 expression in hard palate, thereby resembling
plaques. Rather than viewing psoriasis as a nonspecific response to
inflammation, we postulate a metaplastic switch by which prepsoriatic
skin is converted to a distinct adult tissue type resembling hard
palate. In summary, many lessons can be learned by focusing on complex
processes involved in regulation of inflammation, tissue repair, and
remodeling.

Journal of Investigative Dermatology Symposium Proceedings (2006) 11,
16-29. doi:10.1038/sj.jidsymp.5650010.

PMID: 16983353

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

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Identification of susceptibility Loci for skin disease in a murine
psoriasis model.

* Kess D,
* Lindqvist AK,
* Peters T,
* Wang H,
* Zamek J,
* Nischt R,
* Broman KW,
* Blakytny R,
* Krieg T,
* Holmdahl R,
* Scharffetter-Kochanek K.

Department of Dermatology and Allergic Diseases, and.

Psoriasis is a frequently occurring inflammatory skin disease
characterized by thickened erythematous skin that is covered with
silvery scales. It is a complex genetic disease with both heritable and
environmental factors contributing to onset and severity. The CD18
hypomorphic PL/J mouse reveals reduced expression of the common chain
of beta(2) integrins (CD11/CD18) and spontaneously develops a skin
disease that closely resembles human psoriasis. In contrast, CD18
hypomorphic C57BL/6J mice do not demonstrate this phenotype. In this
study, we have performed a genome-wide scan to identify loci involved
in psoriasiform dermatitis under the condition of low CD18 expression.
Backcross analysis of a segregating cross between susceptible CD18
hypomorphic PL/J mice and the resistant CD18 hypomorphic C57BL/6J
strain was performed. A genome-wide linkage analysis of 94
phenotypically extreme mice of the backcross was undertaken.
Thereafter, a complementary analysis of the regions of interest from
the genome-wide screen was done using higher marker density and further
mice. We found two loci on chromosome 10 that were significantly linked
to the disease and interacted in an additive fashion in its
development. In addition, a locus on chromosome 6 that promoted earlier
onset of the disease was identified in the most severely affected mice.
For the first time, we have identified genetic regions associated with
psoriasis in a mouse model resembling human psoriasis. The
identification of gene regions associated with psoriasis in this mouse
model might contribute to the understanding of genetic causes of
psoriasis in patients and pathological mechanisms involved in
development of disease.

PMID: 16982899

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

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
The Monoclonal Antibody CHO-131 Identifies a Subset of Cutaneous
Lymphocyte-Associated Antigen T Cells Enriched in P-Selectin-Binding
Cells.

* Ni Z,
* Campbell JJ,
* Niehans G,
* Walcheck B.

Department of Veterinary and Biomedical Sciences, university of
Minnesota, St. Paul, MN 55108;

T cells use the vascular adhesion molecules E- and P-selectin to enter
inflamed skin. Previous studies have indicated the possibility for
diversity in the synthesis of E- and P-selectin glycan ligands by
activated T cells due to their different requirements for the O-glycan
branching enzyme core 2 beta1,6-N-acetylglucosaminyltransferase I and
its independent regulation. It is known that T cell staining by the mAb
HECA-452 (referred to as cutaneous lymphocyte-associated Ag (CLA) T
cells) correlates with E-selectin binding, yet whether these cells
uniformly bind P-selectin is less clear. The mAb CHO-131 and P-selectin
binding require a glycan moiety consisting of a sialylated and
fucosylated oligosaccharide properly positioned on a core-2 O-glycan.
Interestingly, CHO-131 stains a subset of CLA(+) T cells. A direct
comparison of the selectin binding capacity of CHO-131(+) and
CHO-131(-) CLA(+) T cells revealed a significantly greater P-selectin,
but not E-selectin, binding activity by the former subset. Based on the
expression of homing and central and effector memory cell markers,
CHO-131(+) and CHO-131(-) CLA(+) T cells have an overlapping
skin-tropic and memory phenotype. CHO-131(+) T cells were considerably
enriched in psoriatic skin, yet, unlike the peripheral blood of healthy
individuals, HECA-452 and CHO-131 stained a similar proportion of T
cells in the cutaneous lesions, indicating an accumulation advantage by
CHO-131(+) T cells. We conclude that the CHO-131(+)CLA(+) T cell subset
is enriched in P-selectin binding cells. These findings should provide
new insights into the regulation and function of skin homing T cells.

PMID: 16982914

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

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
An Anti-IL-12p40 Antibody Down-Regulates Type 1 Cytokines, Chemokines,
and IL-12/IL-23 in Psoriasis.

* Toichi E,
* Torres G,
* McCormick TS,
* Chang T,
* Mascelli MA,
* Kauffman CL,
* Aria N,
* Gottlieb AB,
* Everitt DE,
* Frederick B,
* Pendley CE,
* Cooper KD.

Department of Dermatology, Case Western Reserve University, Cleveland,
OH 44106.

Psoriasis is characterized by activation of T cells with a type 1
cytokine profile. IL-12 and IL-23 produced by APCs are essential for
inducing Th1 effector cells. Promising clinical results of
administration of an Ab specific for the p40 subunit of IL-12 and IL-23
(anti-IL-12p40) have been reported recently. This study evaluated
histological changes and mRNA expression of relevant cytokines and
chemokines in psoriatic skin lesions following a single administration
of anti-IL-12p40, using immunohistochemistry and real-time RT-PCR.
Expression levels of type 1 cytokine (IFN-gamma) and chemokines (IL-8,
IFN-gamma-inducible protein-10, and MCP-1) were significantly reduced
at 2 wk posttreatment. The rapid decrease of these expression levels
preceded clinical response and histologic changes. Interestingly, the
level of an anti-inflammatory cytokine, IL-10, was also significantly
reduced. Significant reductions in TNF-alpha levels and infiltrating T
cells were observed in high responders (improvement in clinical score,
>/=75% at 16 wk), but not in low responders. Of importance, the levels of APC cytokines, IL-12p40 and IL-23p19, were significantly decreased in both responder populations, with larger decreases in high responders. In addition, baseline levels of TNF-alpha
significantly correlated with the clinical improvement at 16 wk, suggesting that these levels may predict therapeutic responsiveness to anti-IL-12p40. Thus, in a human Th1-mediated disease, blockade of APC cytokines by anti-IL-12p40 down-regulates expres
sion of type 1 cytokines and chemokines that are downstream of IL-12/IL-23, and also IL-12/IL-23 themselves, with a pattern indicative of coordinated deactivation of APCs and Th1 cells.

PMID: 16982934

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

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
CD18 in Monogenic and Polygenic Inflammatory Processes of the Skin.

* Peters T,
* Sindrilaru A,
* Wang H,
* Oreshkova T,
* Renkl AC,
* Kess D,
* Scharffetter-Kochanek K.

1Department of Dermatology and Allergic Diseases, university of Ulm,
Ulm, Germany.

The beta(2) integrin family (CD11/CD18) of leukocyte adhesion molecules
plays a key role in inflammation. Absence of the common beta chain
(CD18) leads to leukocyte adhesion deficiency-1 (LAD1) in humans. We
here summarize data of two genetically defined mice models of beta(2)
integrin deficiency, one with a CD18 null mutation (CD18(-/-)), and the
other one with a hypomorphic CD18 mutation (CD18(hypo)). Firstly, we
focus on the underlying mechanism of a severely impaired wound healing
in CD18(-/-) mice, outlining a scenario in which a defective
extravasation and phagocytosis of CD18(-/-) neutrophils results in
delayed myofibroblast-dependent wound contraction owing to a deficient
transforming growth factor-beta(1) release. Based on this, we have
identified a potential therapy that fully rescued the impaired wound
healing in CD18(-/-) mice. Secondly, we expand on a CD18(hypo) PL/J
mouse model closely resembling human psoriasis. Apart from common
clinical and pathophysiological features, this psoriasiform dermatitis
also depends on the presence of activated CD4(+)T cells. We here
recapitulate the influence of a reduced CD18 gene expression on T-cell
function, also with regard to CD18 gene-dose effects, and its
contribution to the pathogenesis of this disease. Taken together, these
unique features make this model a valuable tool for investigations into
the pathogenesis of human psoriasis - including its polygenic base -
and future preclinical studies.

Journal of Investigative Dermatology Symposium Proceedings (2006) 11,
7-15doi:10.1038/sj.jidsymp.5650006.

PMID: 16983352

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

Thank-you psoriaform mice! Their pointing the way to future studies!
These
P genes are only a few studies away from shedding their clues.

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

Sinus problems? You may have a shortage of two-four genes!
http://www.innovations-report.de/ht...icht-70613.html

[...]
In a study to be described on Sept. 19 at the annual scientific
sessions of the American Academy of Otolaryngology, Head and Neck
Surgery, the Hopkins team found that in chronic sufferers who failed to
respond to treatment, the activity of at least four genes in the body's
nasal immune defense system were severely decreased, and their
production of two proteins critical to this defense was 20 to 200 times
less than normal.

Comparing nasal epithelial cell samples from nine patients who
benefited from surgery with nine who did not, the Hopkins team
discovered suppressed levels of human beta defensin 2 (HBD2) and
mannose binding lectin (MBL) in those whose symptoms returned. The
proteins are naturally produced in the nose whenever the immune system
detects foreign bacteria or fungi, binding to invading pathogens,
inactivating them and making them easily disposed of.

An earlier study published by the same team in the March-April issue of
the American Journal of Rhinology also showed that sinus tissue from
people with chronic sinusitis that resisted treatment had 30 times
lower than normal activity of a so-called toll-like receptor gene,
TLR9. <sniP>

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

TLR9 and myd88 pathways go together.

Let's see if there's anything current in the news.

http://www.bioworld.com/servlet/com...e&forceid=40779

[...]
IC31 contains two components, an immunostimulatory oligodeoxynucleotide
(ODN1a) and an antimicrobial peptide (KLK). It stimulates the innate
immune system and ultimately both arms of the adaptive immune response
via the Toll-like receptor-9 (TLR-9)/MyD88 signaling pathway.

ODN1a is an agonist for TLR-9, which identifies specific CpG-containing
DNA motifs that are characteristic of microbial and viral pathogens.
The oligonucleotide is taken up by dendritic cells in the skin, which
then trigger an immunological cascade. KLK, a cationic anti-bacterial
peptide, acts as a "gating molecule," von Gabain said. It helps to
protect ODN1a against degradation, and it also assists the transport of
foreign antigens into dendritic cells. When used alone, it helps to
elicit a Th2 or antibody-mediated immune response, von Gabain said.
<sniP>

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

And one more abstract.

http://www.ncbi.nlm.nih.gov/entrez/...2&dopt=Abstract

Cytokine responses to CpG DNA in human leukocytes.

Agren J, Thiemermann C, Foster SJ, Wang JE, Aasen AO.

University of Oslo, Faculty Division Rikshospitalet, Institute for
Surgical Research, Oslo, Norway.

Previous studies have implicated a role of bacterial DNA, containing
unmethylated cytosine-phosphate-guanosine (CpG) motifs, in the
initiation of systemic inflammation. This is based on the ability of
CpG-DNA to act in synergy with lipopolysaccharide (LPS) to trigger
tumor necrosis factor alpha (TNFalpha) production in murine monocytes
and to enhance LPS toxicity in rodents. In this study we investigated
the capacity of CpG-DNA to trigger and modulate cytokine responses in
human leukocytes. A human blood assay, as well as isolated cultures of
monocytes and neutrophils, was exposed to the synthetic
oligodeoxynucleotides (ODNs) CpG ODN (2006) and GpC ODN (2006-GC),
alone or in combination with peptidoglycan or LPS. Plasma or
supernatants were isolated and analyzed for TNFalpha, interleukin-1
beta (IL-1beta), IL-6 and IL-8 by ELISA. In the blood, 2006 (but not
2006-GC) induced the release of TNFalpha (P < 0.05) and possibly
IL-1beta and IL-6. IL-8 was induced in a CpG-independent manner. When
co-administered with peptidoglycan, both ODNs enhanced the release of
cytokines, but not consistently CpG dependent. When co-administered
with LPS, only IL-8 values were enhanced, whereas IL-6 was suppressed
at early time points. In monocyte and neutrophil cultures, CpG
dependent induction of cytokine release was not observed. However, both
ODNs inhibited LPS-induced IL-6. In conclusion, the capacity of CpG DNA
to trigger the release of TNFalpha and to enhance LPS-induced release
of this cytokine is confirmed in human whole blood, but not in adherent
human monocytes. Most effects of the ODNs on cytokine release in human
leukocytes were CpG independent.

PMID: 16784492

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

randall...

randall

2006-09-21, 4:26 pm

Hi,

P News from around the world.

http://www.medicalnewstoday.com/med...hp?newsid=52208

Short-term Topical Corticosteroid Use May Offer Relief For Patients
With Acute Form Of Psoriasis

Researchers suggest a short-term application of topical corticosteroids
and maintenance with a less potent agent for patients with
intertriginous psoriasis (IP), according to a study published in the
September issue of Archives of Dermatology, one of the JAMA/Archives
journals.

Psoriasis is an inflammatory skin disease. In a subset of patients,
psoriasis is located in the intertriginous areas, including the skin
folds of the underarms, breasts, groin, buttocks and genitals,
according to background information in the article. "Patients who
exhibit intertriginous psoriasis often complain about intense itching,
irritation from sweating and soreness. These symptoms may have
devastating psychological and emotional consequences." Management of IP
usually includes the application of topical corticosteroids, but those
medications have adverse effects with long-term use.

In this study, Alexander Kreuter, M.D, from Ruhr university of Bochum,
Germany, and colleagues conducted a randomized controlled trial that
compared 1 percent pimecrolimus (a new anti-inflammatory drug), 0.005
percent calcipotriol, 0.1 percent betamethasone and the vehicle (a
similarly appearing cream with no active drug) in the treatment of IP
with a four-week treatment period and a six-week follow-up without
therapy. A total of 80 adult patients with the clinical diagnosis of IP
were included, 20 patients in each of the four treatment groups.

"After four weeks of treatment, the three active compounds and the
vehicle resulted in a significant decrease in mean (average) M-PASI
score [Modified Psoriasis Area and Severity Index] (86.4 percent for
0.1 percent betamethasone, 62.4 percent for 0.005 percent calcipotriol,
39.7 percent for 1 percent pimecrolimus and 21.1 percent for vehicle),"
the researchers found. "The 0.1 percent betamethasone was significantly
more effective than 1 percent pimecrolimus during the study period."
The researchers report 25 percent of patients treated with pimecrolimus
reported an increase in itching and burning shortly after application,
however, most reactions lasted less than 30 minutes and resolved in a
few days.

"In conclusion, this study indicated the efficacy of all three active
compounds, 1 percent pimecrolimus, 0.1 percent betamethasone, and 0.005
percent calcipotriol (as well as the vehicle) in the treatment of IP.
The 0.1 percent betamethasone was clearly more effective than 1 percent
pimecrolimus, confirming that treatment with corticosteroids is still
the most effective topical approach for psoriasis. However, their use
in long-term management, particularly for the treatment of
intertriginous areas, which are more prone to steroid adverse effects,
is limited. To combine the rapid anti-inflammatory effects of a topical
corticosteroid with the favorable long-term effects and safety profile
of pimecrolimus or calcipotriol, short-term application of topical
corticosteroids for acute disease followed by maintenance treatment
with one of these agents seems to be a reasonable approach in the
treatment of IP."

###

(Arch Dermatol. 2006:142:1138-1143.)

Co-author Dr. Brautigam is an employee of Novartis Pharma GmbH. This
study was supported by a financial grant from Novartis Pharma GmbH.
Please see the article for additional information, including other
authors, author contributions and affiliations, financial disclosures,
funding and support, etc.

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

If the people at UCLA can figure out how to slow inflammation with
sleep, i'm awaken just dreaming about it.

http://www.newsroom.ucla.edu/page.asp?RelNum=7335
Sleepless Night Triggers Immune System's Inflammatory Response;
Findings Reveal New Avenue for Fighting Autoimmune Disorders

Researchers at UCLA are the first to show how sleep loss affects the
immune system's inflammatory response and suggest sleep interventions
as a possible way to address problems associated with inflammation and
autoimmune disorders.

Reporting in the Sept. 6 edition of the peer-reviewed journal Archives
of Internal Medicine, the research team finds that even modest sleep
loss triggers cellular and genetic processes involved in the immune
system's inflammatory response to disease and injury.

The findings increase understanding of sleep's role in altering immune
cell physiology and suggest sleep interventions as a possible way to
address inflammation associated with risk of cardiovascular disease,
arthritis, diabetes and other autoimmune disorders.

"This study shows that even a modest loss of sleep for a single night
increases inflammation, which is a key factor in the onset of
cardiovascular disease and autoimmune disorders such as rheumatoid
arthritis." said Dr. Michael Irwin, professor and director of the
Cousins Center for Psychoneuroimmunology at the Semel Institute for
Neuroscience and Human Behavior at UCLA. <sniP>

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

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum

Expression of keratinocyte growth factor and its receptor in clear cell
acanthoma.

* Kovacs D,
* Cota C,
* Cardinali G,
* Aspite N,
* Bolasco G,
* Amantea A,
* Torrisi MR,
* Picardo M.

Istituto Dermatologico San Gallicano, IRCCS, Rome, Italy.

The aetiopathogenic mechanism underlying clear cell acanthoma (CCA) is
not completely clear and it has been postulated that CCA and psoriasis
may have a similar pathogenesis because of the common features shared
by the two diseases. As it has been recently demonstrated that in
psoriatic lesions the paracrine epithelial growth factors [keratinocyte
growth factor (KGF)/fibroblast growth factor (FGF)-7 and FGF-10] are
involved in promoting and sustaining the keratinocyte
hyperproliferation, the aim of this study was to analyse the expression
of KGF on CCA lesions and to search for a role of this growth factor in
CCA pathogenesis. Immunohistochemical analysis showed an up-modulation
of KGF in CCA, although the immunostaining was variable among the
different samples collected. Positive immunoreactivity for KGF was
detected mainly on dermal areas where the inflammatory infiltrate was
more pronounced suggesting a relationship between lymphocyte activation
and KGF up-modulation. Real-time quantitative RT-PCR assay performed on
mRNA extracted from formalin-fixed paraffin-embedded CCA and normal
skin (NS) samples further demonstrated the overexpression of the
KGF/FGF-7 gene in all CCA samples compared with NS. Moreover, the
evaluation by immunohistochemistry of KGF receptor distribution, the
high-affinity tyrosine kinase receptor for KGF, showed a
down-modulation of this receptor, as previously reported in the
presence of increased levels of KGF. Taken together these results
suggest the inflammatory nature of CCA and further support the
hypothesis that this disease may represent, like psoriasis, an
inflammatory dermatosis in which KGF up-modulation may be responsible
for keratinocyte hyperproliferation and may represent a new common
feature of both diseases.

PMID: 16984257

Doesn't look like P much, unless you rip off all flakes,
http://tray.dermatology.uiowa.edu/D...anthoma-001.htm

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

randall..

randall

2006-09-23, 4:26 pm

Hi,

P News from around the world.

First stop the middle east.

http://www.ameinfo.com/97122.html

60 Dermatologists from across the Middle East attend Psoriasis lecture
at the JW Marriot.

The lecture, sponsored by Wyeth Pharmaceuticals and in coordination
with The Dubai Dermatology Club, was given by Prof. Richard Langley,
Associate Professor of Medicine & Director of Research at Dalhouise
University, Halifax, Canada. Prof. Langley discussed the British
Association of Dermatologists Guidelines, along with his personal
guidelines on the use of Biological therapies on Psoriasis patients.

The objective of the lecture was to increase awareness of the practical
aspects of 'biologics', by clarifying who should be treated and how to
initiate biological therapy. Prof. Langley also gave an overview on the
results of a study conducted on 300 patients. One of the results
discussed, showed the link between psoriasis and obesity.

'Psoriasis has a profound negative impact on the quality of life and in
many cases it may lead the sufferer into a state of depression' says
Prof. Langley, 'there is a need for new therapies with fewer side
effects, especially for patients with severe psoriasis that are
undergoing extensive therapies'

Biological therapies or 'biologics' have emerged over the last 3-5
years as a potentially therapeutic option to psoriasis, but since
clinical history and long-term results are limited certain guidelines
have been developed to guarantee a systematic, safe and effective
treatment process for psoriasis patients.

'The results I have seen from biologics have been terrific on most of
my patients, especially when treating moderate to severe psoriasis'
adds Prof. Langley, 'but guidelines prescribing biologics is a must, to
maximize treatment effectiveness and ensure that the correct biologic
treatment is presented for the patient.'

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

Depression? No one around here gets that? do we?

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

NOT, when you can shuffle off to the blue lagoon in Greenland. Lets say
all that searing sun in the middle east isn't enough to tan your hide.
And you need
northern exposure to get closer to those rays.

http://www.dailyrecord.co.uk/news/t...od=3Dfull&site=
id=3D66633&headline=3Dnorthern-exposure--name_page.html

NORTHERN EXPOSURE
Don't be put off by the high prices, Iceland has some things money just
can't buy
By Jack Mathieson

I WAS up to my chest in pale blue water, but the undercurrent that
gently pummelled the back of my legs was as hot as a bath tub.

Through the clouds of vapour rising from the surface, I could see the
rugged lava formations which defined the edges of the world-famous
lagoon.

A waiter - clad only in bathing trunks and a bow tie - waded out to us
holding a tray of drinks high above his head.

I took a glass and the sweet cocktail slipped down smoothly, its
striking blue hue an identical match to the waters which were lapping
around us.

However, this was no tropical paradise. The Blue Lagoon geothermal spa
is one of the most popular attractions in Iceland, and is only a
40-minute drive from Reykjavik, the northernmost capital in the world.

Cynics may claim that the lagoon amounts to no more than a pool of
effluent from the nearby power plant.

Advertisement
Falk AdSolution

But the chemical waste dump jibes are easily shrugged off by those who
say the landmark, which has spawned a line of skin-care products, has
eased the effects of psoriasis. It's certainly great fun.

And it has also become an essential item on the itinerary for visitors
to Iceland as well as an interesting stopover spot for British visitors
on their way to the USA.

With Keflavik Airport only a couple of hours away from Glasgow, bosses
at Icelandair are very keen to see even more of us enjoying what their
country has to offer.

A Celebrate Iceland festival, to be held in Glasgow's Princes Square
from October 12-15, will showcase Icelandic food, artwork and music.

Chef Steinar Thorfinnsson will take up temporary residence at Darcy's
restaurant with a specially-created menu. Visitors will also be able to
enjoy painting, photography, storytelling and even get a massage
Icelandic-style.

Most tourists come to Iceland to enjoy its natural beauty and vast open
spaces. The snow-capped peaks, glaciers and abundant birdlife are a
huge draw.

On a previous trip, I enjoyed the I sight of a rainbow through the I
spray given off by the waterfalls at Gullfoss, and experienced the
thrill of trying to capture on camera the frequent but short-lived
eruptions of spouting hot springs nearby. However, the small but lively
capital Reykjavik, located on the island's south-west corner, has now
emerged as a captivating destination in its own right.

No less than a quarter of the city area is devoted to open space, but
the array of museums and galleries, fine dining and bustling nightlife
also suits those who are motivated by more metropolitan pursuits.

A new city centre exhibition, based on exhibits unearthed in
archaeological excavations, uses multi-media technology to portray what
life was like during the time of the Vikings.

But contemporary Reykjavik - now in the middle of a huge building boom
- is no less interesting, as I found out on my most recent visit.

The city can be pricey, but don't let that put you off visiting. Even
the most upmarket bars and restaurants are no more expensive than, for
example, London's west end.

We began our night on the town with a few liveners at the Hotel
Nordica, just outside the city centre.

The Panorama Lounge on the eighth floor offers spectacular views across
the nearby Laugardalur Valley and beyond, and drinks there set us up
nicely for dinner at one of the best restaurants in the city centre.

Einar Ben is named after a leading Icelandic poet and, as befits a
country whose fishing industry generates about half of the nation's
export earnings, the menu on the night had a distinctly sea food
flavour. Suitably fortified, our group rounded off the night by
visiting some of the trendier bars in town, including one which was
doing a roaring trade in Mojitos.

I had last tasted the cocktail amid the sultry heat of a tropical
evening in its spiritual home of Cuban capital Havana.

It seemed odd to say the least to be quaffing the rum-based drink so
close to the Arctic Circle, but it hit the spot nonetheless.

The natives were very friendly, although one group of teenage revellers
did overstep the mark by mistakenly identifying us as English and
continually asking, in their best Queen Elizabeth accents, if we would
like tea and biscuits.

Icelandair offers up to five direct flights each week from Glasgow
Airport to Reykjavik. Return flights from =A3163, including taxes.

'The small capital of Reykjavik has emerged as a captivatng
destination'=20

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

randall

JXStern

2006-09-30, 9:30 pm

On 30 Sep 2006 13:23:56 -0700, "randall" <ranhub11@aol.com> wrote:

>The Vegas nerve. Is it craPPing out on us?

I dunno, call CSI!

Some really good stuff below, not the meditation stuff, the mobo
stuff.

Meanwhile, my mantra:
One of these days we're gonna have some seriously good treatments.
Hope I'm still around to see them. Hope some at least pretty good new
treatments come along (a lot) sooner.

J.

randall

2006-10-01, 4:27 pm

JXStern wrote:
> On 30 Sep 2006 13:23:56 -0700, "randall" <ranhub11@aol.com> wrote:
>
>
> I dunno, call CSI!

We need doctor HOUSE, not CSI!

I'm waiting for him to out FOX it. But first he needs to heal that
criPPled leg.

Here's a switch, why don't they give him late onset psoriasis?

He already is on the level of the singing detective on many levels.lol

>
> Some really good stuff below, not the meditation stuff, the mobo
> stuff.
>
> Meanwhile, my mantra:
> One of these days we're gonna have some seriously good treatments.
> Hope I'm still around to see them. Hope some at least pretty good new
> treatments come along (a lot) sooner.

It felt like those drugs were here with biologicals. But when you
waited for
the reports to come back, the price and side effects took some serious
weighing.
Maybe not so much for those severely afflicted of course.

I guess beyond biological is what's next.

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

P NEWs_____________________

Eureka! A major theory to explain inflammation.
Our dead immune cells become sponges. YIKES!

http://www.newscientist.com/article...inflammation-o=
ff-switch.html
Body reveals its inflammation 'off switch'

Researchers have shed light on how the body switches off its immune
response, a key step towards understanding autoimmune diseases and
controlling inflammation.

When immune cells die, they transform into "sponges" that soak up
the molecules responsible for causing inflammation, researchers have
discovered. The new information may lead to better drugs to treat
inflammatory disorders, such as eczema.

Inflammation is characterised by a red, painful swelling around a wound
caused by blood fluids, proteins and immune cells flooding into an area
of the body in response to germs or damage. Its biological purpose is
to allow immune cells to get from the blood to the trouble spot to
fight infection.

But too much inflammation can be devastating. It is what causes death
in diseases such as flu, while chronic, misdirected inflammation causes
conditions from eczema to arthritis. As a result, researchers have been
looking for ways to "turn-off" the inflammatory response.
Ultimate scavengers

Now, Charles Serhan and colleagues at Harvard university in Boston, US,
have discovered an important natural braking mechanism. In a healthy
inflammatory response, immune cells called leukocytes are attracted to
the site of injury, where they are activated by molecules called
chemokines. The leukocytes emit powerful germ-killing chemicals, and
then commit suicide.

The researchers discovered that _dying leukocytes_ act like _sponges_,
soaking up chemokines, preventing them from attracting more leukocytes.
It is the body's way of controlling inflammation - a good thing,
since too much of their germ-killing chemicals can damage healthy
surrounding tissue.

These dying leukocytes are the "ultimate scavenging entity", Serhan
says. As they die, they even produce more of the molecules - called
__CCR5__ - that help them soak up chemokines. Then the whole lot is
gobbled by debris-removing cleaner cells called macrophages.
Complete turnaround

This system is just one part of a complicated web of inflammation
controls. But understanding this natural chemokine-soaking mechanism is
vital to learning more about how inflammation and autoimmune disorders
progress, the team says. For example, mice bred to lack another
molecule that soaks up chemokines develop a skin inflammation similar
to ___psoriasis__ in humans.

Serhan told New Scientist that one day it may be possible to control
chronic inflammatory disease by making drugs that promote the natural
signals that turn inflammation off.

Such drugs could also be used to turn off the chronic inflammation
underlying many auto-immune diseases. "This is a complete 180=B0 turn
from the drugs sought today and used in the last century," he says,
which have focused on drugs that block the signals that turn
inflammation on in the first place.
Journal reference: Nature Immunology (DOI: 10.1038/ni13920

-------------------
Oral Vitamin D3

http://www.medicalnewstoday.com/med...?newsid=3D52974
Oral Treatment With A Vitamin D3 Analogue (BXL628) Has
Anti-inflammatory Effects In Rodent Model Of Interstitial Cystitis
The active form of vitamin D, calcitriol or 1,25(OH)2D3, is a
secosteroid hormone that has been extensively studied over several
years. Its biological effects in vivo include regulation of bone
metabolism, cellular proliferation, and immune response. These
characteristics led to therapeutic applications in osteoporosis,
secondary hyperparathyroidism, and psoriasis. Many reports show
beneficial effects of vitamin D in animal models of diabetes, organ
graft rejection, experimental allergic encephalomyelitis, lupus
nephritis, and in allergic experiment asthma.

Benigni and colleagues from Milan, Vermont, and Lund report a very
interesting study in which they devised a mouse model of
allergen-induced allergic cystitis that is associated with the
up-regulation of genes for interleukin-13, FC?RI? and mast
cells-derived proteases, a massive inflammatory reaction in the bladder
tissue, and augmented levels of mast cell-derived protease 1 detected
in mouse sera. Oral administration of a vitamin D3 analogue (BXL628)
reduced the expression of interleukin-13, FC?RI?, and mast cell-derived
protease 1 in the bladder. At histology there was decreased edema and
leukocyte infiltration in the bladder wall. There was a preventative
effect on mast cell degranulation in vivo.

The authors believe that the data in this detailed manuscript clearly
support the hypothesis that the vitamin D3 derivative BXL628 is
effective in modulating the Th2-type inflammatory response in the
bladder by down-modulating the expression of typical markers such as
interleukin-13 or FC?RI?. Also, a reduced inflammatory cell infiltrate
is detected within the ovalbumin-challenged bladders on drug treatment,
indicating that migration of inflammatory cells might be reduced. It is
suggested because oral treatment with the vitamin D3 analogue BXL628
has anti-inflammatory effects on the urinary bladder in a model of
allergic cystitis, that vitamin D3 analogues may represent a new
therapeutic option for BPS/IC.

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

Cancer sees the light
http://www.news.com.au/entertainmen...5006012,00.html

randall...UVR =3DD3 and UVB/UVR =3D increased clarity... can we really eat
sunlight with D3?

>=20
> J.

randall

2006-10-03, 4:28 pm

JXStern wrote:
> On 1 Oct 2006 14:22:16 -0700, "randall" <ranhub11@aol.com> wrote:
>
>
> I dunno, the House paradigm is to kill the patient in order to save
> him, don't know that I need that.

What? You wouldn't die for a few minutes to be cured? LOL

How about vaccinated?

Most type II psoriatics could make due with less obesity and
thusly TNF from adipose cells.

http://www.usaweekend.com/06_issues...ealthsmart.html
& the abstract to go with it,
http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum

>
> The current anti-TNF biologicals are pretty far downstream, blocking
> symptoms, not causes. Plenty of room to move upstream.
>
>
> ...
>
> I think they are saying sponge = good. We need more sponges! But
> this is very interesting, maybe we lack normal amounts of sponge!?!
>
> Calling Dr. Squarepants ...

Indubitably! Small molecules to turn them on, applied topically sounds
plausible. Or vaccination every few months would be uPstream of the
biologicals.

Or how about RNAi or even a simple DNA fix?

Yeah right! lol

__________________________________________________________

P NEWS

http://phgu.org.uk/ecard.php?link_ID=2665

The major histocompatibility complex (MHC) is a set of genes on
chromosome 6 that are highly polymorphic; multiple alternative genetic
variants (alleles) are present in human populations. Many of the Human
Leukocyte Antigen or HLA genes within the MHC region play a crucial
role in the human immune system; specifically, in the processes by
which the body distinguishes ?self? and foreign or ?non-self?
cells or agents and targets the latter for destruction. HLA variation
is a key factor in determining individuals? susceptibility to
multiple infectious and autoimmune diseases, such as malaria, SARS, TB,
diabetes, multiple sclerosis, psoriasis and Crohn?s disease. No other
region of the human genome has been associated with susceptibility to
so many diseases. However, identifying the exact genetic variants
associated with disease is extremely difficult due to the high degree
of genetic diversity in human populations with respect to this region,
and a high level of variation in linked, neighbouring alleles that
effectively masks that of the causal alleles. <sniP>

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

http://releases.usnewswire.com/GetRelease.asp?id=73634

Psoriasis Cure Now Releases New Podcast Discussing Remicade as a
Psoriasis Treatment

10/3/2006 7:30:00 AM

To: National Desk, Health Reporter

Contact: Michael Paranzino of Psoriasis Cure Now, 202-253-4863,
mike@psoriasis-cure-now.org ; Web: http://www.psoriasis-cure-now.org

KENSINGTON, Md., Oct. 3 /U.S. Newswire/ -- "Psoriasis Cure Now," a
nonprofit patient advocacy group, today released the newest in its
series of psoriasis podcasts, this one focused on Remicade (infliximab)
for the treatment of psoriasis. Last week, the U.S. Food and Drug
Administration approved Centocor's Remicade for the treatment of adults
with severe psoriasis. The free podcast is available on the Psoriasis
Cure Now website at http://www.psoriasis-cure-now.org/podcasts.php , or
through iTunes.

The podcast includes a pair of interviews. Alan Menter, M.D., Chairman
of the Division of Dermatology at Baylor university Medical Center and
a renowned dermatologist, speaks about Remicade's efficacy and safety
profile. Dr. Menter was the lead investigator for Remicade's U.S.
psoriasis study. The podcast also includes an interview with Mike
Hills, a Remicade patient from Virginia, who shares his experience with
the treatment and walks us through an infusion from the patient
perspective. Remicade is delivered via intravenous infusion in a
medical setting, a procedure with which many patients are not yet
familiar.

"Remicade is an important new treatment option for people with severe
psoriasis, so we put together interviews with a top psoriasis expert
and a man treating his psoriasis with Remicade to help people
understand what Remicade is and whether it might be appropriate for
them," said Michael Paranzino, president of Psoriasis Cure Now. "That
psoriasis patient waited a quarter century to clear his skin, and many
psoriasis patients have been waiting even longer than that. People who
are not satisfied with their current condition owe it to themselves to
speak with their physician about all the new treatment options that
have appeared in recent years."

Remicade is also approved for several other diseases, including
psoriatic arthritis, rheumatoid arthritis and Crohn's disease. Previous
Psoriasis Cure Now podcasts have covered topics including strategies
for treating children with psoriasis, and the future of psoriasis
treatments. The next one, to be released near the end of October, will
be an introduction to psoriatic arthritis. They are all available free
from the Psoriasis Cure Now website and via iTunes.

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

randall...

>
> J.

randall

2006-10-04, 4:28 pm

Hi,

P News from around the world.

Abstracts today and ending with one food article for J.

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

Oh boy gut flora!

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Intestinal flora and psoriatic arthritis.

* Vasey FB,
* Carter JD.

Department of Internal Medicine, Division of Rheumatology, University
of South Florida, Tampa, FL, USA.

PMID: 17014029

Darn! I hate these abstracts without any meat in the taco. Let's check
the related links
box.

Vasey FB also did another study previous to this one. Back in 1982!
Interesting that he may have found something 24 years later. That
abstract from way back then,
http://www.ncbi.nlm.nih.gov/entrez/...st_uids=6757423
1982 Sep-Oct;9(5):719-22.

Possible involvement of group A streptococci in the pathogenesis of
psoriatic arthritis.

* Vasey FB,
* Deitz C,
* Fenske NA,
* Germain BF,
* Espinoza LR.

Bacteria have been implicated in the form of Reiter's syndrome, known
as reactive arthritis. If bacteria are important in the related
spondyloarthropathy psoriatic arthritis, they may be those comprising
skin flora. We found elevated levels of antibody to the streptococcal
exotoxin antideoxyribonuclease-B in psoriatic arthritis patients in
comparison to patients with psoriasis without arthritis, rheumatoid
arthritis, other forms of dermatitis, and normal controls. Patients
with peripheral arthritis were more likely than psoriatic spondylitis
patients to be antideoxyribonuclease-B positive. Streptococci or
streptococcal products may be involved in the pathogenesis of psoriatic
arthritis in some patients.

PMID: 6757423

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

Oh boy, chinese herbs now!

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Successful Treatment of Pediatric Psoriasis with Indigo naturalis
Composite Ointment.

* Lin YK,
* Yen HR,
* Wong WR,
* Yang SH,
* Pang JH.

Department of Traditional Chinese Medicine, Center for Traditional
Chinese Medicine, Chang Gung Memorial Hospital, Taoyuan, Taiwan.

The treatment of psoriasis in children is still an intractable problem
and demands a long-term therapy with prolonged efficacy that is free
from serious adverse events. Many modes of therapy are currently in use
but the disease is often resistant to treatment owing to the
unacceptable toxicity that leads to poor compliance. Therefore, to
develop an alternative treatment is indispensable. Traditional Chinese
medicine has been documented for over 1000 years to provide various
effective treatments for inflammatory skin diseases. Herein, we report
an 8-year-old boy with recalcitrant pediatric psoriasis who, after
multiple treatment failures with conventional antipsoriatic
medications, showed remarkable clinical improvement with 8 weeks of
topical treatment with Indigo naturalis composite ointment. Remission
has lasted for over 2 years until now. Our patient's response suggests
that topical Indigo naturalis composite ointment may provide a safe and
effective alternative treatment for pediatric psoriasis.

PMID: 17014654

I wonder whats in it? Checking the patent should turn up ingredients.
YeP

http://appft1.uspto.gov/netacgi/nph...o+AND+naturalis

[...]

We claim:

1. A method for treating psoriasis comprising: applying a topical
treatment to a selected portion of a person's body according to a
selected schedule; said topical treatment comprised of an extract of at
least one of the following compounds: Rhizoma Curcumae Aeruginosae
Curcumae Aeruginosae, Pericarpium Citri Reticulatae Citrus reticulata
blanco, Radix Angelicae Hangbaizhi or Radix Angelicae Qibaizhi
Angelicae dahuricae, Herba Artemisiae Anomalae Artemisia anomala,
Ramulus Euonymi Euonymus alatus, Radix Tripterygiim Wilfordii
Tripterygium Wilfordi, and a topical medicinal carrier.

[...]

6. The method for treating psoriasis of claim 1 wherein said topical
treatment for psoriasis comprises: an extract from a combination of all
of the following compounds, Caulis Spatholobi (Spatholobus suberectus),
Radix Rehmanniae Exsiccata (Rehmanniae glutinosa), Radix lithospermi
(Lithospermum erythrorhizon), Radix Salviae Miltiorrhizae (Salviae
Miltiorrhiza), Radix Paeoniae Veitchii (Paeonia Veitchii), Rhizoma
Imperatae (Imperata cylindrica), Flos Sophorae (Sophora japonica) and a
topical medicinal carrier.

[...]

[0007] CTMs (Chinese traditional medicines) have been extensively used
to treat psoriasis and have acquired considerable favor among many of
the patients. The earliest description of psoriasis in ancient Chinese
medical literature may be found in Sui-Dynasty, 581-618 AD. According
to Chinese literatures, "Bian Zheng Shi Zhi", Lin X R. J. Dermato. 20,
746-55, 1993 collected a number of clinical psoriasis cases report, and
distinguished psoriasis into 2 or 3 types, namely "Blood-Heat" type and
"Blood deficiency-Dryness" type or "Blood-Heat," "Blood
deficiency-Dryness" and "Blood stasis" type. While in also described
prescription (I) to treat "Blood-Heat" type, that including Caulis
Spatholobi 2, Radix Rehmanniae Exsiccata 6, Radix Lithospermi 13, Radix
Salviae Miltiorrhizae 14, Radix Paeoniae Veitchii 17, Rhizoma Imperatae
23, and Flos Sophorae 27. Prescription (II) to treat "Blood
deficiency-Dryness" type that including Caulis Spatholobi 2, Radix
Angelicae Sinensis 3, Rhizoma Smilacis Glabrae 4, Radix Rehmanniae
Exsiccata 6, Radix Ophiopogonis Japonici 7, Radix Asparagi 8, Nidus
Vaspae 10, and Radix Salviae Miltiorrhizae 14. Prescription (III) to
treat "Blood stasis" type that including Canlis Spatholob 2, Rhizoma
Sparganii 5, Herba Hedyotis 11, Rhizoma Curcumae Aeruginosae 15,
Pericarpium Citri Reticulatae 18, Flos Carthami 19, Semen Amygdalus
Persicae 20, and Ramulus Euonymi 26. <sniP>

Well You get the idea by now. A bunch of chinese herbs help bad p and
Indigo naturalis composite ointment has a lot more in it then Indigo.

I want to try it!

In late december or January 07. But heck, i want to try kalawalla still
as well.

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

If you have PsA, have your thyroid checked for low fluid levels. You
may need a grain or two to toP it off.

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
High prevalence of thyroid autoimmunity and hypothyroidism in patients
with psoriatic arthritis.

* Antonelli A,
* Sedie AD,
* Fallahi P,
* Ferrari SM,
* Maccheroni M,
* Ferrannini E,
* Bombardieri S,
* Riente L.

>From the Department of Internal Medicine and the Rheumatology Unit,
University of Pisa; and the Endocrinological Laboratory, Azienda
Ospedaliera Pisana, Pisa, Italy.

OBJECTIVE:To evaluate the prevalence of thyroid disorders in a group of
patients with psoriatic arthritis (PsA). METHODS: A complete thyroid
investigation was carried out in 80 patients with PsA, in gender- and
age-matched subjects (1:5) drawn from the general population
(controls), and in 112 patients with rheumatoid arthrtitis (RA) with
similar iodine intake. RESULTS: Anti-thyroid peroxidase antibodies
(AbTPO), a hypoechoic thyroid, and subclinical hypothyroidism were
significantly more frequent in women with PsA than in control women,
and their frequency was similar to that in patients with RA (positive
AbTPO titer 28%, 12%, and 31%; hypoechoic thyroid 31%, 16%, and 36%;
subclinical hypothyroidism 25%, 8%, and 12%, respectively). Among men,
positive AbTPO titers and a hypoechoic thyroid were found more
frequently in the patients with PsA and RA than in controls (positive
AbTPO titer 14%, 5%, and 2%; hypoechoic thyroid 16%, 10%, and 3%,
respectively). All patients with PsA with subclinical hypothyroidism
had polyarticular involvement (p </= 0.05) and a longer disease
duration (years 19 +/- 15 vs 11 +/- 8, p = 0.03) than patients with
euthyroid PsA. The prevalence of subclinical hyperthyroidism, thyroid
nodules, and thyroid enlargement was not significantly different among
the 3 groups.CONCLUSION: Our results demonstrate a significantly higher
prevalence of thyroid autoimmunity (positive AbTPO, hyoechoic thyroid)
findings in men and women with PsA and of subclinical hypothyroidism in
women with PsA than in the general population. Therefore, thyroid
function tests, an AbTPO assay, and thyroid ultrasound should be
performed as part of the clinical evaluation, particularly in women
with PsA.

PMID: 17014017

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

And just for J today.

http://www.aicr.org/site/News2?JSer...Article&id=9331
Stronger Than Iron, Curcumin May Prevent Tumors
Curcumin is the phytochemical in the spice turmeric that gives curry
its yellow color. In animal studies, it has prevented the growth of
several types of cancers. It has even been tested in clinical trials as
a way to prevent cancer in humans.

Suzy V. Torti, Ph.D., Associate Professor of Biochemistry at Wake
Forest university School of Medicine in Winston-Salem, N.C., has
studied curcumin's protective effect against cancer. In collaboration
with her research colleagues, Dr. Torti recently found a possible
explanation for how curcumin inhibits tumor growth.

Cancer Cells Deprived of Iron

"We made the unexpected observation that curcumin binds and isolates
iron in cells and tissues," says Dr. Torti. The process of binding and
isolating a metal ion such as iron is known as chelation. Her group
made this discovery after studying the effects of several natural
products.

How chelation of iron by curcumin may prevent cancer is unknown. It may
involve the special need of tumor cells for iron. Although iron is
essential for the body to function, cancer cells are avid for iron. It
is required for their growth and DNA synthesis. In conditions of excess
iron storage, the risk of liver cancer is greatly increased.

Dr. Torti notes, however, that chelation is probably only a part of how
curcumin affects tumors. "Studies have shown lots of partial answers to
the question of why curcumin inhibits tumor growth. Its property of
chelating iron is just another piece of the puzzle of how this simple
molecule works." <sniP>

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

randall... curcumin chelates iron! YMMV depends on ros and anti-ros
then!

randall

2006-10-05, 4:27 pm

Hi,

P News from around the world.

>From downunder today.

Eat your way to clear glowing skin,
http://seven.com.au/todaytonight/story/?id=29961

[...]

So what exactly do the experts recommend then?

The recommended skin-friendly foods are:
Wholegrain bread
Porridge
Muesli
Basmati rice
Sweet potatoes
Lean red meat at least 3-4 times a week
Fish
Green vegetables
Fruit
Nuts
Eggs
Avocadoes

Foods to avoid are:
White bread
Sweet biscuits
Sugary breakfast cereals
White rice
Potatoes
Cakes and sweet biscuits
Pies
Lollies
Chocolate
Hot chips

But if you're worried convincing your teen to swap chips for carrots
will be an impossible task, then listen to those who have seen the
results first-hand.

"If they want to help themselves and their skin, they will change their
habits," Andrea said.

And Daniel's advice?

"I would say try it and when you see the results you won't care.

"Instead of stopping at McDonald's you'll have an apple, you won't
care cause the results speak for themselves."

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

But, for P you may need more. Some of us, a LOT more.

Here's a new one.

ToPical Niacin,
http://www.prnewswire.com/cgi-bin/s...04446212&EDATE=

[...]

Dr. Jacobson's research, performed in collaboration with Dr. Myron K.
Jacobson, has been continuously funded by the National Institutes of
Health
for more than 28 years, and has led to more than 150 published papers
and
invited book chapters, and 25 patent applications. Together, their
research
has led to the discovery of new functions of niacin in skin biology,
and
the development of novel compounds designed for topical delivery of
niacin.
One of these compounds has proven so effective that it has been
selected by
the National Cancer Institute for evaluation as a possible skin cancer
prevention agent under the Rapid Access to Prevention Intervention
Development (RAPID) program.

[...]

About Niadyne, Inc.
Niadyne, Inc., a privately held company, is involved in the
discovery
of uniquely efficacious molecules that penetrate the skin to address
unmet
health care needs. Product development is focused on the treatment and
prevention of sun damage to skin and the optimization of scalp and hair
follicle function. Recently, the company created NIA 24(TM), a
niacin-powered skin care line, based on more than 25 years of
biomedical
research. The Drs. Jacobson and colleagues developed a patented niacin
molecule called Pro-Niacin(TM), the main ingredient in the NIA 24
products.
Pro-Niacin facilitates the delivery of niacin deep into the skin, where
it
helps to stimulate DNA repair and build the skin barrier from the
inside
out. This remarkable molecule also assists in energy metabolism and
stimulation of Leptin release. NIA 24 products are available through
leading dermatologists and plastic surgeons and select medi- spas
nationwide. For more information about NIA 24 and Niadyne, Inc., visit
http://www.nia24.com.

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

Cute DNA story and a nobel prize for Roger Kornberg
http://www.latimes.com/news/nationw...la-story-footer

Rogers cousin, Dr. Richard Kornberg is a dermatologist in San Diego.
http://www.signonsandiego.com/news/...99-7m5bell.html

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

Dna vaccine to prevent allergy for two years.
http://www.timesonline.co.uk/articl...2388981,00.html
A NEW DNA-based allergy vaccine can offer long-lasting relief to hay
fever sufferers after just six injections, American scientists have
claimed.

Patients receiving the experimental vaccine showed an average 60 per
cent reduction in typical allergy symptoms, such as sneezing, runny
nose, watering eyes and itching for at least two years, compared with
those receiving a placebo.

Researchers at the Johns Hopkins university School of Medicine, in
Baltimore, Maryland, believe that a six-injection treatment with the
new vaccine, known as AIC, could offer a significant improvement over
traditional allergen immunotherapy, which can require several years of
weekly or bi-weekly injections.

AIC contains a short piece of DNA known as an "immunostimulatory
sequence" that can modify immune system reactions and reduce the
typical symptoms of ragweed allergy, more commonly known as hay fever.

[...]

In allergic individuals, antibodies known as IgE are responsible for
mediating the allergic response.

In the current study, the researchers found that, like standard
immunotherapy, AIC blocks the seasonal rise in ragweed-specific IgE in
people who are allergic.

Investigators at the university of California, in San Diego, had
observed previously that a particular sequence of DNA, derived from
bacteria, shuts down a T-helper cell (Th2) involved in the body's
inflammatory response.

It is thought that the vaccine lessens the immune system's excessive
reactions to inhaled allergens by stimulating protective cells that
turn off the Th2 helper cells.

[...]

"Long-lasting relief can be achieved with a concise, six-week
injection regimen, as opposed to the current, tedious, four to
five-year course of treatment with allergen immunotherapy," Dr
Creticos said. "And we're not just treating the symptoms, we're
targeting the fundamental defects in the immune system that cause
allergy."

Further studies are under way to examine the drug's lasting effects
in a larger group of participants.

"Our hope is that we can one day provide a long-term cure for hay
fever and other chronic inflammatory diseases," Dr Creticos said.

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

$10M reward for super fast DNA tests from Archon X-prize (Ansari)
http://news.bbc.co.uk/1/hi/sci/tech/5404678.stm

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

Pick up an extra $13M from the National Human Genome Research Institute
for faster and more cost-effective DNA sequencing technology.

http://www.upi.com/NewsTrack/view.p...04-041125-2216r

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

P Abstracts in the NEWs

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Structural requirements of heparin and related molecules to exert a
multitude of anti-inflammatory activities.

* Ludwig RJ,
* Alban S,
* Boehncke WH.

Department of Dermatology, Johann Wolfgang Goethe University,
Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany.
r.ludwig@em.uni-frankfurt.de.

Chronic inflammatory diseases are common and still remain a therapeutic
challenge for both efficacy and safety reasons. Hence, novel
therapeutics addressing these issues would for example improve
treatment of severe diseases such as psoriasis, rheumatoid arthritis,
inflammatory bowel disease and multiple sclerosis. Inappropriate
leukocyte homing to the affected compartments is a common feature of
these diseases. Heparin and related polysaccharides have been shown to
interfere with leukocyte homing through a variety of effects distinct
from their anticoagulant properties. In this review, data on heparin as
an anti-inflammatory agent are presented. In addition,
structure-activity requirements for the anti-inflammatory properties of
heparin are discussed, which should aid the drug development based on
structurally modified heparin or other sulfated carbohydrates for
treatment of inflammatory diseases.
PMID: 17018000

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

Here's a small plus for those of you taking Remicade. Increased HDL
level's may
offer a small degree of protection against cardiovascular disease.

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Modest But Sustained Increase of Serum High Density Lipoprotein
Cholesterol Levels in Patients with Inflammatory Arthritides Treated
with Infliximab.

* Spanakis E,
* Sidiropoulos P,
* Papadakis J,
* Ganotakis E,
* Katsikas G,
* Karvounaris S,
* Bizaki A,
* Kritikos H,
* Boumpas DT.

OBJECTIVE: Tumor necrosis factor-a (TNF-a) is a key cytokine in the
pathogenesis of chronic inflammatory arthritides, has proatherogenic
effects, and may be positively correlated with impairment of the action
of insulin. Patients with chronic inflammatory arthritides have an
increased risk for cardiovascular diseases. We assessed whether
anti-TNF-a treatment modifies the unfavorable lipid profile induced by
chronic inflammatory arthritides. METHODS: Sixty patients (24 with
rheumatoid arthritis, 26 ankylosing spondylitis, and 10 psoriatic
arthritis) receiving infliximab because of ongoing disease activity
despite disease modifying drugs (DMARD) were prospectively studied for
6 months. Lipid profile, total cholesterol/high density lipoprotein
cholesterol (TC/HDL-C), and low density lipoprotein cholesterol
(LDL-C)/HDL-C ratios, as well as disease activity indices (DAS28 and
BASDAI), were assessed. RESULTS: A sustained increase of serum HDL-C
was observed [mean increase (95% CI)] 5 (3-7) mg/dl, 3.5 (1-6) mg/dl,
and 3 (1-5) mg/dl at 1, 3, and 6 months, respectively (p < 0.01).
Compared to nonresponders, HDL-C increased significantly more in EULAR
or BASDAI responders (0.8 vs 5.8 mg/dl; p = 0.05). Serum TC was
significantly increased [11 (4-8) mg/dl; p = 0.001] only after the
first month of treatment. TC/HDL-C and LDL-C/HDL-C decreased only after
the first month [0.3 (0.1-0.4), p < 0.01, and 0.2 (0.1-0.4), p < 0.01,
respectively]. For patients with baseline LDL-C > 130 mg/dl,
LDL-C/HDL-C decreased (p < 0.05) during the whole study period and
TC/HDL-C decreased (p < 0.05) at 1 and 3 months. CONCLUSION: Anti-TNF-a
treatment in patients with chronic inflammatory arthritides induces a
modest, but sustained, increase in serum HDL-C levels, which may have a
favorable effect in reducing the cardiovascular risk in these patients.

PMID: 17014005

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

randall..

randall

2006-10-06, 4:27 pm

Hi,

P News from around the world.

http://www.ncbi.nlm.nih.gov/entrez/...l=pubmed_docsum
Phosphodiesterase 7A: a new therapeutic target for alleviating chronic
inflammation?

* Giembycz MA,
* Smith SJ.

Department of Pharmacology and Therapeutics, Respiratory Research
Group, Faculty of Medicine, university of Calgary, Calgary, Alberta,
Canada. giembycz@ucalgary.ca

Over the last fifteen years there has been much excitement in the idea
that targeting phosphodiesterase (PDE) 4 with small molecule inhibitors
could lead to the discovery of novel, steroid-sparing compounds with
utility in treating a multitude of diseases associated with chronic
inflammation. However, dose-limiting side effects, of which nausea and
vomiting are the most common are worrisome, have hampered their
clinical development. Indeed, a fundamental obstacle that still is to
be overcome by the pharmaceutical industry is to make compounds that
dissociate beneficial from the adverse events. Unfortunately, both of
these activities of PDE4 inhibitors represents an extension of their
pharmacology and improving the therapeutic ratio has proved to be a
major challenge. Several strategies have been considered, with some
degree of success, but compounds with an optimal pharmacophore still
have not been reported. An alternative approach to targeting PDE4 is to
inhibit other cAMP PDE families that are also expressed in immune and
pro-inflammatory cells in the hope that the beneficial activity can be
retained at the expense of side effects. One such candidate is PDE7A.
In this article we review the literature on PDE7A and explore the
possibility that selective small molecule inhibitors of this enzyme
family could provide a novel approach to alleviate the inflammation
that is associated with many inflammatory diseases including asthma,
chronic obstructive pulmonary disease, atopic dermatitis, psoriasis,
lupus, rheumatoid arthritis and multiple sclerosis.

PMID: 17020529

What is it?
http://www.ncbi.nlm.nih.gov/entrez/...hodiesterase+7A

OK,
http://www.ncbi.nlm.nih.gov/entrez/...t_uids=14662840
Phosphodiesterase 7A-deficient mice have functional T cells.

Yang G, McIntyre KW, Townsend RM, Shen HH, Pitts WJ, Dodd JH, Nadler
SG, McKinnon M, Watson AJ.

Immunology and Inflammation Drug Discovery, Bristol-Myers Squibb
Pharmaceutical Research Institute, Princeton, NJ 08543, USA.
guchen.yang@bms.com

Phosphodiesterases (PDEs) are enzymes which hydrolyze the cyclic
nucleotide second messengers, cAMP and cGMP. In leukocytes, PDEs are
responsible for depletion of cAMP which broadly suppresses cell
functions and cellular responses to many activation stimuli. PDE7A has
been proposed to be essential for T lymphocyte activation based on its
induction during cell activation and the suppression of proliferation
and IL-2 production observed following inhibition of PDE7A expression
using a PDE7A antisense oligonucleotide. These observations have led to
the suggestion that selective PDE7 inhibitors could be useful in the
treatment of T cell-mediated autoimmune diseases. In the present
report, we have used targeted gene disruption to examine the role PDE7A
plays in T cell activation. In our studies, PDE7A knockout mice
(PDE7A(-/-)) showed no deficiencies in T cell proliferation or Th1- and
Th2-cytokine production driven by CD3 and CD28 costimulation.
Unexpectedly, the Ab response to the T cell-dependent Ag, keyhole
limpet hemocyanin, in the PDE7A(-/-) mice was found to be significantly
elevated. The results from our studies strongly support the notion that
PDE7A is not essential for T cell activation.

PMID: 14662840

TiPs from the psoriasis newsgroup?
http://groups-beta.google.com/group...osphodiesterase

More info in a pdf then you really want?
http://ajplung.physiology.org/cgi/r...sterase%207A%22

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

New Data On Co-Morbidities In Psoriasis Highlight That Skin
Inflammation May Be The Tip Of The Iceberg

http://www.medicalnewstoday.com/med...hp?newsid=53471

Initial research shows that there may be a link between psoriasis and
co-morbid conditions (cardiovascular, liver disease, depression and
obesity). The International Psoriasis Council (IPC) will hold a
collaborative Consensus Meeting, bringing together medical
professionals from across different disease areas, to look at the
inflammatory nature of psoriasis and how it might be linked with
obesity and other co-morbid con