2% of HANs on Psor DECK - STRESS - Indigo Herb - Candida on P40 KO mice -IBD & P40 - Mercola - P60 binds FoxP3 with TREGs being skewed - Selenium -
randall
The chinese HAN's raise their PSOR hands and they've got them thar
psor GENEs...
http://www.ncbi.nlm.nih.gov/pubmed/20875477
Hum Immunol. 2010 Sep 24.
Replication of association between interleukin-23 receptor (IL23R) and
its ligand (IL12B) polymorphisms and psoriasis in the Chinese Han
population.
Wu Y, Lu Z, Chen Y, Xue F, Chen X, Zheng J.
Department of Dermatology, Ruijin Hospital, Jiao Tong University
school of Medicine, Shanghai, China.
Abstract
Psoriasis is an inflammatory skin disease with a multifactorial
genetic basis. A recent whole-genome association (GWA) study
identified several psoriasis predisposing loci including IL12B which
encodes the common p40 subunit of IL-12 and IL-23 and the IL-23
receptor gene (IL23R). To investigate the relationships of these
predisposing polymorphisms with psoriasis in the Chinese Han
population, we genotyped three representative variants, rs6887695,
rs11465817 and rs1343152, in 217 unrelated patients and 288 control
subjects using direct sequencing and we further replicated the
positive polymorphism, rs6887695, in a larger combined sample
including 578 patients and 1422 controls. We found the SNP, rs6887695
[OR=1.33 (95% CI 1.03~1.73), p=0.028] of IL12B to be significantly
associated with psoriasis and a novel halotype A-A of rs11465817-
rs1343152 also showed positive association. Our study confirms the
effects of IL12B and IL23R variants on psoriasis in East Asian
populations and provides a reference point for further investigation
of the role of the IL12/IL23 pathway in chronic epithelial
inflammation in Asian and other ethnic populations.
PMID: 20875477
I suPPose i should study this?
But not right now. :)
-----------------
The genetics of STRESS?
Is this a epigenetical thingy BOB?
http://www.wellnessresources.com/health/articles/early_life_stress_more_detrimental_than_previously_thought/
Early Life Stress More Detrimental than Previously Thought
Thursday, September 30, 2010 - Byron Richards, CCN
Several recent gene studies are demonstrating the life-long impact
that early life stress has while in the womb and early childhood. The
studies are showing that the influence of stress on the developing
baby can turn on inappropriate gene settings that can lead to poor
health, even poor mental health.
In the first study researchers at the University of Copenhagen showed
that stress turned on the wrong genes during fetal development. “We
found that stress-activating factors can control our genes by turning
on certain genes that were supposed to be silenced. It is very
important that some genes are on and others are off in order to ensure
normal foetal development and correct function of our cells later in
life,” says Dr. Klaus Hansen, lead study author.
The researchers pinpointed that methyl groups needed to be attached to
various proteins in order for DNA to have proper gene settings. In
plain English this means that the B vitamins, especially folic acid,
B12, and B6 are needed to ensure an adequate supply of methyl groups
in the face of stress. If a pregnant mother is lacking B vitamins,
and thus methyl groups, it causes a different chemistry reaction and
inappropriate gene settings to establish themselves. While little
stress is best during pregnancy, stress can be offset to some degree
with intake of B vitamins which would appear to be quite protective
for the developing fetus.
Another study from McGill University shows that a lack of a mother’s
caring affection following birth caused the offspring to have DNA that
was altered to that GABA was lacking. GABA is needed to relax the
nerves. An inability to make GABA causes later life insomnia,
anxiety, and in more advanced cases mental illness (such as
schizophrenia). Once again, the lack of love in a critical time
period shortly following birth induces gene-related methylation
problems. This study also supports the idea that a mother needs
adequate nutrition to manage mood during and after pregnancy in a way
that supports positive emotions that in turn fortify the correct
settings for genes.
Setting gene switches, a field of research known as epigenetics, has a
powerful influence on future health as these genes are not easily
reset later in life to a healthy status. While improvements can be
made later on, it takes a lot of work. It is much better to get the
genes set properly in the first place, which places a whole new
emphasis on the need for healthy pregnancy and a stable and loving
environment for both mother and child. The future well being of
everyone depends on it.
This is the new era of mind-body medicine, linking directly to the
emerging field of mind-social medicine.
Related Entries:
<see above link for these>
---------------
Ok, ok so is there a LINK or do the 2% of psor folks get it regardless
or does the stress
increase severity?
Easily discovered with some nice psor mice i'd surmise.
http://www.ncbi.nlm.nih.gov/pubmed/20877306
Nat Rev Rheumatol. 2010 Sep 28.
Psoriasis: what we have learned from mouse models.
Wagner EF, Schonthaler HB, Guinea-Viniegra J, Tschachler E.
Fundación Banco Bilbao Vizcaya Argentaria (F-BBVA)-CNIO Cancer Cell
Biology Program, Centro Nacional de Investigaciones Oncológicas,
Melchor Fernández Almargo 3, 29029 Madrid, Spain.
Abstract
Psoriasis is a common inflammatory skin disease of unknown etiology,
for which there is no cure. This heterogeneous, cutaneous,
inflammatory disorder is clinically characterized by prominent
epidermal hyperplasia and a distinct inflammatory infiltrate.
Crosstalk between immunocytes and keratinocytes, which results in the
production of cytokines, chemokines and growth factors, is thought to
mediate the disease. Given that psoriasis is only observed in humans,
numerous genetic approaches to model the disease in mice have been
undertaken. In this Review, we describe and critically assess the
mouse models and transplantation experiments that have contributed to
the discovery of novel disease-relevant pathways in psoriasis.
Research performed using improved mouse models, combined with studies
employing human cells, xenografts and patient material, will be key to
our understanding of why such distinctive patterns of inflammation
develop in patients with psoriasis. Indeed, a combination of genetic
and immunological investigations will be necessary to develop both
improved drugs for the treatment of psoriasis and novel curative
strategies.
PMID: 20877306
But, but what if the stress makes you Bitter and NOT BETTER?
Easy.....----> use indigo Naturalis<-----?
http://www.ncbi.nlm.nih.gov/pubmed/20877233
Molecules. 2010 Sep 14;15(9):6423-35.
Inhibitory Effect of Indigo Naturalis on Tumor Necrosis Factor-α-
Induced Vascular Cell Adhesion Molecule-1 Expression in Human
Umbilical Vein Endothelial Cells.
Chang HN, Pang JH, Yang SH, Hung CF, Chiang CH, Lin TY, Lin YK.
Department of Traditional Chinese Medicine, Chang Gung Memorial
Hospital, 222 Mai Chin Road, Keelung 204, Taiwan.
lin...@adm.cgmh.org.tw.
Abstract
The use of indigo naturalis to treat psoriasis has proved effective in
our previous clinical studies. The present study was designed to
examine the anti-inflammatory effect of indigo naturalis in primary
cultured human umbilical vein endothelial cells (HUVECs). Pretreatment
of cells with indigo naturalis extract attenuated TNF-α-induced
increase in Jurkat T cell adhesion to HUVECs as well as decreased the
protein and messenger (m)RNA expression levels of vascular cell
adhesion molecule-1 (VCAM-1) on HUVECs. Indigo naturalis extract also
inhibited the protein expression of activator protein-1 (AP-1)/c-Jun,
a critical transcription factor for the activation of VCAM-1 gene
expression. Since the reduction of lymphocyte adhesion to vascular
cells by indigo naturalis extract could subsequently reduce the
inflammatory reactions caused by lymphocyte infiltration in the
epidermal layer and help to improve psoriasis, this study provides a
potential mechanism for the anti-inflammatory therapeutic effect of
indigo naturalis extract in psoriasis.
PMID: 20877233
http://www.ncbi.nlm.nih.gov/pubmed/20387086
Eur J Clin Microbiol Infect Dis. 2010 Aug;29(8):913-6. Epub 2010 Apr
13.
Mutative expression in Candida albicans infection and cytokine
signaling network in gene knockout mice.
He H, Cong Y, Yang H, Dong Y.
Department of Stomatology, Second Affiliated Hospital, School of
Medicine, Zhejiang University, Hangzhou, China.
Abstract
The interactions of Candida species with host cells are crucial for
candidiasis. Recognition and adherence to host constituents are the
keys to initial colonization of mucosal surfaces and the invasion of
host cells. Resistance to mucosal candidiasis is mediated by cell-
mediated immunity. Knowledge about host receptors on immune cells and
the adhesins on the surface of C. albicans are more redundant,
respectively, than about the ligands on the fungal surface and the
structures on the host cells bound by adhesions. Silencing or
disrupting specific genes both in the pathogen and the host are
developing optimistically. The research on IL-12/23 p40 knockout (KO)
mice is sound in providing preliminary array data about the principal
pathways in oral C. albicans infection and clues about the molecular
differences between wild-type (WT) and p40 KO mice of candidiasis in
different sites, thus, hints that certain specific drug targets
accessible to topical agents for the clinical treatment of oral
candidiasis and relevant mucocutaneous precancerous lesions.
PMID: 20387086
92 hits for keywords: candida AND psoria* - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+candida
The most receent with dectin-1 blows it off?
And i thought LOWER?
But, butt is it all coming from the bowel?
http://www.ncbi.nlm.nih.gov/pubmed/19897961
Dig Dis. 2009;27(4):465-9. Epub 2009 Nov 4.
Targeted therapies in inflammatory bowel disease.
Siegmund B.
Charité, Campus Benjamin Franklin, Medizinische Klinik I, Berlin,
Germany. britta....@charite.de
Abstract
The pathogenesis of inflammatory bowel disease (IBD) is still not
completely understood, however the ongoing research of the last decade
is allowing the hypothesis that in genetically predisposed individuals
distinct environmental factors result in a dysregulation of the
mucosal immune system and thus IBD. Until today the majority of
patients are being treated with rather unspecific medications exerting
suppressive effects on the mucosal immune system. Nevertheless, theses
substances including azathioprine and steroids have proven excellent
efficacy for defined subgroups of patients. However, the better
understanding of the underlying pathogenesis resulted in the clinical
development of novel therapeutic strategies with specific targets. The
most prominent example being antibodies targeting tumor necrosis
factor-alpha which are routinely administered in patients suffering
from either Crohn's disease (CD) or ulcerative colitis. A second
strategy is targeting the protein subunit p40 which heterodimerizes
either with p35 resulting in the pro-inflammatory cytokine IL-12 or
with p19 thus forming the pro-inflammatory IL-23. Experimental data
suggest a crucial role for both cytokines in experimental colitis.
Various antibodies against p40 are currently in clinical trials for
patients with CD. In areas of inflammation, the blood vessel
endothelial cells upregulate adhesion molecules resulting in the
infiltration of leukocytes into the respective area. Natalizumab
blocks these adhesion molecules. Treatment with natalizumab was
associated with clinical improvement in patients with CD and has been
approved in the USA. In summary, several therapeutic targets have
already entered our clinical routine and have for some patients
resulted in significant changes of the disease course.
PMID: 19897961
We certainly get that gut feelings don't we?
And the chinese HANs (IL-12 p40 subunits) are helPing out. LOL
85 hits: IL-12 p40 mucosal - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=IL-12+p40+mucosal
Is the GUT key?
Or not?
http://www.ncbi.nlm.nih.gov/pubmed/19737136
Clin Exp Immunol. 2009 Nov;158(2):205-18. Epub 2009 Aug 12.
A novel population of human CD56+ human leucocyte antigen D-related
(HLA-DR+) colonic lamina propria cells is associated with inflammation
in ulcerative colitis.
Ng SC, Plamondon S, Al-Hassi HO, English N, Gellatly N, Kamm MA,
Knight SC, Stagg AJ.
Antigen Presentation Research Group, Faculty of Medicine, Imperial
College London, Northwick Park and St Mark's Campus, Watford Road,
Harrow, UK.
Abstract
Ulcerative colitis (UC) involves inappropriate mucosal immune
responses to intestinal microbiota. Gut dendritic cells (DC) are
central immunoregulators of the response to commensal bacteria, and
the subset of CD11c(+) cells within the human leucocyte antigen D-
related (HLA-DR(+)) lineage (lin)(-/dim) population are activated in
inflammatory bowel disease. We hypothesized that CD11c(-) cells within
this population may also be involved in intestinal inflammation. HLA-
DR(+) lin(-/dim) cells were identified in freshly isolated lamina
propria mononuclear cells by multi-colour flow cytometry in 54 UC
patients and 22 controls. Proportion and number of CD11c(+) and
CD11c(-) cells, and surface expression of activation markers CD40,
CD86, Toll-like receptor (TLR)-2, TLR-4, and CD56(+)[natural killer
(NK) marker], were determined. Cytokine production was assessed by
intracellular staining. Lamina propria colonic CD11c(-) HLA-DR(+)
lin(-/dim) cells were increased significantly in inflamed and 'non-
inflamed' UC tissue, compared with control tissue. CD11c(+) HLA-DR(+)
lin(-/dim) cells were unchanged. Fewer CD11c(-) cells expressed
activation markers and produced intracellular cytokines than their
CD11c(+) counterparts, and they were weakly stimulatory in mixed
leucocyte reactions. Few CD11c(-) cells expressed blood plasmacytoid
DC markers, but a major subset expressed high levels of CD56. CD11c(-)
cells decreased after inflammation resolved. Intestinal inflammation
in UC is associated with the presence of cells that share phenotypic
features of both DC and NK cells. This novel population of human
colonic CD56(+) HLA-DR(+) cells may play a role in immune regulation
or tissue repair. Their increase in quiescent UC may be a marker of
subclinical inflammation.
PMID: 19737136
If psor folks have anything close to CD56+ it might answer a question
or TEN, i've got. LOL
In particular how come it's inside skin (lamina propria for UCi folks
and outer epidermal skin for psor folks?
----------
Just the HAN HLA (B, C or D) genes?
see:
http://www.ncbi.nlm.nih.gov/pubmed/19680446
pmid: 19680446
Hla-dr psoria* - 331 hits
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=Hla-dr+psoria*
So psor is such an HLA gene thing STILL... LOL
-------------------
Mercola says today:
Deadlier than AIDS: Why is This Travesty Allowed to Continue in the
U.S.?
http://articles.mercola.com/sites/articles/archive/2010/09/29/is-this-the-end-of-antibiotics.aspx
and it's in the FOOD we eat.
How can it be deadlier then aids?
Mercola argues with the death statistics actually.
[...] Antibiotic-resistant infections now claim more lives each year
than the "modern plague" of AIDS, and cost the American health care
system some $20 billion a year! According to a study published in
October, 2007 in the Journal of the American Medical Association,
there were close to 100,000 cases of invasive MRSA infections in the
United States in 2005, which lead to more than 18,600 deaths.
Meanwhile, HIV/AIDS killed 17,000 people that same year...
<snip>
Drunks kill more then that iirc on the roads...
------------------
Bigger than Any Transplant Story You’ve Heard Before…
http://articles.mercola.com/sites/articles/archive/2010/09/29/star-trek-medicine-is-here-organs-made-to-order.aspx
Organ printing.
Imagine your printer placing your cells in to positions to grow a new
lung or kidney?
Yep
six part interview:
part one:
http://www.youtube.com/watch?v=GQFNKycCb00&feature=related
part two
http://www.youtube.com/watch?v=DYYm954F50c
Organ Printing with Dr. Gabor Forgacs (Part 3 of 6)
http://www.youtube.com/watch?v=5EUYSRnCHd8
part four
http://www.youtube.com/watch?v=3a-k7j_D9rk&feature=related
part five
http://www.youtube.com/watch?v=X6ZQdGrGEoE&feature=related
part six
http://www.youtube.com/watch?v=e9fItSv27nU&feature=related
---
A device to print body organs
http://www.youtube.com/watch?v=NQ2aEfhti28&feature=related
Another kewl forgacs youtube:
Organ printing with bioink:
http://www.youtube.com/watch?v=80DhBLEhdzk&feature=related
xxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxxx
This looks good.
Do Th1 skewed folks already have this peptide?
Did they find it in my DNA at the psor DNA bank?
I'm serious.
http://www.ncbi.nlm.nih.gov/pubmed/20870946
J Immunol. 2010 Sep 24.
A Peptide Inhibitor of FOXP3 Impairs Regulatory T Cell Activity and
Improves Vaccine Efficacy in Mice.
Casares N, Rudilla F, Arribillaga L, Llopiz D, Riezu-Boj JI, Lozano T,
López-Sagaseta J, Guembe L, Sarobe P, Prieto J, Borrás-Cuesta F,
Lasarte JJ.
Gene Therapy and Hepatology Area.
Abstract
Immunosuppressive activity of regulatory T cells (Treg) may contribute
to the progression of cancer or infectious diseases by preventing the
induction of specific immune responses. Using a phage-displayed random
peptide library, we identified a 15-mer synthetic peptide, P60, able
to bind to forkhead/winged helix transcription factor 3 (FOXP3), a
factor required for development and function of Treg. P60 enters the
cells, inhibits FOXP3 nuclear translocation, and reduces its ability
to suppress the transcription factors NF-κB and NFAT. In vitro, P60
inhibited murine and human-derived Treg and improved effector T cell
stimulation. P60 administration to newborn mice induced a
lymphoproliferative autoimmune syndrome resembling the reported
pathology in scurfy mice lacking functional Foxp3. However, P60 did
not cause toxic effects in adult mice and, when given to BALB/c mice
immunized with the cytotoxic T cell epitope AH1 from CT26 tumor cells,
it induced protection against tumor implantation. Similarly, P60
improved the antiviral efficacy of a recombinant adenovirus expressing
NS3 protein from hepatitis C virus. Functional inhibition of Treg by
the FOXP3-inhibitory peptide P60 constitutes a strategy to enhance
antitumor and antiviral immunotherapies.
PMID: 20870946
Another reason besides avoiding protate cancer?
What?
Eat some foods with selenium:
http://www.desiblitz.com/content/eating-tips-for-healthy-skin
[...] Eating wholegrain foods such as wholemeal bread, Brazil nuts,
walnuts, turkey, chicken, oysters and tuna will give your skin a
Selenium boost.
Rich sources of Selenium skin experts claim is key to healthy skin
cells. High levels of the mineral may even protect the skin from sun
damage, skin inflammation problems and dry skin related problems such
as Eczema and Psoriasis.
Any dietary changes you make will take time to show up in your skin.
Your skin is also a reflection of other lifestyle factors such as lack
of sleep, stress, physical activity levels and air conditioning. An
overall lifestyle change is the best way to make your skin bloom
whilst safeguarding your health.
If you have a persistent skin condition you may need medical attention
so consult your doctor for the best course of action.
<sniP>
Whole body irradiation?
Yep... get it on YOU and make TREGs go UP?
They say so here:
http://www.ncbi.nlm.nih.gov/pubmed/20871628
Cell Mol Immunol. 2010 Sep 27.
2-Gy whole-body irradiation significantly alters the balance of
CD4(+)CD25(- )T effector cells and CD4(+)CD25(+)Foxp3(+ )T regulatory
cells in mice.
Qu Y, Zhang B, Liu S, Zhang A, Wu T, Zhao Y.
Transplantation Biology Research Division, State Key Laboratory of
Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese
Academy of Sciences, Beijing, China.
Abstract
CD4(+)CD25(+) T regulatory (Treg) cells are critical in inducing and
maintaining immunological self-tolerance as well as transplant
tolerance. The effect of low doses of whole-body irradiation (WBI) on
CD4(+)CD25(+)Foxp3(+) Treg cells has not been determined. The
proportion, phenotypes and function of CD4(+)CD25(+) Treg cells were
investigated 0.5, 5 and 15 days after euthymic, thymectomized or
allogeneic bone marrow transplanted C57BL/6 mice received 2-Gy γ-rays
of WBI. The 2-Gy WBI significantly enhanced the ratios of
CD4(+)CD25(+) Treg cells and CD4(+)CD25(+)Foxp3(+) Treg cells to
CD4(+) T cells in peripheral blood, lymph nodes, spleens and thymi of
mice. The CD4(+)CD25(+) Treg cells of the WBI-treated mice showed
immunosuppressive activities on the immune response of CD4(+)CD25(-) T
effector cells to alloantigens or mitogens as efficiently as the
control mice. Furthermore, 2-Gy γ-ray WBI significantly increased the
percentage of CD4(+)CD25(+)Foxp3(+) Treg cells in the periphery of
either thymectomized mice or allogeneic bone marrow transplanted mice.
The in vitro assay showed that ionizing irradiation induced less cell
death in CD4(+)CD25(+)Foxp3(+) Treg cells than in CD4(+)CD25(-) T
cells. Thus, a low dose of WBI could significantly enhance the level
of functional CD4(+)CD25(+)Foxp3(+) Treg cells in the periphery of
naive or immunized mice. The enhanced proportion of
CD4(+)CD25(+)Foxp3(+) Treg cells in the periphery by a low dose of WBI
may make hosts more susceptible to immune tolerance induction.Cellular
& Molecular Immunology advance online publication, 27 September 2010;
doi:10.1038/cmi.2010.45.
PMID: 20871628
============================
randall... moooo over i'm in the clover NOW... LOL