Microbiome and ROS --> Small Intestinal (LMW-PTP and SHP-2) Trick or TREAT? --> NF-kB -- ABSTRACTS --SFB theory<--- By RANDALL - mercola & Byron Richards links
randall
gut stuff -- AGAIN ---> And it's GOOD<---
And certainly refutes GFII's contention that someone in the psoriasis
newsgroup is
a shill for BiG pILL pharma... HA... as if.
If your brain cells are in the ON position, you'll find the exact
opposite in this post.
Sadly, if your eyes glaze over it's due to turned off and tuned out
brain cells, most likely. LoL
COME ON FOLKs and get this stuff and then harbor and protect the good
flora in your GUTs.
I've called this terrain of life in the voltaire quote --> tending to
your OWN garden, before.
randall terrain - 157 hits - P NG
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=terrain+randall&start=0&hl=en&
NINE times i've said it in the P NG: voltaire AND cultivate :
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=voltaire+cultivate&start=0&hl=en&
NOW TEN times:
Voltaire: Candide; "but let us cultivate our garden”
love it...
more voltaire Quotes please?
ok
“Judge a man by his questions rather than by his answers”
“Prejudices are what fools use for reason.”
“The best government is a benevolent tyranny tempered by an
occasional assassination.”
“Each player must accept the cards life deals him or her: but once
they are in hand, he or she alone must decide how to play the cards
in order to win the game.”
------
Wow. that voltaire guy said some kewl things.
Unlike the guy who murders the truth every time he opens his 747 oval
office wanna be
a second term contemptuous pie hole.
LOL
-------------------------------
Which truths did you double TAP today oh MAMA?
hey
hey
segue please?
OK...
I've got a gut fool of this maroon goon.
Yet i could read about candide going viral in 1759 all day long:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=randall+voltaire+candide+viral+1759&start=0&hl=en&
========================
OK---> time for the truth in YOUR garden of paradise which is east of
eden or right under your nostrils.
People these days.... sheesssh...
Even some of the SMART ones are dumber then DIRT...
Yeah, so eat dirt and do the hh theory... <w>
You won't get autism then. LoL
Hey i'll do the hygiene hypothesis by ucsd's dick gallo right after
this salient gut post.
Just so you KNOW what or which card your dealt is MOST imPortant.
=========================================
http://www.eurekalert.org/pub_releases/2011-05/eu-bbh051011.php
Beneficial bacteria help repair intestinal injury by inducing reactive
oxygen species
-------------------
http://shared.web.emory.edu/whsc/news/img/whsc/neish_cell_195.jpg
IMAGE: Intestinal epithelial cells exposed to probiotic bacteria. Red
indicates focal adhesions that help the cells migrate and repair gaps.
-----------------
The gut may need bacteria to provide a little bit of oxidative stress
to stay healthy, new research suggests.
Probiotic bacteria promote healing of the intestinal lining in mice by
inducing the production of reactive oxygen species, researchers at
Emory University School of Medicine have shown.
The results, published online this week in Proceedings of the National
Academy of Sciences Early Edition, demonstrate a mechanism by which
bacterial cultures in foods such as yogurt and kimchi have beneficial
effects on intestinal health. The insights gained could also guide
doctors to improved treatments for intestinal diseases, such as
necrotizing enterocolitis in premature babies or intestinal injury in
critically ill adults.
The laboratories of Andrew Neish, MD and Asma Nusrat, MD, both
professors of pathology and laboratory medicine, teamed up for the
study. The paper's co-first authors are postdoctoral fellow Philip
Swanson, PhD and associate research professor Amrita Kumar, PhD.
"It's been known for years that probiotic bacteria can have these
kinds of helpful effects, but it wasn't really clear how this worked,"
Neish says. "We've identified one example, among many, of how certain
kinds of bacteria have specific biochemical functions in the body."
Recent research has shown that the bacteria in our intestines
influence our metabolism and immune systems. For example, an imbalance
in the proportions of harmful and beneficial bacteria seems to over-
activate immune cells in the intestines, driving inflammatory bowel
disease.
Intestinal epithelial cells, the cells that line the intestine, live
in close contact with bacteria and normally form a barrier that keeps
bacteria away from other organs. They can repair small gaps in the
barrier, which breaks down in intestinal diseases, by migrating into
the gaps.
The researchers showed that Lactobacillus rhamnosus bacteria can
accelerate this healing process, both in culture dishes and in mice
with intestines damaged by chemicals. Lactobacillus rhamnosus, a
species of bacteria found naturally in human intestines and often used
as a probiotic, is a relative of other kinds of Lactobacillus bacteria
found in fermented foods.
"Unlike most cell types that can not tolerate bacterial contact,
intestinal epithelial cells respond to Lactobacillus rhamnosus by
increasing their motility," Neish says.
Using a fluorescent dye that is sensitive to reactive oxygen species
(ROS), the researchers showed that intestinal epithelial cells produce
ROS internally when in contact with Lactobacillus rhamnosus. The ROS
induced by the bacteria stimulate the formation of focal adhesions,
structures on intestinal epithelial cells that act as anchors for
their movement.
"Focal adhesions are where cells attach to the matrix that surrounds
them," Neish says. "The cells lay them down on one side and remove
them on the other side, like the tracks of a bulldozer."
In studying the effect of Lactobacillus rhamnosus on intestines in
mice, Neish's team focused on the small intestine, which normally has
fewer bacteria than the colon. This allowed them to avoid using
antibiotics to remove naturally existing bacteria beforehand, and to
see ROS production in tissue from live animals.
Antioxidants that mop up ROS prevent the bacteria from promoting wound
healing in the laboratory, the researchers showed. Neish says his
team's finding suggests that large amounts of antioxidants by humans
could interfere with the ability of bacteria to promote intestinal
healing.
Previously, it was known that immune cells respond to bacteria by
producing ROS, but Neish and his colleagues believe the ROS production
they observed stimulates tissue maintenance and is a marker of
cohabitation and adaptation, rather than defense.
Oxidative stress, or an imbalance of reactive oxygen species
throughout the body, has been linked to diseases such as heart disease
and stroke. However, scientists have learned in recent years that
cells can also use reactive oxygen species in a controlled, local way
to send signals needed for normal functions.
Neish says his team is working to determine which part of the bacteria
is responsible for inducing cells to produce ROS. Once identified,
this component could be used to encourage intestinal healing in
situations where contact with large amounts of live bacteria might be
dangerous, such as in premature babies or critically ill adults.
###
The research was supported by the National Institutes of Health.
Reference:
P.A. Swanson II et al. Enteric commensal bacteria potentiate
epithelial restitution via reactive oxygen species-mediated
inactivation of focal adhesion kinase phosphatases. PNAS Early Edition
(2011).
<snip>
OK we do our work on Lactobacillus rhamnosus first. Since i've been
all over Lactobacillus PLANTARUM recently it will be nice to spend
time with another Lactobacilli.
And we can't leave this T3SS (Type three secretion system) unTOUCHED
either:
http://en.wikipedia.org/wiki/Type_three_secretion_system
Type three secretion system (often written Type III secretion system
and abbreviated TTSS or T3SS) is a protein appendage found in several
Gram-negative bacteria.
In pathogenic bacteria, the needle-like structure is used as a sensory
probe to detect the presence of eukaryotic organisms and secrete
proteins that help the bacteria infect them. The proteins are secreted
directly from the bacterial cell into the eukaryotic cell, also known
as "the host" cell.
wow.. you can really see it:
http://upload.wikimedia.org/wikipedia/commons/0/05/TEM_of_isolated_T3SS_needle_complexes.jpg
http://en.wikipedia.org/wiki/File:T3SS_needle_complex.svg
http://upload.wikimedia.org/wikipedia/commons/2/2a/Basal_body_of_T3SS_needle_complex.jpg
WOW a lot of stuff in this t3ss wiki page that may pertain to
psoriatics.
One might be calcium ions (or calmodulin) and t3ss.
And certainly it indicts LPS (endogenous endotoxins) and t3ss as they
go hand in gland with gram negative bacteria:
http://en.wikipedia.org/wiki/Gram-negative
<randall note: i don't know if it indicts but does bite as there are
five hits for gram-negative on the t3ss wiki page>
467 hits on pubmed: t3ss
http://www.ncbi.nlm.nih.gov/pubmed?term=T3SS
Anyway let's move on to the authors:
-----------------
So---> Andrew Neish has 68 hits -pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Neish%20AS%22%5BAuthor%5D
OOp'S he's got 70 now.. GOOD thing i waited one more DAY to bring you
this...:)
The new #1 is here: (but no meat in this taco:( ]
http://www.ncbi.nlm.nih.gov/pubmed/21555952
J Clin Gastroenterol. 2011 May 6.
The Microbiota and Colonic Neoplasia: An Emerging Link?
Neish AS.
Source
Department of Pathology, Emory University School of Medicine, Atlanta,
GA.
PMID: 21555952
WOW, colonic neoplasia has some hits in pubmed:
86,061 - keywords: colonic neoplasia - pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=colonic%20neoplasia
#2 in that list is Neish's pmid 21555952 right above.
If we add autoimmun* as the kicker to the above search, we get
204 hits for : colonic neoplasia AND autoimmun* - pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=colonic%20neoplasia%20autoimmun*
#1 tells the tale:
it's genius as the SCIENTISTs are right on top of curing cancer with
gut flora:
<randall note: this negates any and all comments that randall is a
pharma shill... eat that pill GFII.. LOL>
http://www.ncbi.nlm.nih.gov/pubmed/21278760
Cell Mol Immunol. 2011 Mar;8(2):110-20. Epub 2011 Jan 31.
The role of gut microbiota (commensal bacteria) and the mucosal
barrier in the pathogenesis of inflammatory and autoimmune diseases
and cancer: contribution of germ-free and gnotobiotic animal models of
human diseases.
Tlaskalová-Hogenová H, Stěpánková R, Kozáková H, Hudcovic T, Vannucci
L, Tučková L, Rossmann P, Hrnčíř T, Kverka M, Zákostelská Z, Klimešová
K, Přibylová J, Bártová J, Sanchez D, Fundová P, Borovská D, Srůtková
D, Zídek Z, Schwarzer M, Drastich P, Funda DP.
Source
Institute of Microbiology, Academy of Sciences of the Czech Republic,
v.v.i., Prague, Czech Republic. tlas...@biomed.cas.cz
Abstract
Metagenomic approaches are currently being used to decipher the genome
of the microbiota (microbiome), and, in parallel, functional studies
are being performed to analyze the effects of the microbiota on the
host. Gnotobiological methods are an indispensable tool for studying
the consequences of bacterial colonization. Animals used as models of
human diseases can be maintained in sterile conditions (isolators used
for germ-free rearing) and specifically colonized with defined
microbes (including non-cultivable commensal bacteria). The effects of
the germ-free state or the effects of colonization on disease
initiation and maintenance can be observed in these models. Using this
approach we demonstrated direct involvement of components of the
microbiota in chronic intestinal inflammation and development of
colonic neoplasia (i.e., using models of human inflammatory bowel
disease and colorectal carcinoma). In contrast, a protective effect of
microbiota colonization was demonstrated for the development of
autoimmune diabetes in non-obese diabetic (NOD) mice. Interestingly,
the development of atherosclerosis in germ-free apolipoprotein E
(ApoE)-deficient mice fed by a standard low-cholesterol diet is
accelerated compared with conventionally reared animals. Mucosal
induction of tolerance to allergen Bet v1 was not influenced by the
presence or absence of microbiota. Identification of components of the
microbiota and elucidation of the molecular mechanisms of their action
in inducing pathological changes or exerting beneficial, disease-
protective activities could aid in our ability to influence the
composition of the microbiota and to find bacterial strains and
components (e.g., probiotics and prebiotics) whose administration may
aid in disease prevention and treatment.
PMID: 21278760
#3 is also saying cancer is due to high TREGs (Th2 skew) fixable with
gut flora. Duh..
I've only said this for a decade now. LoL
http://www.ncbi.nlm.nih.gov/pubmed/20924111
Conditional regulatory T-cell depletion releases adaptive immunity
preventing carcinogenesis and suppressing established tumor growth.
[...] pmid: 20924111
===================================
**************************this is it for *****************
OK this is the **ONE** that goes with the above eurekalert i'm SURE
this TIME. (<w><G>)
http://www.ncbi.nlm.nih.gov/pubmed/21555563
Proc Natl Acad Sci U S A. 2011 May 9.
Enteric commensal bacteria potentiate epithelial restitution via
reactive oxygen species-mediated inactivation of focal adhesion kinase
phosphatases.
Swanson PA 2nd, Kumar A, Samarin S, Vijay-Kumar M, Kundu K, Murthy N,
Hansen J, Nusrat A, Neish AS.
Source
Departments of Pathology and Pediatrics, Emory University School of
Medicine, Atlanta, GA 30322.
Abstract
The mechanisms by which enteric commensal microbiota influence
maturation and repair of the epithelial barrier are relatively
unknown. Epithelial restitution requires active cell migration, a
process dependent on dynamic turnover of focal cell-matrix adhesions
(FAs). Here, we demonstrate that natural, commensal bacteria stimulate
generation of reactive oxygen species (ROS) in intestinal epithelia.
Bacteria-mediated ROS generation induces oxidation of target cysteines
in the redox-sensitive tyrosine phosphatases, LMW-PTP and SHP-2, which
in turn results in increased phosphorylation of focal adhesion kinase
(FAK), a key protein regulating the turnover of FAs. Accordingly,
phosphorylation of FAK substrate proteins, focal adhesion formation,
and cell migration are all significantly enhanced by bacterial contact
in both in vitro and in vivo models of wound closure. These results
suggest that commensal bacteria regulate cell migration via induced
generation of ROS in epithelial cells.
PMID: 21555563
ok & more gut stuff from neish recently:
http://www.ncbi.nlm.nih.gov/pubmed/21352463
Cell Microbiol. 2011 May;13(5):670-6. doi: 10.1111/j.
1462-5822.2011.01579.x. Epub 2011 Feb 24.
Recognition of bacterial pathogens and mucosal immunity.
Jones RM, Neish AS.
Source
Epithelial Pathobiology Unit, Department of Pathology and Laboratory
Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Abstract
Rapid detection and elimination of pathogens invasive to intestinal
tissue is essential to avoid prolonged gut inflammation, or systemic
sepsis. The discovery of transmembrane or intracytoplasmic pattern
recognition receptors that detect the presence of conserved microbial
macromolecular structures has significantly advanced the understanding
of how metazoans respond to and eliminate bacteria that have entered
the intestinal mucosa. In this review, we highlight recent advances in
the field of host recognition of bacterial pathogens and subsequent
mucosal innate immune response. Additionally, some bacteria are
pathogenic because they have evolved sophisticated mechanisms to evade
the host mucosal innate immune response. We discuss advances in
identifying the mechanisms by which pathogens evade detection by
dampening the immune response.
PMID: 21352463
This next ONE is gut related as well:
http://www.ncbi.nlm.nih.gov/pubmed/20838961
Curr Top Microbiol Immunol. 2011;349:145-58.
NF-κB and Mucosal Homeostasis.
Eckmann L, Neish AS.
Source
Department of Medicine, University of California, 9500 Gilman Drive,
La Jolla, San Diego, CA, 92093-0063, USA, leck...@ucsd.edu.
Abstract
NF-κB is well characterized as a primary mediator of inflammatory
responses during infection and immune reactions, but it has recently
become evident that NF-κB also mediates a potent cytoprotective,
homeostatic function under basal conditions. This role is especially
evident in the mammalian intestine, which is challenged not only with
a range of microbial pathogens, but is also in constant contact with
potent proinflammatory commensal bacteria and their products. Present
data lead to the overall conclusion that antiapoptotic actions of NF-
κB in intestinal epithelial cells dominate tissue responses to many
acute inflammatory and injurious challenges, whereas proinflammatory
and cell survival functions of NF-κB in macrophages and T cells govern
chronic intestinal inflammation. This review focuses on the protective
and homeostatic functions of NF-κB, and the importance of NF-κB in
determining host-microbe interactions in the intestinal tract.
PMID: 20838961
Nusrat also has GUT stuff, i'm proud of him, and his 111 hits -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Nusrat%20A%22%5BAuthor%5D
http://www.ncbi.nlm.nih.gov/pubmed/21440550
Gastroenterology. 2011 Mar 24.
The Wnt Antagonist Dkk1 Regulates Intestinal Epithelial Homeostasis
and Wound Repair.
Koch S, Nava P, Addis C, Kim W, Denning TL, Li L, Parkos CA, Nusrat A.
Source
Epithelial Pathobiology Unit, Department of Pathology and Laboratory
Medicine, Emory University, Atlanta, GA.
Abstract
BACKGROUND & AIMS: Dkk1 is a secreted antagonist of the Wnt-β-catenin
signaling pathway. It is induced by inflammatory cytokines during
colitis and exacerbates tissue damage by promoting apoptosis of
epithelial cells. However, little is known about the physiological
role of Dkk1 in normal intestinal homeostasis and during wound repair
following mucosal injury. We investigated whether inhibition of Dkk1
affects the morphology and function of the adult intestine.
METHODS: We used doubleridge mice (Dkk1(d/d)), which have reduced
expression of Dkk1, and an inhibitory Dkk1 antibody to modulate Wnt-β-
catenin signaling in the intestine. Intestinal inflammation was
induced with dextran sulfate sodium (DSS), followed by a recovery
period in which mice were given regular drinking water. Animals were
sacrificed before, during, or after DSS administration; epithelial
homeostasis and the activity of major signaling pathways were
investigated by morphometric analysis, bromo-2'-deoxyuridine
incorporation, and immunostaining.
RESULTS: Reduced expression of Dkk1 increased proliferation of
epithelial cells and lengthened crypts in the large intestine, which
was associated with increased transcriptional activity of β-catenin.
Crypt extension was particularly striking when Dkk1 was inhibited
during acute colitis. Dkk1(d/d) mice recovered significantly faster
from intestinal inflammation, but exhibited crypt architectural
irregularities and epithelial hyper-proliferation, compared with wild-
type mice. Survival signaling pathways were concurrently upregulated
in Dkk1(d/d) mice, including the AKT-β-catenin, ERK-Elk-1, and c-Jun
pathways.
CONCLUSIONS: Dkk1, an antagonist of Wnt-β-catenin signaling, regulates
intestinal epithelial homeostasis under physiological conditions and
during inflammation. Depletion of Dkk1 induces a strong proliferative
response that promotes wound repair after colitis.
PMID: 21440550
http://www.ncbi.nlm.nih.gov/pubmed/21411630
Mol Biol Cell. 2011 Apr 1.
Tight Junction Zonula Occludens-3 regulates Cyclin D1 dependent cell
proliferation.
Capaldo CT, Koch S, Kwon M, Laur O, Parkos CA, Nusrat A.
Source
Epithelial Pathobiology Research Unit, Dept. of Pathology, Emory
University, Atlanta, GA, 30322 Yerkes-Microbiology Emory University
Atlanta, Ga, 30329.
Abstract
Coordinated regulation of cell proliferation is vital for epithelial
tissue homeostasis, and uncontrolled proliferation is a hallmark of
carcinogenesis. A growing body of evidence indicates that epithelial
Tight Junctions (TJs) play a role in these processes, although the
mechanisms involved are poorly understood. In this study, we identify
and characterize a novel plasma membrane pool of cyclin D1 with cell
cycle regulatory functions. We have determined that the Zonula
Occludens (ZO) family of TJ plaque proteins sequester cyclin D1 at TJs
during mitosis, through an evolutionarily conserved class II PSD-95/
Dlg/ ZO-1 (PDZ)-binding motif within cyclin D1. Disruption of the
cyclin D1/ZO complex through mutagenesis or siRNA-mediated suppression
of ZO-3, resulted in increased cyclin D1 proteolysis and G(0)/G(1)
cell cycle retention. This study highlights an important new role for
ZO family TJ proteins in regulating epithelial cell proliferation
through stabilization of cyclin D1 during mitosis.
PMID: 21411630
Free Article (use above link to have this for FREE:)
-----------------
OK i just noticed this one.... if they did it again and noticed the
effects of SFB it would
be more then NICE, it would be the sPice for nailing autoimunity once
and for ALL.
And this was Oct. 15 of 2010 no less...
How come i didn't see it sooner?
I'm clueless?.. i could have been on top of these guys a lot sooner
and their cooking and by that i mean their doing xlnt work.
http://www.ncbi.nlm.nih.gov/pubmed/21091507
Mol Microbiol. 2010 Dec;78(5):1232-45. doi: 10.1111/j.
1365-2958.2010.07400.x. Epub 2010 Oct 15.
Enteropathogenic E. coli non-LEE encoded effectors NleH1 and NleH2
attenuate NF-κB activation.
Royan SV, Jones RM, Koutsouris A, Roxas JL, Falzari K, Weflen AW, Kim
A, Bellmeyer A, Turner JR, ___Neish AS___, Rhee KJ, Viswanathan VK,
Hecht GA.
Source
Department of Medicine, Section of Digestive Diseases and Nutrition,
University of Illinois at Chicago, Chicago, IL 60612, USA.
Abstract
Enteric bacterial pathogens have evolved sophisticated strategies to
evade host immune defences. Some pathogens deliver anti-inflammatory
effector molecules into the host cell cytoplasm via a type III
secretion system (T3SS). Enteropathogenic Escherichia coli (EPEC)
inhibits inflammation by an undefined, T3SS-dependent mechanism. Two
proteins encoded outside of the EPEC locus of enterocyte effacement
(LEE) pathogenicity island, non-LEE-encoded effector H1 (NleH1) and H2
(NleH2), display sequence similarity to Shigella flexneri OspG, which
inhibits activation of the pro-inflammatory transcription factor NF-
κB. We hypothesized that the anti-inflammatory effects of EPEC were
mediated by NleH1 and NleH2. In this study, we examined the effect of
NleH1/H2 on the NF-κB pathway. We show that NleH1/H2 are secreted via
the T3SS and that transfection of cells with plasmids harbouring nleH1
or nleH2 decreased IKK-β-induced NF-κB activity and attenuated TNF-α-
induced degradation of phospho-IκBα by preventing ubiquitination.
Serum KC levels were higher in mice infected with ΔnleH1H2 than those
infected with WT EPEC, indicating that NleH1/H2 dampen pro-
inflammatory cytokine expression. ΔnleH1H2 was cleared more rapidly
than WT EPEC while complementation of ΔnleH1H2 with either NleH1 or
NleH2 prolonged colonization. Together, these data show that NleH1 and
NleH2 function to dampen host inflammation and facilitate EPEC
colonization during pathogenesis.
PMID: 21091507
i'd like to say i'm over WOW'ed by nusrat and neish RIGHT NOW..
Bravo... your almost as KEY as kenya honda and dan littman (SFB
inducts Th17 in the small intestines).
=============================================
OK so what about getting cancer of the colon or intestines?
BIG PHARMA ALeRT... randall speaks... is he shilling now?
http://www.ncbi.nlm.nih.gov/pubmed/21553077
Cancer Causes Control. 2011 May 7.
Association between psoriasis and incident cancer: the Iowa's Women's
Health Study.
Prizment AE, Alonso A, Folsom AR, Ahmed RL, Virnig BA, Warshaw EM,
Anderson KE.
Source
Division of Epidemiology and Community Health, University of
Minnesota, 1300 2nd Street South, Suite 300, Minneapolis, MN, 55455,
USA, priz...@umn.edu.
Abstract
INTRODUCTION: Studies have reported higher cancer risk in individuals
with psoriasis, a chronic inflammatory autoimmune disease; however,
adjustment for potential confounders was lacking.
METHODS: We examined the association of psoriasis with cancer
incidence in 32,910 women after age 65 in the IWHS cohort linked to
Medicare. Psoriasis was defined as: 2+ psoriasis claims from any
Medicare file during 1991-2004 or 1+ psoriasis claim from a
dermatologist (n = 719). Severe psoriasis was defined as 4+ psoriasis
claims from a dermatologist in any year (n = 121). Cox proportional
hazards regression, with psoriasis as a time-dependent variable was
conducted to calculate hazard ratios (HR) and 95% confidence intervals
(CI) of total (n = 6,488), breast (n = 2,066), lung (n = 742), and
colon cancers (n = 947).
RESULTS: With age-adjustment, psoriasis (yes vs. no) was associated
with increased risk of lung 1.9 (95% CI: 1.2-3.0), colon 1.6 (95% CI:
1.1-2.5), and total cancer 1.2 (95% CI, 1.0-1.4). After further
adjustment for smoking, body mass index, education, physical activity,
and hormone therapy use, only the association for colon cancer
remained statistically significant (HR = 1.6, 95% CI: 1.0-2.4) and was
stronger for severe psoriasis.
CONCLUSION: The observed association between psoriasis and colon
cancer may reflect inflammatory or unidentified processes.
PMID: 21553077
MAYBE if you treat an autoimmune disease, that meay be compensatory
for detoxification pathways, topically you drive the condition back
where it starts, the colon and that is the CAUSE of this cancer?
I raised this with a doctor (Krueger) with the NPF many moons ago and
asked him if he saw a colon cancer increase to which he said, if there
was he didn't know as the patients went to the next specialist or
something sorta to that effect iirc.
IOWs treatment may drive the toxins (for godfather that would be
antigenic dairy products) back in to your colon and without flaking
your skin to burn off the DAIRY products [LoL] your screwed.
Etiology can be more then an itch, it can be a bi itch. duh
WILL the godfather call me a shill for pharma with this answer?
Yes, as his eyes are so OLD they glaze over to quickly LOL
Don't worry randall... i'm sure he's gone again. <w>
==========================
http://www.ncbi.nlm.nih.gov/pubmed/21551409
Invest Ophthalmol Vis Sci. 2011 May 6.
Expression and regulation of antimicrobial peptide psoriasin (S100A7)
at the ocular surface and in the lacrimal apparatus.
Garreis F, Gottschalt M, Schlorf T, Gläser R, Harder J, Worlitzsch D,
Paulsen FP.
Source
Department of Anatomy II, Friedrich Alexander University Erlangen-
Nuremberg, Erlangen, Germany.
Abstract
Purpose. Psoriasin, originally isolated as an overexpressed molecule
of unknown function from psoriasis, has recently been identified as a
principal Escherichia coli-killing antimicrobial peptide of healthy
skin. The aim of this study was to investigate the expression and
antimicrobial role of psoriasin at the ocular surface and in the
lacrimal apparatus. Methods. Different tissues of the lacrimal
apparatus and ocular surface were systematically analyzed by means of
RT-PCR, Western blot and immunohistochemistry for their ability to
express and produce psoriasin. Inducibility and regulation of
psoriasin were studied in human corneal as well as conjunctival
epithelial cell lines after challenge with frequent ocular pathogens
and proinflammatory cytokines. Real-time RT-PCR were performed to
evaluate the expression and induction of psoriasin. Additionally, we
examined tear fluid obtained from different healthy volunteers for its
psoriasin concentration by ELISA. Results. RT-PCR and Western blot
analyses revealed a constitutive expression of psoriasin in cornea,
conjunctiva, nasolacrimal ducts and lacrimal gland.
Immunohistochemistry showed strong staining of Meibomian glands for
psoriasin. No induction of psoriasin was observed after stimulation
with supernatants of E. coli whereas supernatants of Staphylococcus
aureus and Haemophilus influenzae significantly increased the
psoriasin mRNA expression. Stimulation with IL-1β and VEGF also
strongly increased the psoriasin transcription. Highest amounts of
psoriasin protein were detected in tear fluid (∼170 ng/ml) of healthy
volunteers. Conclusions. Our results suggest that psoriasin is
produced by the structures of the ocular surface and is part of the
innate immune system at the ocular surface and tear film.
PMID: 21551409
I'd like to know if they ran D3 and LL27 levels in this trial. Just a
thought that might be key.
===========================
http://www.ncbi.nlm.nih.gov/pubmed/21550282
Joint Bone Spine. 2011 May 5
HLA-DR17 is associated with enthesitis in psoriatic arthritis.
[...] PMID: 21550282
ONLY 40 total hits for HLA-DR17 - pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=hla-dr17
===========================
OK, ok i know this next one is a fish study which makes my guess fishy
at best.
But these FISH have SFB in their gut tracts and we KNOW via Littman/
Honda et al that SFB inducts Th17 cells.
So maybe it's NOT so FISHY as one may jumP to conclusions before
thinking correctly.
http://www.ncbi.nlm.nih.gov/pubmed/21488908
J Fish Dis. 2011 Jun;34(6):433-43. doi: 10.1111/j.
1365-2761.2011.01254.x. Epub 2011 Apr 13.
Mucosal CD3ε+ cell proliferation and gut epithelial apoptosis:
implications in rainbow trout gastroenteritis (RTGE).
Ronza P, Bermúdez R, Losada AP, Robles A, Quiroga MI.
SourceDepartamento de Ciencias Clínicas Veterinaria, Facultad de
Veterinaria, Universidad de Santiago de Compostela, Lugo, Spain
Departamento de Anatomía y Producción Animal, Facultad de Veterinaria,
Universidad de Santiago de Compostela, Lugo, Spain División de
acuicultura, Isidro de la Cal s.l., Cambre, A Coruña, Spain.
Abstract
Rainbow trout gastroenteritis (RTGE) is an emerging disease that has
acquired new relevance in European rainbow trout, Oncorhynchus mykiss
(Walbaum), culture, because of the economic losses it causes. Disease
aetiology and pathogenesis remain unclear. The lesions appear
restricted to the gastrointestinal tract where extensive mucosal
detachment associated with high numbers of segmented filamentous
bacteria (SFB) can be detected. In this study, an RTGE outbreak in
north-western Spain was investigated, and findings observed in
diseased trout were compared with control fish. PAS stain and
immunohistochemical assays with anti-CD3ε and anti-active caspase-3
antibodies were performed. The results showed that CD3ε+ inflammatory
infiltrates were present in the intestine of diseased trout both in
the lamina propria-submucosa and within the epithelium. Moreover, an
increased number of caspase-3+ cells in the intestinal mucosa and also
strong anti-caspase-3 immunoreactivity in desquamated cells in the gut
lumen were observed. Changes in the number of goblet cells were also
found, resulting in an increase or depletion of mucous cells depending
on the severity of the intestinal lesions. These findings suggest that
T cells and apoptosis play an important role in the development and
pathogenesis of RTGE.
PMID: 21488908
OK my BIG fishy GUESS now. What if we're like these trout and less
mucous cells increase the leaky gut (permeable or translocation of
endogenous endotoxins or zonulin with loose junctions etc) and this is
the cause of the SKEW towards Th1 via SFB induction of Th17 cells in
the lamina propria?
I'm only GUESSing our guts are like these rainbow trouts NOW, just
another unEDUCATED GUESS.
But, but, what if i'm entirely CORRECT?
What then?
Big pharma takes a DUMP on ALL their billion dollar mAbs they spent
millions on, to survive to see daylight after the rectal FDA
examinations.
So tell us randall, why would big pharma take this potty [dump if you
will] trip if SFB is punching holes in your small intestine lamina
propria regions?
EASY we now have etiological reason for why most autoimmune diseases
exist.
If your Th1 skew is preventing treg's from turning off autoimmunity
then bingo is the gut holes and their easily treated with L. plantarum
for instance.
Which is cheap..
So godfather once again is either unable to form correct conclusions
or gaming me to understand TRUTH, perhaPs? LoL
================
http://www.ncbi.nlm.nih.gov/pubmed/21545794
Dev Biol. 2011 Apr 28.
Hedgehog signaling controls homeostasis of adult intestinal smooth
muscle.
<snip>
Hh and lamina propria and Ai time?
Hh and autoimmun* - 13 hits - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=hedgehog%20autoimmun*
OK so Hh is hedgehog and hh is hygiene hypothesis?
OK... don't forget to post the hh next.
huh? DUH... OK.. LoL
===================
by VRP Staff
There’s no question about the benefits of a healthy weight. Being
overweight negatively impacts just about every possible aspect of your
body’s functions—which is why so many Americans are currently
struggling to shed a few (or more than a few) pounds.1 But what you
may not know is that melting off that fat comes with its own set of
concerns… and they might pose a far bigger worry to your health than
you think.
That’s because adipose tissue is a common hiding place of so-called
“xenobiotics”—chemical compounds such as pesticides, industrial
compounds, cosmetic additives, hormones and drugs, which creep into
your body from environmental exposure and can hang around for decades
in your fat cells.2-4 What’s worse, research shows that fat loss can
unleash these xenobiotics into your system—resulting in levels of
these chemicals that can put a burden on the body’s normal
detoxification processes.5
One study showed that serum chemical levels were higher in adults
undertaking long-term weight management when compared to those
experiencing long-term weight gain.5 Another showed that older men who
lost fat mass were more likely to experience a higher level of health
risks—a link that may be due to the increasing detoxification
difficulties that arise with age.6-7 And even more research has linked
stored environmental chemicals in the body to blood sugar imbalances…
not to mention waning energy, inflammatory imbalances, cognitive
concerns and suboptimal mood.8-13
A good look at the data is probably enough to scare you off of your
weight loss efforts for good. But luckily, you can effectively balance
the potential impacts of long-term fat loss by nurturing your body’s
own detoxification systems—allowing you to achieve your healthiest
weight without taking on unwanted chemical levels in the process.
In order for your body to successfully eliminate xenobiotics, your
liver must first convert these fat-soluble chemicals into water-
soluble compounds that can be easily excreted through fecal
elimination with the activity of bile or through the urine. This
requires two phases of metabolism: Phase 1, which converts the
chemical into a more water-soluble, but also more reactive form to
prime it for removal—and Phase 2, in which the newly reactive
substance is “conjugated” with a neutralizing substance to facilitate
its safe excretion from your body.14-16
Both phases of detox are essential—but adequate Phase 2 support is
especially critical if you’re faced with higher levels of unwanted
chemicals. And that’s precisely when targeted supplements can come to
the rescue.
Glycine, taurine, and glutamine, for example, are all Phase 2
conjugating agents—while methylsulfonylmethane (MSM) and betaine
perform a similar role by acting as methyl donors.16,17-19 These
nutrients support your body’s methylation and amino acid conjugation
pathways, while calcium D-glucarate promotes the Phase 2
glucuronidation pathway, in which glucuronic acid joins with chemicals
to help usher them out of your body.20-21
The glutathione conjugation pathway is equally important, as
glutathione is one of the most powerful natural weapons you have
against xenobiotics—unfortunately, your stores of this crucial
antioxidant are also easily depleted. The good news is that you can
enhance your body’s glutathione synthesis with a number of natural
compounds, including n-acetyl L-cysteine (NAC), R-lipoic acid and milk
thistle (silymarin).22-29
Each of the nutrients above can help to strengthen your body’s natural
defense against the chemical challenges that accompany a shrinking
waistline—which is why you’ll find them combined in the formulas Detox
365 and HepatoGen™, available from Vitamin Research Products®.
Finally, don’t forget to fill up on fiber, which will keep you regular
and help to ensure that the chemical metabolites dumped into your
intestines aren’t reabsorbed right back into your body. A hydrolyzed
guar gum fiber supplement—such as VRP’s EZ Fiber™—offers the added
benefit of supporting intestinal microflora balance, for optimal bowel
health and complete detox support you can count on.30
References:
<snip>
====================
mercola - n3, w3 or omega-3
http://articles.mercola.com/sites/articles/archive/2011/05/10/omega3-fats-shown-to-decrease-risk-of-dying-from-inflammatory-diseases.aspx
American Journal of Clinical Nutrition May 2011; 93(5): 1073-1079
http://www.ajcn.org/content/93/5/1073.abstract?etoc
----------
mercola The 7 Tricks Restaurants Play to Separate You From Your Money
http://articles.mercola.com/sites/articles/archive/2011/05/10/7-ways-restaurant-menus-trick-you-to-spend-more.aspx
=======================
http://www.wellnessresources.com/weight/articles/nobiletin_and_tangeretin_prevent_insulin_resistance_by_improving_fat_fitnes/
Nobiletin and Tangeretin Prevent Insulin Resistance by Improving Fat
Fitness
Sunday, May 08, 2011
Nobiletin Type of citrus bioflavonoid shown to have anti-inflammatory,
anti-oxidant, and blood sugar support properties. and Tangeretin
Special type of citrus bioflavonoid shown to reduce the risk for
certin cancers, protecting nerve cells, and involved with healthy
cholesterol function. are citrus-derived polymethoxyflavonoids,
uniquely structured Flavonoids Plant compound that is associated with
pigmentation. Flavonoids have been shown to modify allergens, viruses,
inflammation, and various carcinogens. Found in green tea, citrus,
berries, onions, parsley, red wine, dark chocolate, and others. that
are now shown to directly interact with white adipose tissue in a way
that makes your stored fat much healthier, including the prevention of
insulin resistance.
The fat cells that are in your white adipose tissue are in a continual
state of turnover, meaning that new ones are formed and old ones die
off. In an overweight person the new ones are rapidly filled with fat
(triglycerides) and quickly become unfit – making it difficult to lose
weight and easy to gain weight. In fact, in order to have stable
weight loss over time, it is necessary to have a new supply of fat
cells that are more metabolically fit. Part of this is not eating too
much once you have lost some weight. Cramming your fat cells full is a
fast track to getting nowhere fast.
A new study with fat cells shows that Nobiletin Type of citrus
bioflavonoid shown to have anti-inflammatory, anti-oxidant, and blood
sugar support properties. and Tangeretin Special type of citrus
bioflavonoid shown to reduce the risk for certin cancers, protecting
nerve cells, and involved with healthy cholesterol function.1 have a
profound impact on how fat cells develop. The study showed that as
baby fat cells matured under the influence of these nutrients, they
had less fat in them. Furthermore, the level of Adiponectin Protein
hormone that modulates metabolism including glucose and fatty acid
catabolism. High levels are associated with low body fat., which
prevents insulin resistance, was boosted and the level of another fat
cell hormone, resistin, which causes insulin resistance, was
decreased. Nobiletin Type of citrus bioflavonoid shown to have anti-
inflammatory, anti-oxidant, and blood sugar support properties. even
helped kill off some of the older and more unfit fat cells.
This study is significant because the fitness of your fat is key to
managing your body weight and maintaining your cardiovascular health –
not to mention preventing type 2 diabetes. An earlier study also
showed that these nutrients helped insulin resistance2 by decreasing
inflammation coming from fat cells. Collectively, these studies show
that Nobiletin Type of citrus bioflavonoid shown to have anti-
inflammatory, anti-oxidant, and blood sugar support properties. and
Tangeretin Special type of citrus bioflavonoid shown to reduce the
risk for certin cancers, protecting nerve cells, and involved with
healthy cholesterol function. are novel nutrients that support healthy
metabolism by helping to improve the fitness of your fat.
<snip>
Nobiletin Helps Prevent Fatty Liver, High Cholesterol, Weight Gain,
and Insulin Resistance
Monday, May 09, 2011 - Byron Richards,
A new study with mice1 that are programmed to rapidly develop insulin
resistance, fatty liver, and atherosclerosis found that Nobiletin Type
of citrus bioflavonoid shown to have anti-inflammatory, anti-oxidant,
and blood sugar support properties., a citrus-derived
polymethoxylatedflavone, prevented the development of all three
problems.
Nobiletin Type of citrus bioflavonoid shown to have anti-inflammatory,
anti-oxidant, and blood sugar support properties. was found to lower
LDL cholesterol Low-density lipoprotein. It is a group of lipids and
proteins that allow lipids like cholesterol, triglycerides, and fat
soluble nutrients (Vitamin A, D, E , K, Q 10, carotenes) to be
transported with the water-based bloodstream. by suppressing the
production of triglyceride-rich VLDL cholesterol. Furthermore,
Nobiletin Type of citrus bioflavonoid shown to have anti-inflammatory,
anti-oxidant, and blood sugar support properties. actually turned on
genes in the liver that induced fat burning, thus preventing a build
up of unhealthy fat in the liver. And Nobiletin Type of citrus
bioflavonoid shown to have anti-inflammatory, anti-oxidant, and blood
sugar support properties. was found to promote insulin sensitivity,
the opposite of insulin resistance, not only in the liver but at other
locations around the body. In comparison to a control group that
rapidly gained weight, the animals on Nobiletin Type of citrus
bioflavonoid shown to have anti-inflammatory, anti-oxidant, and blood
sugar support properties. did not gain any extra weight even though
they were fed the exact same diet. These beneficial effects
“dramatically attenuated atherosclerosis.”
“The Nobiletin Type of citrus bioflavonoid shown to have anti-
inflammatory, anti-oxidant, and blood sugar support properties.-
treated mice were basically protected from obesity,” says Murray Huff,
the Director of the Vascular Biology Research Group at Robarts. “And
in longer-term studies, Nobiletin Type of citrus bioflavonoid shown to
have anti-inflammatory, anti-oxidant, and blood sugar support
properties. also protected these animals from atherosclerosis, the
buildup of plaque in arteries, which can lead to a heart attack or
stroke. This study really paves the way for future studies to see if
this is a suitable treatment for metabolic syndrome and related
conditions in people
<snip>
http://www.wellnessresources.com/weight/articles/melatonin_supports_weight_management/
Melatonin Supports Weight Management
Friday, May 06, 2011 - Byron Richards,
One problem in overweight individuals is the loss of 24-hour rhythm
patterns (circadian rhythms), a problem that is central to the
clocking operations of every cell and consequently to the coordinated
calorie burning efforts of your body as a whole. This aspect of the
issue has lead researchers to focus on the use of melatonin1,
especially to help protect against the slide into diabetes and
cardiovascular problems. A new animal study confirms that melatonin
may be a potent nutrient2 for weight management efforts.
The study was carried out using well-studied Zucker diabetic fatty
rats, a type of rat that readily develops high blood pressure, high
cholesterol, insulin resistance, and has rapidly expanding white
adipose tissue due to leptin receptor gene mutations. In the melatonin-
treated group less weight was gained, there was a reduction in
triglycerides and LDL cholesterol Low-density lipoprotein. It is a
group of lipids and proteins that allow lipids like cholesterol,
triglycerides, and fat soluble nutrients (Vitamin A, D, E , K, Q 10,
carotenes) to be transported with the water-based bloodstream. , and a
boost in HDL Cholesterol High-density lipoprotein that is one of five
lipoproteins that enable cholesterol and triglycerides to be
transported within the bloodstream to the liver and to the adrenals,
ovaries, or testes for the production of steroid hormones. . The
treatment was performed in young rats, prior to the onset of
cardiovascular disease, indicating the potential benefit in helping to
reduce risk for health complications from the now-raging obesity
epidemic in this country.
It is known that melatonin levels decline with age. As little as 0.5
mg of melatonin may be all that it takes to help improve sleep, while
others may benefit from doses in the 3 mg – 12 mg range. This
information is likely to be of help to any person who is overweight
and has trouble sleeping.
Nighttime issues and daytime issues, are highly interdependent in
terms of linked rhythms. This means that as you manage stress better
during the day and become consistent with exercise, you tend to sleep
better. On the other hand, any time you sleep better you have more
energy to deal with stress and to exercise. Thus, looking for entry
points to help solve the energy/rhythm aspect of this problem is
valuable. For some, melatonin may be a workable strategy to help
sleep. You tend to need more in the winter and less in the summer, but
many people over the age of 40 tend to benefit from at least 0.5 mg
per night. You can tell it is of help because when you use it you
sleep better.
<snip>
---
http://www.wellnessresources.com/health/articles/the_antioxidant_properties_of_caffeine/
The Antioxidant Properties of Caffeine
Saturday, May 07, 2011 - Byron Richards
Caffeine is known to have antioxidant properties and may be protective
against a variety of health problems. For example, coffee contains
various Flavonoids Plant compound that is associated with
pigmentation. Flavonoids have been shown to modify allergens, viruses,
inflammation, and various carcinogens. Found in green tea, citrus,
berries, onions, parsley, red wine, dark chocolate, and others. that
participate in antioxidant processes. A new study shows that caffeine
directly acts as an antioxidant1, independent of such Flavonoids Plant
compound that is associated with pigmentation. Flavonoids have been
shown to modify allergens, viruses, inflammation, and various
carcinogens. Found in green tea, citrus, berries, onions, parsley, red
wine, dark chocolate, and others., by binding on to the hydroxyl
radical and rendering it inert.
The hydroxyl radical (OH) is one of the most damaging free radicals
that can occur in your body. This free radical is not deactivated by
an enzyme system and typically requires antioxidant nutrients such as
melatonin or vitamin E to take care of it. It is readily produced when
iron and copper interact with hydrogen peroxide. If hydroxyl radicals
are not neutralized then they readily damage large molecules such as
fatty membranes of cells, carbohydrates, and structural proteins – not
to mention that they also damage DNA leading to cell mutation.
The new study shows that caffeine works by directly binding to the
hydroxyl radical and neutralizing it. This means that caffeine is not
only a metabolic stimulant it is also a protective antioxidant – good
in moderation if desired.
<snip>
=======================
randall.... wow ... wow... these things are getting so GOOD
my mind is almost BLOWing in the wind...