Trillium Gut BActeria & BEhavioural illnesses --RNF114 -->PSORs12 -- Gut Bullets-->LAB master<--->GLENN GIBSON -->Microbiome & Metabonomics --> Jeffrey GORDON --NM DELZENNE - GLP-2 _ Chitin Glucan Fiber
randall
Notice how a little missPELLing travels from link to link?
Both of these next two say we HAVE a TRILLIUM bacteria in our guts.
XcuseME isn't that a flower?
Lilly of our GUTs?
http://en.wikipedia.org/wiki/Trillium
Or is a thousand trillion a trillium?
NOpE it's a quadrillion.
OK check it out::
http://www.eurekalert.org/pub_releases/2011-05/mu-tam051711.php
and/or
http://www.sciencedaily.com/releases/2011/05/110517110315.htm
Gut Bacteria Linked to Behavior: That Anxiety May Be in Your Gut, Not
in Your Head
ScienceDaily (May 17, 2011) — For the first time, researchers at
McMaster University have conclusive evidence that bacteria residing in
the gut influence brain chemistry and behaviour.
---------------
http://images.sciencedaily.com/2011/05/110517110315-large.jpg
Rendering of bacteria. For the first time, researchers at McMaster
University have conclusive evidence that bacteria residing in the gut
influence brain chemistry and behavior. (Credit: © Irochka / Fotolia)
---------------
The findings are important because several common types of
gastrointestinal disease, including irritable bowel syndrome, are
frequently associated with anxiety or depression. In addition there
has been speculation that some psychiatric disorders, such as late
onset autism, may be associated with an abnormal bacterial content in
the gut.
"The exciting results provide stimulus for further investigating a
microbial component to the causation of behavioural illnesses," said
Stephen Collins, professor of medicine and associate dean research,
Michael G. DeGroote School of Medicine. Collins and Premysl Bercik,
assistant professor of medicine, undertook the research in the
Farncombe Family Digestive Health Research Institute.
The research appears in the online edition of the journal
Gastroenterology.
For each person, the gut is home to about 1,000 _____trillium____
bacteria with which we live in harmony. These bacteria perform a
number of functions vital to health: They harvest energy from the
diet, protect against infections and provide nutrition to cells in the
gut. Any disruption can result in life-threatening conditions, such as
antibiotic-induced colitis from infection with the "superbug"
Clostridium difficile.
Working with healthy adult mice, the researchers showed that
disrupting the normal bacterial content of the gut with antibiotics
produced changes in behaviour; the mice became less cautious or
anxious. This change was accompanied by an increase in brain derived
neurotrophic factor (BDNF), which has been linked, to depression and
anxiety.
When oral antibiotics were discontinued, bacteria in the gut returned
to normal. "This was accompanied by restoration of normal behaviour
and brain chemistry," Collins said.
To confirm that bacteria can influence behaviour, the researchers
colonized germ-free mice with bacteria taken from mice with a
different behavioural pattern. They found that when germ-free mice
with a genetic background associated with passive behaviour were
colonized with bacteria from mice with higher exploratory behaviour,
they became more active and daring. Similarly, normally active mice
became more passive after receiving bacteria from mice whose genetic
background is associated with passive behaviour.
While previous research has focused on the role bacteria play in brain
development early in life, Collins said this latest research indicates
that while many factors determine behaviour, the nature and stability
of bacteria in the gut appear to influence behaviour and any
disruption , from antibiotics or infection, might produce changes in
behaviour. Bercik said that these results lay the foundation for
investigating the therapeutic potential of probiotic bacteria and
their products in the treatment of behavioural disorders, particularly
those associated with gastrointestinal conditions such as irritable
bowel syndrome.
The research was funded by grants from the Canadian Institutes of
Health Research (CIHR) and the Crohn's and Colitis Foundation of
Canada (CCFC).
Journal Reference:
Emmanuel Denou, Wendy Jackson, Jun Lu, Patricia Blennerhassett, Kathy
McCoy, Elena F. Verdu, Stephen M. Collins, Premysl Bercik. The
Intestinal Microbiota Determines Mouse Behavior and Brain BDNF Levels.
Gastroenterology, Vol. 140, Issue 5, Supplement 1, Page S-57
http://download.journals.elsevierhealth.com/pdfs/journals/0016-5085/PIIS0016508511602308.pdf
--------
The case of the mysterious trillium bacterium.
It's making me/we MISS be HAVE?
Almost as strange as SFB (segmented filamentous bacterium) that induct
Th17 cells.
Trillium and SFB are driving me CRAZY> LoL
=============================
A new monkey wrench in the cytoplasm makes a monkey outa randall's
craPazoid?
Huh?
Your already a monkey dude and rude and GFII thinks your a shill for
BIG pILL.<G>
So what have i got?
OK, at the risk of my rePutation this is a DNA psor GENE, maybe.
http://www.ncbi.nlm.nih.gov/pubmed/21571784
Hum Mol Genet. 2011 May 13.
Functional analysis of the RNF114 psoriasis susceptibility gene
implicates innate immune responses to double-stranded RNA in disease
pathogenesis.
Bijlmakers MJ, Kanneganti SK, Barker JN, Trembath RC, Capon F.
Source
Division of Immunology, Infection and Inflammatory Disease, King's
College London, London, SE1 9RT, UK.
Abstract
Psoriasis is an immune-mediated skin disease, the aetiology of which
remains poorly understood. In recent years, genome-wide association
studies (GWAS) have helped to illuminate the molecular basis of this
condition, by demonstrating the pathogenic involvement of multiple
genes from the IL-23 and NF-κB pathways. A GWAS carried out by our
group also identified RNF114, a gene encoding a novel ubiquitin
binding protein, as a determinant for psoriasis susceptibility.
Although the function of RNF114 is unknown, its paralogue RNF125 has
been shown to regulate the RIG-I/MDA5 innate antiviral response. This
signalling cascade, which is activated by the presence of double-
stranded RNA (dsRNA) within the cytoplasm, induces the production of
type I interferon (IFN) through the activation of the IRF3 and NF-κB
transcription factors. Here, we explore the hypothesis that RNF114 may
also modulate RIG-I/MDA5 signalling. We show that RNF114 associates
with ubiquitinated proteins and that it is a soluble cytosolic protein
that can be induced by interferons and synthetic dsRNA. Moreover, we
demonstrate that RNF114 over-expression enhances NF-κb and IRF3
reporter activity and increases type I and type III IFN mRNA levels.
These results indicate that RNF114 regulates a positive feedback loop
that enhances dsRNA induced production of type I IFN. Thus, our data
point to a novel pathogenic pathway, where dysregulation of RIG-I/MDA5
signalling leads to the over-production of type I IFN, a key early
mediator of epithelial inflammation.
PMID: 21571784
A total of six hits for RNF114 (a zinc ring finger not a cubic
zurconium. LOL)
http://www.ncbi.nlm.nih.gov/pubmed?Db=gene&Cmd=retrieve&dopt=full_report&list_uids=55905
Also known as ZNF313; PSORS12; RNF114
<snip>
ALL 17 hits for RNF114 (might appear as ZNF313 or PSORS12)
http://www.ncbi.nlm.nih.gov/pubmed?Db=pubmed&DbFrom=gene&Cmd=Link&LinkName=gene_pubmed&LinkReadableName=PubMed&IdsFromResult=55905
---
http://www.ncbi.nlm.nih.gov/omim/612950
MIM ID %612950
PSORIASIS SUSCEPTIBILITY 12; PSORS12
http://www.ncbi.nlm.nih.gov/omim/177900
http://www.ncbi.nlm.nih.gov/pubmed/18364390
Hum Mol Genet. 2008 Jul 1;17(13):1938-45. Epub 2008 Mar 25.
Identification of ZNF313/RNF114 as a novel psoriasis susceptibility
gene.
[...] pmid: 18364390
free full text:
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/18364390/?tool=pubmed
pmid: 18364390 has been posted one time previously:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=pmid%3A+18364390&start=0&hl=en&
Same link -> goes straight to the post:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/47d7425281a2af27?hl=en&&q=pmid%3A+18364390
--------
19 hits for keywords: zinc finger protein - P NG
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=zinc+finger+protein&start=0&hl=en&
I pick up a few more with ALL groups:
http://groups.google.com/groups/search?hl=en&q=zinc+finger+protein+psoriasis+randall&btnG=Search&sitesearch=groups.google.com
http://en.wikipedia.org/wiki/Zinc_finger_protein
A zinc finger protein is a DNA-binding protein domain consisting of
zinc fingers ranging from two in the Drosophila regulator ADR1, the
more common three in mammalian Sp1 up to nine in TFIIIA. They occur in
nature as the part of transcription factors conferring DNA sequence
specificity as the DNA-binding domain.
They have also found use in protein engineering due to their
modularity and have prospects as components of tools for use in
therapeutic gene modulation[1] and zinc finger nucleases.[2]
Structure
Zinc finger protein consists of anti-parallel hairpin motif. It
consists of 2 beta strands, one alpha helix and a hairpin structure.
The first Zn binds to Cys-3 of 1st beta strand, second Zn binds to
Cys-6 that is present in the tight loop that separates the two beta
strands. The other two Zn is coordinated to Cys 19 & 23 which are
present in C-terminal half of the alpha helix. The hairpin is followed
by alpha helix of about 3.5 turns. The binding of Zn at the last two
positions mentioned causes distortion in alpha helix between these
positions to form a 3-10 complex in which H bonding occurs between 1st
and 3rd amino acid instead of 1-4 amino acid bonding. Zn in buried in
the interior of the protein and is necessary for the formation of a
stable finger structure in aqueous solution. The zinc does not
interact with DNA.
<snip>
http://en.wikipedia.org/wiki/Zinc_finger
http://en.wikipedia.org/wiki/Zinc_finger_inhibitor
Zinc finger inhibition is the process by which the synthesis of zinc
fingers is blocked. Zinc finger inhibitors have been tested for their
efficacy in treating AIDS and HIV.
http://en.wikipedia.org/wiki/Zinc_finger_nuclease#Applications
http://en.wikipedia.org/wiki/Zinc_finger_nuclease#Gene_therapy
=====
http://www.ncbi.nlm.nih.gov/pubmed/18256691
J Invest Dermatol. 2008 Jul;128(7):1662-8. Epub 2008 Feb 7.
A promoter sequence variant of ZNF750 (zinc-finger protein 750 ) is
linked with familial psoriasis.
[....] pmid: 18256691
----
104 hits - keywords: zinc finger protein autoimmun* - pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=zinc%20finger%20protein%20autoimmun*
#1 of these 104:
J Immunol. 2011 Feb 15;186(4):2138-47. Epub 2011 Jan 19.
Essential role of E3 ubiquitin ligase activity in Cbl-b-regulated T
cell functions.
Paolino M, Thien CB, Gruber T, Hinterleitner R, Baier G, Langdon WY,
Penninger JM.
Source
Institute of Molecular Biotechnology of the Austrian Academy of
Science, A-1030 Vienna, Austria.
Abstract
E3 ubiquitin ligases have been placed among the essential molecules
involved in the regulation of T cell functions and T cell tolerance.
However, it has never been experimentally proven in vivo whether these
functions indeed depend on the catalytic E3 ligase activity. The
Casitas B-cell lymphoma (Cbl) family protein Cbl-b was the first E3
ubiquitin ligase directly implicated in the activation and tolerance
of the peripheral T cell. In this study, we report that selective
genetic inactivation of Cbl-b E3 ligase activity phenocopies the T
cell responses observed when total Cbl-b is ablated, resulting in T
cell hyperactivation, spontaneous autoimmunity, and impaired induction
of T cell anergy in vivo. Moreover, mice carrying a Cbl-b E3 ligase-
defective mutation spontaneously reject tumor cells that express human
papilloma virus Ags. These data demonstrate for the first time, to our
knowledge, that the catalytic function of an E3 ligase, Cbl-b, is
essential for negative regulation of T cells in vivo. Thus, modulation
of the E3 ligase activity of Cbl-b might be a novel modality to
control T cell immunity in vaccination, cancer biology, or
autoimmunity.
PMID: 21248250
http://en.wikipedia.org/wiki/Ubiquitin_ligase
http://en.wikipedia.org/wiki/Cbl-b
Cbl (named after Casitas B-lineage Lymphoma) is a mammalian gene
encoding several proteins including E3 ubiquitin-protein ligase CBL
involved in cell signalling and protein ubiquitination.
http://en.wikipedia.org/wiki/Cbl-b#Structure
--------------------
#2
http://www.ncbi.nlm.nih.gov/pubmed/20886122
PLoS One. 2010 Sep 23;5(9):e12904.
EGR-2 is not required for in vivo CD4 T cell mediated immune
responses.
[...] pmid: 20886122
http://en.wikipedia.org/wiki/EGR2
Early growth response protein 2 is a protein that in humans is encoded
by the EGR2 gene.
The early growth response protein 2 is a transcription factor with
three tandem C2H2-type zinc fingers.
<snip>
==============
OK so somehow i've come back towards runx and autoimmun*
runx - 35 hits - P NG
runx - relevance
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=runx+&start=0&scoring=d&hl=en&
runx chrono order:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=runx+&start=0&hl=en&
Is autoimmunity more dependent on runx genes or SFB in the small
intestine (lamina propria) inducting Th17?
Good question, as a over protective Th2 (skew) is breeding grounds for
cancer and hiv/aids
8 hits: runx AND autoimmun* - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=runx%20autoimmun*
#1 of EIGHT:
http://www.ncbi.nlm.nih.gov/pubmed/19800266
Immunity. 2009 Oct 16;31(4):609-20. Epub 2009 Oct 1.
Indispensable role of the Runx1-Cbfbeta transcription complex for in
vivo-suppressive function of FoxP3+ regulatory T cells.
Kitoh A, Ono M, Naoe Y, Ohkura N, Yamaguchi T, Yaguchi H, Kitabayashi
I, Tsukada T, Nomura T, Miyachi Y, Taniuchi I, Sakaguchi S.
Source
Department of Experimental Pathology, Institute for Frontier Medical
Sciences, Graduate School of Medicine, Kyoto University, Kyoto
606-8507, Japan.
Abstract
Naturally arising regulatory T (Treg) cells express the transcription
factor FoxP3, which critically controls the development and function
of Treg cells. FoxP3 interacts with another transcription factor Runx1
(also known as AML1). Here, we showed that Treg cell-specific
deficiency of Cbfbeta, a cofactor for all Runx proteins, or that of
Runx1, but not Runx3, induced lymphoproliferation, autoimmune disease,
and hyperproduction of IgE. Cbfb-deleted Treg cells exhibited impaired
suppressive function in vitro and in vivo, with altered gene
expression profiles including attenuated expression of FoxP3 and high
expression of interleukin-4. The Runx complex bound to more than 3000
gene loci in Treg cells, including the Foxp3 regulatory regions and
the Il4 silencer. In addition, knockdown of RUNX1 showed that RUNX1 is
required for the optimal regulation of FoxP3 expression in human T
cells. Taken together, our results indicate that the Runx1-Cbfbeta
heterodimer is indispensable for in vivo Treg cell function, in
particular, suppressive activity and optimal expression of FoxP3.
PMID: 19800266
#4 of the 8:
http://www.ncbi.nlm.nih.gov/pubmed/16124855
Annu Rev Genomics Hum Genet. 2005;6:93-122.
The genetics of psoriasis and autoimmunity.
Bowcock AM.
Source
Department of Genetics, Washington University School of Medicine, St.
Louis, Missouri 63110, USA. bow...@genetics.wustl.edu
Abstract
Psoriasis is an inflammatory/autoimmune disease and, as with many
autoimmune diseases, is associated with alleles from the major
histocompatibility complex (MHC). With psoriasis and autoimmune
disease, the penetrance of the MHC-associated alleles is never 100%,
even for monozygotic twins. This may be because development requires
additional environmental and/or genetic modifiers or requires specific
T-cell receptor arrangements. Families segregating single or
multilocus susceptibility alleles other than the MHC have also been
reported. Overlapping genetic locations of loci for different
autoimmune diseases have been known for several years and are starting
to reveal common genes or genetic variants. These include genes
normally involved in preventing spontaneous T-cell activation or
proliferation, immune synapse formation, or cytokine production via
pathways such as those mediated by NFkappaB and those involved in
thymic selection. Autoimmunity may also involve dysregulation of genes
or pathways regulated by the RUNX family of transcription factors.
RUNX is involved in hematopoietic cell development, development of T
cells in the thymus, chromatin remodeling, and gene silencing. Hence,
its effect on cells of the immune system may be due to variable
changes in gene expression and could account for variable body surface
involvement and waxing and waning of disease.
PMID: 16124855
#7 of 8:
http://www.ncbi.nlm.nih.gov/pubmed/15225361
Arthritis Res Ther. 2004;6(4):169-73. Epub 2004 Jun 21.
Role of RUNX in autoimmune diseases linking rheumatoid arthritis,
psoriasis and lupus.
Alarcón-Riquelme ME.
Source
Department of Genetics and Pathology, Rudbeck Laboratory, University
of Uppsala, Uppsala, Sweden. marta....@genpat.uu.se
Abstract
Recent studies investigating the genetic susceptibility of systemic
lupus erythematosus, rheumatoid arthritis and psoriasis have revealed
a potential role for the RUNX proteins in the development of
autoimmune disease. A new pathway of disease pathogenesis opens new
avenues of research with thousands of questions that remain to be
answered. In this review I attempt to propose how the RUNX proteins
might be involved in these diseases and review current knowledge on
this very interesting trio of transcription factors that was
previously only suspected to be involved in cancer.
PMID: 15225361
PMCID: PMC464920
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/15225361/?tool=pubmed
-----------------
161 hits - tregs AND Th17 - pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=tregs%20th17
spend the time and let me know if something jumPs your bones for Th1
or Th2.
But don't forget Th17 is inducted by SFB.
================================
I don't KNOW about foolproofing, as taking L-glutamine has been a
negative experience
while having a Th1 skew and psor flares 24/7.
I'd certainly like to BULLET Proof my gut with LAB (lactic acid
bacteria)
http://www.vrp.com/digestive-health/for-foolproof-digestive-health-keep-your-guts-fortress-strong?utm_content=article3213
For Foolproof Digestive Health, Keep Your Gut’s Fortress Strong
When it comes to maximizing GI health, certain rules are golden.
Practically everyone knows to keep an eye on portion sizes and to
avoid food that may cause imbalances within your gut—but while you
probably work pretty hard to keep the bad stuff out of your gut, a lot
less thought usually goes into keeping the good stuff in. And
unfortunately, this is a mistake… because whether you’re dealing with
a weak intestinal wall or an imbalance of friendly bacteria, the end
result may be trouble, where both your digestive health and your
immune system are concerned.
At its healthiest, your intestinal wall is a veritable fortress—always
keeping the contents of your gut properly quarantined for maximum
nutrient uptake and seamless, efficient digestion. But when the “tight
junctions”—the spaces between the cells of your intestinal lining,
which are normally sealed—become irritated by an unbalanced
inflammatory response, they can start to loosen. As a result, larger
molecules than usual are allowed to permeate your gut, triggering a
domino effect of immune responses and cellular distress in reaction to
the arrival of perceived foreign particles in your bloodstream.
Appropriately, this is known as “leaky gut”—and the consequences can
range from abdominal discomfort, gas, bloating, occasional
indigestion, diarrhea and constipation to brain fog, joint discomfort,
nervousness and a noticeable dip in your mood, your energy and your
immune health. This last point is especially important, because
believe it or not, your GI tract—and more specifically, your gut-
associated lymphoid tissue (GALT)—hosts a whopping 70 percent of your
body’s immune cells.1-2 GALT consists of lymphoid follicles called
“Peyer’s patches,” which act as your intestines’ immune sensors—and
which can also upset your gastrointestinal health if not functioning
properly.
Ultimately, your GI tract needs ample nutrient support and a steady
supply of good bacteria if it’s going to keep your digestion running
smoothly and your immune system working at its peak. And the easiest
way to ensure that you’re giving your gut the reinforcement it needs
is to keep your bases covered with the right daily supplements.
For starters, stock up on a high-quality probiotic blend—such as VRP’s
BioPRO™—to keep your body’s bacterial balance in check. Imbalances in
your gut’s microbial population is a leading cause of occasional lower
GI tract irritation—but research shows that probiotics can promote the
colonization of friendly bacteria and support both digestive and
overall health in situations where microbiota balance and intestinal
wall strength are compromised.3
Select botanicals and nutrients can also help you to strengthen your
intestinal wall and support normal gut permeability. Glutamine, for
example, nourishes the cells that line your colon and is critical for
maintaining intestinal structure—while deglycyrrhizinated licorice
(DGL) has been shown to promote gastric and duodenal health.4-7
Similarly, N-acetyl-glucosamine plays a vital role in the synthesis of
protective intestinal mucosa, while marshmallow, berberine, cabbage,
slippery elm, phosphatidylcholine and gamma oryzanol all contribute to
optimal colon health.5-17
<snip>
=====================
http://www.nutraingredients-usa.com/Research/The-prebiotic-pioneer-Prof-Glenn-Gibson
The prebiotic pioneer: Prof Glenn Gibson
By Stephen Daniells, 17-May-2011
Related topics: Research, Prebiotics , Probiotics and prebiotics, Bone
& joint health, Gut health, Weight management
Harnessing modern technologies like metabonomics will ‘provide the
answers’ to questions about how the gut microflora affect human
health, says the scientist who co-coined the term ‘prebiotic’.
has spent the majority of his professional career at the business end
of the digestive tract. He is currently Professor of Food Microbial
Sciences at the University of Reading in the UK.
Since the coining of the term ‘prebiotic’ in a paper in 1995, Prof
Gibson has continued to lead research in the field. Talking to
NutraIngredients-USA, Gibson professed his excitement over the
potential of new technologies, and metabonomics
http://www.nutraingredients-usa.com/content/search?SearchText=metabonomics&FromNews
in particular, to “provide the answers” to the subjects unanswered
questions.
Metabonomics is part of the bigger subject of nutrigenomics, which
includes transcriptomics and proteomics: In other words, changes to
messenger RNA (transcriptomics) and the corresponding proteins
(proteomics) control the transport of certain nutrients and
metabolites (metabonomics) in the biochemical pathway.
“I do think going from molecular to metabolic is a sea change.”
“We’re on the verge of understanding the role of this big organ [the
gut] on health and disease,” he said. Gut health is no longer just
about how regular your bowel movements are, but has reported
implications for immunity, brain health, and weight gain.
“I’m not amazed by the potential health benefits of modifying gut
microflora because of the sheer numbers of cells involved,” said Prof
Gibson. “Bacteria will come to play a major role in health and
wellness.”
A long and winding road
Prof Gibson’s PhD was in the field of marine and estuarine sediments
at the University of Dundee in Scotland, and he’s quick to note that
sediments and the human gut have more in common than you’d think: Both
contain bacteria that can produce hydrogen sulfide (H2S) – a noxious
gas that smells like rotten eggs.
His interest in H2S-producing bacteria led him to look at how these
may promote human conditions such as ulcerative colitis.
Probiotics were the obvious next step in his research, and attempts to
change the microbial populations to produce health benefits.
Belgian sugar company Orafti (now Beneo) then came calling with an
ingredient called inulin, funding a PhD student under Prof Gibson’s
guidance.
Prof Gibson’s interactions with Orafti introduced him to Marcel
Roberfroid from the Catholic University of Louvain, who was working as
a consultant to the Belgian company.
Working together in a hotel room near Victoria train station in
London, Roberfroid and Gibson produced a landmark paper in the Journal
of Nutrition and introduction of the concept of ‘prebiotics’ (Vol.
125, pp. 1401-1412).
http://www.nutraingredients-usa.com/content/search?SearchText=prebiotics&FromNews
The same paper also introduced the term ‘synbiotic’, which is a
synergistic combination of prebiotic fibers and probiotic bacterial
strains.
Leap forward
The early Orafti-sponsored project was time consuming, and involved
hours of culturing bacteria in Petri dishes. The advent of molecular
biology allowed the research, which had been ‘stagnating’, to leap
forward.
“This was a big step,” said Gibson, “and allowed us to do volunteer
trials.”
Even as the quantity of data grows and our understanding more complex,
moves are being made to simplify the subject: An international team of
researchers recently reported in Nature that microflora in our guts
may fit into one of three distinct groups, called enterotypes:
Bacteroides, Prevotella and Ruminococcus.
Prof Gibson is quick to point out that such a study was based on data
from only 22 people and notes that Bifidobacteria were not shown.
“What this paper did show was the value of high throughput
sequencing,” he said.
Obesity
An interesting development in recent years stems from a study from the
lab of Jeffrey Gordon at the University of Washington in St Louis. In
articles published in Nature in December 2006 (Vol. 444, pp.
1022-1023, 1027-1031) Dr Gordon and his team reported that microbial
populations in the gut are different between obese and lean people,
and that when the obese people lost weight their microflora reverted
back to that observed in a lean person, suggesting that obesity may
have a microbial component.
“By playing with the gut microflora, can we drag people from obese to
lean?” asks Prof Gibson. “Obesity is related to genetics, the diet,
and exercise… and there are gut flora difference. We can do something
about gut flora, and this can affect appetite, it can affect the
calories extracted from food.”
Prof Gibson is quick to add that the changes to gut microflora
produced by prebiotics “only last as long as you take the
intervention”. In other words, stop taking the prebiotics and, within
about a week, the gut microflora returns to what it was before you
started taking it.
This represents an opportunity for the food and nutrition industries –
“you can put prebiotics into food people eat anyway”.
The EFSA issue
The science appears impressive, and the potential immense, but mention
EFSA and Prof Gibson’s tone changes. The prebiotic pioneer has watched
while the European Food Safety Authority (EFSA) released negative
opinion after negative opinion for pre- and probiotics.
Commenting on the recent EFSA document, Guidance on the scientific
requirements for health claims related to gut and immune function ,
http://www.efsa.europa.eu/en/efsajournal/doc/1984.pdf
Prof Gibson suggests there is a lack of understanding from EFSA’s
Panel on Dietetic Products, Nutrition and Allergies (NDA), and cites
guidance on end-point measures for interventions, one of which is a 1-
log decrease in specific gut pathogens.
The 1-log pathogen reduction rule (in order to produce an effect
against pathogenic bacteria, the intervention must display a reduction
in population of 1-log) is “nonsense”, he says, “because it doesn’t
take into account of starting populations.
“If one of my undergraduates made such a statement, they’d fail.
“If you have 10 million Campylobacter, you have food poisoning. If you
then reduce this by 1-log to one million you’d still have food
poisoning. Where’s the benefit?”
Bifido-bashing
EFSA’s dismissal that a promotion of Bifidobacteria populations does
not relate to a health benefit is “rubbish”, said Prof Gibson.
“I could cite hundreds of studies that contradict this.
“The literature is overwhelmingly in favor of probiotics and
prebiotics.”
So how does he rationalize EFSA’s decisions? He doesn’t: “I’m very,
very puzzled”.
“People who make good prebiotics and do the work in building the
science will walk [away from Europe],” he predicts. “They’ll go to
Asia and America where the legislation is hard and fair and clear.”
Comments from EFSA suggest that the science is not developed enough to
answer all of their questions, but Prof Gibson dismisses suggestions
that health claims came too soon for pro- and prebiotics, and he
points eastward for evidence: “The Japanese have their act together,”
he says, “and they have 100s of foods with FOSHU status, and these
include prebiotics and probiotics.”
<snip>
----------------
OK so Jeffrey GORDON has 405 hits in pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Gordon%20JI%22%5BAuthor%5D
And 25 of these 405 have keyword: microbiome (making him mister
microbiome no doubt)
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Gordon%20JI%22%5BAuthor%5D%20microbiome
And if you wish to doubt, then add kicker: colon* for 83 hits -pubmed
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Gordon%20JI%22%5BAuthor%5D%20colon*
From 2006:
http://www.ncbi.nlm.nih.gov/pubmed/17183309
Nature. 2006 Dec 21;444(7122):1022-3.
Microbial ecology: human gut microbes associated with obesity.
Ley RE, Turnbaugh PJ, Klein S, Gordon JI.
Source
Washington University School of Medicine, St Louis, Missouri 63108,
USA.
Abstract
Two groups of beneficial bacteria are dominant in the human gut, the
Bacteroidetes and the Firmicutes. Here we show that the relative
proportion of Bacteroidetes is decreased in obese people by comparison
with lean people, and that this proportion increases with weight loss
on two types of low-calorie diet. Our findings indicate that obesity
has a microbial component, which might have potential therapeutic
implications.
Comment in
Nature. 2006 Dec 21;444(7122):1009-10.
PMID: 17183309
This ONE from 2005 is particularly SALIENT to the above article:
http://www.ncbi.nlm.nih.gov/pubmed/16033867
Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):11070-5. Epub 2005 Jul
20.
Obesity alters gut microbial ecology.
Ley RE, Bäckhed F, Turnbaugh P, Lozupone CA, Knight RD, Gordon JI.
Source
Center for Genomes Sciences, Washington University School of Medicine,
St. Louis, MO 63108, USA.
Abstract
We have analyzed 5,088 bacterial 16S rRNA gene sequences from the
distal intestinal (cecal) microbiota of genetically obese ob/ob mice,
lean ob/+ and wild-type siblings, and their ob/+ mothers, all fed the
same polysaccharide-rich diet. Although the majority of mouse gut
species are unique, the mouse and human microbiota(s) are similar at
the division (superkingdom) level, with Firmicutes and Bacteroidetes
dominating. Microbial-community composition is inherited from mothers.
However, compared with lean mice and regardless of kinship, ob/ob
animals have a 50% reduction in the abundance of Bacteroidetes and a
proportional increase in Firmicutes. These changes, which are division-
wide, indicate that, in this model, obesity affects the diversity of
the gut microbiota and suggest that intentional manipulation of
community structure may be useful for regulating energy balance in
obese individuals. The sequences reported in this paper have been
deposited in the GenBank database [accession nos. DQ 014552--DQ 015671
(mothers) and AY 989911--AY 993908 (offspring)].
PMID: 16033867
PMCID: PMC1176910
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/16033867/?tool=pubmed
------------
Let's look at more recent studies:
http://www.ncbi.nlm.nih.gov/pubmed/19491241
J Physiol. 2009 Sep 1;587(Pt 17):4153-8. Epub 2009 Jun 2.
The core gut microbiome, energy balance and obesity.
Turnbaugh PJ, ____Gordon JI.____
Source
Center for Genome Sciences, Washington University School of Medicine,
St Louis, MO 63108, USA.
Abstract
Metagenomics is an emerging field focused on characterizing the
structures, functions and dynamic operations of microbial communities
sampled in their native habitats without the need for culture. Here,
we present findings from a 16S rRNA gene sequence- and whole community
DNA shotgun sequencing-based analysis of the adult human gut
microbiomes of lean and obese mono- and dizygotic twins. Our findings
indicate that a core microbiome can be found at the gene level,
despite large variation in community membership, and that variations
from the core are associated with obesity. These findings have
implications for ongoing Human Microbiome Project(s), and highlight
important challenges to the field of metagenomics.
PMID: 19491241
free full text
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19491241/?tool=pubmed
---------
http://www.ncbi.nlm.nih.gov/pubmed/17943116
Nature. 2007 Oct 18;449(7164):804-10.
The human microbiome project.
Turnbaugh PJ, Ley RE, Hamady M, Fraser-Liggett CM, Knight R,
____Gordon JI.____
Source
Center for Genome Sciences, Washington University School of Medicine,
St Louis, Missouri 63108, USA.
Abstract
A strategy to understand the microbial components of the human genetic
and metabolic landscape and how they contribute to normal physiology
and predisposition to disease.
PMID: 17943116
-----------
http://www.ncbi.nlm.nih.gov/pubmed/16497592
Cell. 2006 Feb 24;124(4):837-48.
Ecological and evolutionary forces shaping microbial diversity in the
human intestine.
Ley RE, Peterson DA, _____Gordon JI._____
Source
Center for Genome Sciences, Washington University School of Medicine,
St. Louis, MO 63108, USA.
Abstract
The human gut is populated with as many as 100 trillion cells, whose
collective genome, the microbiome, is a reflection of evolutionary
selection pressures acting at the level of the host and at the level
of the microbial cell. The ecological rules that govern the shape of
microbial diversity in the gut apply to mutualists and pathogens
alike.
PMID: 16497592
Does he mean trillium cells?
========================
So all these Gordon links/abstracts led me to this other scientist:
83 hits - "Delzenne NM"[Author] -pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Delzenne%20NM%22%5BAuthor%5D
This guy is HOT..he gives tiPs on what to close the gaP with.
LOOK at this one from Aug 2009 on HOW to CLOSE GUT HOLES with GLP-2:
http://www.ncbi.nlm.nih.gov/pubmed/19240062
Gut. 2009 Aug;58(8):1091-103. Epub 2009 Feb 24.
Changes in gut microbiota control inflammation in obese mice through a
mechanism involving GLP-2-driven improvement of gut permeability.
Cani PD, Possemiers S, Van de Wiele T, Guiot Y, Everard A, Rottier O,
Geurts L, Naslain D, Neyrinck A, Lambert DM, Muccioli GG, Delzenne NM.
Source
Unit of Pharmacokinetics, Metabolism, Nutrition and Toxicology,
Louvain Drug Research Institute, Université catholique de Louvain,
Brussels, Belgium. patric...@uclouvain.be
Abstract
BACKGROUND AND AIMS: Obese and diabetic mice display enhanced
intestinal permeability and metabolic endotoxaemia that participate in
the occurrence of metabolic disorders. Our recent data support the
idea that a selective increase of Bifidobacterium spp. reduces the
impact of high-fat diet-induced metabolic endotoxaemia and
inflammatory disorders. Here, we hypothesised that prebiotic
modulation of gut microbiota lowers intestinal permeability, by a
mechanism involving glucagon-like peptide-2 (GLP-2) thereby improving
inflammation and metabolic disorders during obesity and diabetes.
METHODS: Study 1: ob/ob mice (Ob-CT) were treated with either
prebiotic (Ob-Pre) or non-prebiotic carbohydrates as control (Ob-
Cell). Study 2: Ob-CT and Ob-Pre mice were treated with GLP-2
antagonist or saline. Study 3: Ob-CT mice were treated with a GLP-2
agonist or saline. We assessed changes in the gut microbiota,
intestinal permeability, gut peptides, intestinal epithelial tight-
junction proteins ZO-1 and occludin (qPCR and immunohistochemistry),
hepatic and systemic inflammation.
RESULTS: Prebiotic-treated mice exhibited a lower plasma
lipopolysaccharide (LPS) and cytokines, and a decreased hepatic
expression of inflammatory and oxidative stress markers. This
decreased inflammatory tone was associated with a lower intestinal
permeability and improved tight-junction integrity compared to
controls. Prebiotic increased the endogenous intestinotrophic
proglucagon-derived peptide (GLP-2) production whereas the GLP-2
antagonist abolished most of the prebiotic effects. Finally,
pharmacological GLP-2 treatment decreased gut permeability, systemic
and hepatic inflammatory phenotype associated with obesity to a
similar extent as that observed following prebiotic-induced changes in
gut microbiota.
CONCLUSION: We found that a selective gut microbiota change controls
and increases endogenous GLP-2 production, and consequently improves
gut barrier functions by a GLP-2-dependent mechanism, contributing to
the improvement of gut barrier functions during obesity and diabetes.
Comment in
Gut. 2009 Aug;58(8):1044-5.
Gastroenterology. 2010 Feb;138(2):779-81.
PMID: 19240062
PMCID: PMC2702831
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19240062/?tool=pubmed
http://en.wikipedia.org/wiki/Glucagon-like_peptide-2
Glucagon-like peptide-2 (GLP-2) is a 33 amino acid peptide with the
sequence HADGSFSDEMNTILDNLAARDFINWLIQTKITD in humans. GLP-2 is created
by specific post-translational proteolytic cleavage of proglucagon in
a process that also liberates the related glucagon-like peptide-1
(GLP-1). GLP-2 is produced by the intestinal endocrine L cell and by
various neurons in the central nervous system. Intestinal GLP-2 is co-
secreted along with GLP-1 upon nutrient ingestion.
When externally administered, GLP-2 produces a number of effects in
humans and rodents, including intestinal growth, enhancement of
intestinal function, reduction in bone breakdown and neuroprotection.
GLP-2 may act in an endocrine fashion to link intestinal growth and
metabolism with nutrient intake. GLP-2 and related analogs may be
treatments for short bowel syndrome, Crohn's disease, osteoporosis and
as adjuvant therapy during cancer chemotherapy.
-----------------
http://www.ncbi.nlm.nih.gov/pubmed/21411304
J Nutr Biochem. 2011 Mar 14.
Dietary modulation of clostridial cluster XIVa gut bacteria (Roseburia
spp.) by chitin-glucan fiber improves host metabolic alterations
induced by high-fat diet in mice.
Neyrinck AM, Possemiers S, Verstraete W, De Backer F, Cani PD,
Delzenne NM.
Source
Metabolism and Nutrition Research Group, Louvain Drug Research
Institute, Université catholique de Louvain, B-1200 Brussels, Belgium.
Abstract
Recent studies have provided new evidence that alterations in the
composition of the gut microbiota - known as dysbiosis - participate
in the development of obesity. The aim of the present study was to
investigate the ability of chitin-glucan (CG) from a fungal source to
modulate both the gut microbiota and glucose and lipid metabolism in
high-fat (HF) diet-induced obese mice. Supplementation of the HF diet
with fungal CG (10% w/w) induced caecal enlargement with prominent
changes in gut microbiota: it restored the number of bacteria from
clostridial cluster XIVa including Roseburia spp., which were
decreased due to HF feeding. Furthermore, CG treatment significantly
decreased HF-induced body weight gain, fat mass development, fasting
hyperglycemia, glucose intolerance, hepatic triglyceride accumulation
and hypercholesterolemia, independently of the caloric intake. All
those parameters were negatively correlated with specific bacteria of
clostridial cluster XIVa, i.e., Roseburia spp. (Pearson's correlations
analysis). In contrast to prebiotics that more specifically target the
bifidobacteria species, CG effects on obesity appear to be independent
of the incretin glucagon-like peptide 1 (GLP-1) production, since
portal GLP-1 and proglucagon (its precursor) expression were not
modified by the dietary intervention. In conclusion, our findings
support the view that chronic consumption of CG has potential
beneficial effects with respect to the development of obesity and
associated metabolic diabetes and hepatic steatosis, through a
mechanism related to the restoration of the composition and/or the
activity of gut bacteria, namely, bacteria from clostridial cluster
XIVa.
PMID: 21411304
---------
http://regulatoryandfoodsafety.food-business-review.com/news/fda-grants-gras-status-to-chitin-glucan-fiber-ingredient-of-stratum-nutrition-100211
Stratum Nutrition achieves self-affirmed GRAS status for chitin-glucan
fiber ingredient
Stratum Nutrition,a Novus International owned provider of functional
and specialty ingredients for manufacturers of food, beverages and
dietary supplements, has obtained self affirmed Generally Recognized
As Safe (GRAS) status for its chitin-glucan fiber ingredient, ARTINIA.
ARTINIA is said to be a high-purity, natural, chitin-glucan fiber
featuring the benefits of both soluble and insoluble fibers.
The company noted that a 12-week animal and 30-day human pilot study
have been completed, and each study demonstrates that ARTINIA provides
substantial benefits for arterial and overall heart health, including
a reduction in oxidized-LDL.
The GRAS designation will allow ARTINIA to be used in various food and
beverage categories including beverage and beverage bases such as
energy and sports drinks, fruit juices, and meal replacement drinks;
milk products such as smoothies, yogurt and yogurt drinks; cereal and
energy bars, breakfast cereals, pastas, and baked goods among others.
Stratum Nutrition pharmacology manager Joseph Evans said achieving
GRAS approval is a major milestone and a testament to the rigorous and
extensive scientific and technical information associated with
ARTINIA.
The Allowable Daily Intake (ADI) for ARTINIA is up to 70mg/kg per day
for food use and intake.
<snip>
20 something hits: glucagon randall psoriasis - ALL GrouPs
http://groups.google.com/groups/search?hl=en&q=psoriasis+randall+glucagon&sitesearch=
http://en.wikipedia.org/wiki/Glucagon
===================================
mercola - multiple sclerosis (MS) - vitamin D3 -Epstein-Barr Virus
(EBV)
http://articles.mercola.com/sites/articles/archive/2011/05/17/american-cancer-society-and-dermatologists-dead-wrong-about-the-sun.aspx
Sources:
BBC News April 19, 2011
http://www.bbc.co.uk/news/health-13092524
Neurology April 19, 2011;76(16):1410-4
http://www.ncbi.nlm.nih.gov/pubmed/21502600
<snip>
==========================
http://www.ncbi.nlm.nih.gov/pubmed/21573897
Int J Legal Med. 2011 May 15.
Good shedder or bad shedder-the influence of skin diseases on forensic
DNA analysis from epithelial abrasions.
Kamphausen T, Schadendorf D, von Wurmb-Schwark N, Bajanowski T,
Poetsch M.
Source
Institute of Legal Medicine, University Hospital Essen, Hufelandstr.
55, 45122, Essen, Germany.
Abstract
The successful analysis of weak biological stains by means of highly
sensitive short tandem repeat (STR) amplification has been increased
significantly over the recent years. Nevertheless, the percentage of
reliably analysable samples varies considerably between different
crime scene investigations even if the nature of the stains appears to
be the same. It has been proposed that the amount and quality of DNA
left at a crime scene may be due to individual skin conditions (among
other factors). Therefore, we investigated DNA from handprints from 30
patients acutely suffering from skin diseases like atopic dermatitis,
psoriasis or skin ulcer before and after therapy by STR amplification
using the new and highly sensitive Powerplex® ESX17 kit in comparison
to 22 healthy controls. Handprints from atopic dermatitis patients
showed a correct and reliable DNA profile in 90% and 40% of patients
before and after therapy, respectively. Regarding psoriasis patients,
we detected full DNA profiles in only 64% and 55% of handprints before
and after therapy. In contrast, in ulcus patients and controls, full
DNA profiles were obtained in much lower numbers. We conclude that
active skin diseases like atopic dermatitis or psoriasis have a
considerable impact on the amplificable DNA left by skin contact with
surfaces. Since up to 7% of adults in European countries suffer from
one of these diseases, this could explain at least partially the
varying quality of DNA from weak stains.
PMID: 21573897
randall... gosh mister wizard... did you lose your black hole god
particle shedder?