Hearts with SOUL? - Psor ABstractions --Autoimmune ODDs (SEE PsA!)- SFB/Th17/& more -FoxP3 & TREGs - Plantarum & Kimchi - Aspirin -DEFA5 & Crohn's- DRD4 SnP - Crazy MAN why? -IL-10 Th2 Skew? - Gut Microbiota redux -
randall
Mercola - HEART Disease - LINK:
Modify Your Diet so You Feel Terrific
http://www.mercola.com/article/heart_disease/index.htm
<there must be 5 dozen links on this one link>
I guess one has gotta have HEART.
Those Deccan health guys must think so to push their wares in
the groups.
But let's face it. I do the same thing while having zero economic kick
backs
any way, shape or form from those i SPAM . LOL
Here's one and it's anti spam.
I'm helping you to avoid drugs. LOL
Mercola Dangerous DRUGs
http://articles.mercola.com/sites/articles/archive/2011/01/11/the-year-in-pills.aspx
How to Solve Nearly Any Illness - Without Drugs
OK so i started to run/jog/walk before xmas time this year.
Why?
I want to LIVE...
But i wasn't happy with recovery times being so middle aged and all.
AND
I didn't want that to slow me down.
Nothing is gonna slow me down and break my stride
Break My Stride(Old Version)
http://www.youtube.com/watch?v=8XxBbcrs5KY
That was weird....Never met a squirrel like you. LoL
OK, that was FUN.
Back to xxxercise.
Talking squirrely i'm watching LAW of DEsIRE by Director: Pedro
Almodóvar
http://www.imdb.com/title/tt0093412/
Only watched a few minutes. It LOOKs HOT. Maybe too hot? Not sure
yet...
XXXercise please.
OK..
So i'm on this mini traPmoline thing and it seems GOOD as long as i'm
catching a few UVB's simultaneously.
I can bust a gut on this thing and i'm loving it.
And my RA & PsA joints are A OK as well.
Swell....
Let's do abstracts for why were HERE.
Right.
Don't have a heart xxx ON attack. LOL
======================
I won't. I promise. I'm exxxxxercising instead.
Genetics to the rescure?
Of curse.
All part of the psor course to a cure?
http://www.ncbi.nlm.nih.gov/pubmed/21214922
BMC Dermatol. 2011 Jan 7;11(1):1.
Psoriasis prediction from genome-wide SNP profiles.
Fang S, Fang X, Xiong M.
Abstract
ABSTRACT:
BACKGROUND: With the availability of large-scale genome-wide
association study (GWAS) data, choosing an optimal set of SNPs for
disease susceptibility prediction is a challenging task. This study
aimed to use single nucleotide polymorphisms (SNPs) to predict
psoriasis from searching GWAS data.
METHODS: Totally we had 2,798 samples and 451,724 SNPs. Process for
searching a set of SNPs to predict susceptibility for psoriasis
consisted of two steps. The first one was to search top 1,000 SNPs
with high accuracy for prediction of psoriasis from GWAS dataset. The
second one was to search for an optimal SNP subset for predicting
psoriasis. The sequential information bottleneck (sIB) method was
compared with classical linear discriminant analysis(LDA) for
classification performance.
RESULTS: The best test harmonic mean of sensitivity and specificity
for predicting psoriasis by sIB was 0.674(95% CI: 0.650-0.698), while
only 0.520(95% CI: 0.472-0.524) was reported for predicting disease by
LDA. Our results indicate that the new classifier sIB performs better
than LDA in the study.
CONCLUSIONS: The fact that a small set of SNPs can predict disease
status with average accuracy of 68% makes it possible to use SNP data
for psoriasis prediction.
PMID: 21214922
Cool, gwas and psor make sense to me.
At least we gain perspective on inflammation and evolution btw. :)
http://en.wikipedia.org/wiki/Genome-wide_association_study
In genetic epidemiology, a genome-wide association study (GWA study,
or GWAS), also known as whole genome association study (WGA study, or
WGAS), is an examination of all or most of the genes (the genome) of
different individuals of a particular species to see how much the
genes vary from individual to individual. Different variations are
then associated with different traits, such as diseases. In humans,
this technique has led to discovery of associations of particular
genes with diseases such as the eye disease known as age-related
macular degeneration and diabetes. In humans, hundreds or thousands of
individuals are tested, usually for single DNA mutations (single-
nucleotide polymorphisms, or SNPs). About 600 human GWASs have
examined 150 diseases and traits, and found 800 SNP associations.[1]
They are useful in finding the molecular pathways of disease, but
usually not useful in finding genes that predict risks of disease.[2]
[3][4]
<snip>
-----------------
http://www.ncbi.nlm.nih.gov/pubmed/21221615
Arch Dermatol Res. 2011 Jan 11.
Cyclosporin A induces the unfolded protein response in keratinocytes.
Hibino M, Sugiura K, Muro Y, Shimoyama Y, Tomita Y.
Department of Dermatology, Nagoya University Graduate School of
Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.
Abstract
Psoriasis vulgaris is a chronic inflammatory disorder of the skin, in
which activation of keratinocytes and crosstalk between keratinocytes
and T cells or dendritic cells are considered to be involved in the
pathogenesis of psoriasis vulgaris. Cyclosporin (Cy) A, an
immunomodulator, has been used for the treatment of psoriasis
vulgaris, but the mechanism of its action on keratinocytes has not
been well elucidated as its function on T cells is well known.
Previous study indicated that the expression of the unfolded protein
response (UPR) markers, GRP78/Bip and HRD1 were poorly expressed in
psoriasis vulgaris. To investigate if the UPR in keratinocytes is
involved in the pathogenesis of psoriasis vulgaris we assessed
immunocytochemistry of normal human skin and psoriatic lesions,
quantitative PCR of keratinocyte cell line (HaCaT) treated with TGFβ.
Moreover, to elucidate how CyA effects on the UPR in keratinocytes, we
set out quantitative PCR and western blotting, HaCaT and squamous cell
carcinoma cell lines (HSC-1) treated with CyA and CyA analog,
cyclosporin D. Furthermore, the siRNA-mediated knockdown effect of
cyclophilin (Cyp) A, Cyp B and Cyp C on HaCaT cells were also
examined. As a result, the UPR was downregulated in keratinocytes from
psoriatic lesions, characterized by immunocytochemical staining of
GRP78/Bip, CHOP/GADD153, HRD1 and C/EBPβ. TGFβ induced UPR markers in
HaCaT cells. CyA treatment and siRNA-mediated knockdown of Cyp B
induced the UPR in HaCaT cells or HSC-1 cells. Altogether, we
demonstrate that in psoriasis vulgaris CyA or reduction in Cyp B by
RNA interference might induce the UPR in keratinocytes.
PMID: 21221615
http://en.wikipedia.org/wiki/Protein_folding
http://en.wikipedia.org/wiki/Intrinsically_unstructured_proteins
http://en.wikipedia.org/wiki/Intrinsically_unstructured_proteins#Sequence_signatures_of_disorder
--------------
OK so we got some folded protein issue?
Don't take CyA?
YeP... smoke pot instead.
What and become like JARED?
No thankx, i'll stay with butt ugly plaques.
Or you should?
My psor plaques are so diminutive i'm having a hard time doing my next
LAB (as in plantarum this time again) trial.
And with the mini me tramPoline i'm not losing my heart except for
that nine year old Christina Taylor Green who
was born on 9-11. :(
And left the world a few days before 1-11-11.
http://www.ncbi.nlm.nih.gov/pubmed/21216492
J Am Acad Dermatol. 2011 Jan 7.
Increased risk of acute myocardial infarction in patients with
psoriasis: A 5-year population-based study in Taiwan.
Lin HW, Wang KH, Lin HC, Lin HC.
Biostatistics Research and Consulting Center, Taipei Medical
University, Hospital, Taipei, Taiwan.
Abstract
BACKGROUND: No previous study has investigated the incidence or risk
of acute myocardial infarction (AMI) developing after the diagnosis of
psoriasis in Asian populations.
OBJECTIVE: We sought to evaluate the association between psoriasis and
subsequent AMI during a 5-year follow-up period, using a nationwide
Taiwanese population-based claims database, and taking clinical and
demographic characteristics into consideration.
METHODS: Our study cohort consisted of all patients with a first
recorded diagnosis of psoriasis (N = 4752) between 1999 and 2001 and
of patients without a diagnosis of psoriasis (N = 23,760) who were
matched by age and sex (1:5) to the patients with psoriasis. Each
patient was tracked using hospitalization data from 2001 until the end
of 2006. Stratified Cox proportional hazard regressions (stratified by
age and sex) were performed as a means of computing the 5-year AMI-
free survivals after adjusting for possible confounding factors.
RESULTS: Of the total sample, 70 patients (0.2%) had AMIs during the 5-
year follow-up period: 22 (0.5% of the patients with psoriasis) from
the study cohort and 48 (0.2%) from the comparison cohort. After
adjusting for other factors, the hazard of AMI during the 5-year
follow-up period was 2.10 times greater (95% confidence interval
1.27-3.43, P = .004) for patients with psoriasis than for comparison
patients.
LIMITATIONS: We could not take into account some known risk factors
for AMI, such as smoking and body mass index.
CONCLUSIONS: Psoriasis may confer an independent risk of AMI in Asian
populations. We suggest that patients with psoriasis be made aware of
the increased risk of AMI.
PMID: 21216492
------------
http://www.ncbi.nlm.nih.gov/pubmed/21214631
Efficacy and safety of adalimumab in patients with psoriasis
previously treated with anti-tumour necrosis factor agents:
subanalysis of BELIEVE.
[...] Conclusion Adalimumab was effective and well-tolerated in
patients with psoriasis previously treated with anti-TNF therapy.
pmid: 21214631
HUMIRA
http://en.wikipedia.org/wiki/Adalimumab
---------------
http://www.ncbi.nlm.nih.gov/pubmed/21219290
Comparison of drug survival rates for adalimumab, etanercept and
infliximab in patients with psoriasis vulgaris.
[...] Conclusion The overall efficacy of anti-TNFα drugs diminishes
with time, as envisaged by the progressive loss of patient adherence
to treatment. The major reasons for stopping treatment were loss of
efficacy, followed by adverse events. Infliximab had the best patient
retention ability with 70% patients being still on drug after 4 years
of treatment.
pmid: 21219290
I don't DO anti TNF blockers.
Never have and never WILL by cracky.
I use LIFE to fight my psor DEATH.
And having to much SFB in the Gi tract (small intestines/lamina
propria et al) is skewing T helper one cells.
And if you have cancer or hiv that would BE NICE to have in sPades.
So my studies have morphed to help those of you with Th2 skews,
besides autoimmune folks like me with severe Th1 skews.
All due to SFB in the Gi tract and Th17 generation which prevents
TREGs from slowing excess inflammation called autoimmunity.
-----------------
http://www.ncbi.nlm.nih.gov/pubmed/21219637
Risk of venous thromboembolism in people admitted to hospital with
selected immune-mediated diseases: record-linkage study.
[...] Although it is mainly considered a complication of surgery, it
often occurs in people who have not undergone surgery, with recent
evidence suggesting that immune-mediated diseases may play a role in
VTE risk. We, therefore, decided to study the risk of deep vein
thrombosis (DVT) and pulmonary embolism (PE) in people admitted to
hospital with a range of immune-mediated diseases.
[...] CONCLUSIONS: People admitted to hospital with immune-mediated
diseases may be at an increased risk of subsequent VTE. Our findings
need independent confirmation or refutation; but, if confirmed, there
may be a role for thromboprophylaxis in some patients with these
diseases.
PMID: 21219637
=============
Seeing inflammation in REAL TIME?
Yikes... might change your diet or something radical like that? LOL
http://www.ncbi.nlm.nih.gov/pubmed/21221071
Q J Nucl Med Mol Imaging. 2010 Dec;54(6):639-53.
The role of radiolabelled anti-TNFa monoclonal antibodies for
diagnostic purposes and therapy evaluation.
Glaudemans AW, Dierckx RA, Kallenberg CG, Anzola Fuentes KL.
Department of Nuclear Medicine and Molecular Imaging, University
Medical Center Groningen, University of Groningen, Groningen, The
Netherlands - a.w.j.m.g...@ngmb.umcg.nl.
Abstract
Radiolabelled cytokines and monoclonal antibodies are an emerging
class of radiopharmaceuticals for imaging inflammation. These
radiopharmaceuticals bind to their targets with high affinity and
specificity and therefore have excellent diagnostic potential for
imaging of patients with chronic inflammatory diseases. One of the key
cytokines involved in the process of inflammation is tumor necrosis
factor alpha (TNFα). With the introduction of anti-TNFα monoclonal
antibodies over the past decade, treatment of inflammatory diseases
has evolved, which allowed remarkable advances in controlling signs
and symptoms of inflammation and in slowing destruction. However,
drugs may lose efficacy over time in patients or induce adverse
events. Using immediately the right medication tailored to the
patient's molecular status avoids unnecessary costs and side effects.
Significant differences in mechanisms of action and in therapy
outcome, depending on the disease to be treated, exist among the
different TNFα antagonists. Labelling these agents may help to find
out if TNFα is present in the inflammatory process and will therefore
help in therapy prediction and stratification in the individual
patient. This review describes the role of cytokines and in particular
of TNFα in the process of inflammation as well as the influence of
TNFα in some well-known and common inflammatory diseases, such as
rheumatoid arthritis, ankylosing spondylitis, inflammatory bowel
diseases, psoriasis and sarcoidosis. The main focus of this article is
to review the role of molecular imaging with radiolabelled anti-TNFα
monoclonal antibodies for diagnostic purposes, and in therapy
precision, decision-making and evaluation.
PMID: 21221071
========================
What are your odds of autoimmunity?
#1 - don't BE FEMALE
#2 - Being MALE decreases your ODDs.
http://www.webmd.com/rheumatoid-arthritis/news/20110110/1-in-12-women-will-have-autoimmune-disease
1 in 12 Women Will Have Autoimmune Disease
Study Estimates Lifetime Risk of Rheumatoid Arthritis and Other
Autoimmune Diseases
By Jennifer Warner
WebMD Health NewsReviewed by Laura J. Martin, MD
Jan. 11, 2011 -- One in 12 women and one in 20 men in the U.S. will
develop some sort of autoimmune disease in their lifetime, according
to new estimates.
Inflammatory autoimmune diseases, such as rheumatoid arthritis (RA),
are relatively common conditions, especially among adults aged 50 and
older.
Researchers say the risk of developing an autoimmune disease depends
on a number of factors, including age and gender, but until now there
hasn’t been an easy-to-understand average risk over a person’s
lifetime for adults in the U.S.
The results suggest that one in 28 women (3.6%) and one in 59 (1.7%)
of men will develop rheumatoid arthritis, the most common autoimmune
disease, in their lifetime. The second most common autoimmune disorder
in the study was polymyalgia rheumatica (PMR) with a lifetime risk of
2.4% for women and 1.7% for men.
"We estimated the lifetime risk for rheumatic disease for both sexes,
something that had not been done before," researcher Cynthia Crowson,
a biostastician at the Mayo Clinic, says in a news release.
"Prevalence and incidence rates existed, but prevalence figures
underestimate individual risk and incidence rates express only a
yearly estimate."
Researchers say the risk of autoimmune diseases changes at every age,
but the results can serve as a guide in counseling people regarding
their overall risk of these conditions.
New RA Risk Estimates
The study, published in Arthritis and Rheumatism, determined the
average risk of developing one of seven of the most common autoimmune
disorders over a person’s lifetime, including: rheumatoid arthritis,
systemic lupus erythematosus, psoriatic arthritis, polymyalgia
rheumatica, giant cell arteritis, ankylosing spondylitis, and
Sjögren’s syndrome.
Researchers based their estimates on the number of autoimmune diseases
diagnosed between 1955 and 2007 among 1,179 residents of Olmstead
County, Minn., and then extrapolated their results to the general
population.
Overall, researchers estimate 8.4% of women (1 in 12) and 5.1% (1 in
20) of men will develop some type of autoimmune disease in their
lifetime.
Specifically, the lifetime risk of the six autoimmune diseases
examined in the study were:
Disease
Women Men (mean are under the women- right)
LOL
Rheumatoid Arthritis 3.6% or 1 in 28
1.7% or 1 in 59
Polymyalgia Rheumatica 2.4%
1.7%
Systemic Lupus Erythematosus 0.9%
0.2%
Giant Cell Arteritis 1.0%
0.5%
Psoriatic Arthritis 0.5%
0.6% (wow-- men have a .1% greater chance of PsA then women? Didn't
know that i betcha?)
Primary Sjögrens syndrome 0.8%
0.04%
Ankylosing Spondylitis 0.1%
0.6%
Researchers say these figures represent a substantial risk and could
have implications on national disease awareness campaigns and research
into diagnosis and treatments for autoimmune diseases.
<snip>
===========================
Many folks get RA after the age of 50. Is it the genes and what makes
them fire
for early autoimmune onset?
And at this AGE do syndrome X (metabolic disorder) folks also GET PsA?
How about SFB?
SFB inducts Th17 and that is stopping TREGs from forming.
And that might also be an effect of syndrome X then?
I don't KNOW.
But....
I believe it... get the L. Plantarum please?
It eats SFB btw...
Sweet! I know and its my sweet whey to stay UN psor. LOL
http://www.ncbi.nlm.nih.gov/pubmed/21221592
Rheumatol Int. 2011 Jan 11.
The Th17/Treg imbalance and cytokine environment in peripheral blood
of patients with rheumatoid arthritis.
Wang W, Shao S, Jiao Z, Guo M, Xu H, Wang S.
Department of Pathogenic Biology, School of Medical Science and
Laboratory Medicine, Jiangsu University, 212001, Zhenjiang, China.
Abstract
Broken Th17/Treg balance has been reported contributing to several
inflammatory autoimmune diseases. The objective of the study was to
investigate whether the Th17/Treg balance was impaired in the
peripheral blood of patients with rheumatoid arthritis (RA). The
frequencies of Treg cells and Th17 cells and mRNA expression of
transcription factor RORγt and FoxP3 in peripheral blood of RA
patients (n = 37) and healthy controls (n = 30) were determined by
flow cytometry and real-time PCR, respectively. Eleven serum cytokines
were analyzed by using cytometeric bead array (CBA). The results
demonstrated that active RA patients exhibited increased peripheral
Th17 cells, Th1- and Th17-related cytokines and RORγt expression while
decreased Treg cells and FoxP3 expression. In addition, Th17/Treg
ratios were positively correlated with serum concentrations of Th1-
and Th17-related cytokines. In conclusion, our results indicated that
Th17/Treg balance was broken in peripheral blood, which may play an
important role in the development of RA.
PMID: 21221592
Does L. Plantarum dictate immune health or homeostasis?
Perhaps.
But the facts are getting clearer. But not as FAST as my skin did with
L. plantarum rich kimchi.
http://www.ncbi.nlm.nih.gov/pubmed/21219575
Am J Transplant. 2011 Jan 10. doi: 10.1111/j.1600-6143.2010.03389.x.
Distinct Inflammatory Signals Have Physiologically Divergent Effects
on Epigenetic Regulation of Foxp3 Expression and Treg Function.
Lal G, Yin N, Xu J, Lin M, Schroppel S, Ding Y, Marie I, Levy DE,
Bromberg JS.
Department of Surgery and Microbiology and Immunology and the Center
for Vascular and Inflammatory, University of Maryland, Baltimore, MD
Recanati/Miller Transplantation Institute, Mount Sinai School of
Medicine, New York, NY Division of Nephrology, Mount Sinai School of
Medicine, New York, NY Pathology and Microbiology, New York University
School of Medicine, New York, NY.
Abstract
Foxp3 expression in regulatory T cells (Treg) is required for their
development and suppressive function. How different inflammatory
signals affect Foxp3 chromatin structure, expression and Tregs
plasticity are not completely known. In the present study, the Toll-
like receptor 2 (TLR2) ligand peptidoglycan inhibited Foxp3 expression
in both natural Treg (nTreg) and TGFβ-driven adaptive Treg (aTreg).
Inhibition was independent of paracrine Th1, Th2 and Th17 cytokines.
PGN-induced T cell-intrinsic TLR2-Myd88-dependent IFR1 expression and
induced IRF1 bound to IRF1 response elements (IRF-E) in the Foxp3
promoter and intronic enhancers, and negatively regulated Foxp3
expression. Inflammatory IL-6 and TLR2 signals induced divergent
chromatin changes at the Foxp3 locus and regulated Treg suppressor
function, and in an islet transplant model resulted in differences in
their ability to prolong graft survival. These findings are important
for understanding how different inflammatory signals can affect the
transplantation tolerance and immunity.
PMID: 21219575
-------------
Will it be possible to correct Th2 (cancer and HIV aids) skews and Th1
(autoimmunity) with L. Plantarum?
Time will tell as the FACTS add uP.
http://www.ncbi.nlm.nih.gov/pubmed/21217015
J Immunol. 2011 Jan 7.
TLR1/TLR2 Agonist Induces Tumor Regression by Reciprocal Modulation of
Effector and Regulatory T Cells.
Zhang Y, Luo F, Cai Y, Liu N, Wang L, Xu D, Chu Y.
Department of Immunology, Shanghai Medical College, Key Laboratory of
Molecular Medicine of Ministry of Education, Fudan University,
Shanghai 200032, People's Republic of China.
Abstract
Using TLR agonists in cancer treatment can have either beneficial or
detrimental effects. Therefore, it is important to determine their
effect on the tumor growth and understand the underlying mechanisms in
animal tumor models. In this study, we report a general
immunotherapeutic activity of a synthetic bacterial lipoprotein (BLP),
a TLR1/TLR2 agonist, on established lung carcinoma, leukemia, and
melanoma in mice. Systemic treatment of 3LL tumor-bearing mice with
BLP, but not LPS, led to a dose-dependent tumor regression and a long-
lasting protective response against tumor rechallenge. The BLP-
mediated tumor remission was neither mediated by a direct tumoricidal
activity nor by innate immune cells, because it lacked therapeutic
effect in immunodeficient SCID mice. Instead, BLP treatment reduced
the suppressive function of Foxp3(+) regulatory T cells (Tregs) and
enhanced the cytotoxicity of tumor-specific CTL in vitro and in vivo.
Furthermore, adoptive cotransfer of BLP-pretreated but not untreated
CTL and Tregs from wild-type but not from TLR2(-/-) mice was
sufficient to restore antitumor immunity in SCID mice by reciprocally
modulating Treg and CTL function. These results demonstrate that the
TLR1/TLR2 agonist BLP may have a general tumor therapeutic property
involving reciprocal downregulation of Treg and upregulation of CTL
function. This property may play an important role in the development
of novel antitumor strategies.
PMID: 21217015
==================
http://www.ncbi.nlm.nih.gov/pubmed/21218855
ACS Chem Biol. 2011 Jan 11.
Fluorescence and atomic force microscopy imaging of wall teichoic
acids in Lactobacillus plantarum.
Andre G, Deghorain M, Bron P, van Swam I, Kleerebezem M, Hols P,
Dufrene YF.
Abstract
Although teichoic acids are major constituents of bacterial cell
walls, little is known about the relationships between their spatial
localization and their functional roles. Here, we used single-molecule
atomic force microscopy (AFM) combined with fluorescence microscopy to
image the distribution of wall teichoic acids (WTAs) in Lactobacillus
plantarum, in relation with their physiological roles. Phenotype
analysis of the wild-type strain and of mutant strains deficient for
the synthesis of WTAs (ΔtagO) or cell wall polysaccharides (Δcps1-4)
revealed that WTAs are required for proper cell elongation and cell
division. Nanoscale imaging by AFM showed that strains expressing WTAs
have a highly polarized surface morphology, the poles being much
smoother than the side walls. AFM and fluorescence imaging with
specific lectin probes demonstrated that the polarized surface
structure correlates with a heterogeneous distribution of WTAs, the
latter being absent from the surface of the poles. These observations
indicate that the polarized distribution of WTAs in L. plantarum plays
a key role in controlling cell morphogenesis (surface roughness, cell
shape, elongation, and division).
PMID: 21218855
==================
Kimchi to the resCURE of your Qi?
Time will TELL and so WILL i. :)
Going, going GONG with Qi cure. LOL
http://www.ncbi.nlm.nih.gov/pubmed/21215484
Int J Food Microbiol. 2010 Dec 13.
Functional properties of Lactobacillus strains isolated from kimchi.
Lee H, Yoon H, Ji Y, Kim H, Park H, Lee J, Shin H, Holzapfel W.
Abstract
The objective of this study was to evaluate the functional properties
of lactic acid bacteria (LAB) from kimchi, a traditional Korean
fermented vegetable product generally consumed raw as a side-dish with
practically every meal. Twelve mild acid producing facultatively
heterofermentative Lactobacillus strains were selected for their
potential as starter cultures for fermentation of kimchi, and
evaluated for their functional properties. Eleven strains were
identified as Lactobacillus sakei and one as Lactobacillus plantarum.
The strains identified as L. sakei differed in some physiological
features; of particular interest was the fact that 9 of these strains
produced L(+) lactic acid from glucose in presence of acetate. All
strains were able to survive gastrointestinal conditions simulating
stomach and duodenum passage. In addition, they showed higher
adherence to HT-29 cells than Lactobacillus rhamnosus GG, a commercial
probiotic strain used worldwide. These strains also showed
antimicrobial activity against a number of food-borne pathogens. Their
ability to lower cholesterol was demonstrated by BSH (bile salt
hydrolytic) activity, and cholesterol assimilation tests in vitro. The
results suggest the probiotic potential of these strains for use in
kimchi fermentation.
PMID: 21215484
full text costs money
http://linkinghub.elsevier.com/retrieve/pii/S0168-1605(10)00693-8
pay it and send me the pdf please. :)
===================================
Aspirin again and again.
WILL IT SAVE my LIFE?
Maybe or someone you KNOW and LOVE?
That would be COOL.
While i could never take so much as a baby aspirin without flaring a
patch of psor plaque, i can NOW.
snopes.com: Aspirin and Heart Attacks
Variations: Some versions of this message include a picture of a box
of Bayer Aspirin Extra Strength Quick Release Crystals,
<snip>
Go there:
http://www.snopes.com/medical/drugs/aspirin.asp
http://www.fda.gov/Drugs/ResourcesForYou/Consumers/QuestionsAnswers/ucm071879.htm
http://www.fda.gov/Drugs/EmergencyPreparedness/BioterrorismandDrugPreparedness/ucm133431.htm
http://www.fda.gov/Drugs/EmergencyPreparedness/BioterrorismandDrugPreparedness/ucm133505.htm
<snip>
==================
OK time for secret stuff. I don't want the morons to get this.
They might exPlode a brain cell. LOL
Don't you want to go ALL jared on mediots?
Don't answer that. LOL
http://www.ncbi.nlm.nih.gov/pubmed/19855381
Nat Immunol. 2010 Jan;11(1):76-83. Epub 2009 Oct 22.
Enteric defensins are essential regulators of intestinal microbial
ecology.
Salzman NH, Hung K, Haribhai D, Chu H, Karlsson-Sjöberg J, Amir E,
Teggatz P, Barman M, Hayward M, Eastwood D, Stoel M, Zhou Y, Sodergren
E, Weinstock GM, Bevins CL, Williams CB, Bos NA.
Division of Gastroenterology, Medical College of Wisconsin, Milwaukee,
Wisconsin, USA. nsal...@mcw.edu
Comment in:
Nat Immunol. 2010 Jan;11(1):49-50.
Abstract
Antimicrobial peptides are important effectors of innate immunity
throughout the plant and animal kingdoms. In the mammalian small
intestine, Paneth cell alpha-defensins are antimicrobial peptides that
contribute to host defense against enteric pathogens. To determine if
alpha-defensins also govern intestinal microbial ecology, we analyzed
the intestinal microbiota of mice expressing a human alpha-defensin
gene (DEFA5) and in mice lacking an enzyme required for the processing
of mouse alpha-defensins. In these complementary models, we detected
significant alpha-defensin-dependent changes in microbiota
composition, but not in total bacterial numbers. Furthermore, DEFA5-
expressing mice had striking losses of segmented filamentous bacteria
and fewer interleukin 17 (IL-17)-producing lamina propria T cells. Our
data ascribe a new homeostatic role to alpha-defensins in regulating
the makeup of the commensal microbiota.
PMID: 19855381
PMCID: PMC2795796
Free PMC Article
http://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19855381/?tool=pubmed
But, but, but shouldn't hot kofi see this one?
You mean for the crohn's effects?
Yes, of course. They call it paneth's disease in the first of these 14
hits.
OK, i'll warn him... i think i just did. LOL
DEFA5 - 14 hits - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=DEFA5
I'm sure i've posted this one.
http://www.ncbi.nlm.nih.gov/pubmed/21122555
pmid: 21122555
Oh well i don't see it.
So i'll post it now.
J Crohns Colitis. 2010 Nov;4(5):523-31. Epub 2010 Jul 6.
Paneth's disease.
Wehkamp J, Stange EF.
Robert-Bosch-Krankenhaus Stuttgart, Auerbachstr 110, 7076 Stuttgart,
Germany. jan.w...@ikp-stuttgart.de
Abstract
In about 70% of patients Crohn's disease (CD) affects the small
intestine. This disease location is stable over time and associated
with a genetic background different from isolated colonic disease. A
characteristic feature of small intestinal host defense is the
presence of Paneth cells at the bottom of the crypts of Lieberkühn.
These cells produce different broad spectrum antimicrobial peptides
(AMPs) most abundantly the α-defensins HD-5 and -6 (DEFA5 und DEFA6).
In small intestinal Crohn's disease both these PC products are
specifically reduced. As a functional consequence, ileal extracts from
Crohn's disease patients are compromised in clearing bacteria and
enteroadherent E. coli colonize the mucosa. Mechanisms for defective
antimicrobial Paneth cell function are complex and include an
association with a NOD2 loss of function mutation, a disturbance of
the Wnt pathway transcription factor TCF7L2 (also known as TCF4), the
autophagy factor ATG16L1, the endosomal stress protein XBP1, the toll-
like receptor TLR9, the calcium mediated potassium channel KCNN4 as
well as mutations or inactivation of HD5. Thus we conclude that small
intestinal Crohn's disease is most likely a complex disease of the
Paneth cell: Paneth's disease.
PMID: 21122555
The secret is the SFB in the lamina propria cells. Duh.
And get some kimchi to eAT it.
EAT it.
Eat It - Weird Al Yankovic (with lyrics)
http://www.youtube.com/watch?v=E8Nv5hWd-Js
Really?
You've got randall's disease... you dork.
I do?
What is it?
http://www.wrongdiagnosis.com/r/randall_disease/intro.htm#whatis
Randall disease: A rare disorder involving the deposition of light and
heavy chain monoclonal immunoglobulins which can lead to kidney
disease. More detailed information about the symptoms, causes, and
treatments of Randall disease is available below.
Just BEAT it, id squid or i'll starve you to life.
And then you can't act like a DRD4 e7 libby pooh anymore.
What? I've got to grow up?
Yikes... beING libby pooh is FUN and why the main stream media is so
stuPidly. :)
What do you mean?
Take the latest crap their feeding you regarding the 22 y/o moron who
killed people and looks like charles manson with that stupid grin.
Slate nailed it: (they even mentioned chucky manson another--->
nut case:
http://articles.cnn.com/2009-03-20/justice/charles.manson.prison_1_charles-manson-murders-family-prison-interview?_s=PM:CRIME
]
i must think LIKE (nay - say love?) this salon guy?
http://img.slate.com/media/1/123125/123019/2279921/2279922/110111_PRESS_loughnerTN.jpg
http://www.slate.com/id/2280806/
But after reading the article it's CLEAR i'm clearer thinking?
No way?
Yes WAY and it's not sweet, though evil i nail him in udder ways.
He hates his father and life is easiest to see:
Whose got the grin might tell the tale?
Slate and free republic has it.
So does this site called patdollard?
http://patdollard.com/2011/01/psycho-killer-smiles-for-mug-shot-and-first-court-appearance/
[...] Loughner has invoked his right to remain silent for the last 48
hours, saying “not a word,” Pima County Sheriff Clarence Du pnik said.
<snip>
MaYBE DUPNIK should keep his trap shut as WELL?
Swell...
He said that this guy was a victim of sarah plain and right wing talk
radio?
Dupnik is a typiCOW pig and shill for obama think, then?
How so far fetched juan?
Dig it.
======================
While the main stream media is busy blaming right wing talk radio the
actual truth is more perverse.
Jared the 22y/o guy who shot the congresswoman and other folks liked
zeitgeist (the movie) ?
It's on youtube
Zeitgeist - The Movie: Federal Reserve (Part 1 of 5) 4,201,199 views
http://www.youtube.com/watch?v=_dmPchuXIXQ
HOLY CRAP, 4 million people will NOW buy a gun and go NUTZ?
He, JHARED DIDN'T listen to right or left wing TALK radio or the
NEWs...
Maybe jared thinks his name is ji HAD a gun or got a gun?
Is this the new terrorism of the middle east or is this some sort of
humanism on steroids?
Or simply a poor attempt to make our failure of a prez more
impressive?
Johnny got his gun and you know what that meant:
code for left wing wannabe's to tell the gov to screw off with
their wars?
http://en.wikipedia.org/wiki/Johnny_Got_His_Gun
http://en.wikipedia.org/wiki/Johnny_Got_His_Gun#In_popular_culture
http://en.wikipedia.org/wiki/Johnny_Got_His_Gun_(film)
Jared's best friend said:::
"I really think that this 'Zeitgeist' documentary had a profound
impact upon Jared Loughner's mindset and how he viewed the world that
he lives in," he said
Also something called _____loose change_____ which i haven't watched
YET.
So?
Do i need to keeP my TRAp SHUT or what? LOL
After watching Zeit i can't see HOW that might inspire anything close
to murder---> old and young people or
congress people???
But otoh, is loose change mind manipulative somehow?
I'll check it out.
NOW?
YES NOW..
OK wiki it?
http://en.wikipedia.org/wiki/Loose_Change_(film)
Holy T----->URD batman... this is pure stupidly <g>
[...] Loose Change is a series of films released between 2005 and 2009
which argue that the September 11, 2001 attacks were planned and
conducted by elements within the United States government, and base
the claims on perceived anomalies in the historical record of the
attacks. The films were written and directed by Dylan Avery, and
produced by Korey Rowe, Jason Bermas and Matthew Brown.
The original 2005 film was edited and re-released as Loose Change: 2nd
Edition (2006), and then subsequently edited a third time for the 2nd
Edition Recut (2007), each time to tighten the focus on certain key
areas and to correct some inaccurate claims and remove copyrighted
material. Loose Change: Final Cut, deemed "the third and final release
of this documentary series"[1] was released on DVD and Web-streaming
format on November 11, 2007.[2][3]
Another version of the film, Loose Change 9/11: An American Coup,
released on September 22, 2009, is narrated by Daniel Sunjata and
distributed by Microcinema International.[4]
Coverage for the film increased in 2006 with the recut release having
airings on U.S. and European television stations and over 4 million
views online in four months,[5] leading Vanity Fair to say it could be
the first internet blockbuster.[6] Loose Change puts the 9/11 attacks
within a context of a false flag operation and goes on to question the
plausibility of the Pentagon attack, World Trade Center collapse and
United 93 phone calls and crash. The film's main claims have been
disputed by journalists,[7] independent and 9/11 Truth researchers,[8]
[9] and prominent members of the scientific and engineering community.
<snip>
Does this mean jared was mind maniPulated by left wing insane-or's?
Pushing their crap to keep young people in the dark and scamming their
vote for left wing insane-iac's like
that guy who said he'd be better then a BUSH then spent more on then a
bush? LOL
I don't need to watch this birtheror truther nonsense.
So my TRAP remains OPEN for the truth to invade your BRAIN cells. LOL
Morons who live opposite of TRUTH & reality, need to pull or extract
said craniums from their rectums:
http://en.wikipedia.org/wiki/9/11_Truth_movement
But ONE does need to watch out for PEOPLE who believe LIES.
Most of these folks have hide the pride issues or dRD4 e7 snps.
<randall note: hide the pride is #1 sin in the bible?>
Loose Change 9/11 documentary part 1 - 1,740,724 views
http://www.youtube.com/watch?v=CDx1GLqvBO8
It's youtube that caused these murders by JARED the TOOL and FOOL of
the LEFT wING ding a lings?
YOU THINK?
You don't?
Sarah P got porked by the mediots (media + idiot)
Sarah Palin - 'Blood Libel'
http://www.youtube.com/watch?v=Jb0VW8vnMhQ
Dershowitz Gives Palin the Go-Ahead on "Blood Libel"
Posted Wednesday, January 12, 2011 1:49 PM | By David Weigel
http://www.slate.com/blogs/blogs/weigel/archive/2011/01/12/dershowitz-gives-palin-the-go-ahead-on-blood-libel.aspx
Hey! I've got some weigel in me.... WEEEEE... LOL
Does the Weigel have some DRD4 snp in HIM?
Weeee?
Can i tell by simply reading him?
http://www.slate.com/blogs/search/searchresults.aspx?u=2539
I can try. :)
BUT the latest on DRD4 and IL-10 which causes a Th2 skew and cancer
and exacerbates hiv/aids seems more timely.
I bet you can't FIND my other ones (drd4 posts/threads) now.
It's very very very EXPLOSIVE.
And i don't mean anally.
Is it anal or anally retentive?
http://en.wikipedia.org/wiki/Anal_retentive
H'mm both i guess?
OK move on dork dot.
OK, ok, ok, push off id squid.
Shut up and why call me (you) that?
Easy it's to shut YOU UP.
http://en.wikipedia.org/wiki/Id,_ego,_and_super-ego
And that makes you only part of the holy trinity. LOL
are you id, ego, super duPer pooper ego or squid age?
Your all 3... like G the father and son and holy gheist?
OK, ok, i get it and i'm shutting up, so don't go zeitgheist on ME jar
ed head.
Move it.
Right now and here:
http://www.ncbi.nlm.nih.gov/pubmed/21216474
Psychiatry Res. 2011 Jan 7.
The interleukin 10 promoter haplotype ACA and the long-form variant of
the DRD4 uVNTR polymorphism are associated with vulnerability to
schizophrenia.
Lung FW, Yang MC, Shu BC.
Department of Psychiatry, Kaohsiung Armed Forces General Hospital,
Kaohsiung, Taiwan; Department of Psychiatry, National Defense Medical
Center, Taipei, Taiwan; Department of Neurology, Kaohsiung Medical
University, Kaohsiung, Taiwan.
Abstract
A total of 934 patients with schizophrenia and 433 controls were
genotyped for the interleukin-10 (IL-10) promoter and DRD4 uVNTR
polymorphisms. DRD4 long-form variants (namely, those with ≥5
repeats), homozygosity for the 4-repeat allele, and the IL-10
haplotype ACA were associated with schizophrenia, respectively. No
obvious interactions among the potential polymorphisms were found,
which suggests that IL-10 and DRD4 confer vulnerability to
schizophrenia independently.
PMID: 21216474
OK but the drd4 and IL-10 snp's don't jive.
Right i am. LOL
Ham i ate or am?
OK pork MORK from DORK. LOL
Jejune oh gloomy id spid...
LOOK at this instead:
http://www.ncbi.nlm.nih.gov/pubmed/21135754
Pediatr Res. 2010 Dec 3.
Pulse Probiotic Administration Induces Repeated Small Intestinal Muc3
Expression in Rats.
Dykstra NS, Hyde L, Adawi D, Kulik D, Ahrne S, Molin G, Jeppsson B,
Mackenzie A, Mack DR.
Children's Hospital of Eastern Ontario Research Institute [N.S.D.,
L.H., D.K., A.M., D.R.M.], Ottawa, Ontario, K1H 8L1, Canada;
Department of Surgery [D.A., B.J.], Malmo University, Malmo, SE-205
02, Sweden; Department of Food Science [S.A., G.M.], Lund University,
Lund, S-221 00, Sweden; Department of Pediatrics [A.M., D.R.M.],
University of Ottawa, Ottawa, Ontario, K1H 8M5, Canada.
Abstract
Upon ingestion, probiotics may act to protect the host through a
number of protective mechanisms including modulation of genes involved
in intestinal innate mucosal defense such as epithelial cell derived
mucin glycoproteins and inhibitor of apoptosis proteins. To determine
the specificity of effect and sustainability of response in vivo,
Lactobacillus plantarum 299v (Lp299v), Lactobacillus rhamnosus R0011
(LrR0011) and Bifidobacterium bifidum R0071 (BbR0071) were added
repeatedly or intermittently to the drinking water of Sprague-Dawley
rats. Following sacrifice via CO2 suffocation, Muc2, Muc3, NAIP, HIAP1/
cIAP2 and HIAP2/cIAP1 mRNA and protein levels were analyzed via RT-PCR
and immunohistochemistry. Live Lp299v, BbR0071 and LrR0011 increased
Muc3 protein and mRNA expression in jejunum and ileum. Heat-killed and
a non-adherent derivative of Lp299v failed to induce Muc3 expression.
Lp299v did induce expression of HIAP2/cIAP1 and NAIP expression. Muc3
mucin expression was elevated for 5 days following oral administration
of Lp299v but this effect was not sustained despite ongoing daily
ingestion of a probiotic. Intermittent pulse ingestion of probiotics
however, was found to repeatedly increase Muc3 expression. We conclude
that selected probiotics can induce protective genes of mucosal
intestinal epithelial cells, an effect that is reproducible with pulse
probiotic administration. ABBREVIATIONS:
PMID: 21135754
If figures. I was talking with an ICU nurse from Rady Hospital
(Childrens - San Diego) who
said they give L. plantarum to some patients. And wondered wHY.
NOW i KNOW sis.
Why use antibios when you can jujitsu with live benefical bios or LAB
(lactic acid [loving] bacteria)?
http://www.ncbi.nlm.nih.gov/pubmed/20721536
Intensive Care Med. 2010 Aug 19.
Probiotics versus antibiotic decontamination of the digestive tract:
infection and mortality.
Oudhuis GJ, Bergmans DC, Dormans T, Zwaveling JH, Kessels A, Prins MH,
Stobberingh EE, Verbon A.
Department of Medical Microbiology, NUTRIM School for Nutrition,
Toxicology and Metabolism, Maastricht University Medical Centre, PO
Box 5800, 6202 AZ, Maastricht, The Netherlands.
Abstract
PURPOSE: Selective decontamination of the digestive tract (SDD) has
been shown to decrease the infection rate and mortality in intensive
care units (ICUs); Lactobacillus plantarum 299/299v plus fibre (LAB)
has been used for infection prevention and does not harbour the
potential disadvantages of antibiotics. The objective was to assess
whether LAB is not inferior to SDD in infection prevention.
METHODS: Two hundred fifty-four consecutive ICU patients with expected
mechanical ventilation >/=48 h and/or expected ICU stay >/=72 h were
assigned to receive SDD: four times daily an oral paste (polymyxin E,
gentamicin, amphotericin B), enteral solution (same antibiotics),
intravenous cefotaxime (first 4 days) or LAB: two times daily L.
plantarum 299/299v with rose-hip.
RESULTS: The primary endpoint was infection rate. A difference <12%
between both groups indicated non-inferiority of LAB. The trial was
prematurely stopped after a study reporting increased mortality in
critically ill pancreatitis patients receiving probiotics. No
significant difference in infection rate [31% in the LAB group, 24% in
the SDD group (OR 1.68, 95% CI 0.91-3.08; p = 0.10)] was found. ICU
mortality was 26% and not significantly different between the LAB and
SDD groups. Gram-positive cocci and Pseudomonas aeruginosa were
significantly more frequently isolated from surveillance cultures in
the SDD group compared to the LAB group (for sputum: 18 vs. 10% and 33
vs. 14%). Significantly more Enterobacteriaceae were found in the LAB
group (23 vs. 50%). No increase in antibiotic resistance was found
during and after SDD or LAB use.
CONCLUSIONS: The trial could not demonstrate the non-inferiority of
LAB compared with SDD in infection prevention. Results suggest no
increased ICU mortality risk in the LAB group.
PMID: 20721536
http://www.ncbi.nlm.nih.gov/pubmed/20699130
Vaccine. 2010 Sep 24;28(41):6714-22. Epub 2010 Aug 8.
Platform technology to deliver prophylactic molecules orally: an
example using the Class A select agent Yersinia pestis.
del Rio B, Fuente JL, Neves V, Dattwyler R, Seegers JF, Gomes-Solecki
M.
Department of Molecular Sciences, UTHSC, Memphis, TN 38163, USA.
Abstract
Consumed for centuries, lactic acid bacteria are excellent candidates
for the development of safe mucosal delivery vehicles for prophylactic
and therapeutic molecules. We have recently reported that the immune
response to an effective OspA-expressing L. plantarum vaccine for Lyme
disease is modulated by the lipid modification of the antigen. In this
study, we investigated if this technology can be applied to developing
vaccines for other diseases by focusing on the Class A select agent,
Yersinia pestis. We used a number of biochemistry and immunology
techniques to determine the localization of the immunogen in our
delivery vehicle and to evaluate the mucosal as well as the systemic
immune response to the immunogen. We found that only LcrV cloned
downstream of the signal sequence of B. burgdorferi OspA ((ss)LcrV),
but not wildtype LcrV (LcrV), is localized to the desired
peptidoglycan layer of the delivery vehicle. In addition, only mice
that received L. plantarum expressing (ss)LcrV produced significant
titers of IgG antibody as well as IgA in distant mucosal sites such as
lungs and vagina. Furthermore, only L. plantarum expressing (ss)LcrV
induced significant amounts of pro-inflammatory cytokines TNFα, IL-12,
IFNγ and IL-6 as well as anti-inflammatory IL-10 in human peripheral
blood mononuclear cells derived dendritic cells, suggesting that the
mechanism by which LcrV-expressing L. plantarum stimulates the immune
response involves polarization to Th1 mediated immunity with some
involvement of Th2. The study reported here proves that this system is
a platform technology to develop oral vaccines for multiple diseases.
PMID: 20699130
This is a nice search:
Plantarum and ORAL - 116 hits - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=plantarum+oral
Is that enough BABE?
what?
Your calling me a porker now?
No, no, stuPidly juan.
Hey! I call you dat and not you calling me DAT.
OK, but i'm YOU. LOL
Right you are. <sigh>
What have you got on me?
Your gutz?
Spill please.
http://www.ncbi.nlm.nih.gov/pubmed/18621050
Gastroenterology. 2008 Sep;135(3):849-60, 860.e1-6. Epub 2008 May 21.
Intestinal deletion of Pofut1 in the mouse inactivates notch signaling
and causes enterocolitis.
Guilmeau S, Flandez M, Bancroft L, Sellers RS, Tear B, Stanley P,
Augenlicht LH.
Department of Oncology, Albert Einstein Cancer Center, Montefiore
Hospital, Bronx, New York 10467, USA. sgui...@montefiore.org
Abstract
BACKGROUND & AIMS: Notch downstream targets are fundamental to
intestinal cell lineage commitment and are suggested as therapeutic
targets for colon cancer cells. However, the role of endogenous Notch
signaling through receptor-ligand interaction, and effects of its
longer term down-regulation on intestinal homeostasis, are unclear.
METHODS: To address these issues, the gene encoding protein O-
fucosyltransferase 1, an enzyme required for Notch ligand binding and
thus activation of all Notch receptors, was deleted in the mouse
intestinal and colonic epithelium, through Villin-Cre-mediated
recombination.
RESULTS: Pofut1 deletion inactivated Notch signaling, giving rise to
smaller but viable mice. These mice exhibited a large increase in all
intestinal secretory cell lineages, which accumulated in the crypts,
resulting in crypt hyperplasia. Although proliferating cells were
largely reduced in the colon, the transit amplifying compartment was
maintained in the upper crypts of the intestinal mucosa. By 9 months,
these perturbations in cell maturation altered mucus-associated gut
microbiota and caused chronic intestinal inflammation, with evidence
of bacterial translocation to the mesenteric lymph nodes, macrophage,
and T-lymphocyte infiltration, and Th1/Th17 immune response.
Dysplastic foci were also observed in Pofut1-deficient small intestine
with occasional progression to tumor formation.
CONCLUSIONS: Mucus hypersecretion upon Pofut1 inactivation is
accompanied by alteration of the mucus-associated flora, which likely
contributes to the development of enterocolitis. Therefore, these data
identify important potential complications in strategies to target
Notch signaling in therapeutic approaches to colon cancer.
PMID: 18621050
143 hits; l. plantarum gi tract - pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=l.%20plantarum%20gi%20tract&cmd=correctspelling
very fertile grounds no doubt.
OK so?
So read em...
OK but i'm in to the sunshine of my LOVE now..
Oh please you can sit under the uvb rays any old time.
Yes i can... but now is part of my golden ratio. LOL
So read this oh FAT HEAD and Gi tract JUAN and check back.
K....
http://www.ncbi.nlm.nih.gov/pubmed/20826633
J Nutr. 2010 Nov;140(11):1963-9. Epub 2010 Sep 8.
Inulin prolongs survival of intragastrically administered
Lactobacillus plantarum No. 14 in the gut of mice fed a high-fat diet.
Takemura N, Hagio M, Ishizuka S, Ito H, Morita T, Sonoyama K.
Graduate School of Life Science, Hokkaido University, Sapporo
060-8589, Japan.
Abstract
We tested whether a high-fat diet (HFD) impairs the survival of
probiotics in mice. In Expt. 1, after feeding either a HFD (62.7%
energy) or a normal-fat diet (NFD; 11.1% energy) for 2 d, C57BL/6 mice
were i.g. administered Lactobacillus plantarum No. 14. Fecal recovery
of viable L. plantarum was significantly decreased 99% by the HFD
compared with the NFD. Total bile acid concentrations in the small
intestine and cecum were significantly higher (1.5- and 2.2-fold of
NFD, respectively) in mice fed HFD than in those fed NFD. Cholic acid
and deoxycholic acid significantly reduced the viability of L.
plantarum No. 14 in culture experiments. In Expt. 2, after feeding HFD
for 2 d, simultaneous administration of inulin (10 mg) with L.
plantarum No. 14 significantly increased (100-fold of that without
inulin) the fecal recovery of viable L. plantarum. Inulin
administration did not alter intestinal bile acid concentrations. In
Expt. 3, after feeding HFD for 2 d, mice were i.g. administered either
inulin (10 mg) or vehicle and, after 6 h, cecal contents were
subjected to culture experiments. Growth of L. plantarum No. 14 was
significantly higher in the cecal contents of inulin-administered mice
than vehicle-administered mice. Inulin supplementation to cecal
contents of vehicle-administered mice significantly enhanced the
growth of L. plantarum No. 14. We propose that HFD impairs the
survival of probiotics in the gut due to increased bile acid stress
and that simultaneous administration of inulin prolongs the survival
of probiotics in mice fed HFD.
PMID: 20826633
------------
http://www.ncbi.nlm.nih.gov/pubmed/15327645
Oral Microbiol Immunol. 2004 Oct;19(5):322-6.
Biofilm growth of Lactobacillus species is promoted by Actinomyces
species and Streptococcus mutans.
Filoche SK, Anderson SA, Sissons CH.
Dental Research Group, Department of Pathology and Molecular Medicine,
Wellington School of Medicine, Wellington, New Zealand.
Abstract
The ability of oral bacteria to integrate within a biofilm is pivotal
to their survival. A dependence on the amount of biofilm growth by
noncoaggregating Lactobacillus rhamnosus and Lactobacillus plantarum
on coculture with Actinomyces naeslundii, Actinomyces gerencseriae,
Streptococcus mutans and Veillonella parvula was investigated using an
artificial-mouth culture system. Biofilm formation by the lactobacilli
in mono-culture was poor. In coculture with Actinomyces species the
amount of L. rhamnosus increased 7-20 times and L. plantarum 4-7 times
compared to its mono-culture biofilm. S. mutans also promoted
substantial biofilm growth of lactobacilli but V. parvula had no
effect. We conclude that these Actinomyces species promoted growth of
key Lactobacillus species in a biofilm, as did S. mutans to a smaller
extent, and that the ability of individual bacteria to form mono-
culture biofilms is not necessarily an indicator of their survival and
pathogenic potential in a complex multispecies biofilm community.
PMID: 15327645
http://www.ncbi.nlm.nih.gov/pubmed/19748696
Int J Food Microbiol. 2009 Oct 31;135(2):90-8. Epub 2009 Aug 26.
In vitro evaluation of Lactobacillus plantarum DSMZ 12028 as a
probiotic: emphasis on innate immunity.
Cammarota M, De Rosa M, Stellavato A, Lamberti M, Marzaioli I,
Giuliano M.
Department of Experimental Medicine, Biotechnology and Molecular
Biology Section, Medical School, Second University of Naples, Italy.
Abstract
In this study, we analyzed the probiotic potential of L. plantarum
DSMZ 12028 in vitro using the pathogen E. coli K4 and a certified
probiotic, L. paracasei F19, as controls. Adhesion to intestinal
epithelial cells was evaluated using two cell lines, CaCo-2 and HT-29,
through the plate dilution method. Moreover, the bacteria/epithelial
dynamic interaction was continuously monitored using time-lapse
microscopy. Expression of the innate immunity receptors, the TLRs, was
evaluated by semi-quantitative PCR on an epithelial/bacteria co-
culture. Real-time PCR was used to monitor expression of TLRs and
cytokines in a monocytic cell line (THP-1) following bacterial
exposure. The adherence of the strain to intestinal epithelial cells
was comparable to that of the probiotic. Time-lapse experiments showed
that E. coli K4 induced cell death while L. plantarum did not affect
proliferation at a 10:1 bacteria/cell ratio. L. plantarum down-
regulated TLR mRNAs with the exception of TLR2, while L. paracasei F19
and E. coli K4 caused a significant (p<0.05) up-regulation of TLR2 and
4, respectively. To simulate the activation of underlying immune cells
in the lamina propria, we analyzed the immunomodulation of L.
plantarum on a monocytic cell line, THP-1. Proinflammatory cytokines,
such as TNFalpha, were increased by the presence of bacteria. The
pathogen E. coli K4 also induced a strong up-regulation of
proinflammatory cytokines, such as IL8, IL1beta and IL23. No
differences were observed between experimental groups for IFNgamma,
IL-10 and IL12p40. Overall, L. plantarum DSMZ 12028 demonstrated
probiotic traits, inducing a proinflammatory response just above the
"threshold level", which could prevent an inflammatory outcome, while
inducing a higher state of alertness in the defense system of the host
intestinal epithelial cells.
PMID: 19748696
http://www.ncbi.nlm.nih.gov/pubmed/19519855
Clin Microbiol Infect. 2010 Mar;16(3):281-6. Epub 2009 Jun 6.
Interleukin-8 production by polymorphonuclear leukocytes from patients
with chronic infected leg ulcers treated with Lactobacillus plantarum.
Peral MC, Rachid MM, Gobbato NM, Huaman Martinez MA, Valdez JC.
Cátedra de Biología, Departamento Biomédico, Facultad de Medicina,
Universidad Nacional de Tucumán, Tucumán, Argentina.
Abstract
Bacterial infection impairs the healing process, promoting the
chronicity of inflammation and wounds. Because antibiotics fail to
eradicate bacteria, especially in biofilm form, new therapeutic
modalities may be required. In the present study, the effectiveness of
bacteriotherapy with Lactobacillus plantarum on infected chronic
venous ulcers was investigated and its effects on interleukin (IL)-8
production by cells from the ulcer bed and neutrophils isolated from
peripheral blood that were previously challenged in vitro with
Pseudomonas aeruginosa and L. plantarum were studied. Topical
application of L. plantarum culture to lesions (25-60 cm(2)) of 14
diabetic and 20 non-diabetic patients induced debridement, granulation
tissue formation and total healing after 30 days in 43% diabetics and
in 50% non-diabetics. No significant differences between the groups
were observed. The cells from ulcer beds collected after treatment
with L. plantarum for 10 days showed a decrease in the percentage of
polymorphonuclear, apoptotic and necrotic cells and an enhancement of
IL-8 production. IL-8 production by isolated neutrophils from these
patients was compared with that in diabetics without ulcers, as well
as normal subjects under basal conditions, and after infection of
polymorphonuclear cells with P. aeruginosa preincubated either with or
without L. plantarum. The basal values in diabetic and ulcer patients
were higher than normal (p <0.001) and were increased by P. aeruginosa
infection in normal, diabetics (p <0.001) and non-diabetics with
ulcers (p <0.01). Preincubation with L. plantarum decreased IL-8
production in patients with ulcers non-diabetic and diabetic (p
<0.001). Lactobacillus plantarum treatment reduced wound bacterial
load, neutrophils, apoptotic and necrotic cells, modified IL-8
production and induced wound healing.
PMID: 19519855
Actinomyces naeslundii in the mouths of infants 4 months after the
arival of teeth?
What about it and LAB?
right on and it might be KEY..
Why?
I wasn't breast fed and was a severe early onset autoimmunoiac.
http://www.ncbi.nlm.nih.gov/pubmed/15327645
Oral Microbiol Immunol. 2004 Oct;19(5):322-6.
Biofilm growth of Lactobacillus species is promoted by Actinomyces
species and Streptococcus mutans.
Filoche SK, Anderson SA, Sissons CH.
Dental Research Group, Department of Pathology and Molecular Medicine,
Wellington School of Medicine, Wellington, New Zealand.
Abstract
The ability of oral bacteria to integrate within a biofilm is pivotal
to their survival. A dependence on the amount of biofilm growth by
noncoaggregating Lactobacillus rhamnosus and Lactobacillus plantarum
on coculture with Actinomyces naeslundii, Actinomyces gerencseriae,
Streptococcus mutans and Veillonella parvula was investigated using an
artificial-mouth culture system. Biofilm formation by the lactobacilli
in mono-culture was poor. In coculture with Actinomyces species the
amount of L. rhamnosus increased 7-20 times and L. plantarum 4-7 times
compared to its mono-culture biofilm. S. mutans also promoted
substantial biofilm growth of lactobacilli but V. parvula had no
effect. We conclude that these Actinomyces species promoted growth of
key Lactobacillus species in a biofilm, as did S. mutans to a smaller
extent, and that the ability of individual bacteria to form mono-
culture biofilms is not necessarily an indicator of their survival and
pathogenic potential in a complex multispecies biofilm community.
PMID: 15327645
So microbiota is key or what?
http://en.wikipedia.org/wiki/Human_flora
http://en.wikipedia.org/wiki/Human_flora#Gut_flora
[...] Bacteria make up most of the flora in the colon[25] and 60% of
the dry mass of feces.[22] This fact makes feces an ideal source to
test for gut flora for any tests and experiments by extracting the
nucleic acid from fecal specimens, and bacterial 16S rRNA gene
sequences are generated with bacterial primers. This form of testing
is also often preferable to more invasive techniques, such as
biopsies. Somewhere between 300[22] and 1000 different species live in
the gut,[20] with most estimates at about 500.[23][26] However, it is
probable that 99% of the bacteria come from about 30 or 40 species.
[27] Fungi and protozoa also make up a part of the gut flora, but
little is known about their activities.
Research suggests that the relationship between gut flora[28] and
humans is not merely commensal (a non-harmful coexistence), but rather
is a mutualistic, symbiotic relationship.[20] Though people can
survive with no gut flora,[23] the microorganisms perform a host of
useful functions, such as fermenting unused energy substrates,
training the immune system, preventing growth of harmful species,[22]
regulating the development of the gut, producing vitamins for the host
(such as biotin and vitamin K), and producing hormones to direct the
host to store fats. However, in certain conditions, some species are
thought to be capable of causing disease by causing infection or
increasing cancer risk for the host.[22][25]
Some bacteria found in the large intestine of humans:
Bacterium--------- --------Range of Incidence
Bacteroides fragilis-------- 100
Bacteroides melaninogenic---- 100
Bacteroides oralis -----------100
Lactobacillus ----------------20-60
Clostridium perfringens -------25-35
Clostridium septicum--------- 5-25
Clostridium tetani------------ 1-35
Bifidobacterium bifidum -------30-70
Staphylococcus aureus------ 30-50
Enterococcus faecalis--------- 100
Escherichia coli --------------100
Salmonella enteritidis--------- 3-7
Klebsiella sp.-------------- 40-80
Enterobacter sp.------------ 40-80
Proteus mirabilis--------------- 5-55
Pseudomonas aeruginosa --------3-11
Peptostreptococcus sp.----------- ?common
Peptococcus sp. ?common
<snip>
http://en.wikipedia.org/wiki/List_of_human_flora
http://en.wikipedia.org/wiki/List_of_human_flora#Gastro-intestinal_tract
http://en.wikipedia.org/wiki/Lactobacillus
LAB
http://en.wikipedia.org/wiki/Lactic_acid_bacteria
zzzzzzzzzzzzzzzzzzzzzzzzz
http://www.ncbi.nlm.nih.gov/pubmed/15327645
Oral Microbiol Immunol. 2004 Oct;19(5):322-6.
Biofilm growth of Lactobacillus species is promoted by Actinomyces
species and Streptococcus mutans.
Filoche SK, Anderson SA, Sissons CH.
Dental Research Group, Department of Pathology and Molecular Medicine,
Wellington School of Medicine, Wellington, New Zealand.
Abstract
The ability of oral bacteria to integrate within a biofilm is pivotal
to their survival. A dependence on the amount of biofilm growth by
noncoaggregating Lactobacillus rhamnosus and Lactobacillus plantarum
on coculture with Actinomyces naeslundii, Actinomyces gerencseriae,
Streptococcus mutans and Veillonella parvula was investigated using an
artificial-mouth culture system. Biofilm formation by the lactobacilli
in mono-culture was poor. In coculture with Actinomyces species the
amount of L. rhamnosus increased 7-20 times and L. plantarum 4-7 times
compared to its mono-culture biofilm. S. mutans also promoted
substantial biofilm growth of lactobacilli but V. parvula had no
effect. We conclude that these Actinomyces species promoted growth of
key Lactobacillus species in a biofilm, as did S. mutans to a smaller
extent, and that the ability of individual bacteria to form mono-
culture biofilms is not necessarily an indicator of their survival and
pathogenic potential in a complex multispecies biofilm community.
PMID: 15327645
whoops... now i know i'm getting tired.
I just heard that gas or a barrel of oil has gone over $90 bucks.
Is that those gold and silver bugs looking for a bargain or inflation?
Yikes...
If i spent haft of my gut time on stocks and commodities i'd be filthy
rich. LOL
randall... doing the gold bug jig like a rich man pig? (<w> <G>)