Hey Cruiser
manfred
Other Uses
One of the wonderful attributes of alternative non-toxic cancer
treatments in general is that they often can be used to treat or cure
other conditions as well. And Protocel is no different. As described
earlier, ******Protocel works by interfering with the cell respiration
(energy production) of anaerobic cells. Cancer cells happen to be
primarily anaerobic. But there are other types of anaerobic cells in
the body that are not necessarily cancer cells. These are always
damaged cells in one way or another and often involved in conditions
such as auto-immune disorders***** and viral infections. Protocel
breaks down these damaged anaerobic cells the same way it breaks down
cancer cells.
Thus, people have also had success using Protocel to either fully
recover from or gain significant relief from many different chronic
illnesses. Some examples are:
Arthritis
Psoriasis
Mononucleosis
Ulcerative Colitis
Crohn’s disease
Multiple Sclerosis
Viral Infections
Of these, the intestinal disorders and viral conditions tend to be the
fastest responders, with multiple sclerosis and other auto-immune
disorders taking longer.
randall
Manfred,
Can you find out from cruiser how his topical luteolin trial worked
out?
With over a 100 hits and the first one being YOU/HIM i'd love
to know.
OTOH if your both talking internal and not topical external, luteolin
is still good as a pde4 inhibitor.
Works for me.
I'll check pubmed.
I'm working a day late with posting the PSOR day for the NPF
yesterday. :(
randall.. and will post again in less then a shake or a celery stalk.
randall
Whoops psor day was two days ago on Thursday.
I didn't call or talk to one other psor person. What kinda big deal is
that? LOL
Do they have a big party at psor HQ's or what?
I might go if they did. LOL
http://www.prnewswire.com/news-releases/millions-mark-world-psoriasis-day-on-oct-29-67156902.html
Millions Mark World Psoriasis Day on Oct. 29
National Psoriasis Foundation asks Americans affected by psoriatic
diseases to take action
PORTLAND, Ore., Oct. 29 /PRNewswire-USNewswire/ -- Today is World
Psoriasis Day and the National Psoriasis Foundation is asking all
Americans affected by psoriasis and psoriatic arthritis to raise
awareness about these diseases by going to www.psoriasis.org/wpd and
taking action.
[...]
To learn more about World Psoriasis Day activities in the U.S., visit
About World Psoriasis Day
Held on Oct. 29, the purpose of World Psoriasis Day is to raise
awareness of psoriasis and psoriatic arthritis. World Psoriasis Day is
sponsored by the International Federation of Psoriasis Associations, a
global consortium of patient associations, including the National
Psoriasis Foundation. Visit www.worldpsoriasisday.com to learn more.
About the National Psoriasis Foundation
The National Psoriasis Foundation is the world's largest nonprofit
patient advocacy organization, and the voice for millions of Americans
who are affected by psoriasis and psoriatic arthritis. Our mission is
to find a cure for psoriasis and psoriatic arthritis and to eliminate
their devastating effects through research, advocacy and education.
For more information, call the Psoriasis Foundation, headquartered in
Portland, Ore., at 800.723.9166,
or visit www.psoriasis.org.
<sniP>
I suppose i could have gone to the npf forum and chatted with a psor
person or more?
===========
OK, The NFP guys are making a day of PsoRiaSIS.
And i'm looking for a CURE via L. plantarum.
And i love luteolin/aPigenin to game some psor territory in the psor
war.
Randall is nutz... LOL
Makes wanna be oval office denizens look rather DULL in the process.
LOL
Duh, we saved almost a million jobs and it only cost 4 million per
job. LOL
Who KNOWs health cure deals? :)
I do... and want a psor CURE so i can eat celery without thinking
how much it's gonna help. LOL
=========
Are we having FUN gus?
For the longest time I thought psoriasis was a fungal infection.
There are over 500 hits for fungal infection on the psoriasis support
group.
'
But only five WITH ME. gee!
And those are GOOD ones. LOL
So what's NEW for CARD, fungal infections and psoriasis?
Will topical luteolin or systemic wide or both block NF-kappaB?
www.ncbi.nlm.nih.gov/pubmed/19699229
Structure and expression pattern of teleost caspase recruitment domain
(CARD) containing proteins that are potentially involved in NF-kappaB
signalling.
Chang MX, Chen WQ, Nie P.
State Key Laboratory of Freshwater Ecology and Biotechnology, and
Laboratory of Fish Diseases, Institute of Hydrobiology, Chinese
Academy of Sciences, Wuhan, Hubei Province 430072, PR China.
Caspase-associated recruitment domain (CARD) proteins play critical
roles in regulation of caspase activation, or regulation of NF-kappaB
activation. In the present study, 9 CARD-genes, which may be involved
in NF-kappaB activation, were identified in teleost fish. Phylogenetic
analysis showed that the orthologs to mammalian RIPK2, NOD1, PYCARD,
CARD9, CARD10, CARD11, CARD14, NOD2 and BCL10 were evident in teleost
fish, but clear orthologs to mammalian CARD6 and CARD8 were not found
in teleost fish. In zebrafish, most CARD-genes were expressed in
embryos and larvae. In adult zebrafish, zfRIPK2, zfNOD1, zfPYCARD,
zfCARD9 and zfNOD2 transcripts were constitutively expressed in
kidney, gill, intestine, liver, brain and spleen whilst zfCARD11,
zfCARD14 and BCL10 exhibited limited tissue distribution. A CARD-
related gene (zfCARD-rel), containing a single CARD domain, was
identified in the zebrafish genome and the EST databases and its
transcripts were detected only in spleen and kidney. Phylogenetic
analysis suggested that zfCARD-rel might be the ortholog of mammalian
CARD8 or the short isoform of NLRP1. Overexpression of zfCARD-rel had
a significantly inhibitory effect on NF-kappaB activity, demonstrating
the zfCARD-rel protein might serve as a negative regulator of cell
death and inflammatory response.
PMID: 19699229
Isn't this GREAT now that I know and NOW YOU know about sFB?
SAY yes...
It's the truth. And i'm gonna prove it. :)
Unless you refuse to believe and you doctor says, **JR open your trap
and swallow**. LOL
Which BRINGs uP...
===============
Let's prolong the JR susPense?
OK, i'll try this...
How can we look day after day at abstracts like this one?
www.ncbi.nlm.nih.gov/pubmed/19863376
The role of angiogenesis in the pathogenesis of psoriasis.
Chua RA, Arbiser JL.
Department of Dermatology, Emory University School of Medicine,
Atlanta Veterans Administration Hospital, Atlanta, GA 30322, USA.
Psoriasis is a multifactorial skin disorder with known systemic
consequences. While most recent studies point to a predominantly Th17-
driven process, psoriasis also lies at the crossroads linking the
pathways of angiogenesis and inflammation. Mediators such as VEGF and
angiopoietin-2 play significant roles in the pathophysiology and may
even account for the maintenance of the chronic inflammatory state.
Targets in this shared pathway may offer alternative avenues for
therapy.
PMID: 19863376
Day after day without a rEASON for Th17 being out of control....
So?
Well...
Now we KNOW.
And if you don't accept it, who cares?
Once you eat a drug or take a gut bug that turns OFF SFB from making
an
inordinate amount of Th17 YOU'LL be HAPPY.
So?
OK?
But?
Those ARE JR questions? LOL
YeP...
Because he CAN'T take or make the TRUTH?
YeP..
So?
Let's put some gut fiber in to this thing?
Yes, let's
http://www.eurekalert.org/pub_releases/2009-10/ra-nfc102809.php
New findings connect diet and intestinal bacteria with healthier
immune systems
Insoluble dietary fibre, or roughage, not only keeps you regular, say
Australian scientists, it also plays a vital role in the immune
system, keeping certain diseases at bay.
The indigestible part of all plant-based foods pushes its way through
most of the digestive tract unchanged, acting as a kind of internal
broom. When it arrives in the colon, bacteria convert it to energy and
compounds known as 'short chain fatty acids'. These are already known
to alleviate the symptoms of colitis, an inflammatory gut condition. 1
Similarly, probiotics and prebiotics, food supplements that affect the
balance of gut bacteria, reduce the symptoms of asthma and rheumatoid
arthritis, also inflammatory diseases. Until now no-one has understood
why.
Published tomorrow in Nature, breakthrough research by a Sydney-based
team makes new sense of such known facts by describing a mechanism
that links diet, gut bacteria and the immune system.
PhD student Kendle Maslowski and Professor Charles Mackay from the
Garvan Institute of Medical Research, in collaboration with the Co-
operative Research Centre for Asthma and Airways, have demonstrated
that GPR43, a molecule expressed by immune cells and previously shown
to bind short chain fatty acids, functions as an anti-inflammatory
receptor,
"The notion that diet might have profound effects on immune responses
or inflammatory diseases has never been taken that seriously" said
Professor Mackay. "We believe that changes in diet, associated with
western lifestyles, contribute to the increasing incidences of asthma,
Type 1 diabetes and other autoimmune diseases. Now we have a new
molecular mechanism that might explain how diet is affecting our
immune systems."
"We're also now beginning to understand that from the moment you're
born, it's incredibly important to be colonised by the right kinds of
gut bacteria," added Kendle. "The kinds of foods you eat directly
determine the levels of certain bacteria in your gut."
"Changing diets are changing the kinds of gut bacteria we have, as
well as their by-products, particularly short chain fatty acids. If we
have low amounts of dietary fibre, then we're going to have low levels
of short chain fatty acids, which we have demonstrated are very
important in the immune systems of mice."
"Mice that lack the GPR43 gene have increased inflammation, and poor
ability to resolve inflammation, because their immune cells can't bind
to short chain fatty acids.
There is plenty of evidence to suggest that bacteria and their by-
products play an important role in people. An American study published
in Nature in 2006 2 compared the bacteria in the guts of obese and
lean people. The obese people were put on a diet, and as they lost
weight their bacteria profile gradually came to match that of the lean
people.
Another study 3 looked at what diets might do to short chain fatty
acid levels. Obese people were put on three different diets over time
– high, medium and low fibre – and there was a direct correlation
between the level of carbohydrate, or fibre, in the diet and the level
of short chain fatty acids.
The conclusions drawn from the current research provide some of the
most compelling reasons yet for eating considerably more unprocessed
whole foods - fruits, vegetables, grains, nuts and seeds. 4
Dietary fibre, of course, has many known health benefits in addition
to those discussed above, including reduced risk of cardiovascular
disease and certain cancers 5, and various health organizations around
the world recommend daily minimum levels. 6 It is certain that the
majority of people in countries like Australia, the United States and
Britain eat much less fibre than they need to stay healthy.
"The role of nutrition and gut intestinal bacteria in immune responses
is an exciting new topic in immunology, and recent findings including
our own open up new possibilities to explore causes as well as new
treatments for inflammatory diseases such as asthma", said Professor
Mackay.
<sniP>
-----
I'm Not stoPPing with sFB, Littman et al.
It's total common sense and the whole immune theory based on the gut
is looking more and more elegant.
Oh?
So NOW the couP de grace?
Why NOT?
Once AGAIN. (i've posted this a dozen times i bet. LOL)
OR
http://www.labspaces.net/100198/In_shaping_our_immune_systems__some__friendly__bacteria_may_play_inordinate_role
In shaping our immune systems, some 'friendly' bacteria may play
inordinate role
http://upload.wikimedia.org/wikipedia/commons/2/29/T_cell_activation.png
Thursday, October 15, 2009
Out of the trillions of "friendly" bacteria - representing hundreds of
species -that make our intestines their home, new evidence in mice
suggests that it may be a very select few that shape our immune
responses. The findings detailed in two October 16th reports appearing
in the journals Cell and Immunity, both Cell Press publications, offer
new insight into the constant dialogue that goes on between intestinal
microbes and the immune system, and point to a remarkably big role for
a class of microbes known as segmented filamentous bacteria (SFB).
"It's the first example of a commensal bacteria that can induce
accumulation in the gut of a highly specific branch of the immune
system," said Dan Littman of the Howard Hughes Medical Institute and
the New York University School of Medicine, who led the study reported
in Cell. "We're headed into an exciting new area, and we hope more
pieces of how the microbial-host interaction contributes to health
will begin to fall into place."
"Our study provides the surprising result that among the hundreds of
bacterial species composing the gut microbiota -- only a very small
number, the prototype of which is SFB -- can efficiently stimulate the
post-natal physiologic maturation of the immune barrier," added
Valérie Gaboriau-Routhiau of INSERM in France, who led the Immunity
report. "A unique feature of SFB appears to be its capacity to
simultaneously stimulate a large spectrum of intestinal immune
responses -- innate and adaptive, pro-inflammatory and regulatory --
which complete and balance each other."
Notably, those SFBs stimulate particular types of helper T cells,
known as Th17 cells, the studies show.
In Littman's case, the findings by his group were something of an
accidental discovery. They were studying T cells in the intestine and
were getting some inconsistencies in their results. Those
inconsistencies could be traced to differences in the gut floras of
mice obtained from different sources, and specifically, they found, in
the presence or absence of SFB.
Introduction of SFB, but not other bacteria, stimulated the production
of Th17 cells in mice who were otherwise deficient in them, they show.
The bacteria also set in motion a pro-inflammatory gene program. That
SFB-induced immune response protected the mice from becoming ill with
an intestinal pathogen, supporting a role for the SFBs in setting up
the intestine's immunity barrier.
Gaboriau-Routhiau similarly found in studies of conventional and germ-
free mice that colonization of the gut induced a broad spectrum of pro-
inflammatory and T cell responses, including the emergence of Th17
cells. That occurred despite the fact that most bacteria, in
combination or on their own, didn't lead to such a reaction. Rather,
that function appeared limited to a restricted number of bacteria, her
team reports, the prototype of which is the SFB. All on its own, SFB
could largely recapitulate the coordinated maturation of T cell
responses normally induced by the whole mouse microbiota.
Gaboriau-Routhiau suspects that SFBs may have some special attributes
that explain their importance.
"For us, it was first a surprise to observe so little redundancy in
the role of commensal bacteria on stimulating immune responses,"
Gaboriau-Routhiau said. "One striking feature of SFB, which makes it
very different from the vast majority of the members of the
microbiota, is its capacity to adhere to epithelial cells notably in
the ileum, a property normally more the prerogative of pathogens." The
ileum is the final section of the small intestine and is distinguished
by many folds, giving it a very substantial surface area.
The findings also suggest how such commensal bacteria might sometimes
go from beneficial inhabitants, helping to fend off nasty bugs, to
ones that may tip the balance of the immune system toward the
development of inflammatory, autoimmune disease, such as Crohn's
disease, psoriasis and even arthritis, according to the researchers.
Indeed, the Th17 cells observed in the new studies have been noted in
recent years because of their importance in autoimmune diseases,
Littman explained. Animals with defects in those Th17 cells generally
don't develop autoimmune disease or develop disease that is less
severe, earlier studies showed.
"Th17 cells make cytokines that can be highly protective in the case
of infection," he said. "At the same time, in the wrong context or in
the wrong amount [they can lead to disease]. You need to have the
right balance."
Given the bacterial diversity found within our guts, the new results
show how much there still is to learn about this important aspect of
the immune system. While probiotic products on the market today don't
have the benefit of such a thorough understanding, says Littman, there
is little doubt that down the road we may be able to manipulate our
immune system in beneficial ways with microbes. Alternatively, he
said, some of the molecular products of those bacteria – particular
sugars or peptides, for instance – might ultimately serve as useful
therapies on their own.
----
http://news.biocompare.com/News/NewsStory/294399/NewsStory.html
=============
http://www.labspaces.net/96494/Plastic_protein_protects_bacteria_from_stomach_acid_s_unfolding_power
[...]
However, disease-causing bacteria such as the notorious E. coli are
protected from stomach acid by a tiny protein called HdeA. In the PNAS
paper, James Bardwell and coworkers describe how this protein works to
protect bacteria. Like other proteins, HdeA unfolds and becomes more
flexible when exposed to acid. But in a clever twist, the unfolding
process that inactivates most other proteins activates HdeA. Once
unfolded, this plastic protein molds itself to fit other bacterial
proteins that have been made sticky by acid- induced unfolding.
<sniP>
HdeA looks important now as well.
Only 41 hits i'll read them tomorrow.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=hdea&log$=activity
==============
How important are blood tests?
I bet Susan would say very. She knows her D3 levels and most hormones
certainly.
Blood tests, testing protocols
http://www.lef.org/protocols/appendix/blood_testing_01.htm
Blood Testing Protocols
Too often, people fall victim to a disease that could have been
prevented if their blood had been tested once a year.
For instance, we know that prescription drugs can cause liver and
kidney problems, but other factors (alcohol, over-the-counter drugs,
excess niacin, hepatitis C) can make a person susceptible to liver or
kidney damage. These conditions often smolder for years until a life-
threatening medical crisis occurs. Because of a phenomenon known as
“individual variability,” some people are especially vulnerable to
liver and kidney damage. The good news is that a simple blood
chemistry test can detect an underlying problem in time to take
corrective actions.
<sniP>
keywords: TSH values hormones DHEA Insulin (fasting) Free testosterone
Estradiol Thyroid stimulating hormone bun creatinine potassium uric
acid cbc Alkaline Phosphatase
AST (SGOT) SLT (SGPT) HDL LDL Hemoglobin Hematocrit C-Peptide C-
Reactive Protein (CRP) Dehydroepiandrosterone (DHEA) Sulfate Ferritin
Interleukin-1 beta (IL-1b) TIB PSA Selenium TSH Tumor Necrosis Factor-
alpha (TNF-alpha)
===================
http://www.news-medical.net/news/20091030/Online-resource-to-illustrate-genetic-networks-in-common-autoimmune-diseases-published.aspx
Online resource to illustrate genetic networks in common autoimmune
diseases published
30. October 2009 02:15
New tool to accelerate discovery of autoimmune disease mechanisms and
therapies
Currently, 5-8% of the U.S. population is afflicted with an autoimmune
disease (www.niaid.nih.gov). Many of these are chronic and require
life-long care. Moreover, different autoimmune diseases aggregate
within a single family, suggesting they are caused by disruptions in
common biological pathways.
To help researchers investigate these common pathways, The Jackson
Laboratory has published "Pathways to Discovery: Autoimmune
Diseases" (www.jax.org/jaxmice/pathways/autoimmune), a unique,
interactive, and publicly accessible online resource that illustrates
the genetic networks involved in five common autoimmune diseases:
inflammatory bowel disease, rheumatoid arthritis, asthma, multiple
sclerosis, and psoriasis.
The backbone of the new tool is five "spider-web" diagrams that depict
the gene/proteins involved in two or more of the five diseases. The
symbols in the diagrams represent cytokines, transmembrane receptors,
enzymes, nuclear receptors, and transcriptional regulators. The
resource also provides gene- and disease-specific references, links to
JAX- Mice strains (including inducible mouse models) that can be used
to research the five diseases, and descriptions of JAX- In Vivo
Services for compound efficacy testing.
"Pathways to Discovery: Autoimmune Diseases" promises to accelerate
the discovery of autoimmune disease mechanisms and therapeutic
interventions for both new and existing targets.
<sniP>
This looks cool...
http://jaxmice.jax.org/pathways/autoimmune/
Pathways to Discovery: Autoimmune Diseases
To assist researchers in investigating molecular commonalities among
different autoimmune diseases, in silico data mining and pathway
software were used to integrate the gene/pathway interactions between
inflammatory bowel disease (IBD), rheumatoid arthritis, asthma,
multiple sclerosis (MS), and psoriasis.
This new, comprehensive resource facilitates the identification of
novel therapeutic targets, or the exploration of alternate therapeutic
areas for existing targets, by providing the following:
Schematics of gene/pathway associations common to IBD, arthritis,
asthma, MS, and psoriasis
<sniP>
http://jaxmice.jax.org/pathways/autoimmune/psoriasis.html
========================
http://www.signaling-gateway.org/update/updates/200910/nri2645.html
gamma delta T cells: Innate source of IL-17
Gamma delta T cells produce IL-17 without ligation of their T cell
receptor (TCR), which contributes to a first line of defense against
pathogens and to the early stages of autoimmune inflammation.
Interleukin-17 (IL-17) has been the subject of a great deal of recent
research, mainly as the cytokine that characterizes the CD4+ T helper
cell subset known as TH17 cells. Now, two studies published in
Immunity show that T cells are also an important source of IL-17,
which is produced by these cells without ligation of their T cell
receptor (TCR) and contributes to a first line of defence against
pathogens and to the early stages of autoimmune inflammation.
Characterization of IL-17-producing T cells by both groups revealed
similarities of these cells to TH17 cells. These include the
expression of CC-chemokine receptor 6 (CCR6), IL-23 receptor, retinoic
acid receptor-related orphan receptor-t (RORt) and aryl hydrocarbon
receptor, as well as the production of IL-17 and IL-22. However, in
contrast to TH17 cells, T cells did not require TCR ligation to
induce IL-17 production in the presence of IL-1 and IL-23, cytokines
that can be produced by dendritic cells (DCs) following triggering of
Toll-like receptor 2 (TLR2), NOD-like receptors or dectin 1. Indeed,
Martin et al. showed that the IL-17-producing T cell subset rapidly
expanded following injection of mice with heat-killed Mycobacterium
tuberculosis or Candida albicans hyphae (which activate TLR2 and
dectin 1, respectively).
Evidence for a direct role of IL-17-producing T cells in the defence
against pathogens was provided by Martin et al., who showed that CCR6+
IL-17-producing T cells, but not other T cell subsets or TH17 cells,
express TLR1, TLR2 and dectin 1 and proliferate in vitro following
stimulation with ligands for these innate immune receptors but not
with the TLR4 ligand lipopolysaccharide — an effect that was further
enhanced in the presence of IL-23. Moreover, transfer of wild-type T
cells into TLR2-deficient mice followed by intraperitoneal injection
of the TLR1 and TLR2 ligand Pam3CysSerLys4 led to the recruitment of
IL-17-expressing T cells and neutrophils, suggesting that T cells
can sense certain pathogens and initiate an appropriate immune
response.
Sutton et al. described an important role for IL-17-producing T cells
in the early stages of experimental autoimmune encephalomyelitis
(EAE). Large numbers of these cells infiltrated the brain 7 days after
induction of EAE, and peak levels were reached at day 10–14. The IL-17-
producing T cells were found to be required for the subsequent
infiltration by autoantigen-specific CD4+ T cells during the
development of EAE; accordingly, EAE was less severe in T cell-
deficient mice. IL-17 produced by T cells following exposure to IL-1
and IL-23 establishes an amplification loop by acting directly on TH17
cells to promote their IL-17 production and indirectly on DCs to
promote their IL-23 production, which in turn supports the production
of further TH17 and T cells. So, T cells provide an innate source of
IL-17 in response to pathogenic signals to amplify immune responses in
certain infectious or inflammatory disease settings.
Lucy Bird
Ref:
www.ncbi.nlm.nih.gov/pubmed/19682928
www.ncbi.nlm.nih.gov/pubmed/19682929
www.ncbi.nlm.nih.gov/pubmed/19699169
www.ncbi.nlm.nih.gov/pubmed/19699170
Since we first looked at Wendy Havran and gamma delta T cells it's
clear that this area of immunity is critical and now with SFB to test
out gut theory, we'll shortly understand more about these early
immune cells. :)
==============
I love resveratrol besides luteolin from celery and apigenin et al:
http://groups.google.com/groups/search?hl=en&qt_s=1&q=apigenin+psoriasis
But resveratrol is VERY SPECIAL... to me any WHEY...
SWEET. ;~/
Resveratrol:
www.longevinex.com [the only product i'll take]
Resveratrol Produces “Vaccine-Like” Immunity Against Cancer
The provision of high-dose resveratrol to laboratory mice not only
cures many of them of metastatic (spreading) cancer, but produces
complete immunity towards future cancer among surviving animals, even
when tumor cells are intentionally re-injected into their bodies.
This astounding discovery has cancer researchers buzzing about a
nutriceutical cancer vaccine that could revolutionize modern cancer
therapy.
Researchers at the Department of Food Science, Chiayi University in
Taiwan, injected laboratory mice twelve times with tumor cells which
ended up in the lungs of the animals, mimicking metastatic colon
cancer.
The animals were then fed the human equivalent of 1050 milligrams of
resveratrol for 100 days. Fifty-percent (50%) of these animals
survived compared to 0% in untreated animals. That result is
remarkable in itself, but there was a longer-lasting effect, as
researchers go on to explain.
The surviving animals then had tumor cells injected once again, only
this time without resveratrol being given to them. No tumors were
noted in the lungs or elsewhere. The animals appeared to be “cancer-
proof.” Researchers called it a “vaccine-like” effect.
---------
These microscopic photos show slices of mouse lung tissue. A2
represents lung tissue in healthy mice that were not injected with
cancer cells. Photo B2 shows lung tissue laden with tumors after
cancer cells were injected into the animals. Photo C2 represents lung
tissue injection of tumor cells when resveratrol was administered.
The cancer eradication effect was achieved at a human equivalent dose
of 1050 milligrams of resveratrol.
Inexplicably, the inhibitory effects of resveratrol on tumor growth
and lung metastasis could not be explained by natural killer or
cytotoxic T-lymphocyte stimulation, typically seen when the immune
system is activated. Researchers say the underlying mechanisms remain
unclear, at least for now.
In 1893 Dr. William P. Coley was the first to link immunity to
cancer therapy by observing that tumor size decreases when
cancer patients are injected with infectious bacteria.
Based upon work by other researchers, mega-dose resveratrol should
only be used for treatment of existing cancer. Mega-dose resveratrol
has been shown to weaken the heart and shorten the lifespan of healthy
lab animals. Animal studies suggest 175-300 mg of resveratrol exerts
beneficial effects. Even lower doses have been demonstrated to exert
far greater biological effect when combined with other molecules such
as quercetin and rice bran.
The report is published in an early online edition of Molecular
Nutrition & Food Research [Volume 53, pages 1-9, 2009].
======================
Did i put this one up already?
Goes with dectin and card and Th17 et al.
www.ncbi.nlm.nih.gov/pubmed/19703985
Dectin-2 is a Syk-coupled pattern recognition receptor crucial for
Th17 responses to fungal infection.
Robinson MJ, Osorio F, Rosas M, Freitas RP, Schweighoffer E, Gross O,
Verbeek JS, Ruland J, Tybulewicz V, Brown GD, Moita LF, Taylor PR,
Reis e Sousa C.
Immunobiology Laboratory, Cancer Research UK, London Research
Institute, Lincoln's Inn Fields Laboratories, London WC2A 3PX,
England, UK.
Innate immune cells detect pathogens via pattern recognition receptors
(PRRs), which signal for initiation of immune responses to infection.
Studies with Dectin-1, a PRR for fungi, have defined a novel innate
signaling pathway involving Syk kinase and the adaptor CARD9, which is
critical for inducing Th17 responses to fungal infection. We show that
another C-type lectin, Dectin-2, also signals via Syk and CARD9, and
contributes to dendritic cell (DC) activation by fungal particles.
Unlike Dectin-1, Dectin-2 couples to Syk indirectly, through
association with the FcRgamma chain. In a model of Candida albicans
infection, blockade of Dectin-2 did not affect innate immune
resistance but abrogated Candida-specific T cell production of IL-17
and, in combination with the absence of Dectin-1, decreased Th1
responses to the organism. Thus, Dectin-2 constitutes a major fungal
PRR that can couple to the Syk-CARD9 innate signaling pathway to
activate DCs and regulate adaptive immune responses to fungal
infection.
PMID: 19703985 [PubMed - indexed for MEDLINE]
But SFB isn't FUNGAL...
www.ncbi.nlm.nih.gov/pubmed/19767757
CARD9 facilitates microbe-elicited production of reactive oxygen
species by regulating the LyGDI-Rac1 complex.
Wu W, Hsu YM, Bi L, Songyang Z, Lin X.
Department of Molecular and Cellular Oncology, University of Texas MD
Anderson Cancer Center, Houston, Texas, USA.
In response to invading microorganisms, macrophages engage in
phagocytosis and rapidly release reactive oxygen species (ROS), which
serve an important microbicidal function. However, how phagocytosis
induces ROS production remains largely unknown. CARD9, a caspase-
recruitment domain (CARD)-containing protein, is important for
resistance to fungal and bacterial infection. The mechanism of CARD9-
mediated bacterial clearance is still mostly unknown. Here we show
that CARD9 is required for killing intracellular bacteria in
macrophages. CARD9 associated with the GDP-dissociation inhibitor
LyGDI in phagosomes after bacterial and fungal infection and binding
of CARD9 suppressed LyGDI-mediated inhibition of the GTPase Rac1,
thereby leading to ROS production and bacterial killing in
macrophages. Thus, our studies identify a key pathway that leads to
microbe-elicited ROS production.
PMID: 19767757
But Crohn's genetics does tie in. Is it due to sFB directing that
genetics?
The genetics of Crohn's disease.
www.ncbi.nlm.nih.gov/pubmed/19453248
Van Limbergen J, Wilson DC, Satsangi J.
Department of Pediatric Gastroenterology and Nutrition, Royal Hospital
for Sick Children, Edinburgh EH9 1LF, United Kingdom.
johanvan...@hotmail.com
From epidemiological data, based on concordance data in family
studies, via linkage analysis to genome-wide association studies, we
and others have accumulated robust evidence implicating more than 30
distinct genomic loci involved in the genetic susceptibility to
Crohn's disease (CD). These loci encode genes involved in a number of
homeostatic mechanisms: innate pattern recognition receptors (NOD2/
CARD15, TLR4, CARD9), the differentiation of Th17-lymphocytes (IL-23R,
JAK2, STAT3, CCR6, ICOSLG), autophagy (ATG16L1, IRGM, LRRK2),
maintenance of epithelial barrier integrity (IBD5, DLG5, PTGER4,
ITLN1, DMBT1, XBP1), and the orchestration of the secondary immune
response (HLA-region, TNFSF15/TL1A, IRF5, PTPN2, PTPN22, NKX2-3,
IL-12B, IL-18RAP, MST1). While many of these loci also predispose to
pediatric CD, an additional number of childhood-onset loci have been
identified recently (e.g., TNFRSF6B). Not only has the identification
of these loci improved our understanding of the pathophysiology of CD,
this knowledge also holds real promise for clinical practice.
PMID: 19453248
But card goes to BCL and we can't not look at that.
53 hits for keywords: psoria* + BCL* [on pubmed]
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+bcl*&log$=activity
www.ncbi.nlm.nih.gov/pubmed/19359218
CARD9 versus CARMA1 in innate and adaptive immunity.
Hara H, Saito T.
Department of Biomolecular Sciences, Faculty of Medicine, Saga
University, 5-1-1 Nabeshima, Saga 849-8501, Japan. ha...@cc.saga-
u.ac.jp
Nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein
kinases (MAPKs) are activated upon engagement of a wide variety of
immunoreceptors. Accumulating evidence has demonstrated that B-cell
lymphoma 10 (BCL10) and mucosa-associated lymphoid tissue (MALT1) are
essential signaling components for NF-kappaB and MAPK activation
mediated by immunoreceptor tyrosine-based activation motif (ITAM)-
coupled receptors in both adaptive and innate immunity. Recent studies
have revealed that two caspase-recruitment domain (CARD) family
adaptor molecules, CARD-containing MAGUK protein 1 (CARMA1) and CARD9,
are crucial regulators of the ITAM-mediated signaling pathway by
forming a complex with BCL10-MALT1 in lymphoid and myeloid cells,
respectively. Here, we describe the immune responses and the cell-type-
specific regulation mechanisms for NF-kappaB and MAPK activation
controlled by CARMA1 and CARD9 through innate and adaptive
immunoreceptors.
PMID: 19359218
Wow... this one ties the whole taco to-gether.
I love apigenin for it's anti inflammtory work.
REALLY, REALLY love it. :)
And now look..
www.ncbi.nlm.nih.gov/pubmed/19405952
Apigenin, a non-mutagenic dietary flavonoid, suppresses lupus by
inhibiting autoantigen presentation for expansion of autoreactive Th1
and Th17 cells.
Kang HK, Ecklund D, Liu M, Datta SK.
Department of Medicine and Microbiology-Immunology, Division of
Rheumatology, Northwestern University Feinberg School of Medicine,
Chicago, IL 60611, USA. hkk...@northwestern.edu
INTRODUCTION: Lupus patients need alternatives to steroids and
cytotoxic drugs. We recently found that apigenin, a non-mutagenic
dietary flavonoid, can sensitize recurrently activated, normal human T
cells to apoptosis by inhibiting nuclear factor-kappa-B (NF-kappaB)-
regulated Bcl-xL, cyclooxygenase 2 (COX-2), and cellular FLICE-like
inhibitory protein (c-FLIP) expression. Because sustained immune
activation and hyperexpression of COX-2 and c-FLIP contribute to
lupus, we treated SNF1 mice that spontaneously develop human lupus-
like disease with apigenin. METHODS: SNF1 mice with established lupus-
like disease were injected with 20 mg/kg of apigenin daily and then
monitored for development of severe nephritis. Histopathologic changes
in kidneys, IgG autoantibodies to nuclear autoantigens in serum and in
cultures of splenocytes, along with nucleosome-specific T helper 1
(Th1) and Th17 responses, COX-2 expression, and apoptosis of lupus
immune cells were analyzed after apigenin treatment. RESULTS: Apigenin
in culture suppressed responses of Th1 and Th17 cells to major lupus
autoantigen (nucleosomes) up to 98% and 92%, respectively, and
inhibited the ability of lupus B cells to produce IgG class-switched
anti-nuclear autoantibodies helped by these Th cells in presence of
nucleosomes by up to 82%. Apigenin therapy of SNF1 mice with
established lupus suppressed serum levels of pathogenic autoantibodies
to nuclear antigens up to 97% and markedly delayed development of
severe glomerulonephritis. Apigenin downregulated COX-2 expression in
lupus T cells, B cells, and antigen-presenting cells (APCs) and caused
their apoptosis. Autoantigen presentation and Th17-inducing cytokine
production by dendritic cells were more sensitive to the inhibitory
effect of apigenin in culture, as evident at 0.3 to 3 muM, compared
with concentrations (10 to 100 microM) required for inducing
apoptosis. CONCLUSIONS: Apigenin inhibits autoantigen-presenting and
stimulatory functions of APCs necessary for the activation and
expansion of autoreactive Th1 and Th17 cells and B cells in lupus.
Apigenin also causes apoptosis of hyperactive lupus APCs and T and B
cells, probably by inhibiting expression of NF-kappaB-regulated anti-
apoptotic molecules, especially COX-2 and c-FLIP, which are
persistently hyperexpressed by lupus immune cells. Increasing the
bioavailability of dietary plant-derived COX-2 and NF-kappaB
inhibitors, such as apigenin, could be valuable for suppressing
inflammation in lupus and other Th17-mediated diseases like rheumatoid
arthritis, Crohn disease, and psoriasis and in prevention of
inflammation-based tumors overexpressing COX-2 (colon, breast).
PMID: 19405952 [PubMed - indexed for MEDLINE]
I've only posted this one FIVE times. LOL
Duh
==============
But how do we know it's fungal?
http://www.medicalnewstoday.com/articles/169247.php
Researchers Identify Genetic Links To Fungal Infection Susceptibility
New research has identified two genetic mutations that may put
individuals at increased risk for fungal infections. The research
focused on patients with severe fungal infections (primarily of the
genus Candida), but the findings may also have implications for
patients who have more common mild infections.
The research is published in two studies that appear together in the
October 29, 2009 issue of The New England Journal of Medicine. The two
independent research teams, one led by Prof. Mihai Netea (Radboud
University Nijmegen Medical Centre, The Netherlands) and one led by
Prof. Bodo Grimbacher (University College London, Royal Free Campus
Hampstead, United Kingdom) discovered that mutations in two proteins
involved in the pathway responsible for recognition of fungal beta-
glucans substantially impaired the immune system's ability to control
fungi. Dr. Netea's team discovered the relationship with mutations in
the protein Dectin-1, and Dr. Grimbacher's team identified the
relationship with mutations in the CARD9 protein.
The new results show that the mechanisms to protect against fungal
infections have been largely conserved by evolution between mice and
humans, which is not necessarily the case for other microbes. After
sensing the presence of Candida by specialised recognition proteins
such as Dectin-1, immune cells send signals from their surface to the
inside, where CARD9 acts as an adaptor molecule that integrates those
signals. CARD9 then initiates several molecular response mechanisms of
the innate and adaptive immune system to protect us from those
microorganisms. If Dectin-1 or CARD9 are mutated or missing, our
immune system struggles to control Candida and may allow local or even
systemic infections to develop.
"These findings are a first step in understanding the genetic
susceptibility to common and disabling fungal diseases such as
onychomycosis and recurrent vulvovaginal candidiasis," said Dr. Bart
Ferwerda, Radboud University, who first identified the Dectin-1
mutations in a family suffering from mucocutaneous fungal infections.
Dr. Erik-Oliver Glocker, first author of the CARD9 paper, noted the
potential for this research to lead to treatment advances. "This
discovery enables further insights in the interaction between fungi
and the human immune system and may pave the way for future
therapeutical options in patients suffering from Candida infections,"
he said.
Both studies involved researchers from across the world. Professor
Netea's research group specializes, among other things, in how the
human immune system defends itself against fungal infections. The
Marie-Curie Excellence Research Group, under the guidance of Prof.
Grimbacher, has specialised in inborn errors of the human immune
system. Both studies made important usage of a variety of biological
database resources at the National Center for Biotechnology
Information (NCBI), which is part of the National Library of Medicine
at the National Institutes of Health (United States). Dr. Alejandro
Schaffer, a researcher at NCBI and a co-author on the paper by Dr.
Grimbacher's team, helped identify CARD9 as the mutated gene. Critical
experiments to prove the causality of the CARD9 mutation were done in
the laboratory of Prof. Jurgen Ruland (Technical University of Munich,
Germany), where mice lacking the corresponding Card9 gene had been
engineered some years before and had been shown to be susceptible to
fungal infections. Similarly, demonstration of the molecular
mechanisms leading to the loss of beta-glucan recognition by mutated
Dectin-1 had been performed earlier in the laboratory of Prof. Gordon
Brown (University of Aberdeen, United Kingdom).
==========================
Time to KILL sFB again. LOL
Segmented filamentous bacterium MUST die...
Wit L. Plantarum no LESS...
http://www.bodyecology.com/07/08/16/lactobacillus_plantarum_benefits.php
[...]
Right now, you have a variety of these good bacteria and yeast
(microflora) in your body; however, Lactobacillus plantarum is a
"superstar" probiotic that you absolutely need in your inner ecosystem
to keep you healthy and strong.
Lactobacillus Plantarum
Lactobacillus plantarum (or L. plantarum) is one kind of beneficial
bacteria that is commonly found in Korean kimchi, sauerkraut, cultured
vegetables and even human saliva!
L. plantarum can live in your gut and keep pathogenic disease-causing
microorganisms from flourishing.
And similar to the way icing sticks to a cake, L. plantarum creates a
healthy barrier in your colon to keep dangerous bacteria from
penetrating the lining of your intestines and entering your blood
stream.
Besides maintaining the integrity of your intestinal lining, L.
plantarum can:3
Be a treatment for Irritable Bowel Syndrome (IBS)
Ease symptoms of Crohn's disease
Help heal colitis
L. plantarum is one of the best probiotics to address digestive
distress!
In fact, some people NEED Lactobacillus plantarum to improve their
health:
Pregnant women can ensure that they have healthy bacteria in their
birth canal to inoculate their newborn babies.
Newborn babies benefit from tiny spoonfuls of cultured vegetable juice
soon after birth to prevent colic and to ensure their inner ecosystem
is well established.
Autistic children benefit from L. plantarum as it helps clear up
common digestive issues.
Children with ADD/ADHD often find relief when using probiotics.
Anyone Taking Antibiotics (see why below)
Studies have consistently shown that L. plantarum was resistant to
most antibiotics. As readers of this newsletter are well aware,
antibiotics are causing severe yeast overgrowth in millions of people
including our children. Yet, if you must take an antibiotic (and
sometimes they are essential and do save lives) the L. plantarum in
your intestines will survive ensuring that a yeast overgrowth will not
occur there.
L. Plantarum is a bacteria we all need in or diet from birth to the
day we draw or last breath.
Research results also indicate that L. plantarum might be effective as
a probiotic with cholesterol-lowering activities.
<sniP>
============
Stop high blood pressure::
This can GO with that other blood pressure thing up above...
Two Hidden Factors Affecting Blood Pressure
Health News
By VRP Staff
You watch your stress levels and your salt intake… you exercise
regularly… you’ve even tried several different antihypertensive drugs…
and still your blood pressure just keeps on rising. It’s a frustrating
scenario for doctors and patients—but it’s also a surprisingly common
one.
Why? Well as it turns out, there’s more than one factor that can send
your blood pressure soaring. It could be high levels of the enzyme
renin, which converts into the hypertensive peptide angiotensin. On
the other hand, Parathyroid Hypertensive Factor (PHF)—which is
produced by your parathyroid gland and increases intracellular calcium
levels—could be to blame.1-3 Trouble is, there aren’t any easily
accessible and affordable tests to identify which factor is causing
your high blood pressure… meaning that you could hop from medication
to medication for months without any noticeable improvement.
The good news? There are two natural substances that are clinically
proven to support healthy blood pressure levels in both patients with
high-PHF and high-renin: shark cartilage and the medicinal mushroom
Cordyceps sinesis.
Research has shown that shark cartilage is able to lower blood
pressure by inhibiting PHF and regulating intracellular calcium in rat
models.4 Animal studies on Cordyceps have delivered similar results,
showing that this mushroom can both lower blood pressure and relax
calcium-dependent muscle contractions in a dose-dependent manner.5 And
together, their effects are even more pronounced—in fact, preliminary
trials suggest that this combination may be one of the most powerful
heart-protective solutions you can get.
In a study of 102 hypertensive patients, all with blood pressure
concerns ranging from mild to moderate, researchers studied the
effects of one to three capsules of a patented blend of shark
cartilage and Cordyceps (called PRESSURE-fX™) on mean systolic and
diastolic readings over three to 12 months. In addition to the
PRESSURE-fX, all the subjects increased consumption of vegetables,
legumes and fruits, avoided foods linked to lipid peroxidation and
supplemented with calcium, magnesium, potassium and vitamin C.
At the end of the study, the results were dramatic. In the absence of
the shark cartilage/Cordyceps combination, 50 to 60 percent of the
subjects responded to the mineral supplementation and lifestyle
modifications. However, once PRESSURE-fX was added, a total of 88
percent of the patients responded with significantly reduced blood
pressure.6
In this group of patients, mean systolic measurements dropped by
approximately 45 mm/Hg and mean diastolic measurements dropped by an
equally impressive 42 mm/Hg. What’s more, 63 of the patients
supplementing with PRESSURE-fX were able to maintain this healthy
blood pressure range without the assistance of any medication at all.6
The bottom line: If you’ve been struggling in vain to maintain healthy
blood pressure levels, PRESSURE-fX—available now through Vitamin
Research Products—could be the answer you’ve been looking for.
=========
Should we take boron for HB?
randall.. this one is to long... see part II in a few minutes..
manfred
> Manfred,
>
> Can you find out from cruiser how his topical luteolin trial worked
> out?
>
I have had no contact with Cruiser since he disappeared from here.
Hope he's OK.