PSOR News -- Phosphorylated Dihydroceramides (DHCs)- Sugared Polymers--EP4- L-Theanine
randall
PSORIASIS News
New Type Of Immune Cells Discovered That Regulate Inflammation In
Chronic
Diseases (This must be Th22, if so then previously posted)
http://www.medicalnewstoday.com/articles/171828.php
Basilea's Toctino(R) Receives Marketing Authorization In Canada
http://www.medicalnewstoday.com/articles/171358.php
International Psoriasis Council Hosts Second Educational Symposium To
Increase
Global Knowledge Of Psoriasis
http://www.medicalnewstoday.com/articles/171221.php
Are you a fox or a STUD?
Check your skin first:
Skin Color Gives Clues To Health
http://www.medicalnewstoday.com/articles/171109.php
=================
http://www.sciencedaily.com/releases/2009/11/091123171418.htm
Factors from Common Human Bacteria May Trigger Multiple Sclerosis
ScienceDaily (Nov. 24, 2009) — Current research suggests that a common
oral bacterium may exacerbate autoimmune disease. Multiple sclerosis
(MS), a disease where the immune system attacks the brain and spinal
cord, affects nearly 1 in 700 people in the United States. Patients
with multiple sclerosis have a variety of neurological symptoms,
including muscle weakness, difficulty in moving, and difficulty in
speech.
Porphyromas gingivalis, a common oral bacterium in humans, produces a
unique type of lipid, phosphorylated dihydroceramides (DHCs), which
enhance inflammatory responses. These lipids are also likely produced
by bacteria found in other parts of the body including the
gastrointestinal tract. To determine if these lipids accentuate immune-
mediated damage in autoimmune disease, researchers led by Robert B.
Clark and Frank C. Nichols of the University of Connecticut Health
Center administered phosphorylated DHCs in a mouse model of MS. The
severity of disease was significantly enhanced by the addition of
these lipids in a manner that was dependent on activation of the
immune system. These data suggest that phosphorylated DHCs from
bacteria commonly found in humans may trigger or increase the severity
of autoimmune diseases such as multiple sclerosis.
The authors state that "while it is clear that the immune system in
most individuals has the potential to attack self-tissues, the
"tipping" factors that initiate and propagate autoimmune diseases such
as multiple sclerosis in only a subset of individuals remain unknown.
Overall, [their] results represent the first description that
phosphorylated DHCs derived from common human bacteria are capable of
enhancing autoimmune disease." Thus, these lipids may function as
"tipping" factors, playing a previously unrecognized role in
initiating or exacerbating human autoimmune diseases. In future
studies, Dr. Clark and colleagues plan to characterize the effects of
phosphorylated DHCs on specific cells of the immune system and to
identify how and where these lipids are deposited in tissues
throughout the body. In addition to the role of these lipids in
triggering and worsening MS, the authors believe that phosphorylated
DHCs may have the potential to serve both as new markers of MS disease
activity and as new targets for therapeutic intervention.
This work was supported by grants from the National MS Society (RG4070-
A-6) (RBC) and the Patterson Trust Foundation (FN).
-----------
What? I've always thought that omega-6 was a kicker for psoriasis
inflammation.
Let's wiki...
go
http://en.wikipedia.org/wiki/Sphingolipid
see
http://en.wikipedia.org/wiki/Sphingolipid#Mammalian_sphingolipid_metabolism
also
http://en.wikipedia.org/wiki/Phosphorylation
furthermore
http://en.wikipedia.org/wiki/Vitamin_B6#Lipid_metabolism
----------
Their abstract for the above story.
www.ncbi.nlm.nih.gov/pubmed/19850890
Unique Lipids from a Common Human Bacterium Represent a New Class of
Toll-Like Receptor 2 Ligands Capable of Enhancing Autoimmunity.
Nichols FC, Housley WJ, O'Conor CA, Manning T, Wu S, Clark RB.
From the Division of Periodontology,* Department of Oral Health and
Diagnostic Sciences, and the Center for Immunotherapy of Cancer and
Infectious Diseases, Department of Immunology, University of
Connecticut Health Center, Farmington, Connecticut.
Recent reports suggest that commensal bacteria may play a down-
regulatory role in autoimmune disease. In the present studies, we
demonstrate that phosphorylated dihydroceramides, uniquely structured
lipids derived from the common human oral bacterium Porphyromonas
gingivalis and from bacteria commonly found in the gastrointestinal
tract and other organs, are capable of enhancing autoimmunity. We have
previously reported that these lipids have proinflammatory effects on
human fibroblasts in vitro and, in preliminary studies, have recovered
these lipids from surgically removed human carotid atheroma,
suggesting that they may play a role in human inflammatory disease. To
investigate whether these lipids have functional effects on
autoimmunity, we administered phosphorylated dihydroceramides to mice
with the murine model of multiple sclerosis, experimental allergic
encephalomyelitis (EAE). We find that these lipids, and particularly
the phosphoethanolamine dihydroceramide (PE DHC) fraction,
significantly enhanced EAE. Mechanistically, PE DHC enhances EAE in
mice lacking natural killer T cells, fails to enhance EAE in Toll-like
receptor 2 (TLR2)-deficient mice and, in vitro, induces dendritic cell
interleukin-6 secretion in a TLR2-dependent manner. Finally, PE DHC-
treated mice with EAE demonstrate a decreased percentage of spinal
cord Foxp3+ T cells, suggesting that these lipids may affect
regulatory aspects of adaptive immune responses. Overall, our results
suggest that phosphorylated dihydroceramides derived from common human
bacteria function as TLR2 ligands and may play a previously
unrecognized role in human autoimmune diseases.
PMID: 19850890
Some others from the same group of scientists.
Porphyromonas gingivalis lipids and diseased dental tissues.
Nichols FC, Rojanasomsith K.
Department of Oral Health and Diagnostic Sciences, University of
Connecticut School of Dental Medicine, Farmington, CT, USA.
nic...@nso.uchc.edu
BACKGROUND/AIM: Porphyromonas gingivalis synthesizes several classes
of dihydroceramides and at least one of these lipid classes promotes
proinflammatory secretory reactions in gingival fibroblasts as well as
alters fibroblast morphology in culture. The purpose of this
investigation was to determine whether the dihydroceramide lipids of
P. gingivalis are recovered in lipid extracts of subgingival plaque,
diseased teeth, and diseased gingival tissue samples. METHODS: Lipids
were extracted from P. gingivalis, subgingival plaque, subgingival
calculus, teeth laden with gross accumulations of subgingival
calculus, and gingival tissue samples obtained from chronic severe
periodontitis sites. Lipid samples were analyzed by gas chromatography-
mass spectrometry as trimethylsilyl derivatives or by electrospray-
mass spectrometry as underivatized products. High-performance liquid
chromatography fractions of P. gingivalis lipids and gingival tissue
lipids were also analyzed by electrospray-mass spectrometry analysis.
RESULTS: P. gingivalis phosphorylated dihydroceramides were recovered
in lipid extracts of subgingival plaque, subgingival calculus,
calculus contaminated teeth, and diseased gingival tissue samples.
However, the distribution of phosphorylated dihydroceramides varied
between these samples. CONCLUSION: Subgingival plaque, subgingival
calculus, diseased teeth, and gingival tissue are contaminated with
phosphorylated dihydroceramides produced by P. gingivalis. The
previously reported biological activity of these substances together
with the recovery of these lipids at periodontal disease sites argues
strongly for their classification as virulence factors in promoting
chronic inflammatory periodontal disease.
PMID: 16476017
www.ncbi.nlm.nih.gov/pubmed/16439807
Structures and biological activities of novel phosphatidylethanolamine
lipids of Porphyromonas gingivalis.
Nichols FC, Riep B, Mun J, Morton MD, Kawai T, Dewhirst FE, Smith MB.
Department of Periodontology, University of Connecticut School of
Dental Medicine, Farmington, CT 06030, USA. nic...@nso.uchc.edu
The Gram-negative periodontal pathogen Porphyromonas gingivalis
synthesizes several classes of novel phosphorylated complex lipids,
including the recently characterized phosphorylated dihydroceramides.
These sphingolipids promote the interleukin-1 (IL-1)-mediated
secretion of inflammatory mediators from fibroblasts, including
prostaglandin E2 and 6-keto prostaglandin F2alpha, and alter gingival
fibroblast morphology in culture. This report demonstrates that one
additional class of phosphorylated complex lipids of P. gingivalis
promotes IL-1-mediated secretory responses and morphological changes
in cultured fibroblasts. Structural characterization identified the
new phospholipid class as 1,2-diacyl phosphatidylethanolamine, which
substituted predominantly with isobranched C15:0 and C13:0 fatty
acids. The isobranched fatty acids, rather than unbranched fatty
acids, and the phosphoethanolamine head group were identified as the
essential structural elements required for the promotion of IL-1-
mediated secretory responses. These structural components are also
observed in specific phosphorylated sphingolipids of P. gingivalis and
likely contribute to the biological activity of these substances, in
addition to the phosphatidylethanolamine lipids described in this
report.
PMID: 16439807
www.ncbi.nlm.nih.gov/pubmed/15466368
Structures and biological activity of phosphorylated dihydroceramides
of Porphyromonas gingivalis.
Nichols FC, Riep B, Mun J, Morton MD, Bojarski MT, Dewhirst FE, Smith
MB.
<sniP>
www.ncbi.nlm.nih.gov/pubmed/19394759
Dihydroceramide intracellular increase in response to resveratrol
treatment mediates autophagy in gastric cancer cells.
Signorelli P, Munoz-Olaya JM, Gagliostro V, Casas J, Ghidoni R,
Fabriàs G.
Laboratory of Biochemistry and Molecular Biology, San Paolo University
Hospital, Medical School, University of Milan, Italy.
Resveratrol has both apoptosis and autophagy-promoting activities in
different cancer cells. Dihydroceramide is the immediate precursor of
the apoptotic mediator ceramide in the de novo sphingolipid synthesis
pathway. Here we demonstrate that resveratrol induces autophagy in
HGC-27 cells, with no sign of cell death. Autophagy occurs after an
increase in dihydroceramides by inhibition of dihydroceramide
desaturase. The effects of resveratrol are mimicked by a
dihydroceramide desaturase inhibitor. These results demonstrate that
resveratrol-induced autophagy occurs with a rise in intracellular
dihydroceramide levels as the result of inhibition of dihydroceramide
desaturases activity and that dihydroceramide accumulation is
responsible for autophagy promotion.
PMID: 19394759
Nichols has been busy with these oral presentations. LOL
====================
Sweet combat with autoimmunity?
What?
http://news.biocompare.com/News/NewsStory/300299/NewsStory.html
Sweet -- sugared Polymer A New Weapon Against Allergies And Asthma
Scientists at Johns Hopkins and their colleagues have developed sugar-
coated polymer strands that selectively kill off cells involved in
triggering aggressive allergy and asthma attacks. Their advance is a
significant step toward crafting pharmaceuticals to fight these often
life-endangering conditions in a new way.
For more than a decade, a team led by Bruce S. Bochner, M.D., director
of the Division of Allergy and Clinical Immunology at the Johns
Hopkins University School of Medicine, has studied a unique protein
known as Siglec-8. This protein, whose name is an acronym for Sialic
Acid-binding, Immunoglobulin-like LECtin number 8, is present on the
surfaces of a few types of immune cells, including eosinophils,
basophils and mast cells. These different cell types have diverse but
cooperative roles in normal immune function and allergic diseases.
When functioning correctly, they are a valuable aid to keeping the
body healthy and infection-free. However, in allergic reactions and
asthma attacks, the cells unleash an overwhelming response that
typically harms the body more than it helps.
The researchers found in previous studies that when they bound
antibodies that specifically target Siglec-8 to the protein on
eosinophils, the cells promptly died, an effect that might be useful
in stemming an allergy or asthma attack. Since producing antibodies
can be expensive—a potential roadblock to using them as
pharmaceuticals in the future—the researchers sought another way to
activate this protein.
Several years ago, Bochner and his colleagues discovered an unusual
sugar that could uniquely and selectively attach to and activate
Siglec-8. "The trick is that you need to engage several clusters of
Siglec-8 on each cell at once to trigger cell death. You're not going
to be able to do that with individual sugar molecules in solution,"
Bochner says.
To accomplish this goal, the team developed soft, flexible polymer
strands coated with the sugar, "like microscopic spaghetti candy,"
says Bochner.
Using cells genetically modified to produce Siglec-8 on their surfaces
and cells without the protein, the researchers tested whether the
polymer bound when applied to the cells. As expected, the polymer
bound only to the cells that produced Siglec-8. Polymer strands
without the sugar, or with different attached sugars, could not bind
to the cells. Additionally, when the researchers pretreated Siglec-8-
producing cells with antibodies that target the protein, the polymer
couldn't attach, suggesting that it specifically targets Siglec-8 and
not another protein on the cells.
The researchers validated these results further by testing whether
cells adhered to polymer strands immobilized in a petri dish. Cells
expressing Siglec-8 bound firmly to the polymer, but didn't bind to
polymers without the Siglec-8 specific sugar.
Finally, to test the polymer in a more physiologically relevant
setting, the researchers added the polymer to vials of whole human
blood to see which blood cells it attached to. They found that the
polymer only attached to eosinophils. Using only purified eosinophils,
the researchers examined whether the polymer could kill the cells, as
the targeted antibodies had in previous experiments. While their
results showed that the polymer killed about 65 percent of the
eosinophils over 72 hours, it was not as effective as the antibody,
which killed up to 90 percent of the cells in 24 hours.
"This is initial proof that delivering the sugar through a polymer can
give you the desired result of selectively engaging Siglec-8 and
killing eosinophils, but we still have a long way to go," says
Bochner. He and his team plan to try to optimize these results,
reported in the August Journal of Pharmacology and Experimental
Therapeutics, by experimenting with other formulations to deliver the
sugar to cells, including more rigid polymers, those with denser
sugars, or nanoparticles coated with the sugar instead of polymers.
###
Other researchers who participated in this study include Sherry A.
Hudson and Ronald L. Schnaar of the Johns Hopkins University School of
Medicine; Nicolai V. Bovin of the Shemyakin and Ovchinnikov Institute
of Bioorganic Chemistry in Russia; and Paul R. Crocker of the
University of Dundee in the United Kingdom.
----
You can see a few dozen hits for lectins or selectins in the p n g.
================
Fix the Gut via EP4?
http://news.biocompare.com/News/NewsStory/300062/NewsStory.html
Can EP4 Agonist Alleviate Gastric Lesions?
Over 300 million patients use non-steroidal anti-inflammatory drugs
(NSAIDs) in the world to treat pain, arthritis, fever and other
diseases. Nearly 30% of the users suffer from gastric lesions and
bleeding. To mitigate NSAIDs' adverse effects on the stomach,
misoprostol, a non-selective prostaglandin E1 (PGE1) analogue, has
been prescribed as the first choice for prevention of NSAID-induced
injuries, but often induces severe adverse effects. There remain unmet
medical needs for drugs with improved therapeutic profiles.
A research article published on November 7, 2009 in the World Journal
of Gastroenterology addresses this question. A research team from
United States investigated therapeutic potentials of a highly-
selective EP4 agonist for treatment of a mouse gastric ulcer model in
the presence or absence of indomethacin at various levels.
They found the EP4-selective agonist reduced high dose indomethacin-
induced acute hemorrhagic damage and promoted mucous epithelial
regeneration. Low-dose indomethacin aggravated ulcer bleeding and
inflammation, and delayed the healing of the established chronic
gastric ulcer. The EP4 agonist, when applied locally, not only offset
indomethacin-induced gastric bleeding and inflammation, but also
accelerated ulcer healing. In the absence of indomethacin, the EP4
agonist even accelerated chronic gastric ulcer healing and suppressed
inflammatory cell infiltration in the granulation tissue. In vitro,
the EP4 agonist protected human gastric mucous cells from indomethacin-
induced apoptosis.
Their results suggest that EP4 agonists may mimic the gastric
protective effects of PGE2 in the presence or absence of NSAIDs, and
may show advantages over non-selective analogs such as misoprostol by
minimizing adverse effects arising from activating all 4 subtype
receptors of PGE2.
###
Reference: Jiang GL, Im WB, Donde Y, Wheeler LA. EP4 agonist
alleviates indomethacin-induced gastric lesions and promotes chronic
gastric ulcer healing. World J Gastroenterol 2009; 15(41): 5149-5156
----------
8 hits in the P NG: ep4
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=ep4
-----
http://en.wikipedia.org/wiki/EP4_receptor
Prostaglandin E receptor 4 (EP4) is a prostaglandin receptor encoded
by the PTGER4 gene in humans.
The protein encoded by this gene is a member of the G-protein coupled
receptor family. This protein is one of four receptors identified for
prostaglandin E2 (PGE2). This receptor can activate T-cell factor
signaling. It has been shown to mediate PGE2 induced expression of
early growth response 1 (EGR1), regulate the level and stability of
cyclooxygenase-2 mRNA, and lead to the phosphorylation of glycogen
synthase kinase-3. Knockout studies in mice suggest that this receptor
may be involved in the neonatal adaptation of circulatory system,
osteoporosis, as well as initiation of skin immune responses.[1]
<snip>
http://en.wikipedia.org/wiki/Prostaglandin_receptor
http://en.wikipedia.org/wiki/Eicosanoid_receptor
An eicosanoid receptor is an integral membrane protein which detects
the presence of eicosanoid signaling molecules. Most, though not all,
are G protein-coupled receptors (GPCRs). An example of a non-GPCR
receptor that binds eicosanoids is PPAR-γ.[1]
<sniP>
http://en.wikipedia.org/wiki/Eicosanoid_receptor#Leukotriene
And comes back to AA
http://en.wikipedia.org/wiki/Prostaglandin
http://en.wikipedia.org/wiki/File:Eicosanoid_synthesis.svg
No wonder i spent so much time with arachidonic acid:
Over 1,000 hits for AA in the P NG:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=+arachidonic+acid&qt_g=Search+this+group
I suppose i should do the: arachidonic lipopolysaccharide [837 hits
-- pubmed]
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=arachidonic+lipopolysaccharide&log$=activity
---
There has to be some good ones out of 837?
I'll see what i can find that i like.
www.ncbi.nlm.nih.gov/pubmed/16762028
Prostaglandin E2 is a negative regulator on human plasmacytoid
dendritic cells.
Son Y, Ito T, Ozaki Y, Tanijiri T, Yokoi T, Nakamura K, Takebayashi M,
Amakawa R, Fukuhara S.
The First Department of Internal Medicine, Kansai Medical University,
Osaka, Japan.
Prostaglandin E2 (PGE2), a major lipid derived from the metabolism of
arachidonic acid, is an environmentally bioactive substance produced
by inflammatory processes and acts as a cAMP up-regulator that plays
an important role in immune responses. It has been reported that PGE2
has the ability to inhibit the production of interleukin-12 by myeloid
dendritic cells (MDCs) and macrophages, and then induce preferential T
helper type 2 (Th2) cell responses. However, little is known of the
function of PGE2 for plasmacytoid dendritic cells (PDCs), which may
contribute to the innate and adaptive immune response to viral
infection, allergy and autoimmune diseases. In the present study, we
compared the biological effect of PGE2 on human PDCs and MDCs. PGE2
caused the death of PDCs but MDCs survived. Furthermore, we found
that, whereas PGE2 inhibited interferon-alpha production by PDCs in
response to virus or cytosine-phosphate-guanosine, it inhibited
interleukin-12 production by MDCs in response to lipopolysaccharide
(LPS) or poly(I:C). Although both virus-stimulated PDCs and LPS-
stimulated MDCs preferentially induced the development of interferon-
gamma-producing Th1 cells, pretreatment with PGE2 led both DC subsets
to attenuate their Th1-inducing capacity. These findings suggest that
PGE2 represents a negative regulator on not only MDCs but also PDCs.
PMID: 16762028 [PubMed - indexed for MEDLINE]
www.ncbi.nlm.nih.gov/pubmed/16176925
Toll-like receptor 4 signaling regulates cytosolic phospholipase A2
activation and lipid generation in lipopolysaccharide-stimulated
macrophages.
Qi HY, Shelhamer JH.
Critical Care Medicine Department, Clinical Center, National
Institutes of Health, Bethesda, Maryland 20892, USA.
Inflammatory lipid mediators such as prostaglandins and leukotrienes
play crucial roles in the pathogenesis of bacterial lipopolysaccharide
(LPS)-induced inflammation. Cytosolic phospholipase A(2) (cPLA(2)) is
a key enzyme in the generation of pro-inflammatory lipid mediators.
Here, we found that Toll-like receptor 4 (TLR4) is essential for LPS-
induced cPLA(2) activation and lipid release. Inhibition of TLR4
protein expression by TLR4 small interfering RNA or neutralization of
TLR4 by the specific antibody against TLR4/MD2 blocked cPLA(2)
phosphorylation and cPLA(2)-hydrolyzed arachidonic acid release.
Furthermore, activation of the TLR4 signaling pathway by LPS regulated
cPLA(2) activation and lipid release. cPLA(2) phosphorylation and cPLA
(2)-hydrolyzed lipid release were significantly impaired when TLR4
adaptor protein, either MyD88 or TRIF, was knocked down in LPS-
stimulated macrophages. Similarly, LPS-induced arachidonate release
was inhibited in cells transfected with a dominant-negative MyD88 or
TRIF construct. Subsequently, cPLA(2) activation could be suppressed
by inhibition of the TLR4 adaptor protein-directed p38 and ERK MAPK
pathways. These findings suggest that, in LPS-induced inflammation,
the TLR4-mediated MyD88- and TRIF-dependent MAPK pathways result in
cPLA(2) activation and production of pro-inflammatory lipid mediators.
PMID: 16176925
www.ncbi.nlm.nih.gov/pubmed/19779114
Effect of Sasa senanensis Rehder extract on NO and PGE2 production by
activated mouse macrophage-like RAW264.7 cells.
Zhou L, Hashimoto K, Satoh K, Yokote Y, Kitajima M, Oizumi T, Oizumi
H, Sakagami H.
Meikai Pharmaco-Medical Laboratory (MPL), Meikai University School of
Dentistry, Saitama, Japan.
Alkaline extract of Sasa senanensis Rehder (SE) has shown diverse
biological activity. As an extension, whether SE affects the function
of activated macrophages was investigated. SE inhibited the nitric
oxide (NO) production by lipopolysaccharide (LPS)-activated mouse
macrophage-like RAW264.7 cells. Western blot and RT-PCR analyses
demonstrated that this was due to the inhibition of inducible NO
synthase (iNOS) expression at both protein and mRNA levels. ESR
spectroscopy shows that SE dose-dependently scavenged the NO radical
produced by NOC-7. In order to confirm the anti-inflammatory potency,
possible effects on prostaglandin (PG) E(2) production and expression
of enzymes involved in the arachidonic acid pathway were next
investigated. It was found that SE effectively inhibited the PGE(2)
production by LPS-stimulated RAW264.7 cells, although the extent of
inhibition of PGE(2) was slightly less than that of NO production. SE
inhibited cyclooxygenase (COX)-2 expression at both protein and mRNA
levels, but to much lesser extents as compared with those for iNOS
expression. SE contained much lower concentration of arginine,
precursor of NO, as compared with the culture medium. These data
suggest that SE exerts a weak anti-inflammatory activity.
PMID: 19779114
Bamboo extract (Sasa senanensis Rehder) to cool things down on the
inflammation FRONT.
Five hits on pubmed including the above (most recent).
http://www.ncbi.nlm.nih.gov/pubmed?term=senanensis%20Rehder&itool=QuerySuggestion
This vitamin C bambooish one is interesting for comp/alt meds
www.ncbi.nlm.nih.gov/pubmed/18712174
I wonder what the active ingredient is?
Big PharmA must be on it by now.
Will some pharma mock up be as potent as the real thing?
Coke it's the real thing. LOL
So why don't i run the obvious.
PGE2 + LPS 118 returns on the PNG:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=pge2+lps
And the first one has luteolin
=============
http://www.life-enhancement.com/article_template.asp
As we have previously reported, L-theanine enhances immune function. A
distinctive amino acid that is found in minute amounts in tea
(Camellia sinensis), theanine exerts a significant effect on the
immune system, by activating—in the event of bacterial infection—
gammadelta T cells to a state of readiness.1 These cells, comprising a
line of defense among total peripheral blood T cells, are mobilized
(expanding by up to 50-fold) in response to bacteria, and theanine
acts as the precursor to an antigen that primes gammadelta T cells in
a manner that is like cocking a gun, pulling its trigger back.
This doesn’t directly result in firing, but it prepares the immune
system to invoke gammadelta T killer activity against bacteria, while
increasing the speed of action.
<sniP>
I take a melatonin/theanine tab spring/summer. Don't need the
melatonin this
time of year. Maybe theanine helps a little?
===========
http://news.biocompare.com/News/NewsStory/300069/NewsStory.html
[...]
results show that patients with recent-onset schizophrenia have raised
levels of a signal substance called interleukin-1beta, which can be
released in the presence of inflammation. In the healthy control
patients, this substance was barely measurable.
<snip>
===============
www.vrp.com/
Three Ways to Improve Memory Before It’s Too Late
Health News
By VRP Staff
Maybe you forget where you parked your car more often than you used
to—or misplace your glasses more commonly than you’d like to admit. At
the end of the day, there’s no denying that these “senior moments” are
a natural part of aging. But how can you know if they’re really
harmless… or a warning sign that the worst is yet to come?
The truth is, you can’t—in fact, emerging research reveals that
serious neurodegenerative conditions like dementia and Alzheimer’s
disease can cause gradual cognitive changes decades before severe
symptoms settle in.1 -2 The good news: Choosing the right
neuroprotective supplements now can make a critical difference to your
brain’s health in the long run.
Your first goal should be to banish both oxidative stress and the
deadly protein cross -linking that promotes amyloid plaque—two well -
known factors in Alzheimer’s disease development.3 -5 The amino acids
carnosine and histidine can be powerful allies in this effort, as
they’re both potent cross -linking inhibitors that are proven to
reduce neurotoxicity—while additional antioxidants like lipoic acid
and n -acetyl -cysteine (NAC) can combat the inflammation -causing
free radical damage.6 -7
Nutrients that nourish your neuronal health can provide your brain
with an extra layer of protection. Acetyl carnitine, for example, has
been shown to increase vital levels of the antioxidant glutathione
during an in vitro study—and in combination with acetyl carnitine
arginate, it can also increase nerve growth factor (NGF) production,
while cutting levels of toxic amyloid beta by as much as 46 percent.8
-11 Similarly, studies have shown that the compound uridine can
restore your neural communication network by encouraging neurite and
dendrite regrowth.12
Botanicals like Gotu kola (Centella asiatica) and Ginkgo biloba play
an equally important role in preserving your brain’s health. Animal
studies show that Gotu kola supplementation can decrease amyloid beta
overproduction in genetically prone mice, while scavenging for free
radicals and reducing cell membrane and DNA damage at the same time.13
-16 Likewise, similar studies on Ginkgo biloba show that it can cut
levels of amyloid precursor protein in half after just 16 months of
use.17
Finally, consider supplementing with natural substances like choline
and DMAE, which can boost your brain’s production of acetylcholine—the
neurotransmitter responsible for muscle control and memory, among
other things. Additionally, nutrients such as pyroglutamic acid, L -
phenylalanine, vinpocetine, and huperzine -A have been shown to boost
levels of essential neurotransmitters and to increase nourishing
oxygen -flow to the brain. Human clinical trials reveal that these
nutrients (singularly or in combination with others) can benefit
patients with mild cognitive impairment, while supporting memory,
mood, attention and focus.18
Adding all of these key neuroprotective compounds into your daily
regimen may sound like a tall order—but luckily, it doesn’t have to
be. In fact, you’ll find each and every ingredient above in just three
brain -boosting formulas—AGEBlock®, Neuron Growth Factors (NGF™) and
Extension IQ—available now through Vitamin Research Products.
================
CBS reporter Sharyl Attkisson blows the lid off swine flu
http://articles.mercola.com/sites/articles/archive/2009/11/24/Superstar-CBS-Reporter-Blows-the-Lid-Off-the-Swine-Flu-Media-Hype-and-Hysteria.aspx
====================
randall....