LaLanne REMEMBERED - Magnesium - Mercola Metabolismisms -96 Y/O Chester REED redux - Gut Bugs -L. Plantarum -SFB - TLR's -IL-10 AGAIN -Curcumin - PILLs & Drugs - MIND pOWERs - IL10 & LPS
randall
After the shocking LOSS of Jack yesterday i'm convinced of ONE thing.
The GOSPEL of longevity should come from those who live the longest..
ACTIONS SPEAK LOUDER THEN WORDs....
Jeanne Calment who lived to 122 and a half sPeaks loudest to ME.
Why?
Cause i know so and her actions (besides DNA) speak loudest.
She smoked and drank and got exercise and ATE stuff. LOL
Could Jack LaLanne have lived to 120 if he ate some animal products
and didn't succumb
to pneumonia?
Why not?
For all we know his vegetarianism might have shortened his life SOME?
Jack and his mentor Paul Bragg both missed the 100 y/o mark by 4 and
nearly 20 years respectively.
Why?
You don't live forever on earth. Even it will die or go bye bye.
Whose bragging about life span now?
http://en.wikipedia.org/wiki/Paul_Bragg#Healthy_Lifestyle_Legacy
Bragg advocated using deep breathing, water fasts, organic foods,
drinking distilled water, juicing, exercise and listening to one's
body as methods of prolonging life span. Although he died at a claimed
age of 95, but believed to be actually 81, he claimed that every human
being could live to 120 by following his regimen.
Patricia Bragg who claims to be Paul's daughter [1] has since taken
over Bragg's health empire. According to official records, she was
actually his former daughter-in-law, having previously been married to
Robert Elton Bragg (1952 to 1956).
[...] Bragg died in South Shore Hospital, Miami Beach, FL on
12/7/1976. According to the public records of the Dade-Miami Medical
Examiner, the official cause of Bragg's death was "Ventricular
Tachycardia and Fibrillation due to Coronary Occlussion".
<sniP>
Patricia must have been bragging about her paternal roots? LOL
Jack LaLanne interview (five years ago):
http://www.shareguide.com/LaLanne.html
[...] Share Guide: George Burns almost made it to 100 but he smoked
cigars, drank alcohol and was not a health nut. How do you account for
his longevity and others like him?
Jack LaLanne: George Burns was more athletic than you think he was.
And he was a very social man--he loved people, he enjoyed life. He
worked at living. Old George was a social lion, he got around and did
things. That's the key right there. It starts with your brain. Some
people, when they get to 60 years old have no interests anymore, have
no friends left. George Burns was busy all the time doing something.
My oldest son, Danny, was in Beverly Hills going down the street in
his brand new car and this guy in a stretch limousine came through a
stop sign and hit him broadside. Danny got out of the car and was
going to punch the guy out. He looks in the car and who is riding in
the limousine? George Burns! Can you believe this? Danny said, "Jack
LaLanne is my Dad!" He said, "Jack LaLanne, That's my buddy! I watch
him all the time. I want you to come over to the house. Don't worry
about the car, I'll pay you cash. I won't tell my insurance, I don't
want to fool with it." So Danny went over to the house and they had a
couple of drinks. He gave him 300 or 400 bucks for the damage to his
car and they became friends. He was a hell of a guy.
Share Guide: Do you see yourself living to be over 100?
Jack LaLanne: I don't care how old I live; I just want to be LIVING
while I am living! I have friends of mine that are in their 80's and
now they are in wheelchairs or they're getting Alzheimer's. Who wants
that? It's terrible. I want to be able to do things; I want to look
good; I don't want to be a drudge on my wife and my kids. And I want
to get my message out to the people. I might live forever or it may
seem like that. I tell people I can't afford to die; it will wreck my
image! I am proud to say I was just voted in to the Hollywood Walk of
Fame. This year I get my star.
For more information about Jack LaLanne and Jack LaLanne's power
juicer, go to www.jacklalanne.com
I'll stick with my sweet whey to save my DAY. LOL
-------
Jack LaLanne Interview - part two
http://www.shareguide.com/LaLanne2.html
===========
Jack's MENTOR was Paul Bragg (1895-1976):
http://naturalhealthperspective.com/tutorials/paul-bragg.html
=======================
Something that every psoriatic whether overweight or not should take
to HEART:
[...] magnesium is vital to many enzymatic processes in your body,
which are governed by gene-signaling instructions. This new study
documents that magnesium is needed for activation of genes and may be
especially important to overweight individuals.
<snip>
http://www.wellnessresources.com/studies/magnesium_homeostasis_and_aging
<good info :>
[...] in adults over age 51 it was found that 320 mg of magnesium
could lower inflammation (C reactive protein) along with helping to
improve sleep. In a second study of children ages 5-12 with attention
deficit disorders it was found that a supplement containing only 80
mgs of magnesium was able to improve focus and was especially helpful
in correcting sleep problems in these children.
It is known that magnesium helps reduce inflammation in the brain,
which in term should help your brain sleep better. These two studies
lend documentation to the frequently observed benefit of magnesium to
assist sleep along with its ability to reduce the general feeling of
inflammatory wear and tear.
-----------
http://www.wellnessresources.com/studies/magnesium_helps_sleep_in_children
====================
http://www.wellnessresources.com/health/articles/jack_lalanne_-_the_passing_of_a_fitness_legend/
Jack LaLanne - the Passing of a Fitness Legend
Monday, January 24, 2011 - Byron Richards, CCN
Jack LaLanne passed away on Sunday at age 96 – a shining example to
one and all that exercise and a healthier diet was a very good way to
live a longer, healthier life. Following is the Reuters press
release:
(Reuters) - Jack LaLanne, a one-time sugar-holic who became a
television fitness guru preaching exercise and healthy diet to a
generation of American housewives, died on Sunday at age 96, his
daughter said.
LaLanne, who became U.S. television fixture in his close-fitting
jumpsuit starting in 1959 and came to be regarded as the father of the
modern fitness movement, succumbed to pneumonia following a brief
illness at his home in Morro Bay, along the California’s central
coast.
“He was surrounded by his family and passed very peacefully and in no
distress ... and with the football game on Sunday, so everything was
normal,” Yvonne LaLanne, 66, told Reuters.
She said her father had remained active until a few months ago,
including the taping of a recent public TV special.
Well into his 90s, LaLanne exercised for two hours a day. A typical
workout would be 90 minutes of weightlifting and 30 minutes of
swimming, changing his routine every 30 days.
He preached the gospel of exercise, raw vegetables and clean living
long after his contemporaries had traded in their bicycles for nursing
home beds.
“I can’t die,” LaLanne would say. “It would ruin my image.”
LaLanne was born Francois Henri LaLanne on September 26, 1914, in San
Francisco, the son of French immigrants. He said he grew into a “sugar-
holic” who suffered terrible headaches, mood swings and depression.
In desperation when he was 14, LaLanne’s mother took him to hear
health lecturer Paul Bragg, who urged followers to exercise and eat
unprocessed foods.
The young LaLanne swore off white flour, most fat and sugar and began
eating more fruits and vegetables. By age 15, he had built a backyard
gym of climbing ropes, chin-up bars, sit-up machines and weights.
Soon, LaLanne, who was only 5 feet, 6 inches tall, was playing high
school football. He added weight-lifting to recover from a football
injury and was hooked.
LaLanne opened the nation’s first modern health club in Oakland,
California, in 1936. It had a gym, juice bar and health food store.
Soon there were 100 gyms nationwide.
Without bothering with patents, LaLanne designed his own exercise
equipment, which he had built by a blacksmith. In 1951, he started
using television to get the first generation of couch potatoes to try
jumping jacks, push-ups and sit-ups.
“The Jack LaLanne Show,” which went national in 1959, showed
housewives how to work out and eat right, becoming a staple of U.S.
daytime television during a 34-year run.
He also was known for a series of promotional fitness stunts. At age
45, in 1959, he did 1,000 push-ups and 1,000 chin-ups in 86 minutes.
In 1984 a 70-year-old LaLanne had himself shackled and handcuffed and
towed 70 boats 1.5 miles in Long Beach Harbor.
LaLanne said in 2007 his focus was always to help people the way Paul
Bragg had helped him, adding, “Billy Graham is for the hereafter, I’m
for the here and now!”
<snip>
Here! here!
i hear you... :)
=============================
What if you put a turbo charger on your life?
Can you live half as long but twice as much?
Nah... LOL
mercola - eight (8) ways to trick out your metabolism?
Want to Boost Your Metabolism? Try These 3 Things Today...
http://articles.mercola.com/sites/articles/archive/2011/01/24/8-tricks-for-boosting-your-metabolism.aspx
Yahoo Shine suggests eight ways to boost your metabolism and keep
unwanted pounds from your waistline. Here are a few of them:
Do Intervals—Periodic fast-paced intervals raise your metabolic rate
higher than a steady cardio workout can.
Drink Green Tea—A study found that people who drank three to five cups
daily for three months cut 5 percent off their body weight.
Consider Caffeine—Coffee drinkers have a 16 percent higher metabolic
rate -- but make sure you take it early to avoid sleeping problems.
Build More Muscle—Lean muscle mass boosts your metabolism and makes
losing weight more easy.
Pick Up Heavier Weights—Use heavy weights at a very slow rate to break
down your muscles. Your metabolism goes up while your body makes
muscle repairs.
In related news, the results of an epidemiological showed that the
metabolic syndrome, a condition associated with cardiovascular disease
and type 2 diabetes, is related to a poor diet low in micronutrients.
Researchers examined the relationship between the metabolic syndrome
and micronutrients such as folate, zinc and vitamins C, B12 and E.
After adjusting for age and sex, they found significant relationships
between the metabolic syndrome and two of the micronutrients, vitamins
C and E.
According to Eurekalert:
"Additionally, [the researchers] observed a significant relationship
between the metabolic syndrome and C-reactive protein (CRP), a marker
of low-grade inflammation that has been associated with cardiovascular
disease risk. High CRP blood concentrations were seen in almost half
of the population."
Sources:
Yahoo Shine December 28, 2010
http://shine.yahoo.com/channel/health/8-tricks-for-boosting-your-metabolism-2433543/
Eurekalert January 2, 2011
http://www.eurekalert.org/pub_releases/2011-01/tuhs-vc010411.php
Public Health Nutrition October 19, 2010:1-10.
http://www.ncbi.nlm.nih.gov/pubmed/20955641
mercola comments:
A few of the techniques mentioned in the Yahoo article have merit,
while others are dubious at best.
<snip>
Peak 8 - sorta like jack lalanne on sPeed
http://fitness.mercola.com/sites/fitness/archive/2010/06/26/10-minutes-of-exercise-yields-hourlong-effects.aspx
Peak 8 Demonstration (Part 1 of 2)
http://www.youtube.com/watch?v=_NmNS75w9hI&feature=player_embedded
I might have to live to 130 to see how long mercola lives. LOL
If he has any self respect he'll die around 93 so i only have to live
in to my early 100's? LOL
But is he that young or YOU that old?
I dunno and don't care.
It's the schism of isms that i profunduate in this red graPe.
Yeah. So i'm going for resveratrolism with www.longevinex.com.
===================
Who was the guy last year who ate onion sandwiches with mayo and
retired from the post office at
95 or 96 y/o?
Google it.
OK i will...
and i see three hits and the one with Chester Reed who eats mayo/onion
everyday.
Chester REED says:
http://www.signonsandiego.com/news/2010/jun/30/oldest-us-postal-worker-retires-in-calif-at-95/.
[...] He believes in drinking alkaline water, to minimize acids that
can
damage digestive system, and eating sandwiches made "with a lot of
mayonnaise and get a big slice of onion" because the vegetable is
closely related to garlic, one of the healthiest foods you can eat,
he
said.
[...] Reed also likes to point out that his personal hero, the fitness
guru
Jack LaLanne whom Reed calls "a fine physical specimen," is only one
month his senior.
<snip>
[...] Nation's Oldest Postal Worker Retires
http://www.youtube.com/watch?v=nTtu24Gblrc
He's got a nice head of hair.
Here's to watermelon, alkaline water and onion sandwiches...
watermelon is one way to increase glutathione levels btw...
Whats that water stuff?
<snip>
And i looked at my P mayo thread... it looks delicious.
Mon, Nov 26 2001 9:19 am
Subject: P Mayo
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/b5ebf7ffa004b01d
And like jeanne calment, i might live to 122 y/o.
But i don't eat a kilo of chocolate every week like her. And i don't
drink port wine and
i most likely don't consume as much olive oil as jeanne?
But i do want to live that long. LOL
Only if i had her GENEs? But her kids died before her and they had
them or half of them?
Half is never enough if the other half is so so. I dunno.
===============
If i had to vote on someone in their mid 90's making it to 120 i'd
have votted for Jack.
LOOK at all my tributes to jack
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=lalanne&start=0&scoring=d&hl=en&
=============
That is kewl...
I know.
But what i wonder about NOW is what did jeanne calments gut microbes
look like?
Did she have just the right amount of SFB to pull the trigger on TNF
and IFN when
a bad guy came along who needed to be zaPPed?
And how much L. plantarum did Jeanne have in her gut or diet?
why?
Just look:
http://www.greenprophet.com/2010/12/love-bugs-how-bacteria-in-our-guts-influence-mate-selection/
Love Bugs: How Bacteria in Our Guts Influence Mate Selection
mate choice determined by bugs in our gut?
The latest research from Israel is revealing some unexpected insights
about attraction and partner selection. If sparks aren’t flying
between you and a potential mate, could the problem may be as close as
the bugs in your gut?
Right now the findings apply only to fruit flies, humble insects that
because of their quick lifespans and genetic uniformity have taught
humankind a thing or two about the inner magic of our bodies and our
world. In this case, they helped Tel Aviv researchers test a new
theory that basically says this: not only do we adapt to our
environments, but so do the symbiotic bacteria living in our bodies,
and our adaptations are actually intertwined as part of a larger
biological milieu.
The gist of the study is as follows: Fruit flies were separated into
two groups and fed different diets, one based on starch, the other on
malt sugar. When the two groups were reintroduced, lo and behold, the
fruit flies tended to prefer mates who shared similar nutritional
backgrounds. This held true for flies kept separated for a year, and
also for only a few lifecycles.
In subsequent studies, the flies were given antibiotics to kill off
the bacterial matchmaker – in this cased called Lactobacillus
plantarum – in their guts, and mate preference became random.
But here’s the intriguing part: when the isolated bacteria were put
back into their gut, preferential mating behavior resumed. Starch-fed
flies once again chose mates who were also raised on starch diets, and
likewise for those who were sugar-fed.
The reason: Scientists explain that something about diet altered the
flies pheromones.
===================
http://www.sciencedaily.com/releases/2010/12/101202124211.htm
Do Our Bodies' Bacteria Play Matchmaker?
ScienceDaily (Dec. 3, 2010) — Could the bacteria that we carry in our
bodies decide who we marry? According to a new study from Tel Aviv
University, the answer lies in the gut of a small fruit fly.
Prof. Eugene Rosenberg, Prof. Daniel Segel and doctoral student Gil
Sharon of Tel Aviv University's Department of Molecular Microbiology
and Biotechnology recently demonstrated that the symbiotic bacteria
inside a fruit fly greatly influence its choice of mates.
The research was done in cooperation with Prof. John Ringo of the
University of Maine, and was recently published in the Proceedings of
the National Academy of Sciences (PNAS).
Love, marriage and fruit flies
Based on a theory developed by Prof. Rosenberg and Dr. Ilana Zilber-
Rosenberg, the scientists propose that the basic unit of natural
selection is not the individual living organism, plant or animal, but
rather a larger biological milieu called a holobiont. This milieu can
include plant or animal life as well as their symbiotic partners. In
the case of animals, these partners tend to be microorganisms like
intestinal bacteria.
"Up to now, it was assumed that the host organism undergoes evolution
on its own, while its symbiotic bacteria undergo their own evolution,"
Prof. Rosenberg says. "The mechanism that we discovered enables
evolution to occur more rapidly in response to environmental changes.
Since a generation is shorter for bacteria than for multicellular
organisms, they genetically adjust more quickly to changes in the
holobiont," says Prof. Rosenberg.
Conducting their experiments on the rapidly-reproducing fruit fly, the
scientists were able to test this new theory. The first experiment
repeated a study carried out two decades ago by a Yale University
researcher, in which a fly population was divided in half and fed
different diets -- malt sugar versus starch. A year later, when the
flies were re-integrated as one group, those who had been fed starch
preferred starch-fed mates, while the sugar-fed flies preferred mates
of a similar nutritional background. The repeat experiment carried out
by the Tel Aviv University researchers shows that this dietary
influence takes effect within just a generation or two rather than
over an entire year.
In their second experiment, the Tel Aviv University team repeated the
first, but with the addition of an antibiotic, which killed the
bacteria and eliminated the specific mate preference. The mating
process became random, with no dietary influence.
In subsequent experiments, the researchers successfully isolated the
bacterial species responsible for reproductive isolation in flies with
diet-related mating preferences, and found the bacteria Lactobacillus
plantarum to be present in greater numbers in starch-fed fruit flies
than in sugar-fed flies. When L. plantarum was reintroduced into the
antibiotic-treated flies, the preferential mating behavior resumed --
proving that this bacterial species is at least partly responsible for
the mating preference.
Rewriting Darwin?
Finally, in cooperation with Prof. Avraham Hefetz of Tel Aviv
University's Department of Zoology, the team analyzed the sexual
pheromones produced by the fruit flies. There turned out to be
differences in pheromone levels between the two groups of flies --
differences that again disappeared after administering antibiotics.
"The finding indicates that pheromone alterations are a mechanism by
which we can identify mating preferences. We therefore hypothesize
that it is the bacteria that are driving this change," Prof. Rosenberg
says. He adds that these discoveries have implications for our entire
understanding of natural selection -- something which may even lead to
the development of a new theory of evolution.
--------------------------------------------------------------------------------
Story Source:
The above story is reprinted (with editorial adaptations by
ScienceDaily staff) from materials provided by American Friends of Tel
Aviv University.
--------------------------------------------------------------------------------
Journal Reference:
G. Sharon, D. Segal, J. M. Ringo, A. Hefetz, I. Zilber-Rosenberg, E.
Rosenberg. Commensal bacteria play a role in mating preference of
Drosophila melanogaster. Proceedings of the National Academy of
Sciences, 2010; DOI: 10.1073/pnas.1009906107
http://www.pnas.org/content/107/46/20051
===========================
And one term i loved recently which i posted iirc is exercise salience
using hormesis. LOL
Just in case---> i'll POST it here and now cows:
http://www.ncbi.nlm.nih.gov/pubmed/21143891
Nutr Metab (Lond). 2010 Dec 9;7:87.
Inflammatory modulation of exercise salience: using hormesis to return
to a healthy lifestyle.
Nunn AV, Guy GW, Brodie JS, Bell JD.
Metabolic and Molecular Imaging Group, MRC Clinical Sciences Centre,
Hammersmith Hospital, Imperial College London, Du Cane Road, London
W12 OHS, UK. alista...@btconnect.com.
Abstract
ABSTRACT: Most of the human population in the western world has access
to unlimited calories and leads an increasingly sedentary lifestyle.
The propensity to undertake voluntary exercise or indulge in
spontaneous physical exercise, which might be termed "exercise
salience", is drawing increased scientific attention. Despite its
genetic aspects, this complex behaviour is clearly modulated by the
environment and influenced by physiological states. Inflammation is
often overlooked as one of these conditions even though it is known to
induce a state of reduced mobility. Chronic subclinical inflammation
is associated with the metabolic syndrome; a largely lifestyle-induced
disease which can lead to decreased exercise salience. The result is a
vicious cycle that increases oxidative stress and reduces metabolic
flexibility and perpetuates the disease state. In contrast, hormetic
stimuli can induce an anti-inflammatory phenotype, thereby enhancing
exercise salience, leading to greater biological fitness and improved
functional longevity. One general consequence of hormesis is
upregulation of mitochondrial function and resistance to oxidative
stress. Examples of hormetic factors include calorie restriction,
extreme environmental temperatures, physical activity and polyphenols.
The hormetic modulation of inflammation, and thus, exercise salience,
may help to explain the highly heterogeneous expression of voluntary
exercise behaviour and therefore body composition phenotypes of humans
living in similar obesogenic environments.
PMID: 21143891
a diagram of this concept:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3009972/bin/1743-7075-7-87-1.jpg
or
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3009972/figure/F1/
[...] Figure 1
The theoretical relationship between the biphasic hormetic curve and
exercise salience. Regular hormetic stressors result in better
mitochondrial function and increased resistance to oxidative stress,
which translates into reduced inflammatory tone, improved metabolic
flexibility and higher exercise salience. Without regular hormetic
stressors and/or with chronic inflammation (e.g. from an injury or
infection), an animal may cross a tipping point and remain in an
inflammatory state due to a feed forward loop (1 and 2). In times of
plenty (but with some stressors), it may exist in zone 3, where
optimal energy storage occurs (mild inflammation induces insulin
resistance) - but it is still relatively metabolic flexible. Beyond
this, regular hormetic stressors would act to induce further exercise
salience (zones 4 and 5). However, as hormetic stressors increased,
damage would result in a gradual decrease in function and reducing
exercise salience (6 and 7) until the animal had to slow down to
recover (8). If
excessive stress continued, it might develop chronic inflammation, and
eventually succumb (9 and 10). The ability to resist transiting zones
may be associated with an epigenetic shifting of the tipping point. In
effect, an animal may adapt over time (or be preprogrammed from the
preceding generations). In a non-hormetic environment, this would
reinforce the inflammatory cycle, while in a hormetic environment, the
anti-inflammatory cycle will predominate. Much of the Western society
appears to reside in zone 2 due to a lack of hormesis and an excess of
calories. Key to zones: 1 = inflammatory induced sickness behaviour; 2
= subclinical inflammation; 3 = remain sedentary and store food; 4 =
active and seek food; 5 = migratory; 6 = late migratory; 7 = stress
induced damage; 8 = sedentary recovery zone; 9 = inflammatory induced
sickness behaviour; 10 = failure of systems and death.
<snip>
=====================
For whom the toll bells and recePtors vs SFB or plantarum?
no hits for sFB and TLR2 or TLR*
But the next best thing is plantarum and TLR
only seven hits tlr but 17 hits for TLR*
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=plantarum+AND+TLR
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=plantarum+AND+TLR*
---------------
Here: mannose receptors are membrane bound AND soluble (as in serum)
"Performing your original search, serum(pattern recognition), in
PubMed will retrieve 636 records.
see:
http://www.ncbi.nlm.nih.gov/pubmed?term=serum%28pattern%20recognition%29&itool=QuerySuggestion
Semin Immunol. 1998 Oct;10(5):363-72.
The serum mannose-binding protein and the macrophage mannose receptor
are pattern recognition molecules that link innate and adaptive
immunity.
Fraser IP, Koziel H, Ezekowitz RA.
Laboratory of Developmental Immunology and Department of Pediatrics,
Massachusetts General Hospital, and Harvard Medical School, Boston,
MA, USA.
Abstract
The innate immune system evolved to protect the host in the early
phases of an infectious challenge. The soluble mannose binding
protein, and the cell surface mannose receptor are two key pattern
recognition molecules of innate immunity. The ligand binding
specificity of these molecules enables them to differentiate 'self'
from 'non-self'. These pattern recognition capabilities are coupled to
effector functions, which enable them to interact with other molecules
of the immune system. In this way, these pattern recognition molecules
are able to serve as a link between the innate and adaptive immune
systems.
PMID: 9799711
(1)Toll-like receptors
Recognition of extracellular or endosomal pathogen-associated
molecular patterns is mediated by an array of transmembrane proteins
known as toll-like receptors (TLRs).[2] Toll-like receptors were first
discovered in Drosophila and are known to trigger a series of
mechanisms leading to the synthesis and secretion of cytokines and
activation of other host defense programs that are crucial to the
development of innate or adaptative immune responses. At present, TLRs
have been found in many species. In mammals, these receptors have been
assigned numbers 1 to 11 (TLR1-TLR11). Interaction of TLRs with their
specific PAMP* induces NF-κB signaling and MAP kinase pathway and
therefore the secretion of pro-inflammatory cytokines and co-
stimulatory molecules. Molecules released following TLR activation
signal to other cells of the immune system making TLRs key elements of
innate immunity and adaptive immunity.[3]
*PAMPs: pathogen-associated molecular patterns
(2)The mannose receptor
The mannose receptor (MR) is a PRR^ primarily present on the surface
of macrophages and dendritic cells. The MR belongs to the multilectin
receptor protein group and, like the TLRs, provides a link between
innate and adaptive immunity.[4] It recognizes and binds to repeated
mannose units on the surfaces of infectious agents and its activation
triggers endocytosis and phagocytosis of the microbe via the
complement system. Specifically, mannose binding triggers recruitment
of MBL**-associated serine proteases (MASPs). The serine proteases
activate themselves in a cascade, amplifying the immune
response:).......
Pattern recognition receptors, or PRRs, are pro teins expressed by
cells of the innate immune system to identify pathogen-associated
molecular patterns, or PAMPs,"
**One very important collectin is mannan-binding lectin (MBL)
And finally secreted or soluble or....serum
(3)Secreted PRRs
A number of PRRs do not remain associated with the cell that produces
them. Complement receptors, collectins, pentraxin proteins such as
serum amyloid and C-reactive protein, lipid transferases,
peptidoglycan recognition proteins (PGRs) and the LRR, XA21D[14] are
all secreted proteins. One very important collectin is mannan-binding
lectin (MBL), a major PRR of the innate immune system that binds to a
wide range of bacteria, viruses, fungi and protozoa. MBL predominantly
recognizes certain sugar groups on the surface of microorganisms but
also binds phospholipids, nucleic acids and non-glycosylated proteins.
[
(from J on high or living high uP) he might live to 122?
In big sky country no less. :)
=================
63 hits for IL-10 P NG:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=IL-10&start=0&scoring=d&hl=en&
But 220 hits on pubmed for the same search: psoria* AND IL-10
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+IL-10
how many snp's?
ONLY freaking ONE?
I can't believe it.
Here it is?
http://www.ncbi.nlm.nih.gov/pubmed/16078336
J Rheumatol. 2005 Aug;32(8):1571-5.
The role of interleukin 10 promoter polymorphisms in the
susceptibility of distal interphalangeal osteoarthritis.
Riyazi N, Kurreeman FA, Huizinga TW, Dekker FW, Stoeken-Rijsbergen G,
Kloppenburg M.
Department of Rheumatology and Clinical Epidemiology, Leiden
University Medical Center, The Netherlands.
Abstract
OBJECTIVE: The interleukin (IL)-10 single nucleotide promoter
polymorphism (SNP) -2849A is associated with decreased IL-10
production as measured by lipopolysaccharide (LPS) stimulated whole
blood cultures. A low innate production of IL-10 using the same assay
is associated with an increased risk of familial osteoarthritis (OA).
We investigated the association of 7 novel SNP located downstream of
the IL-10 transcription start site: -2849,-2763, -1330, -1082, -819,
and -592, constituting the 4 ancient haplotypes, with distal
interphalangeal (DIP) OA.
METHODS: The study population comprised consecutive patients with and
without radiological DIP OA (Kellgren-Lawrence score of > or = 2 in
one joint) aged 40-70 years from a cohort of subjects with different
types of arthritis in an early stage referred to an Early Arthritis
Clinic (EAC). DNA typing for IL-10 SNP as well as radiographs of the
hands were performed at clinic enrolment. Patients with rheumatoid
arthritis, systemic lupus erythematosus, spondyloarthropathies, and
psoriatic arthritis were excluded.
RESULTS: The distribution of DIP OA and IL-10 SNP were comparable to
representative samples of the Dutch population. In the cohort of 172
subjects, 57 had DIP OA (33%) and 115 (67%) had no DIP OA. No
significant association was found between DIP OA and IL-10 SNP and the
4 common haplotypes IL10.1, IL10.2, IL10.3, and IL10.4.
CONCLUSION: Our data suggest that IL-10 SNP, including -2849, which is
associated with differential production, do not play a major role in
the susceptibility of DIP OA.
PMID: 16078336
----------------------
http://www.ncbi.nlm.nih.gov/pubmed/15306847
Genes Immun. 2004 Nov;5(7):592-5.
Interleukin-10 promoter single-nucleotide polymorphisms as markers for
disease susceptibility and disease severity in leprosy.
Moraes MO, Pacheco AG, Schonkeren JJ, Vanderborght PR, Nery JA, Santos
AR, Moraes ME, Moraes JR, Ottenhoff TH, Sampaio EP, Huizinga TW, Sarno
EN.
Leprosy Laboratory, Department of Tropical Medicine, Oswaldo Cruz
Institute, FIOCRUZ, Rio de Janeiro, RJ, Brazil. mmo...@fiocruz.br
Abstract
We have determined IL-10 promoter genotypes of five single-nucleotide
polymorphisms (SNPs): T-3575A, A-2849G, C-2763A, -A-1082G and C-819T.
The haplotype frequencies were defined in healthy subjects compared to
leprosy patients, and analyzed for their occurrence in multi- (MB) vs
paucibacillary (PB) as severe and mild forms of leprosy, respectively.
Haplotypes defined by three SNP positions (-3575, -2849 and -2763)
captured significant differences between controls and patients
(P=0.04). The haplotype carrying -3575A, -2849G and -2763C was
associated with resistance to leprosy and to the development of severe
forms of the disease using either a binomial (controls vs cases,
P=0.005, OR=0.35, CI=0.13-0.91) or ordinal (controls vs PB vs MB,
P=0.006, OR=0.32, CI=0.12-0.83) model. By contrast, the IL-10
haplotype -3575T/-2849A/-2763C was found to be associated with
susceptibility to leprosy per se (P=0.027, OR=2.37, CI=1.04-5.39), but
not leprosy type. The data suggest that the IL-10 locus contributes to
the outcome of leprosy.
PMID: 15306847
leprosy is Th2 and due to a freaking bug. This is zero help. LOL
This next one throws me off a little.
http://www.ncbi.nlm.nih.gov/pubmed/21254178
Hepatology. 2011 Jan;53(1):306-16. doi: 10.1002/hep.24029. Epub 2010
Dec 7.
Apoptotic cells attenuate fulminant hepatitis by priming Kupffer cells
to produce interleukin-10 through membrane-bound TGF-β.
Zhang M, Xu S, Han Y, Cao X.
National Key Laboratory of Medical Immunology & Institute of
Immunology, Second Military Medical University, Shanghai, China;
Institute of Immunology, Zhejiang University School of Medicine,
Hangzhou, China.
Abstract
The liver, a unique tolerogenic organ, is regarded as the site to trap
and destroy aging erythrocytes and activated T cells. However, to
date, the mechanisms for why the liver is tolerogenic and whether
liver Kupffer cells (KC) are critical phagocytes for apoptotic cells
(AC) contributing to the liver immunosuppression remain unclear. Here
we report that KC is the main phagocyte for AC in the liver. Contact
of AC inhibits proinflammatory cytokine but enhances anti-inflammatory
cytokine production of KC in response to lipopolysaccharide (LPS)
stimulation. Membrane-bound transforming growth factor (TGF)-β on AC
is responsible for the increased production of interleukin (IL)-10 in
KC through extracellular signal-regulated kinase (ERK) activation via
the Smad3 pathway. Importantly, KC-derived IL-10 is critical for AC
infusion-mediated protection of endotoxin-induced fulminant hepatitis
through suppression of tumor necrosis factor (TNF)-α and nitric oxide
(NO) production from KC and consequently attenuation of KC-mediated
cytolysis of hepatocytes. Conclusion: AC can be preferentially
phagocytosed by KC in the liver, leading to attenuation of fulminant
hepatitis through IL-10-mediated suppression of KC-derived
inflammatory TNF-α and NO production. These findings demonstrate that
priming of KC by AC may contribute to maintain liver
immunosuppression, providing a new mechanistic explanation for how
immune homeostasis is maintained in the liver. (HEPATOLOGY 2011.).
PMID: 21254178
Should we do a low dose mouthwash or tooth paste with this?
http://www.ncbi.nlm.nih.gov/pubmed/21242275
Innate Immun. 2011 Jan 17.
Curcumin modulates the immune response associated with LPS-induced
periodontal disease in rats.
Guimarães MR, de Aquino SG, Coimbra LS, Spolidorio LC, Kirkwood KL,
Rossa C Jr.
Department of Diagnosis and Surgery, Faculdade de Odontologia de
Araraquara, Univ Estadual Paulista (UNESP), Araraquara, SP, Brazil.
Abstract
Curcumin is a plant-derived dietary spice ascribed various biological
activities. Curcumin therapeutic applications have been studied in a
variety of conditions, but not on periodontal disease. Periodontal
disease is a chronic inflammatory condition initiated by an immune
response to micro-organisms of the dental biofilm. Experimental
periodontal disease was induced in rats by injecting LPS in the
gingival tissues on the palatal aspect of upper first molars (30 µg
LPS, 3 times/week for 2 weeks). Curcumin was administered to rats
daily via oral gavage at 30 and 100 mg/kg body weight. Reverse
transcriptase-qPCR and ELISA were used to determine the expression of
IL-6, TNF-α and prostaglandin E(2) synthase on the gingival tissues.
The inflammatory status was evaluated by stereometric and descriptive
analysis on hematoxylin/eosin-stained sections, whereas modulation of
p38 MAPK and NK-κB signaling was assessed by Western blot. Curcumin
effectively inhibited cytokine gene expression at mRNA and protein
levels, but NF-κB was inhibited only with the lower dose of curcumin,
whereas p38 MAPK activation was not affected. Curcumin produced a
significant reduction on the inflammatory infiltrate and increased
collagen content and fibroblastic cell numbers. Curcumin potently
inhibits innate immune responses associated with periodontal disease,
suggesting a therapeutic potential in this chronic inflammatory
condition.
PMID: 21242275
======================
http://www.counterpunch.org/rosenberg12172010.html
The Year in Pills
By MARTHA ROSENBERG
2010 will go down as the year the diet pill Meridia and pain pill
Darvon were withdrawn from the market and the heart-attack associated
diabetes drug Avandia was severely restricted.
But it was also the year the Justice Department filed the first
criminal, not civil, charges against a drug company executive. Lauren
Stevens, a former VP and assistant general counsel at GlaxoSmithKline,
hid some 1,000 instances of GSK-paid doctors illegally promoting
Wellbutrin to other doctors, say authorities.
It was also the year prominent psychiatrists Charles Nemeroff and Alan
Schatzberg were accused of writing an entire book for GSK called
Recognition and Treatment of Psychiatric Disorders: A
Psychopharmacology Handbook for Primary Care.
Here are the drugs which make 2010's Hall of Shame.
Yaz and Yasmin
Soon after Bayer launched the pill Yaz in 2006, billing it as going
"beyond birth control," 18-year-olds were coming down with blood
clots, gall bladder disease, heart attacks and even strokes. FDA
ordered Bayer to run correction ads that detail the drugs' risks
though Yaz sales are still brisk. In fact, financial analysts
attribute a third quarter slump to a Yaz generic coming online, not
dangerous side effects.
Lyrica, Topamax and Lamictal
In August FDA ordered a warning on the seizure drug Lamictal for
aseptic meningitis (brain inflammation) but it is still the darling of
military and civilian doctors for unapproved pain and migraine uses.
All three drugs increase the risk of suicidal thoughts and behaviors
according to their mandated labels, in addition to the memory and hair
loss patients report.
Humira, Prolia and TNF Blockers
The drug industry's highly promoted biologic drugs are made from
genetically engineered hamster cells and suppress the immune system,
inviting tuberculosis and several cancers. Yet Humira is advertised to
healthy people for "clearer skin" and Prolia is advertised to prevent
osteoporosis in healthy women.
Chantix
After 397 FDA cases of possible psychosis, 227 domestic reports of
suicidal behaviors and 28 actual suicides, the government banned
pilots, air-traffic controllers and interstate truck and bus drivers
from taking the antismoking drug Chantix in 2008. Its neuropsychiatric
effects were immortalized when New Bohemians musician Carter Albrecht
was shot to death in 2007 in Texas by a neighbor after acting
aggressively on the Chantix.
Ambien
The sleeping pill Ambien was immortalized as the drug Tiger Woods
reportedly cavorted with his consorts on and former US Rep. Patrick
Kennedy crashed his Ford Mustang on, while driving to Capitol Hill in
the middle of the night to "vote" in 2006. Law enforcement officials
say it has increased traffic accidents from people who drive in a
black out and don't even recognize arresting officers.
Tamoxifen
Is it a coincidence that Tamoxifen maker AstraZeneca founded Breast
Cancer Awareness Month and makes carcinogenic agrochemicals that cause
breast cancer? As a breast cancer prevention drug, an American Journal
of Medicine study found the average life expectancy increase from
Tamoxifen was nine day . Public Citizen says for every case of breast
cancer prevented on Tamoxifen there is a life-threatening case of
blood clots, stroke or endometrial cancer.
Lipitor and Crestor
Why is Lipitor the best selling drug in the world? Because every adult
with high LDL or fear of high LDL is on it. And also 2.8 million
children, says Consumer Reports. All statins can cause muscle
breakdown called rhabdomyolysis. And Crestor is so linked to the side
effect, Public Citizen calls it a Do Not Use and the FDA's David
Graham named it one of the five most dangerous drugs before at a
Congressional hearing.
Boniva
Boniva and other bisphosphonate bone drugs are a good example of FDA
approving once unapprovable drugs by transferring risk onto the
public's shoulders. The list of dangers on the label includes waiting
60 minutes before eating or drinking anything except plain water,
never taking the drug with mineral water, sparkling water, coffee,
tea, milk, juice or other oral medicine, including calcium, antacids,
or vitamins and not lying down after you take it.
Prempro
Pfizer's hormone drug Prempro is linked to a 26 percent increase in
breast cancer, 41 percent increase in strokes, 29 percent increase in
heart attacks, 22 percent increase in cardiovascular disease and
double the rate of blood clots. But its cognitive and cardiovascular
"benefits" are being tested right now at major universities to debut
an HT "Light," hoping the public has a short memory.
Prozac, Paxil, Zoloft, SSRIs
Selective serotonin reuptake inhibitor (SSRIs) antidepressants like
Prozac, Paxil, Zoloft and Lexapro probably did more to inflate drug
industry profits than Viagra. But many say the drugs have also
inflated police blotters. In addition to 4,200 published reports of
SSRI-related violence, including the Columbine, Red Lake and NIU
shootings, SSRIs can cause serotonin syndrome and gastrointestinal
bleeding when taken with certain drugs. Paxil is linked to birth
defects.
Effexor, Cymbalta, Pristiq, SNRIs
Selective norepinephrine reuptake inhibitors (SNRIs) are like their
SSRIs chemical cousins except their norepinephrine effects can
modulate pain, which has ushered in your-depression-is-really-pain,
your-pain-is-really-depression and other crossover marketing. SNRI's
are also harder to quit than SSRIs. 739,000 web sites address
"Effexor" and "withdrawal."
Seroquel, Zyprexa, Geodon, atypical antipsychotics
The antipsychotic Seroquel tops 71 drugs on the FDA's January 2010
adverse event report and is linked to unexplained troop deaths and
many research scandals. But it's the fifth biggest-selling drug in the
world. Atypical antipsychotics cause weight gain and diabetes, the
tardive dyskinesia they are marketed to prevent and death in the
demented elderly. Yet FDA approved Zyprexa and Seroquel for children
last year and the new atypical antipsychotic, Latuda this year. Maybe
the FDA is bipolar.
Ritalin, Concerta, Strattera, Adderall and ADHD Drugs
ADHD drugs rob "kids of their right to be kids, their right to grow,
their right to experience their full range of emotions, and their
right to experience the world in its full hue of colors," says Anatomy
of an Epidemic author Robert Whitaker. But they are a gold mine for
the drug industry. During an August conference call with financial
analysts, Shire specialty pharmaceuticals president Mike Cola lauded
the "very dynamic ADHD market," and the "co-administration market" (in
which kids don't need one drug but several.
Gardasil and Cervarix Vaccines
A pharma-government plot to inoculate the public with dangerous
vaccines? Maybe not but why are governors like Texas' Rick Perry
mandating vaccination of girls for HPV? And why was University of
Queensland lecturer Andrew Gunn silenced when he questioned the
Gardasil vaccine? The HPV vaccine doesn't work for all viral strains,
requires a boo$ter and is linked to 56 US girls' deaths as of
September, according to the CDC.
Foradil Aerolizer, Serevent Diskus, Advair and Symbicort
Unlike drugs that look safe in trials and develop "safety signals"
postmarketing, the long-acting beta agonists (LABA), salmeterol and
formoterol, found in many asthma drugs, never looked safe. Studies
link them to an increase in asthma deaths, especially in African-
Americans and children. They may have contributed to 5,000 deaths said
Dr. David Graham at FDA hearings about the controversial asthma drugs.
Singulair and Accolate, leukotriene receptor antagonists
Leukotriene receptor antagonists also never looked safe. Original FDA
reviewers said asthma control "deteriorates" on Singulair and it may
not be safe in children. Last month, Fox TV reported Singulair,
Merck's top selling drug, is suspected of producing aggression,
hostility, irritability, anxiety, hallucinations and night-terrors in
kids, symptoms that are being diagnosed as ADHD. It is huckstered to
parents by the trusted educational service Scholastic, Inc. and the
American Academy of Pediatrics.
Martha Rosenberg can be reached at: martharo...@xyz.com
<snip>
==================
This info will ALL be gone in a few seconds from your brain cells.
really?
Yes so just don't try to remember it. LOL
http://www.eurekalert.org/pub_releases/2011-01/m-oom012411.php
Out of mind in a matter of seconds
IMAGE: An activity pattern is comparable to a communication protocol.
It indicates which neuron is active at a given time.
Click here for more information.
http://www.eurekalert.org/multimedia/pub/28980.php?from=177200
The dynamics behind signal transmission in the brain are extremely
chaotic. This conclusion has been reached by scientists from the Max
Planck Institute for Dynamics and Self-Organization at the University
of Göttingen and the Bernstein Center for Computational Neuroscience
Göttingen. In addition, the Göttingen-based researchers calculated,
for the first time, how quickly information stored in the activity
patterns of the cerebral cortex neurons is discarded. At one bit per
active neuron per second, the speed at which this information is
forgotten is surprisingly high. Physical Review Letters, 105, 268104
(2010)
The dynamics behind signal transmission in the brain are extremely
chaotic. This conclusion has been reached by scientists from the Max
Planck Institute for Dynamics and Self-Organization at the University
of Göttingen and the Bernstein Center for Computational Neuroscience
Göttingen. In addition, the Göttingen-based researchers calculated,
for the first time, how quickly information stored in the activity
patterns of the cerebral cortex neurons is discarded. At one bit per
active neuron per second, the speed at which this information is
forgotten is surprisingly high. Physical Review Letters, 105, 268104
(2010)
The brain codes information in the form of electrical pulses, known as
spikes. Each of the brain's approximately 100 billion interconnected
neurons acts as both a receiver and transmitter: these bundle all
incoming electrical pulses and, under certain circumstances, forward a
pulse of their own to their neighbours. In this way, each piece of
information processed by the brain generates its own activity pattern.
This indicates which neuron sent an impulse to its neighbours: in
other words, which neuron was active, and when. Therefore, the
activity pattern is a kind of communication protocol that records the
exchange of information between neurons.
How reliable is such a pattern? Do even minor changes in the neuronal
communication produce a completely different pattern in the same way
that a modification to a single contribution in a conversation could
alter the message completely? Such behaviour is defined by scientists
as chaotic. In this case, the dynamic processes in the brain could not
be predicted for long. In addition, the information stored in the
activity pattern would be gradually lost as a result of small errors.
As opposed to this, so-called stable, that is non-chaotic, dynamics
would be far less error-prone. The behaviour of individual neurons
would then have little or no influence on the overall picture.
The new results obtained by the scientists in Göttingen have revealed
that the processes in the cerebral cortex, the brain's main switching
centre, are extremely chaotic. The fact that the researchers used a
realistic model of the neurons in their calculations for the first
time was crucial. When a spike enters a neuron, an additional electric
potential forms on its cell membrane. The neuron only becomes active
when this potential exceeds a critical value. "This process is very
important", says Fred Wolf, head of the Theoretical Neurophysics
research group at the Max Planck Institute for Dynamics and Self-
Organization. "This is the only way that the uncertainty as to when a
neuron becomes active can be taken into account precisely in the
calculations".
Older models described the neurons in a very simplified form and did
not take into account exactly how and under what conditions a spike
arises. "This gave rise to stable dynamics in some cases but non-
stable dynamics in others", explains Michael Monteforte from the Max
Planck Institute for Dynamics and Self-Organization, who is also a
doctoral student at the Göttingen Graduate School for Neurosciences
and Molecular Biosciences (GGNB). It was thus impossible to resolve
the long-established disagreement as to whether the processes in the
cerebral cortex are chaotic or not, using these models.
Thanks to their more differentiated approach, the Göttingen-based
researchers were able to calculate, for the first time, how quickly an
activity pattern is lost through tiny changes; in other words, how it
is forgotten. Approximately one bit of information disappears per
active neuron per second. "This extraordinarily high deletion rate
came as a huge surprise to us", says Wolf. It appears that information
is lost in the brain as quickly as it can be "delivered" from the
senses.
This has fundamental consequences for our understanding of the neural
code of the cerebral cortex. Due to the high deletion rate,
information about sensory input signals can only be maintained for a
few spikes. These new findings therefore indicate that the dynamics of
the cerebral cortex are specifically tailored to the processing of
brief snapshots of the outside world.
<sniP<
---------------
OK i've forgotten this IL-10 and snips already. LOL
169 hits - IL-10 AND snp - pubmed
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=IL-10+snp
and since people with crohn's and psoriasis have leaky or permeable
membranes in their lamina propria regions, then LPS comes in to play.
7 hits of these 169 have LPS in them like us.
IL-10 and snp LPS - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=IL-10+snp+LPS
But i only have six to look at.
#5 is already posted above:
http://www.ncbi.nlm.nih.gov/pubmed/16078336
#4 is salient for psor heads:
http://www.ncbi.nlm.nih.gov/pubmed/18703108
Hum Immunol. 2008 Sep;69(9):562-6. Epub 2008 Aug 12.
The combined effect of interleukin (IL)-10 and IL-12 polymorphisms on
induced cytokine production.
Miteva L, Stanilova S.
Department of Molecular Biology, Immunology, & Medical Genetics;
Faculty of Medicine, Trakia University, Stara Zagora, Bulgaria.
Abstract
Interleukin (IL)-12 and IL-10 are immunoregulatory cytokines with an
antagonistic effect of the T-helper (Th)1/Th2 cytokine balance and
provide a functional link between innate and adaptive immune
responses. The aim of the study was to investigate the combined effect
of -1082A*G in IL10 and +16974A*C in IL12B single nucleotide
polymorphisms (SNPs) on induced cytokine production by stimulated
peripheral blood mononuclear cells (PBMCs) isolated from healthy
donors. The presence of the high-producer IL-12p40 genotype led to
diminished production of IL-10 as determined by the -1082*G allele of
SNP in IL10. Significantly decreased IL-10 production was detected in
AA+AG/GG in comparison with the low-producer IL-12p40 (AC/CC+AG/GG)
genotype combination after stimulation with C3bgp (2+/-4 vs. 29+/-14.2
pg/ml; p=0.0003) and LPS (33.4+/-13.5 vs. 93.3+/-59.6 pg/ml; p=0.019).
IL-12p40 production was independent of IL10 genotype. The present
results demonstrated that the production of IL-10 from PBMC depended
on both -1082A*G in IL10 and +16974A*C in IL12B polymorphisms.
PMID: 18703108
#2 might be BIG is D3 from oral sources is negated or something?
http://www.ncbi.nlm.nih.gov/pubmed/19811264
Autoimmunity. 2009 Aug;42(5):467-74.
Retinoid X receptor beta polymorphisms do not explain functional
differences in vitamins D and A response in Antineutrophil cytoplasmic
antibody associated vasculitis patients.
Kälsch AI, Peters A, Buhl B, Breedijk A, Prem K, Schmitt WH, Weiss C,
Heeringa P, Kallenberg C, Birck R, Yard BA.
Fifth Department of Medicine, University Hospital Mannheim, Faculty of
Medicine Mannheim, University of Heidelberg, Heidelberg, Germany. anna-
isabelle.kaelsch
@med5.ma.uni-heidelberg.de
Abstract
It has been suggested that the retinoid X receptor beta (RXRB) gene is
a risk factor for Wegener's granulomatosis. We addressed if there is a
functional difference in the response to retinoic acid (RA) and
vitamin D in Antineutrophil cytoplasmic antibody (ANCA) associated
systemic vasculitis (AASV) patients and if this was associated with
RXRB genotypes. TNFalpha and IL-10 production were measured in whole
blood assay from AASV patients (n = 51) and healthy controls (HC, n =
67). One micromolar of 1,25-(OH)(2) D3, 9-cis RA (9c-RA) or all-trans
RA (ATRA) was added to the assay. Genotyping was performed for exons 7
and 2 of the RXRB gene and for a microsatellite in vicinity of the
RXRB gene. Lipopolysaccharide (LPS) mediated TNFalpha production and
IL-10 were significantly lower in patients. Addition of 1,25-(OH)(2)
D3, ATRA or 9c-RA, blunted TNFalpha production, more pronounced in
patients. Although all three compounds inhibited IL-10 production
significantly in HC, only 1,25-(OH)(2) D3 was found to be effective in
patients. Allele distribution of the RXRB microsatellite differed
significantly between patients and HC. This was not found for the SNP
in exons 2 and 7. Genotype of the latter correlated with the ability
of 1,25-(OH)(2) D3 and ATRA to inhibit IL-10 production. We provide
immunological evidence for a functional difference in vitamins D and A
responsiveness in AASV patients. Since the inhibition of TNFalpha was
more effective in patients, vitamin D supplementation might be an
additional therapeutical approach.
PMID: 19811264
#1 looks GOOD... so remember to READ it. LOL
http://www.ncbi.nlm.nih.gov/pubmed/21238472
Mech Ageing Dev. 2011 Jan 13.
LPS-mediated production of pro/anti-inflammatory cytokines and
eicosanoids in whole blood samples: biological effects of +896A/G TLR4
polymorphism in a Sicilian population of healthy subjects.
Balistreri CR, Caruso C, Listì F, Colonna-Romano G, Lio D, Candore G.
Immunosenescence Group, Department of Pathobiology and Medical and
Forensic Biotechnologies, University of Palermo, Palermo, Italy.
Abstract
Toll-like receptors (TLRs) are the principal mediators of rapid
microbial recognition: the lipopolysaccharide (LPS) receptor TLR4
seems to have a paradigmatic role. Single nucleotide polymorphisms
(SNPs) in the TLR4 gene, such as +896A/G, known to attenuate receptor
signaling, have been described. The +896A/G SNP is significantly less
frequent in patients with myocardial infarction, Alzheimer's disease
or prostate cancer, whereas it is overrepresented in centenarians. To
clarify and confirm the biological effects of +896A/G SNP and its role
in the pathophysiology of age-related diseases and longevity, we
assessed the levels of IL-6, TNF-α, IL-10 and eicosanoids (LTB4 and
PGE2) in LPS-stimulated whole blood samples in vitro of 50 young
healthy Sicilians, screened for the presence of this SNP. To evaluate
the possible influence of SNPs in PTGS2 and 5-Lo genes on eicosanoid
production, the enrolled individuals were also genotyped for -765G/C
PTGS2 and -1708G/A 5-Lo SNPs. Both pro-inflammatory cytokines and
eicosanoids were significantly lower in carriers bearing the TLR4
mutation, whereas the anti-inflammatory IL-10 values were higher. On
the basis of data reported herein, some suggestions can be drawn.
First, pathogen load, by interacting with the host genotype,
determines the type and intensity of inflammatory responses, according
to the pro-inflammatory status and tissue injury, implicated in the
pathophysiology of major age-related diseases. Second, adequate
control of inflammatory response might reduce the risk of these
diseases, and, reciprocally, might increase the chance of extended
survival in an environment with reduced antigen (that is, pathogen)
load.
PMID: 21238472
randall.... ok i'm bushed... and obama will BLAME the burning BUSH
tonight . LOL