CD98 -- IP3R1 --IP6 & IP3 -->Deranged Ca2+ Signaling -- SCiaM Worm Article -- SFB - H. Pylori -> M1 (Th1) Nod back to Th2 (M2) Target Th17 or SFB?
randall
OK so i saw the chinese for pax et bonum right after i posted it. LOL
<last post today - link below>
平安幸福! (Chinese tr.)
Yes?.....
Yet i wonder about bantu, Inuit, sotho, showa, swahili, ethiopian and
xhosa variations.
Is that all?
Well NO, what about KLINGON?
http://en.wikipedia.org/wiki/Klingon#Language
Certainly Spock would say:
Live LONG and Prosper and hold his hands sorta like St. FRANCIS di
Bernardone
http://en.wikipedia.org/wiki/Vulcan_salute
Leonard Nimoy as spock:
http://upload.wikimedia.org/wikipedia/en/5/5a/Spock_vulcan-salute.png
Giovanni Francesco di Bernardone; 1181/1182 – October 3, 1226)
http://upload.wikimedia.org/wikipedia/commons/f/fb/Saint_Francis_of_Assisi_by_Jusepe_de_Ribera.jpg
WELL that is a stretch.
Or Giovanni Francesco di Bernardone (aka- St. FRANCIS of Assisi) was
saying the FISH was THIS BIG. LOL
OK so?
And you misspPPelled his name yesterday. You left out the R. Duh..
Hey i notice that stuff when i re-read, but if i used YOU to edit this
stuff
your anal editorial analysis would take a zillion years. <w>
I'm not ANAL yoU are.
Your that and BANAL and a tedious BORE. So go snore already so i can
blow this post OUT.
AND i brought up Tolstoy, Francis of Assisi, William Shakespeare,
Fyodor Mikhaylovich Dostoyevsky and today AmeriCAN Genius Ben
Franklin.
Who do you LOVE?
Who loves YOU?
Later ans on that one. <w>
http://en.wikipedia.org/wiki/St._Francis_of_Assisi
Saint Francis of Assisi (Giovanni Francesco di Bernardone; 1181/1182 –
October 3, 1226)[2] was a Catholic friar and preacher.
<snip>
He had gnosis in sPades.
Did he have the DRD4 snp as his peta and enviro concerns besides GOD
consciousness, and
early death, only 45ish?
I don't gnosis but if he lived to 84 like Big BEN Franklin and ate
with his
relish for life he might hav got psoriasis? <g>
http://en.wikipedia.org/wiki/Shakespeare
http://en.wikipedia.org/wiki/Fyodor_Dostoyevsky
http://en.wikipedia.org/wiki/Fyodor_Dostoyevsky#Death
[...] His tombstone reads; Verily, Verily, I say unto you, Except a
corn of wheat fall into the ground and die, it abideth alone: but if
it die, it bringeth forth much fruit. (Excerpt from John 12:24, which
is also the epigraph of his final novel, The Brothers Karamazov.)
<snip>
Can't forget Voltaire and Candide? The GLASS is too two 2 FULL of
oPtimism, pangloss. LOL
http://en.wikipedia.org/wiki/Candide
http://en.wikipedia.org/wiki/Voltaire
François-Marie Arouet (French pronunciation: [fʁɑ̃swa maʁi aʁuˈwe]; 21
November 1694 – 30 May 1778)
http://en.wikipedia.org/wiki/Benjamin_Franklin
Benjamin Franklin (January 17, 1706 [O.S. January 6, 1705[1]] – April
17, 1790) was one of the Founding Fathers of the United States. A
noted polymath, Franklin was a leading author and printer, political
theorist, politician, postmaster, scientist, inventor, satirist, civic
activist, statesman, and diplomat. As a scientist, he was a major
figure in the American Enlightenment and the history of physics for
his discoveries and theories regarding electricity. He invented the
lightning rod, bifocals, the Franklin stove, a carriage odometer, and
the glass 'armonica'. He formed both the first public lending library
in America and the first fire department in Pennsylvania.
<snip>
Ben had psoriasis later in life. Late ONset.
If your like BEN who called science natural philosophy iirc, then go
for it.
http://en.wikipedia.org/wiki/Natural_philosophy
http://en.wikipedia.org/wiki/Natural_science
Bens museum in boston
http://www.ansp.org/
Why don't the call it MU see them?
Shut up banal anal one. LOL
Mu would mean nothing in Oriental meanings.
See nothing?
Hey sorta a koan?
Let's see?
yeP:
http://en.wikipedia.org/wiki/Mu_(negative)#The_.22Mu.22_koan
The "Mu" koan
The word mu is central to the following well-known Zen Buddhist koan,
which is also known as the Mu koan[1]:
[...] A monk asked, "Does a dog have a Buddha-nature or not?"
traditional Chinese: 僧問：狗子還有佛性也無？
The master said, "Not [Mu]!"
traditional Chinese: 師云：無。
The monk said, "Above to all the Buddhas, below to the crawling bugs,
all have Buddha-nature. Why is it that the dog has not?"
traditional Chinese: 問：上至諸佛，下至螻蟻皆有佛性，狗子為什麼卻無？
The master said, "Because he has the nature of karmic delusions".
traditional Chinese: 師云：為伊有業識在。
<snip>
A monk asked Zhaozhou Congshen, a Chinese Zen master (known as Jōshū
in Japanese), "Has a dog Buddha-nature or not?" Zhaozhou answered,
"Wú" (in Japanese, Mu)
—The Gateless Gate, koan 1, translation by Robert Aitken [5]
And greek mu is just the LETTER M.
How about a MOOO see em?
Back to BF:
He did bifocals besides fly a kite?
Duh...and he had nasty GOUT and didn't exercise enough.
His work BF said forces him to be sedentary.
So his late onset psoriasis was due to syndrome X? LOL <w>
Franklin quotes:
http://www.brainyquote.com/quotes/authors/b/benjamin_franklin.html
PBS has a 3 1/2 hour miniseries on Ben Franklin
I'm only 2 hours in on it (but wrote almost this entire post in that
time. LOL)
and it hasn't mentioned his psoriasis yet.
http://www.pbs.org/benfranklin/about.html
you can have this amazing BF for under $12 bucks
http://www.amazon.com/Benjamin-Franklin-PBS-Home-Video/dp/B00007KE64
I want it. Does Beyonce?
NO.. who wants scurf and turf?
I will EAT most surfy foods. <w>
================
Ok moron boy... how does this do anything for psoriasis?
Yes we know that BIG BEN had Psor on his skin and he called it scurf.
SEE mY post:
HaPPy 4th of JULY --from PSORiatic - BENJAMIN FRANKLIN - Epigenetics -
HDAC Inhibitors -TSA - Options
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/6b9909b46a0a5e2e
STOP...
Git back to the GUT triP or psor hits/
OK... sorry.
But this exemplifys my CD98hc thing.
Which is?
Don't tell kofi.. he might take it as his discovery. LOL
Hey he won't come and read this today. That last post is moooo JAMBus.
So?
http://en.wikipedia.org/wiki/CD98
CD98 is a glycoprotein[1][2] that is a heterodimer composed of SLC3A2
and SLC7A5 that form the large neutral amino acid transporter (LAT1).
LAT1 is a heterodimeric membrane transport protein that preferentially
transports neutral branched (valine, leucine, isoleucine) and aromatic
(tryptophan, tyrosine) amino acids.[3] LAT is highly expressed in
brain capillaries (which form the blood brain barrier) relative to
other tissues.[3]
A functional LAT1 transporter is composed of two proteins encoded by
two distinct genes:
4F2hc/CD98 heavy subunit protein encoded by the SLC3A2 gene [4]
CD98 light subunit protein encoded by the SLC7A5 gene[5]
<snip>
If he sPies this the CAT is outa the BAG. yikes...
http://en.wikipedia.org/wiki/Membrane_transport_protein
http://en.wikipedia.org/wiki/Transmembrane_protein
http://en.wikipedia.org/wiki/Solute_carrier_family#Families
Hey, hey, i want some real meaty psor stuff?
OK don't have a cardio event.
But i wonder if psoriasis is compensatory for strokes now.
So you ___know_sis___(γνῶσις)___ i worry about calcium and stroke.
Fore! LOL
Heads up perhaPs?
So?
Do ER and calcium (Ca2+) research?
OK and i bet dollars to donuts that BEN Franklin had top notch ER's.
<w>
I found this IP3R1 protein in regards to endoplasmic reticulum & Ca2+.
[...] The ER plays a major role in maintaining protein quality in the
cell and conditions that affect this cause it stress, which can
trigger the cell death associated with Huntington's and Alzheimer's.
Scientists indentified a mechanism involved the process that leads to
ER stress inhabiting the activation of the IP3R1 protein.
<snip>
Only 102 hits for IP3R1 protein - pubmed
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=IP3R1+protein
28 of these 102 have kicker term : endoplasmic - pubmed
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=IP3R1+protein+endoplasmic
http://www.ncbi.nlm.nih.gov/pubmed/21071436
J Biol Chem. 2010 Nov 11.
Activated inositol 1,4,5-trisphosphate receptors are modified by
homogenous LYS48- and LYS63-linked ubiquitin chains, but only LYS48-
linked chains are required for degradation.
Sliter DA, Aguiar M, Gygi SP, Wojcikiewicz RJ.
SUNY Upstate Medical University, United States;
Abstract
Inositol 1,4,5-trisphosphate (IP3) receptors (IP3Rs) are large,
ubiquitously expressed endoplasmic reticulum (ER) membrane proteins
that form tetrameric IP3 and Ca2+-gated Ca2+ channels. Endogenous
IP3Rs provide very appealing tools for studying the ubiquitin
proteasome pathway (UPP) in intact mammalian cells, since upon
activation they are rapidly ubiquitinated and degraded. We previously
examined, using mass spectrometry, the ubiquitination of IP3R1 in
αT3-1 pituitary gonadotrophs and found that IP3R1 ubiquitination is
highly complex with receptors being modified at multiple sites by
monoubiquitin and polyubiquitin chains formed through both Lys48 and
Lys63 linkages (Sliter D.A., et. Al., 2008 J. Biol. Chem. 283,
35319-35328). Here, we have extended these studies to determine if
IP3R2 and IP3R3 are similarly modified and if ubiquitination is cell
type dependent. Using mass spectrometry and linkage-specific ubiquitin
antibodies we found that all IP3R types are subject to ubiquitination
at approximately the same locations, and that, independent of cell
type, IP3Rs are modified by monoubiquitin and Lys48- and Lys63-linked
ubiquitin chains, although in differing proportions. Remarkably, the
attached Lys48- and Lys63-linked ubiquitin chains are homogenous, are
segregated to separate IP3R subunits, and Lys48-linked ubiquitin
chains, but not Lys63-linked chains, are required for IP3R
degradation. Together, these data provide unique insight into the
complexities of ubiquitination of an endogenous UPP substrate in
unperturbed mammalian cells. Importantly, while Lys48-linked ubiquitin
chains appear to trigger proteasomal degradation, the presence of
Lys63-linked ubiquitin chains suggests that ubiquitination of IP3Rs
may have physiological consequences beyond signaling for degradation.
PMID: 21071436 Free Article
http://www.jbc.org/cgi/pmidlookup?view=long&pmid=21071436
WE have 9 hits for IP3 in the P NG
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=ip3&start=0&scoring=d&hl=en&
But for IP6 we have 337 hits
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=ip6&start=0&scoring=d&hl=en&
Does our body fliP IP6 to IP3 or vice versa?
http://en.wikipedia.org/wiki/Phytic_acid
Phytic acid (known as inositol hexaphosphate (IP6), or phytate when in
salt form) is the principal storage form of phosphorus in many plant
tissues, especially bran and seeds.[1]
Inositol penta- (IP5), tetra- (IP4), and triphosphate (IP3) are also
called phytates.
<snip>
IP6 does block iron which is iron justice if your prone to cancer?
Don't wake him uP?
Why?
Cause he's like a religious JESUS veggetaboo freak. LOL
Your right. Your almost all wheys RIgHT.
SWEET--->
I know. Eat your sesame seeds as it is it in sPades
http://en.wikipedia.org/wiki/Phytic_acid#Food_science
==============
http://biomedme.com/general/new-mechanism-links-cellular-stress-brain-damage_25567.html
New Mechanism Links Cellular Stress Brain Damage
Written By: Nadia on December 14, 2010
A new study uncovered a mechanism linking a specific type of cellular
stress with brain damage similar to that associated with
neurodegenerative disease.
The research, published by Cell Press in the Dec. 9 issue of the
journal Neuron, is the first to highlight the significance of the
reduction of a specific calcium signal that is directly tied to cell
fate.
Body cells are constantly exposed to various environmental stresses.
Although cells possess some natural defenses, excessive stress can
lead to a type of cell death called apoptosis.
“It is thought that excessive stress impacts brain function by
inducing neuronal apoptosis and may play a role in neurodegenerative
diseases such as Alzheimer’s disease and Huntington’s disease (HD),”
explains senior study author, Dr. Katsuhiko Mikoshiba, from the
Laboratory for Developmental Neurobiology at RIKEN Brain Science
Institute.
HD is also associated with abnormal calcium signaling and the
accumulation of misfolded proteins. Altered function of an
intracellular structure called the endoplasmic reticulum (ER) that
plays a key role in protein “quality control” and is a critical
regulator of intracellular calcium signaling has been implicated in HD
pathogenesis, but the specific underlying mechanisms linking ER stress
with calcium and apoptosis are poorly understood.
Dr. Mikoshiba and colleagues demonstrated that a neuronal protein
called inositol 1,4,5-trisphosphate receptor 1 (IP3R1) which regulates
cellular calcium signaling was destroyed by ER stress and subsequently
induced neuronal cell death and brain damage.
The researchers went on to show that a protective “chaperone” protein
called GRP78 positively regulated IP3R1 and that ER stress led to an
impaired IP3R1-GRP78 interaction, which has also been observed in an
animal model of HD.
“Based on our observation that the functional interaction between
IP3R1 and GRP78 is impaired during ER stress and in the HD model, we
propose that IP3R1 functions to protect the brain against stress and
that the linkage between ER stress, IP3/calcium signaling, and
neuronal cell death are associated with neurodegenerative disease.”
concludes Dr. Mikoshiba.
<snip>
Wow...Mikoshiba calls it ____DERANGED___ Ca2+ ---> signaling. LOL
http://www.ncbi.nlm.nih.gov/pubmed/21145001
Neuron. 2010 Dec 9;68(5):865-78.
Mechanism of ER Stress-Induced Brain Damage by IP(3) Receptor.
Higo T, Hamada K, Hisatsune C, Nukina N, Hashikawa T, Hattori M,
Nakamura T, Mikoshiba K.
Department of Molecular Neurobiology, Institute of Medical Science,
University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639,
Japan; Laboratory for Developmental Neurobiology, Brain Science
Institute, RIKEN, Wako, Saitama 351-0198, Japan.
Abstract
____Deranged Ca(2+)___ signaling and an accumulation of aberrant
proteins cause endoplasmic reticulum (ER) stress, which is a hallmark
of cell death implicated in many neurodegenerative diseases. However,
the underlying mechanisms are elusive. Here, we report that
dysfunction of an ER-resident Ca(2+) channel, inositol 1,4,5-
trisphosphate receptor (IP(3)R), promotes cell death during ER stress.
Heterozygous knockout of brain-dominant type1 IP(3)R (IP(3)R1)
resulted in neuronal vulnerability to ER stress in vivo, and IP(3)R1
knockdown enhanced ER stress-induced apoptosis via mitochondria in
cultured cells. The IP(3)R1 tetrameric assembly was positively
regulated by the ER chaperone GRP78 in an energy-dependent manner. ER
stress induced IP(3)R1 dysfunction through an impaired IP(3)R1-GRP78
interaction, which has also been observed in the brain of Huntington's
disease model mice. These results suggest that IP(3)R1 senses ER
stress through GRP78 to alter the Ca(2+) signal to promote neuronal
cell death implicated in neurodegenerative diseases.
Copyright © 2010 Elsevier Inc. All rights reserved.
PMID: 21145001
"Mikoshiba K"[Author] 635 hits - pubmed:
http://www.ncbi.nlm.nih.gov/pubmed?term=%22Mikoshiba%20K%22%5BAuthor%5D
64 of these have endoplasmic hits... the stress.. the stress in the
eR... stat.
"Mikoshiba K"[Author] AND endoplasmic - 64 hits - pubmed:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=%22Mikoshiba+K%22%5BAuthor%5D+AND+endoplasmic
--------------
I get deranged just thinking about stroking out.
Get the coconut mct's and take B6 with with wit...?
L-Lysine?
Check it out?
Again?
===================================
AS the wORM Turns
The worms within
By Robin Ann Smith | Dec 17, 2010
Some of the worms and germs we’ve been warding off may actually keep
us well. One solution, some scientists say, is to welcome them back
I met William Parker just two days before World Toilet Day, an
international campaign to break taboos about, yes, potties. It’s a
subject not many like to talk about. The cause is a critical one:
access to sanitation and safe drinking water are key to preventing a
host of diseases. But a growing body of research suggests there may be
a dark side to clean living.
[Image: With allergies and autoimmune disorders on the rise,
researchers find hope in some unlikely allies]
According to one theory, first proposed in the 1980s, the super-
sanitized lifestyle of the western world may have curtailed some
diseases but created new ones. The prevalence of asthma, allergies,
and a number of autoimmune-related ills —from rheumatoid arthritis to
Type I diabetes—has skyrocketed in recent decades, especially in
wealthy countries. "Roughly 4 in 10 Americans suffer from allergies,
and nearly 1 in 10 develop an autoimmune disorder," Parker said. "We
generally don’t see these diseases in developing countries."
Duke immunologist William Parker is one of hundreds of scientists who
are trying to figure out exactly what makes healthy immune systems
tick, and why modern living has run them amok.
[Photo: William Parker, Ph.D]
"Certainly there’s a genetic connection. And there can also be
environmental triggers, like viral infections or chemicals," Parker
said. "But there’s something more going on."
The culprit, some scientists say, may be a lack of worms. Not the
worms that dig in your garden, mind you, but the ones that dwell in
your gut.
Old allies?
Until the last century, few people on Earth were parasite-free. For
much of our evolutionary history, humans have played host to an array
of wormy guests. Hookworms, roundworms, and whipworms have long made
their homes in the warm wet folds of our intestines, bathed in a
constant supply of food and nutrients.
Today, intestinal worms still infect more than one third of the
world’s population. Parker, who grew up on a hobby farm in rural
Arkansas, suspects he plays host to a few parasites of his own. "I
probably have things in my gut that most people don’t, because I grew
up drinking creek water," Parker said.
Many intestinal parasites are passed from person to person when
microscopic amounts of human feces get on our fingers, or when we walk
barefoot on contaminated soil. Sewage treatment and running water
prevent parasites from passing from one person to the next, Parker
explains. But it wasn’t always this way.
"We seem to have forgotten that it was only very recently, less than
100 year ago, that our grandparents first acquired indoor plumbing and
access to modern medicine," Parker said. "A number of different worms
used to live in our guts, but they’ve been wiped out."
Too clean for our own good
Parker and other scientists suspect we may be paying a price for our
parasite-free existence. To find out, Parker’s research revolves
around another set of animals scrubbed squeaky clean by modern living:
lab rats.
Scientists started breeding strains of rodents for laboratory
experiments about 150 years ago, Parker says.
"We treat them with anti-parasitic drugs, and we make sure they have
clean drinking water. So in a real sense we’ve done the same things to
our lab animals that we’ve inadvertently done to ourselves."
In the mid 2000’s, Parker began catching wild rats in and around
Durham, NC, and comparing them to rats raised in the lab.
Parker showed me his trapping technique, learned from catching rats in
his parents’ barn as a child. It’s not glamorous work. In urban areas,
wild rats are lured by garbage cans and dog food bins. Parker finds
rat-infested areas and sets out his traps: wire cages the size of a
shoebox, outfitted with trap doors and triggers.
After putting out unarmed live traps for several days to put the beady-
eyed pests at ease, he baits each trap and sets the trigger, returning
later to collect his prey.
"Wild rats aren’t as friendly as the lab rats are," Parker said.
[Image: Photo of wild rat.]
Unlike sterile lab rats, wild rats are riddled with parasites — not
just worms, but bacteria and viruses, lice and mites — which their
immune systems have to contend with.
When Parker compared immune reactions in spleen cells of wild rats
with their squeaky clean cousins, the lab rats were hypersensitive
compared to their wild counterparts.
This hypersensitivity could also explain what happens when people go
parasite free, Parker explained.
Off kilter
To evade eviction, worms secrete chemicals that quiet the bodies’
natural defenses just enough to allow them to avoid attack without
harming their host.
Over millions of years of co-existence, the theory goes, our immune
systems learned to tolerate these live-in guests —or "helminthes," as
Parker prefers to call them —and eventually came to depend on worms to
work properly.
"Ancient adaptations to deal with helminth infection may have left
their mark on the way the immune system is structured and controlled,"
wrote Janette Bradley and co-authors at the University of Nottingham,
in a 2009 article published in Immunology.
With parasites out of the picture, the body’s natural defenses go into
overdrive. Our immune systems are now mounting the alarm for harmless
substances from dust mites to cat dander. In the case of autoimmune
disorders such as Crohn’s disease and Type I diabetes, the body’s
immune system attacks the very thing it was meant to protect: our own
tissues.
"Our immune system doesn’t have enough to do," so it gets bored and
looks for something to fight, Parker explained. "It may be that our
immune system needs the chemicals helminthes produce to function
normally," he added.
Blurring the line between friend and foe
What to do? Some scientists propose a solution that’s not for the
squeamish. If eliminating parasites triggered the rise in allergies
and autoimmune disorders, could reuniting with the worms within
restore our health?
A growing number of studies suggest that for off-kilter immune
systems, a dose of gut worms may be just what the doctor ordered. Lab
rodents were the first trial subjects to test the idea, but studies in
humans have backed up the hunch.
Researchers at the University of Iowa are treating patients with
inflammatory bowel disease (IBD) with "cocktails" laced with
microscopic whipworm eggs. It may sound like a witch’s brew, but for
some patients with IBD — a painful disorder characterized by diarrhea,
bleeding and fever — it’s a worthwhile tradeoff. The patients had
tried multiple treatments to relieve their symptoms, but nothing
worked. After 24 weeks of worm therapy, 23 of the 29 volunteers went
into remission.
[Photo of whipworm eggs.]<see the link above for sciam>
Worm therapy has also proven effective for other diseases. Multiple
sclerosis (MS) is a debilitating disease in which the body attacks its
own nerve cells. Scientists in Argentina followed several hundred
multiple sclerosis patients for 4 to 6 years, a dozen of whom
accidentally developed intestinal parasites during the study. When
they compared the patients who developed intestinal parasites with the
patients who remained parasite-free, the worm-infected patients had
fewer flare-ups over time.
A new spin on health care
These scientists aren’t suggesting we relinquish the loo. Dozens of
communicable diseases, from cholera to typhoid, travel from person to
person in human feces. Waste disposal and treatment mean the
difference between life and death in some parts of the world, where
defecating in the open is a leading cause of contaminated drinking
water.
"Nobody’s suggesting we go back to the Stone Age," Parker said.
Instead, Parker imagines a future where worm therapy is a routine part
of medical care. "You would go to the doctor to get exactly the type
and number of worms you needed," Parker explained. "You would get your
worm levels checked just like you get your cholesterol levels
checked."
Parker acknowledges this is a big shift for doctors, who are normally
in the business of preventing infection. "We usually think it’s not
healthy to have worms. And indeed, people already plagued by anemia or
malnutrition can get sick from them," he acknowledged. But in
controlled doses under medical supervision, Parker says, the parasites
are unlikely to cause problems. "The risks are small compared to the
potential benefits," he explained.
Gut reaction
Why not identify the mystery compounds the worms secrete, and develop
a drug that mimics their effects? When I asked Parker this question,
he was skeptical. "Each worm constantly secretes dozens if not
hundreds of different molecules as it travels through the body. That’s
hard to reproduce with a drug."
With FDA approval for many kinds of worm therapy still a long ways
off, some people are taking their health in their own hands and
deliberately infecting themselves with worms in the hopes of relieving
their symptoms.
But until we have a better understanding of how worm therapy works,
Parker cautions, self-treatment is still a gamble.
"We still don’t know which species of worms you need, or how many, or
what the timing of treatment needs to be to make your immune system
stable," Parker said.
"Some of these diseases are very early onset. Which diseases can be
treated after symptoms have already developed? And which diseases can
be prevented, but not cured?"
With the sun setting fast, Parker loads the last of his traps, and
hands me a peanut. It’s a deadly allergen to some people, but
irresistible to rodents. I debate whether to wash my hands, then I
take the bait.
****
<for the author: robin smith
http://fds.duke.edu/db/aas/Biology/staff/ras10
and references, credits & Jpg's please visit the link>
Oh and three comments so far:
http://www.scientificamerican.com/blog/post.cfm?id=the-worms-within-2010-12-17&WT.mc_id=SA_DD_20101217
=========================
OK here is MY comment.
<randall note: this is what i said to my online BUD who sent the sciam
wormy story>
screw the worms.
As them worms turn.... let them have their day when they plant us. six
feet deep LOL
We want SFB control in the gut.
Then we SAVE hiv'ers, cancer people and autoimmune folks.
SFB is the biggest worm for big pig pharma to choke on in the world,
in MY OPINION.
wow.. where did that come from?
Must have been just waiting to exPlode outa me?
<snip>
OK so what about WHY people get cancer?
Like what? YOU MEAN genes?
NO.. i mean other bugs that promote it in an epigenetic fashion.
So bugs instead of worms are your passion?
YeP.
Take H. pylori.
you take it.
OK take it as mind fodder now.
In my last HUGEST POST almost? I got down with M1, M2 and Th1 & Th2
skews.
See
Fri, Dec 17 2010 11:16 am
Subject: Current ABSTRACTs - Psors4 - - Autophagy --MIF --M1 M2 with
Th1 Th2 -- IL-19 much much turbo on speed more +++++
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/ae9eb064b3090954
Right i might have missed it. LOL
Like 99.9999% of the folks who even try to read it. LOL
OK so i'm writing for me.
Here:
http://www.ncbi.nlm.nih.gov/pubmed/21124899
PLoS One. 2010 Nov 23;5(11):e15018.
Enhanced M1 macrophage polarization in human helicobacter pylori-
associated atrophic gastritis and in vaccinated mice.
M1
Quiding-Järbrink M, Raghavan S, Sundquist M.
Department of Microbiology and Immunology, University of Gothenburg,
Gothenburg, Sweden.
Abstract
BACKGROUND: Infection with Helicobacter pylori triggers a chronic
gastric inflammation that can progress to atrophy and gastric
adenocarcinoma. Polarization of macrophages is a characteristic of
both cancer and infection, and may promote progression or resolution
of disease. However, the role of macrophages and their polarization
during H. pylori infection has not been well defined.
METHODOLOGY/PRINCIPAL FINDINGS: By using a mouse model of infection
and gastric biopsies from 29 individuals, we have analyzed macrophage
recruitment and polarization during H. pylori infection by flow
cytometry and real-time PCR. We found a sequential recruitment of
neutrophils, eosinophils and macrophages to the gastric mucosa of
infected mice. Gene expression analysis of stomach tissue and sorted
macrophages revealed that gastric macrophages were polarized to M1
after H. pylori infection, and this process was substantially
accelerated by prior vaccination. Human H. pylori infection was
characterized by a mixed M1/M2 polarization of macrophages. However,
in H. pylori-associated atrophic gastritis, the expression of
inducible nitric oxide synthase was markedly increased compared to
uncomplicated gastritis, indicative of an enhanced M1 macrophage
polarization in this pre-malignant lesion.
CONCLUSIONS/SIGNIFICANCE: These results show that vaccination of mice
against H. pylori amplifies M1 polarization of gastric macrophages,
and that a similar enhanced M1 polarization is present in human H.
pylori-induced atrophic gastritis.
PMID: 21124899
H. Pylori is very common in the poPulation at large.
http://en.wikipedia.org/wiki/Helicobacter_pylori
Helicobacter pylori (English pronunciation: /ˌhɛlɨkɵˈbæktər pɪˈlɔraɪ/)
is a Gram-negative, microaerophilic bacterium that can inhabit various
areas of the stomach, particularly the antrum. It causes a chronic low-
level inflammation of the stomach lining and is strongly linked to the
development of duodenal and gastric ulcers and stomach cancer. Over
80% of individuals infected with the bacterium are asymptomatic.
[...] More than 50% of the world's population harbor H. pylori in
their upper gastrointestinal tract. Infection is more prevalent in
developing countries, and incidence is decreasing in Western
countries.
[...]
http://en.wikipedia.org/wiki/Helicobacter_pylori#Pathophysiology
[...] Colonization of the stomach by H. pylori results in chronic
gastritis, an inflammation of the stomach lining. The severity of the
inflammation is likely to underlie H. pylori-related diseases.[23]
Duodenal and stomach ulcers result when the consequences of
inflammation allow the acid and pepsin in the stomach lumen to
overwhelm the mechanisms that protect the stomach and duodenal mucosa
from these caustic substances. The type of ulcer that develops depends
on the location of chronic gastritis, which occurs at the site of H.
pylori colonization.[24] The acidity within the stomach lumen affects
the colonization pattern of H. pylori and therefore ultimately
determines whether a duodenal or gastric ulcer will form. In people
producing large amounts of acid, H. pylori colonizes the antrum of the
stomach to avoid the acid-secreting parietal cells located in the
corpus (main body) of the stomach.[8] The inflammatory response to the
bacteria induces G cells in the antrum to secrete the hormone gastrin,
which travels through the bloodstream to the corpus.[25] Gastrin
stimulates the parietal cells in the corpus to secrete even more acid
into the stomach lumen. Chronically increased gastrin levels
eventually cause the number of parietal cells to also increase,
further escalating the amount of acid secreted.[26] The increased acid
load damages the duodenum, and ulceration may eventually result. In
contrast, gastric ulcers are often associated with normal or reduced
gastric acid production, suggesting that the mechanisms that protect
the gastric mucosa are defective.[26] In these patients, H. pylori can
also colonize the corpus of the stomach, where the acid-secreting
parietal cells are located. However chronic inflammation induced by
the bacteria causes further reduction of acid production and,
eventually, atrophy of the stomach lining, which may lead to gastric
ulcer and increases the risk for stomach cancer.[27]
About 50-70% of H. pylori strains in Western countries carry the cag
pathogenicity island (cag PAI).[28] Western patients infected with
strains carrying the cag PAI have a stronger inflammatory response in
the stomach and are at a greater risk of developing peptic ulcers or
stomach cancer than those infected with strains lacking the island.[8]
Following attachment of H. pylori to stomach epithelial cells, the
type IV secretion system expressed by the cag PAI "injects" the
inflammation-inducing agent, peptidoglycan, from their own cell wall
into the epithelial cells. The injected peptidoglycan is recognized by
the cytoplasmic pattern recognition receptor (immune sensor) Nod1,
which then stimulates expression of cytokines that promote
inflammation.[29]
The type IV secretion apparatus also injects the cag PAI-encoded
protein CagA into the stomach's epithelial cells, where it disrupts
the cytoskeleton, adherence to adjacent cells, intracellular
signaling, cell polarity, and other cellular activities.[30] Once
inside the cell, the CagA protein is phosphorylated on tyrosine
residues by a host cell membrane-associated tyrosine kinase (TK).
Pathogenic strains of H. pylori have been shown to activate the
epidermal growth factor receptor (EGFR), a membrane protein with a
tyrosine kinase domain. Activation of the EGFR by H. pylori is
associated with altered signal transduction and gene expression in
host epithelial cells that may contribute to pathogenesis. It has also
been suggested that a C-terminal region of the CagA protein (amino
acids 873–1002) can regulate host cell gene transcription, independent
of protein tyrosine phosphorylation.[16][17] There is a great deal of
diversity between strains of H. pylori, and the strain with which one
is infected is predictive of the outcome.
Two related mechanisms by which H. pylori could promote cancer are
under investigation. One mechanism involves the enhanced production of
free radicals near H. pylori and an increased rate of host cell
mutation. The other proposed mechanism has been called a "perigenetic
pathway"[31] and involves enhancement of the transformed host cell
phenotype by means of alterations in cell proteins, such as adhesion
proteins. It has been proposed that H. pylori induces inflammation and
locally high levels of TNF-α and/or interleukin 6 (IL-6). According to
the proposed perigenetic mechanism, inflammation-associated signaling
molecules, such as TNF-α, can alter gastric epithelial cell adhesion
and lead to the dispersion and migration of mutated epithelial cells
without the need for additional mutations in tumor suppressor genes,
such as genes that code for cell adhesion proteins.[32]
<sniP>
http://en.wikipedia.org/wiki/Pyloric_antrum
Pyloric antrum (antrum, lesser cul-de-sac) is the initial portion of
the pyloric part of the stomach. It is near the bottom of the stomach
on the left side of the pyloric sphincter, which separates the stomach
and the duodenum.
It may temporarily become partially or completely shut off from the
remainder of the stomach during digestion by peristaltic contraction
of the prepyloric sphincter; it is demarcated, sometimes, from the
second part of the pyloric part of the stomach (pyloric canal) by a
slight groove.
Function
The pyloric antrum is the location of several important endocrine
cells including Gastrin-producing G Cells (stimulate acid production)
and the luminal-pH-sensitive population of somatostatin producing of D
cells (responsible for shutting off acid secretion. There is a second
hormone-sensitive population near the fundus.)
<snip>
==================
M1 is a Th1 skew and due to h. pylori in many cases.
While we have the ONE M1 & h. pylori abstract.
WE can LOOK at 256 hits for Th1 h. pylori
h. pylori Th1
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=h.+pylori+Th1
The very first one takes us back to the land of NOD and east of eden
in the GUT.
http://www.ncbi.nlm.nih.gov/pubmed/21152124
Int J Inflam. 2010 Jul 15;2010:476482.
NOD1-Mediated Mucosal Host Defense against Helicobacter pylori.
Watanabe T, Asano N, Kitani A, Fuss IJ, Chiba T, Strober W.
Mucosal Immunity Section, Laboratory of Host Defenses, National
Institute of Allergy and Infectious Diseases, National Institutes of
Health, Building 10-CRC Room 5W3940, 10 Center Drive, Bethesda, MD
20892, USA.
Abstract
Infection of the stomach with Helicobacter pylori is an important risk
factor for gastritis, peptic ulcer, and gastric carcinoma. Although it
has been well established that persistent colonization by H. pylori is
associated with adaptive Th1 responses, the innate immune responses
leading to these Th1 responses are poorly defined. Recent studies have
shown that the activation of nucleotide-binding oligomerization domain
1 (NOD1) in gastric epithelial cells plays an important role in innate
immune responses against H. pylori. The detection of H. pylori-derived
ligands by cytosolic NOD1 induces several host defense factors,
including antimicrobial peptides, cytokines, and chemokines. In this
paper, we review the molecular mechanisms by which NOD1 contributes to
mucosal host defense against H. pylori infection of the stomach.
PMID: 21152124
It does sorta nail the Th1 (M1) skew due to a BUG.
Does the whiP worm of Th2 (M2) eat the h. pylori of Th1 (M1) skews?
YOU tell me?
I'm sold on using SFB to control the may HAM in the Git.
<git gastro intestinal tract>
And not about to eat worms, honey.
Unless i eat it with honey and they eat SFB?
Sorry, i'm also NOT sold on bioLOGICALs for the most part.
So Big Pharma and BIG GOV can suck the same whiP worm eggs.
I want to put both of them OUTA biz. LOL
I'm more about a slightly acidic pH in the colon to control downSTEAM
effects.
Sounds SWEET and your WHEY....
Hey.. what can i say?
You've ony said it 10 million times. LOL
http://www.ncbi.nlm.nih.gov/pubmed/21155836
Ann N Y Acad Sci. 2010 Dec 13. doi: 10.1111/j.1749-6632.2010.05825.x.
[Epub ahead of print]
The IL-17 pathway as a major therapeutic target in autoimmune
diseases.
Hu Y, Shen F, Crellin NK, Ouyang W.
C2N Diagnostics, St. Louis, Missouri. Department of Immunology,
Genentech, Inc., South San Francisco, California.
Abstract
Th17 cells are a subset of T helper cells that have been recently
found to play important functions in host defense and the pathogenesis
of various human autoimmune and inflammatory diseases. Th17 cells
produce IL-17A, IL-17F, IL-22, and IL-21, of which IL-17A and IL-17F
mediate many of the downstream pathologic functions of these cells.
IL-17A and IL-17F signal through IL-17RA and IL-17RC heterodimeric
receptors that are mainly expressed on tissue epithelial cells and
fibroblasts. While IL-17A and IL-17F are important for host defense
against many extracellular pathogens, they can also cause excessive
tissue damage and exacerbate proinflammatory responses during
autoimmunity. The IL-17 pathway, therefore, is a primary therapeutic
target downstream of Th17 cells.
2010 New York Academy of Sciences.
PMID: 21155836
That was my .50 cents today.
But my earlier post was the rossetta stone is some asPects.
randall... hope vs fear... the GLASS is HALF FULL..dr. P an glossy.