Is randy JR (aka- john) right about the CURE, paranoia and pharmA in
regards to P?
Is BIG PIG Pharma suPPressing the el cheaP-Oh cures?
Will everyone start fasting and follow the pied piper of good health R-
JR?
Whose Paul Bragg: (famous FASTer)
http://en.wikipedia.org/wiki/Paul_Bragg
His site with Patricia:
http://www.bragg.com/
Turbo it out:
With a touch of low dose exercise and not the extreme:
http://en.wikipedia.org/wiki/Jack_LaLane
If @ 94 years young, he looks like he's gonna make it to 122 i'll get
excited for sure.
He has only 28 more years to catch 122y/o Jeanne Calment's record. LOL
But what of pharma secrets? Surely neither Jeanne or Jack or Paul
Bragg used
those goodies and lived long vital lives.
Is big pharma holding out on some lowly off label drugs?
Could be. While LDN is used for a ton of off label uses, it is
working.
This next post done the other day (May 22, 2009) has NO political info
in it.
So, unless ALL of my posts are now beCOMING unsearchable, if has to be
due to content.
My LDN content is being questioned?
Which, makes sense. Or I am becoming paranoid. LOL
Quick get me some LDN to cure my paranoia?
http://en.wikipedia.org/wiki/Paranoia
Yet:
http://www.drugs.com/sfx/naltrexone-side-effects.html
Would most of the sides be attenuated by ALA, ALC, NAC, etc?
Certainly Amelioration is the objective and not the reverse or
extreme paranoia and while an opiod addiction requires 300 mg
type dosages, a low dose preparation would be one percent
of that or 3.5 mg's.
So____________________
What's the BIG secret that's being suppresed?
That LDN, ALA, ALC, NAC, plus iodine, citicoline and supplements to
make them work better according to the case
will create homeostasis and long term heath?
How amazing are these?
I've used all but the LDN (low dose na ltrexone). So I know what they
can do.
These are so powerful that they throw off my personal trials, so I
have to AVOID them.
That's powerful.
Is it enough for BIG Pharma to shut me uP?
Or am i simply paranoid?
Will randy JR have to take over?
Damn I forgot to see if he's being rendered ...?
We'll find out later today when I see if this thread is searchable.
LOL
OK, so which is the latest post with LDN in it, that isn't
searchable?
Right here:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/msg/04caf711539135b7
How do we KNOW it's not searchable?
Easy find a pmid # and google it.
Try pmid # 19450178
And nothing for a search of THIS group:
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&group=alt.support.skin-diseases.psoriasis&q=19450178+pmid.&qt_g=Search+this+group
What about the web? (which people don't search to find group info
btw)
Four hits on the web. Two for ncbi which is where pmid #'s originate,
so that's no surprise. But then two from me and one's from china. LOL
And brings up the other non searchable thread.
http://www.google.com/search?hl=en&qt_s=1&q=19450178%20pmid.&sa=N&tab=gw
----------
So you say, hey it's easy to fix.
And i say i'm not a portuguese water dog or mine that bird gelding.
LOL
http://en.wikipedia.org/wiki/Mine_That_Bird
But wouldn't mind his dery odds at 50-1.
Would i be a gelding to get those odds?
It was spectacular:
http://www.youtube.com/watch?v=0jsY2MlDA1c
Would Calvin Borel become a gelding like his horse?
Of course NOT.He'd lose his drive to compete AND feel complete. LOL
Then again he did choose a filly to WIN the preakness and that wasn't
done for over 85 years.
So the triple crown, should he win the breeders, goes to the jock and
not the horse?
This time..it's not the process but who affectuates it? Sounds a
little political. LOL
Is Bo diddley a gelding?
http://en.wikipedia.org/wiki/Portuguese_water_dog#Notable_Portuguese_Water_Dogs
Who cares?
Oh so you want to know how BO was or wasn't neutered?
The horse techinques may interest you:
http://en.wikipedia.org/wiki/Gelding#Castration_techniques
And big Bo's wiki page should turn the trick if there be one?
http://en.wikipedia.org/wiki/Bo_(dog)
[...]
Bo (born October 9, 2008) is the current pet of the Obama family, the
First Family of the United States,[8] and is a _____neutered_____[9]
male Portuguese Water Dog, or Portie
<sniP>
That bo is cool and has his own wiki web page.
=====================
Should the cool
http://en.wikipedia.org/wiki/White_House_Chief_of_Staff
be afforded this treatment?
He could finish the triple crown and not BITE anyone? LOL
========================
But, what about the tax bite?
Sorry, that will grow till it bites YOU. LOL
But by then it will be moot.
Are those sunspots back?
I have another seven hours before i can check.
But we all can check on the web.
http://sohowww.nascom.nasa.gov/sunspots/
Nope... and it's past 50 to one on coming back.
Will it turn in to the long shot of the century?
Or will it become the long shot with IcE AGE coming in First?
randall.. uh scary...no really
========================================================
Whoops-- disregard this info.. just need a few pmid's
http://www.ncbi.nlm.nih.gov/pubmed/19465513
Dimethylfumarate inhibits NF-{kappa}B function at multiple levels to
limit airway smooth muscle cell cytokine secretion.
Seidel P, Merfort I, Hughes JM, Oliver BG, Tamm M, Roth M.
University Hospital Basel.
The anti-psoriatic dimethylfumarate (DMF) has been anecdotically
reported to reduce asthma symtoms and to improve quality of life of
asthma patients. DMF decreases the expression of pro-inflammatory
mediators by inhibiting the transcription factor nuclear factor kappaB
(NF-kappaB) and might therefore be of interest for the therapy of
inflammatory lung diseases. In this study we determined the effect of
dimethylfumarate (DMF) on platelet derived growth factor (PDGF)-BB and
tumor necrosis factor (TNF)-alpha induced asthma relevant cytokines
and NF-kappaB activation by primary human asthmatic and non-asthmatic
airway smooth muscle cells (ASMC). Methods: Confluent non-asthmatic
and asthmatic ASMC were incubated with DMF (0.1-100 microM) and/or
dexamethasone (0.0001-0.1 microM), NF-kappaB p65 siRNA (100 nM), the
NF-kappaB inhibitor helenalin (1 microM) before stimulation with PDGF-
BB or TNF-alpha (10 ng/ml). Cytokine release was measured by enzyme
linked immunosorbent assay. NF-kappaB, MSK-1, and CREB activation was
determined by immuno-blotting and EMSA. Results: TNF-alpha induced
eotaxin, RANTES and interleukin (IL)-6 as well as PDGF-BB induced IL-6
expression was inhibited by DMF and by dexamethasone from asthmatic
and non-asthmatic ASMC, but the combination of both drugs showed no
glucocorticoid sparing effect in either of the two groups. NF-kappaB
p65 siRNA and/or the NF-kappaB inhibitor helenalin reduced PDGF-BB and
TNF-alpha induced cytokine expression, suggesting the involvement of
NF-kappaB signaling. DMF inhibited TNF-alpha induced NF-kappaB p65
phosphorylation, NF-kappaB nuclear entry and NF-kappaB -DNA complex
formation, whereas PDGF-BB appeared not to activate NF-kappaB within
60 min. Both stimuli induced the phosphorylation of mitogen and stress
activated kinase (MSK)-1, NF-kappaB p65 at Ser276, and CREB and all
were inhibited by DMF. These data suggest that DMF down-regulates
cytokine secretion not only by inhibiting NF-kappaB but a wider range
of NF-kappaB linked signaling proteins which may explain its potential
beneficial effect in asthma. Key words: MSK-1, CREB, DMF anti-
inflammatory action, chronic lung inflammation.
PMID: 19465513
Wow, how about some LOW DOSE DMF with LDN?
And add in ALA, ALC, NAC and support suPPlements?
Sounds awesome... and might be able to cancel all future needs for
biologicals?
I don't want to be rude but insurance rates are to high and if we
didn't
require such expensive drugs then we could lower premiums for
everyone.
Isn't that a good idea?
Chop insurance and health costs in half?
Makes cents to me. :)
Will our politico's follow suit?
Or more same OLD?
=====================================
http://www.ncbi.nlm.nih.gov/pubmed/19464955
Stable form of galectin-9, a Tim-3 ligand, inhibits contact
hypersensitivity and psoriatic reactions: A potent therapeutic tool
for Th1- and/or Th17-mediated skin inflammation.
Niwa H, Satoh T, Matsushima Y, Hosoya K, Saeki K, Niki T, Hirashima M,
Yokozeki H.
Department of Dermatology, Graduate School, Tokyo Medical and Dental
University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
Tim-3 is a cell surface molecule preferentially expressed in Th1 and
Th17 cells. Galectin-9 is a ligand for Tim-3 and the binding of
galectin-9 to Tim-3 induces apoptosis. We recently developed a stable
form of galectin-9 (sGal-9) by partial deletion of the linker peptide.
In this study, we characterized the therapeutic effects of sGal-9 on
inflammatory reactions in contact hypersensitivity and IL-23-induced
psoriatic mouse models. In contact hypersensitivity in mice, the ear
swelling response was suppressed by sGal-9. In vitro treatment with
sGal-9 resulted in cell apoptosis of CD4, CD8, and hepatic NK cells.
sGal-9-treated mice had decreased IFN-gamma- and IL-17-producing T
cells. Similarly, sGal-9 reduced epidermal thickness and dermal
cellular infiltrate levels in IL-23-induced psoriasis-like skin
inflammation. This was accompanied by decreased skin lesion levels of
IL-17 and IL-22. sGal-9 may be a unique and useful therapeutic tool
for the treatment of Th1- and/or Th17-mediated skin inflammation.
PMID: 19464955
13 hits for keyword: GALECTIN in the P NG
http://groups.google.com/group/alt.support.skin-diseases.psoriasis/search?hl=en&q=+galectin&start=0&scoring=d&hl=en&
Seven hits for psoria* + galectin [on pubmed]
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=psoria*+AND+galectin&log$=activity
23 hits for tim + galectin
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=DetailsSearch&term=galectin+tim-3&log$=activity
=====================
Tim-3-Galectin-9 pathway involves the suppression induced by CD4+CD25+
regulatory T cells.
Wang F, Wan L, Zhang C, Zheng X, Li J, Chen ZK.
Department of Clinical Laboratory, The First Affiliated Hospital of
Nanchang University, Nanchang, Jiangxi, China. xijia...@163.com
CD4(+)CD25(+) regulatory T cells (Tregs) are considered to play a key
role as suppressors of immune-mediated reactions. The mechanisms of
this suppression in animals and patients with autoimmune, allergic or
oncogenic diseases have been investigated under various conditions.
However, the precise mode of suppression by CD4(+)CD25(+) Tregs is
still not clear. In this report, Tim-3-Galectin-9 pathway was explored
as one of the mechanisms for the suppression and cytotoxicity induced
by Tregs. Here, we demonstrated that Galectin-9 was expressed on CD4(+)
CD25(+) Tregs by reverse transcription-polymerase chain reaction (RT-
PCR) and Western blot. Interestingly, blocking Tim-3-Galectin-9
pathway resulted in an obvious decreased suppression activity of Tregs
and enhanced Th1 cytokine level in vitro. Furthermore, blocking Tim-3-
Galectin-9 pathway negated prolonged survival of allogeneic skin
grafts induced by CD4(+)CD25(+) Tregs in vivo. Our results suggest
that Tim-3-Galectin-9 pathway involves the function of CD4(+)CD25(+)
Tregs.
PMID: 19362679
--------------------
http://www.ncbi.nlm.nih.gov/pubmed/17007105
=========================
randall... whoops. a double sign off? I did iirc do that above. LOL