Hacking The Cold

[Ironjustic]

This seems to be one of the problems associated with trauma.
Unable to handle the cold.

"one minute I was paralyzed and the next I was normal"

Source: Dalhousie University Released: Tue 11-Mar-2008, 15:15
ET

Dermatology Team Finds Treatment for Rare "Life-ruining"
Condition Description

Relief is now available for 600 people around the world who
suffer from a rare genetic condition triggered by exposure to
cold. "It's like you're freezing from the inside out," says
Rachel Doherty, who took part in a clinical trial. In proving
the effectiveness of anakinra, a Dalhousie dermatology team
successfully concluded a 20- year quest to find a treatment
for Familial Cold Autoinflammatory Syndrome (FCAS).

Newswise -- Dalhousie Medical School dermatologist Dr. Barrie
Ross and his colleagues have successfully ended a 20-year
quest to find a treatment for Familial Cold Autoinflammatory
Syndrome (FCAS). The rare condition, triggered by exposure to
cold, causes severe discomfort and physical incapacity.

Through a clinical trial conducted at Capital Health in
Halifax, Dr. Ross and his colleagues proved the overwhelming
effectiveness of anakinra, a receptor-blocking medication, to
ease the pain and suffering caused by FCAS. The study results
were published this week in the Journal of Cutaneous Medicine
and Surgery.

Dr. Ross, an adjunct professor in the Division of Dermatology,
Department of Medicine at Dalhousie and Capital Health,
had the rare honour of seeing his quest through from
beginning to successful end. In 1986, the year her mother
was diagnosed with kidney failure which is linked to FCAS,
Anne Mallais visited Dr. Ross. She was on a crusade to
find a cure for the debilitating condition that afflicts
her and many of her family.

"From the time Anne came to see me, it was serendipity,
the advancement of technology and perseverance that led
to the clinical trial and the discovery of a treatment,"
says Dr. Ross.

FCAS causes hives, fever, chills, myalgias, headache,
stiffness and swelling, among other symptoms. "It's like
you're freezing from the inside out," says Rachel Doherty.
"Your whole body contracts until you warm up, which can take
hours or days." Doherty took over the crusade to find a cure
from her sister and participated in the clinical trial.

Following Mallais' visit, Dr. Ross encouraged a dermatology
resident to research, write and later publish a paper that
detailed the literature on what was then known as Familial
Cold Urticaria. The paper caught the attention of
researchers in Germany. The researchers later teamed up with
Dr. Ross to discover the chromosomal site for FCAS. Six
years after the discovery, Dr. Ross and a group of UK
colleagues pinpointed the specific receptor responsible for
FCAS. When triggered, the tumour necrosis factor (TNF)
receptor starts the symptoms of FCAS.

"Once we pinpointed the pathway, we looked at other
inflammatory conditions with a common pathway in search of
potential treatments," explains Dr. Ross. "A tip from a
colleague turned us on to anakinra. It was an approved therapy
for rheumatoid arthritis in Canada which meant that was safe
to use." The next step was a clinical trial.

Eight adults, all family members with long-standing FCAS,
participated in the clinical trial in the fall of 2005. They
received daily anakinra injections and all experienced
complete symptom relief within 24 hours of their first
injection. The relief lasted through the treatment period
despite participants being subjected to cold on a daily basis.
"The results were phenomenal," says Dr. Ross. For Doherty it
was surreal. "It was like one minute I was paralyzed and the
next I was normal. When I went home, I walked around in
circles not knowing what to do first."

Anakinra (marketed by Amgen Corporation as Kineret) prevents
the symptoms of FCAS by stopping the TNF receptor from being
triggered. The clinical trial showed that it is 100 per cent
effective when injected on a daily basis. About six hundred
people around the world are afflicted by FCAS.

Editors Note: Imagery can be arranged quickly if required

--------------------------------------------------------------
-------------------

(E) 2008 Newswise. All Rights Reserved.

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

[Ironjustic]

On Mar 12, 8:00=A0am, ironjustice <ironjust...@cashette.com>
wrote:Anakinra <<

What is the significance this disease is treated with
Colchicine and when that doesn't work they say Anakinra may?
This disease is recommended to be treated by bloodletting.

"Requires the patient be examined particularly for
hemochromatosis"

Z Rheumatol. 2007 Nov;66(7):573-4, 576-8.Related Articles,
Links [Diagnosis and treatment of calcium pyrophosphate
crystal-induced arthropathy]

[Article in German]

Announ N, Guerne PA.

Division de Rhumatologie, H=F4pital Universitaire de Gen=E8ve,
26 Avenaue de Beau-S=E9jour, 1211, Gen=E8ve, Schweiz.

Calcium pyrophosphate dihydrate deposition (CPPDD) disease is
the term used to describe a group of common and potentially
severe metabolic arthropathies. In these, CPPD crystals form
and are deposited in the cartilage matrix (chondrocalcinosis)
and induce inflammatory and/or destructive mechanisms. Most
cases are idiopathic, but hyperparathyroidism,
hemochromatosis, hypomagnesemia and hypophosphatemia can
promote or cause chondrocalcinosis. Early disease (with onset
before the age of 60 years) thus requires that the patient be
examined for these metabolic conditions, particularly
hemochromatosis. The prevalence of CPPDD disease in the
general population increases with age, being 10-15% in the age
group 65-75 years and more than 40% in the over-80s. Although
frequently asymptomatic, chondrocalcinosis can involve severe
acute attacks of inflammatory arthritis (pseudogout) and also
various types of chronic arthropathy including
pseudorheumatoid arthritis,
pseudo-osteoarthritis, and pseudoneuropathic joint disease.
CPPD crystals can also be deposited in the bursae,
ligaments, and tendons and generate inflammation and/or
ruptures. The diagnosis is based on synovial fluid analysis
(positively birefringent CPPD crystals visualized by
compensated polarized light microscopy) and X- rays
(punctate and linear radiodense areas in fibrocartilage and
hyaline cartilage). Treatment is primarily symptomatic,
since there is no known drug that can prevent progression of
the joint destruction). Nonsteroid anti-inflammatory drugs
(NSAIDs) and intra-articular or systemic glucocorticoids
(amounts must be only small if use is prolonged) are the
most useful treatments. Colchicine can be effective in
recurring pseudogout, and magnesium can be used
prophylactically. In a small uncontrolled series
methotrexate was effective and aroused interest; it can be
used when other treatments fail.

Publication Types: English Abstract

PMID: 17932681 [PubMed - in process]
-----------------------------

=46rom Medscape Rheumatology
Ask the Experts about Rheumatoid Arthritis and Related
Conditions Gout: Treatment Reaction to Allopurinol -- What
Next? Posted 11/08/2007

Arthur Kavanaugh, MD

Author Information

Information from Industry Explore an agent offering persistent
pain relief with extended benefits. Learn about
around-the-clock treatment with potential to reduce the number
of breakthrough pain episodes and a demonstrated improvement
in pain-related sleep parameters. Read more Question A rash
developed on a patient with gout during treatment with both
allopurinol and sulfinpyrazone. Desensitization with
allopurinol was not successful. The patient is intolerant of
nonsteroidal anti- inflammatory drugs and colchicine. What is
the next treatment option, and can anakinra be tried?

Amir Alvi, MBBS, MRCP

Response from Arthur Kavanaugh, MD Professor, Department of
Rheumatology, University of California, San Diego

This question addresses treatment options for gout. The case
described highlights the unmet clinical need for new gout
treatments. In this case, the best available therapy,
allopurinol, cannot be tolerated because of toxicity, and even
desensitization was not successful. In addition, uricosuric
therapy was unsuccessful, as it is in many cases of gout.
Unfortunately, other treatment options are relatively limited.
To lower uric acid, removing contributing factors such as
medications, where possible, can be useful. Alteration in diet
can have a beneficial effect, but compliance can be difficult
for many patients. Other medications with uric acid-lowering
properties, such as losartan and fenofibrate, can be tried if
there are no contraindications. A drug currently in late-phase
development, febuxostat, is a nonpurine xanthine oxidase
inhibitor that has shown promise in clinical trials but has
not yet been approved for gout.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly
used for the treatment of chronic arthritis. Comorbid
conditions commonly found among patients with gout, including
hypertension and renal dysfunction, which in some cases
contribute to the disease, can limit the use of NSAIDs in
patients with gout, however. The questioner also raises the
possibility of using anakinra, an interleukin-1 (IL-1)
inhibitor. There has indeed been a good deal of interest in
this approach. There are data to suggest that uric acid
crystals may drive inflammation, in part through the
'inflammasome,' an inflammatory intracellular pathway that
acts partly through elaboration of IL-1. There is anecdotal
evidence suggesting that IL-1 inhibitors may indeed be
effective in gouty arthritis, and this approach is currently
under study. However, the same caution must be used with
anakinra as one would undertake when using it for its approved
indication of rheumatoid arthritis.

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

> This seems to be one of the problems associated with trauma.
> Unable to handle the cold.
>
> "one minute I was paralyzed and the next I was normal"
>
> Source: Dalhousie University =A0 =A0 Released: Tue
> 11-Mar-2008, 15:15 ET
>
> Dermatology Team Finds Treatment for Rare "Life-ruining"
> Condition Description
>
> Relief is now available for 600 people around the world who
> suffer from a rare genetic condition triggered by exposure
> to cold. "It's like you're freezing from the inside out,"
> says Rachel Doherty, who took part in a clinical trial. In
> proving the effectiveness of anakinra, a Dalhousie
> dermatology team successfully concluded a 20- year quest to
> find a treatment for Familial Cold Autoinflammatory
> Syndrome (FCAS).
>
> Newswise -- Dalhousie Medical School dermatologist Dr.
> Barrie Ross and his colleagues have successfully ended a
> 20-year quest to find a treatment for Familial Cold
> Autoinflammatory Syndrome (FCAS). The rare condition,
> triggered by exposure to cold, causes severe discomfort and
> physical incapacity.
>
> Through a clinical trial conducted at Capital Health in
> Halifax, Dr. Ross and his colleagues proved the overwhelming
> effectiveness of anakinra, a receptor-blocking medication,
> to ease the pain and suffering caused by FCAS. The study
> results were published this week in the Journal of Cutaneous
> Medicine and Surgery.
>
> Dr. Ross, an adjunct professor in the Division of
> Dermatology, Department of Medicine at Dalhousie and
> Capital Health, had the rare honour of seeing his quest
> through from beginning to successful end. In 1986, the
> year her mother was diagnosed with kidney failure which
> is linked to FCAS, Anne Mallais visited Dr. Ross. She
> was on a crusade to find a cure for the debilitating
> condition that afflicts her and many of her family.
>
> "From the time Anne came to see me, it was serendipity,
> the advancement of technology and perseverance that led to
> the clinical trial and the discovery of a treatment," says
> Dr. Ross.
>
> FCAS causes hives, fever, chills, myalgias, headache,
> stiffness and swelling, among other symptoms. "It's like
> you're freezing from the inside out," says Rachel Doherty.
> "Your whole body contracts until you warm up, which can take
> hours or days." Doherty took over the crusade to find a cure
> from her sister and participated in the clinical trial.
>
> Following Mallais' visit, Dr. Ross encouraged a dermatology
> resident to research, write and later publish a paper that
> detailed the literature on what was then known as Familial
> Cold Urticaria. The paper caught the attention of
> researchers in Germany. The researchers later teamed up with
> Dr. Ross to discover the chromosomal site for FCAS. Six
> years after the discovery, Dr. Ross and a group of UK
> colleagues pinpointed the specific receptor responsible for
> FCAS. When triggered, the tumour necrosis factor (TNF)
> receptor starts the symptoms of FCAS.
>
> "Once we pinpointed the pathway, we looked at other
> inflammatory conditions with a common pathway in search of
> potential treatments," explains Dr. Ross. "A tip from a
> colleague turned us on to anakinra. It was an approved
> therapy for rheumatoid arthritis in Canada which meant that
> was safe to use." The next step was a clinical trial.
>
> Eight adults, all family members with long-standing FCAS,
> participated in the clinical trial in the fall of 2005. They
> received daily anakinra injections and all experienced
> complete symptom relief within 24 hours of their first
> injection. The relief lasted through the treatment period
> despite participants being subjected to cold on a daily
> basis. "The results were phenomenal," says Dr. Ross. For
> Doherty it was surreal. "It was like one minute I was
> paralyzed and the next I was normal. When I went home, I
> walked around in circles not knowing what to do first."
>
> Anakinra (marketed by Amgen Corporation as Kineret) prevents
> the symptoms of FCAS by stopping the TNF receptor from being
> triggered. The clinical trial showed that it is 100 per cent
> effective when injected on a daily basis. About six hundred
> people around the world are afflicted by FCAS.
>
> Editors Note: Imagery can be arranged quickly if required
>
> ------------------------------------------------------------
> ---------------=
-=AD-----
>
> (c) 2008 Newswise. =A0All Rights Reserved.
>
> Who loves ya. Tom
>
> Jesus Was A Vegetarian!http://jesuswasavegetarian.7h.com
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk

[Ironjustic]

On Mar 12, 1:03=A0pm, "ironjust...@aol.com"
<ironjust...@aol.com> wrote:In these, CPPD crystals form and
are deposited in the cartilage matrix (chondrocalcinosis) and
induce inflammatory and/or destructive mechanisms. <<

One might wonder since .. crystallization inhibitors are
also called bisphosphonates .. would my free
bisphosphonate work .. ?

http://tinyurl.com/3yqmcn

Hmmm ..

"Etidronate severely inhibits rates of growth and formation of
various forms of calcium pyrophosphate crystals"

http://pubs.acs.org/cgi-bin/abstract.cgi/cgdefu/2003/3/i01/ab-
s/cg025581d.htm= l

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

> On Mar 12, 8:00=A0am, ironjustice <ironjust...@cashette.com>
> wrote:Anakinra <<
>
> What is the significance this disease is treated with
> Colchicine and when that doesn't work they say Anakinra may?
> This disease is recommended to be treated by bloodletting.
>
> "Requires the patient be examined particularly for
> hemochromatosis"
>
> =A0Z Rheumatol. 2007 Nov;66(7):573-4, 576-8.Related
> Articles, Links [Diagnosis and treatment of calcium
> pyrophosphate crystal-induced arthropathy]
>
> [Article in German]
>
> Announ N, Guerne PA.
>
> Division de Rhumatologie, H=F4pital Universitaire de
> Gen=E8ve, 26 Avenaue de Beau-S=E9jour, 1211, Gen=E8ve,
> Schweiz.
>
> Calcium pyrophosphate dihydrate deposition (CPPDD) disease
> is the term used to describe a group of common and
> potentially severe metabolic arthropathies. In these, CPPD
> crystals form and are deposited in the cartilage matrix
> (chondrocalcinosis) and induce inflammatory and/or
> destructive mechanisms. Most cases are idiopathic, but
> hyperparathyroidism, hemochromatosis, hypomagnesemia and
> hypophosphatemia can promote or cause chondrocalcinosis.
> Early disease (with onset before the age of 60 years) thus
> requires that the patient be examined for these metabolic
> conditions, particularly hemochromatosis. The prevalence of
> CPPDD disease in the general population increases with age,
> being 10-15% in the age group 65-75 years and more than 40%
> in the over-80s. Although frequently asymptomatic,
> chondrocalcinosis can involve severe acute attacks of
> inflammatory arthritis (pseudogout) and also various types
> of chronic arthropathy including pseudorheumatoid arthritis,
> pseudo-osteoarthritis, and pseudoneuropathic joint disease.
> CPPD crystals can also be deposited in the bursae,
> ligaments, and tendons and generate inflammation and/or
> ruptures. The diagnosis is based on synovial fluid
> analysis (positively birefringent CPPD crystals visualized
> by compensated polarized light microscopy) and X- rays
> (punctate and linear radiodense areas in fibrocartilage
> and hyaline cartilage). Treatment is primarily
> symptomatic, since there is no known drug that can prevent
> progression of the joint destruction). Nonsteroid
> anti-inflammatory drugs (NSAIDs) and intra-articular or
> systemic glucocorticoids (amounts must be only small if
> use is prolonged) are the most useful treatments.
> Colchicine can be effective in recurring pseudogout, and
> magnesium can be used prophylactically. In a small
> uncontrolled series methotrexate was effective and aroused
> interest; it can be used when other treatments fail.
>
> Publication Types: English Abstract
>
> PMID: 17932681 [PubMed - in process]
> -----------------------------
>
> From Medscape Rheumatology Ask the Experts about Rheumatoid
> Arthritis and Related Conditions Gout: Treatment Reaction to
> Allopurinol -- What Next? Posted 11/08/2007
>
> Arthur Kavanaugh, MD
>
> Author Information
>
> Information from Industry Explore an agent offering
> persistent pain relief with extended benefits. Learn about
> around-the-clock treatment with potential to reduce the
> number of breakthrough pain episodes and a demonstrated
> improvement in pain-related sleep parameters. Read more
> =A0Question A rash developed on a patient with gout during
> treatment with both allopurinol and sulfinpyrazone.
> Desensitization with allopurinol was not successful. The
> patient is intolerant of nonsteroidal anti- inflammatory
> drugs and colchicine. What is the next treatment option, and
> can anakinra be tried?
>
> Amir Alvi, MBBS, MRCP
>
> =A0Response from Arthur Kavanaugh, MD Professor, Department
> of Rheumatology, University of California, San Diego
>
> This question addresses treatment options for gout. The case
> described highlights the unmet clinical need for new gout
> treatments. In this case, the best available therapy,
> allopurinol, cannot be tolerated because of toxicity, and
> even desensitization was not successful. In addition,
> uricosuric therapy was unsuccessful, as it is in many cases
> of gout. Unfortunately, other treatment options are
> relatively limited. To lower uric acid, removing
> contributing factors such as medications, where possible,
> can be useful. Alteration in diet can have a beneficial
> effect, but compliance can be difficult for many patients.
> Other medications with uric acid-lowering properties, such
> as losartan and fenofibrate, can be tried if there are no
> contraindications. A drug currently in late-phase
> development, febuxostat, is a nonpurine xanthine oxidase
> inhibitor that has shown promise in clinical trials but has
> not yet been approved for gout.
>
> Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly
> used for the treatment of chronic arthritis. Comorbid
> conditions commonly found among patients with gout,
> including hypertension and renal dysfunction, which in some
> cases contribute to the disease, can limit the use of NSAIDs
> in patients with gout, however. The questioner also raises
> the possibility of using anakinra, an interleukin-1 (IL-1)
> inhibitor. There has indeed been a good deal of interest in
> this approach. There are data to suggest that uric acid
> crystals may drive inflammation, in part through the
> 'inflammasome,' an inflammatory intracellular pathway that
> acts partly through elaboration of IL-1. There is anecdotal
> evidence suggesting that IL-1 inhibitors may indeed be
> effective in gouty arthritis, and this approach is currently
> under study. However, the same caution must be used with
> anakinra as one would undertake when using it for its
> approved indication of rheumatoid arthritis.
>
> Who loves ya. Tom
>
> Jesus Was A Vegetarian!http://jesuswasavegetarian.7h.com
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > This seems to be one of the problems associated with
> > trauma. Unable to handle the cold.
>
> > "one minute I was paralyzed and the next I was normal"
>
> > Source: Dalhousie University =A0 =A0 Released: Tue
> > 11-Mar-2008, 15:15 ET=

>
> > Dermatology Team Finds Treatment for Rare "Life-ruining"
> > Condition Description
>
> > Relief is now available for 600 people around the world
> > who suffer from a rare genetic condition triggered by
> > exposure to cold. "It's like you're freezing from the
> > inside out," says Rachel Doherty, who took part in a
> > clinical trial. In proving the effectiveness of anakinra,
> > a Dalhousie dermatology team successfully concluded a 20-
> > year quest to find a treatment for Familial Cold
> > Autoinflammatory Syndrome (FCAS).
>
> > Newswise -- Dalhousie Medical School dermatologist Dr.
> > Barrie Ross and his colleagues have successfully ended a
> > 20-year quest to find a treatment for Familial Cold
> > Autoinflammatory Syndrome (FCAS). The rare condition,
> > triggered by exposure to cold, causes severe discomfort
> > and physical incapacity.
>
> > Through a clinical trial conducted at Capital Health in
> > Halifax, Dr. Ross and his colleagues proved the
> > overwhelming effectiveness of anakinra, a
> > receptor-blocking medication, to ease the pain and
> > suffering caused by FCAS. The study results were published
> > this week in the Journal of Cutaneous Medicine and
> > Surgery.
>
> > Dr. Ross, an adjunct professor in the Division of
> > Dermatology, Department of Medicine at Dalhousie and
> > Capital Health, had the rare honour of seeing his
> > quest through from beginning to successful end. In
> > 1986, the year her mother was diagnosed with kidney
> > failure which is linked to FCAS, Anne Mallais visited
> > Dr. Ross. She was on a crusade to find a cure for the
> > debilitating condition that afflicts her and many of
> > her family.
>
> > "From the time Anne came to see me, it was serendipity,
> > the advancement of technology and perseverance that led to
> > the clinical trial and the discovery of a treatment," says
> > Dr. Ross.
>
> > FCAS causes hives, fever, chills, myalgias, headache,
> > stiffness and swelling, among other symptoms. "It's like
> > you're freezing from the inside out," says Rachel Doherty.
> > "Your whole body contracts until you warm up, which can
> > take hours or days." Doherty took over the crusade to find
> > a cure from her sister and participated in the clinical
> > trial.
>
> > Following Mallais' visit, Dr. Ross encouraged a
> > dermatology resident to research, write and later publish
> > a paper that detailed the literature on what was then
> > known as Familial Cold Urticaria. The paper caught the
> > attention of researchers in Germany. The researchers later
> > teamed up with Dr. Ross to discover the chromosomal site
> > for FCAS. Six years after the discovery, Dr. Ross and a
> > group of UK colleagues pinpointed the specific receptor
> > responsible for FCAS. When triggered, the tumour necrosis
> > factor (TNF) receptor starts the symptoms of FCAS.
>
> > "Once we pinpointed the pathway, we looked at other
> > inflammatory conditions with a common pathway in search of
> > potential treatments," explains Dr. Ross. "A tip from a
> > colleague turned us on to anakinra. It was an approved
> > therapy for rheumatoid arthritis in Canada which meant
> > that was safe to use." The next step was a clinical trial.
>
> > Eight adults, all family members with long-standing FCAS,
> > participated in the clinical trial in the fall of 2005.
> > They received daily anakinra injections and all
> > experienced complete symptom relief within 24 hours of
> > their first injection. The relief lasted through the
> > treatment period despite participants being subjected to
> > cold on a daily basis. "The results were phenomenal," says
> > Dr. Ross. For Doherty it was surreal. "It was like one
> > minute I was paralyzed and the next I was normal. When I
> > went home, I walked around in circles not knowing what to
> > do first."
>
> > Anakinra (marketed by Amgen Corporation as Kineret)
> > prevents the symptoms of FCAS by stopping the TNF
> > receptor from being triggered. The clinical trial showed
> > that it is 100 per cent effective when injected on a
> > daily basis. About six hundred people around the world
> > are afflicted by FCAS.
>
> > Editors Note: Imagery can be arranged quickly if required
>
> > ----------------------------------------------------------
> > ---------------=
---=AD=AD-----
>
> > (c) 2008 Newswise. =A0All
>
> ...
>
> read more =BB- Hide quoted text -
>
> - Show quoted text -

[Joan Carte]

On Wed, 12 Mar 2008 19:08:34 -0700 (PDT),
"ironjustice@aol.com" <ironjustice@aol.com> wrote:

>Who loves ya. Tom

Tom, the only person you love is yourself. Now go away.

[Ironjustic]

On Mar 12, 7:16=A0pm, Joan Carter <spamf...@sentex.ca> wrote:

Ever hear the phrase .. "if you have nothing good to say" .. ?

Orrr .. how about .. "if you are not part of the solution" ..

http://www.medicalnewstoday.com/articles/100511.php

What Will You Do? Join The Movement To End Multiple Sclerosis
During MS Awareness Week
---------------------

Maybe iron IS involved ..

There are many studies which have the researchers believing
iron IS involved ..

Sooo .. nurse .. give a couple of studies which DON'T point to
**iron** .. IN .. multiple sclerosis ..

Study Proposes Interferon Beta-1A May Lessen Brain Atrophy in
MS Patients by Minimizing Effects of Toxic Iron Deposits

Release date: Thursday, April 10, 2003 Contact: Lois Baker,
ljba...@buffalo.edu Phone: 716-645-5000 ext 1417 Fax:
716-645-3765

BUFFALO, N.Y. -- Specialists in neuroimaging at the
University at Buffalo have proposed a mechanism by which
interferon beta-1a may limit brain atrophy in multiple
sclerosis (MS) patients.

The positive effect of interferon beta-1a, a standard
treatment for MS, on brain atrophy is well known, but the
process through which that occurs remains a mystery. UB
scientists have shown that the treatment appears to limit
atrophy by minimizing the toxic effect of pathologic iron
deposits found in gray-matter structures of MS patients.

While the treatment did not diminish iron concentrations that
had already accumulated, it appeared to interfere with the
accumulation of iron- induced damage, said Robert A. Bermel, a
fourth-year medical student in UB's School of Medicine and
Biomedical Sciences and lead author on the study.

Bermel presented the research findings on April 3 at the
annual meeting of the American Academy of Neurology in Hawaii.
He also presented the study in March at the annual meeting of
the American Society of Neuroimaging, which selected the work
to receive the society's 2003 Oldendorf Award for the best
research project first-authored by a trainee.

The MRI imaging work was conducted at the Buffalo Neuroimaging
Analysis Center (BNAC) of the Jacobs Neurological Institute,
affiliated with UB's School of Medicine and Biological
Sciences and Kaleida Health. This group reported previously
for the first time that in addition to the characteristic
white-matter lesions that are a traditional marker of the
disease, MS patients show shrinkage, or atrophy, of certain
structures in the brain's deep gray matter.

Their imaging studies have shown also that in MS patients
these deep gray-matter structures appear hypointense, or
darker than normal, signaling the presence of iron
concentrations. The researchers hypothesize that brain atrophy
is linked to these iron deposits.

"We know that MS patients have defective blood-brain barriers,
the filter that keeps chemicals, like iron, from leaking into
the brain," said Bermel. "Our hypothesis is that this defect
allows iron to accumulate in certain parts of the brain, which
then can be directly neurotoxic to cells, causing atrophy."

Knowing that interferon beta-1a treatment has a positive
effect on brain atrophy, Bermel and colleagues set out to
determine if the pathway of action was associated with iron
concentration. They followed 159 patients who were enrolled
in a randomized, double-blind treatment trial for the
relapsing form of the disease for two years. Eighty-one
patients received treatment; 78 who received placebo served
as controls.

Researchers took MRI scans of all patients to determine
hypointensity and brain atrophy at baseline and at two years.
Results showed that hypointensity at baseline was linked to
brain atrophy over that time period in controls, but not in
the treatment group. Hypointensity remained unchanged in the
treatment group, but brain atrophy was significantly less.

"These findings suggest that interferon may disrupt the
relationship between baseline T2H (hypointensity) and atrophy
over time," Bermel said, noting that there may be several
explanations for the finding.

"Interferon beta-1a is known to lower the levels of
inflammatory cytokines in the blood of patients with MS.
When the body is in a state without inflammation, as it is
normally, its cells, including neurons, can better
regulate their contents and byproducts, including iron. In
untreated MS, which is characterized by brain
inflammation, iron may be allowed to build up to toxic
levels in certain brain structures, causing toxic chemical
reactions and death of nerve cells, leading to what we see
as brain atrophy on MRI scans.

"Also, interferon is known to help restore the body's natural
blood- brain barrier, which would keep toxic iron from seeping
into the cells," Bermel said. "This study shows for the first
time that interferon treatment may result in less brain
atrophy in MS through a cascade of events that interferes with
the pathologic iron deposition."

Additional authors on the study from Buffalo were:
Srinivas R. Puli,
M.D., former research associate in the BNAC; Andrew J.
Fabiano, third-year medical student doing research in the
BNAC; Bianca Weinstock-Guttman, M.D., assistant professor
of neurology; Frederick E. Munschauer, M.D., professor
and chair of the Department of Neurology, and Rohit
Bakshi, M.D., associate professor of neurology and
director of the BNAC.

Elizabeth Fisher, Ph.D., and Richard A. Rudick, M.D., from the
Cleveland Clinic, performed measurements of whole brain
atrophy. Jack H. Simon,
M.E., Ph.D., from the University of Colorado, performed
additional analysis.

The research was funded by a grant from Alpha Omega Alpha and
a scholarship from the American Academy of Neurology to
Bermel and by a grant to Bakshi from the National Institutes
of Health.

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk


> On Wed, 12 Mar 2008 19:08:34 -0700 (PDT),
> "ironjust...@aol.com"
>
> <ironjust...@aol.com> wrote:
> >Who loves ya. Tom
>
> Tom, the only person you love is yourself. Now go away.

[Ironjustic]

On Mar 13, 6:47=A0am, "ironjust...@aol.com"
<ironjust...@aol.com> wrote:interferon is known to help
restore the body's natural blood- brain barrier <<

The curious thing here is .. deferoxamine is ALSO known "to
restore the body;s natural blood- brain barrier" ..

Deferoxamine is an iron chelator ..

<<snip>> DFO reduces disruption of the BBB <<snip>>

Ophthalmic Res. 1994;26(5):310-23. Related Articles, Links

Conjugated deferoxamine reduces blood-brain barrier disruption
in experimental optic neuritis.

Guy J, McGorray S, Qi X, Fitzsimmons J, Mancuso A, Rao N.

Department of Ophthalmology, University of Florida,
Gainesville.

The purpose of this paper was to investigate the role of
deferoxamine (DFO) scavenging of hydroxyl radical (.OH) on
disruption of the blood-brain barrier (BBB) and demyelination
in experimental optic neuritis. Eighteen strain-13 guinea pigs
were sensitized for experimental allergic encephalomyelitis.
Nine animals received 100 mg/kg of hydroxyethyl
starch-conjugated (HES) DFO by daily intraperitoneal injection
commencing the day of antigenic sensitization. Nine paired
litter mates received daily IP injections of HES. Serial fat-
suppressed magnetic resonance imaging of the optic nerves was
obtained with a T2 weighting
(T2w) to evaluate demyelination and after intravascular
administration of Gd-DTPA to evaluate BBB disruption.
The intensity of Gd-DTPA enhancement and T2w signal of
the optic nerves was quantitated 3, 7, 10 and 14 days
after antigenic sensitization. Animals were then
sacrificed and the optic nerves processed for light and
transmission electron microscopy with ultracytochemical
localization of endogenous hydrogen peroxide (H2O2) and
immunogold colocalization of extravasated serum albumin.
The area of the optic nerve head, intensity of toluidine
blue staining, and the cellular infiltrate were
digitized and quantitated. Administration of HES-DFO
significantly reduced the intensity of Gd-DTPA
enhancement in the optic nerves of HES-DFO- treated
animals compared to paired control HES animals (p =3D
0.0236), with the mean difference between control and
treated animals of 19.39. The difference in T2w signal
was not significant (p =3D 0.39), with a mean difference
between control and treated animals of -5.51. The
intensity of toluidine blue staining of optic nerve
specimens was slightly less with HES-DFO compared to
untreated animals (mean pair difference 2.48), and the
inflammatory infiltrate was reduced with HES-DFO
compared to untreated animals (mean pair difference =3D
61.57); these differences were not statistically
significant. In the optic nerve specimens of both groups
cerium perhydroxide-derived H2O2 reaction product was
evident in a predominantly perivascular and perineural
distribution. Immunogold- labeled serum albumin showed
extravasation at foci of perivascular inflammation in
both the presence and absence of H2O2-derived reaction
product. Conjugated DFO reduces disruption of the BBB,
as measured by Gd-DTPA enhancement, suggesting the .OH
radical generated from perivascular H2O2 may play a role
in alterations of vascular permeability in experimental
optic neuritis.

PMID: 7533278 [PubMed - indexed for MEDLINE]

--------------------------------------------------------------
-------------
------

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

> On Mar 12, 7:16=A0pm, Joan Carter <spamf...@sentex.ca>
> wrote:
>
> Ever hear the phrase .. "if you have nothing good to
> say" .. ?
>
> Orrr .. how about .. "if you are not part of the
> solution" ..
>
> http://www.medicalnewstoday.com/articles/100511.php
>
> What Will You Do? Join The Movement To End Multiple
> Sclerosis During MS Awareness Week
> ---------------------
>
> Maybe iron IS involved ..
>
> There are many studies which have the researchers believing
> iron IS involved ..
>
> Sooo .. nurse .. give a couple of studies which DON'T point
> to **iron** .. IN .. multiple sclerosis ..
>
> Study Proposes Interferon Beta-1A May Lessen Brain Atrophy
> in MS Patients by Minimizing Effects of Toxic Iron Deposits
>
> Release date: Thursday, April 10, 2003 Contact: Lois Baker,
> ljba...@buffalo.edu Phone: 716-645-5000 ext 1417 Fax:
> 716-645-3765
>
> BUFFALO, N.Y. -- Specialists in neuroimaging at the
> University at Buffalo have proposed a mechanism by which
> interferon beta-1a may limit brain atrophy in multiple
> sclerosis (MS) patients.
>
> The positive effect of interferon beta-1a, a standard
> treatment for MS, on brain atrophy is well known, but the
> process through which that occurs remains a mystery. UB
> scientists have shown that the treatment appears to limit
> atrophy by minimizing the toxic effect of pathologic iron
> deposits found in gray-matter structures of MS patients.
>
> While the treatment did not diminish iron concentrations
> that had already accumulated, it appeared to interfere
> with the accumulation of iron- induced damage, said
> Robert A. Bermel, a fourth-year medical student in UB's
> School of Medicine and Biomedical Sciences and lead
> author on the study.
>
> Bermel presented the research findings on April 3 at the
> annual meeting of the American Academy of Neurology in
> Hawaii. He also presented the study in March at the annual
> meeting of the American Society of Neuroimaging, which
> selected the work to receive the society's 2003 Oldendorf
> Award for the best research project first-authored by a
> trainee.
>
> The MRI imaging work was conducted at the Buffalo
> Neuroimaging Analysis Center (BNAC) of the Jacobs
> Neurological Institute, affiliated with UB's School of
> Medicine and Biological Sciences and Kaleida Health. This
> group reported previously for the first time that in
> addition to the characteristic white-matter lesions that are
> a traditional marker of the disease, MS patients show
> shrinkage, or atrophy, of certain structures in the brain's
> deep gray matter.
>
> Their imaging studies have shown also that in MS patients
> these deep gray-matter structures appear hypointense, or
> darker than normal, signaling the presence of iron
> concentrations. The researchers hypothesize that brain
> atrophy is linked to these iron deposits.
>
> "We know that MS patients have defective blood-brain
> barriers, the filter that keeps chemicals, like iron, from
> leaking into the brain," said Bermel. "Our hypothesis is
> that this defect allows iron to accumulate in certain parts
> of the brain, which then can be directly neurotoxic to
> cells, causing atrophy."
>
> Knowing that interferon beta-1a treatment has a positive
> effect on brain atrophy, Bermel and colleagues set out to
> determine if the pathway of action was associated with iron
> concentration. They followed 159 patients who were enrolled
> in a randomized, double-blind treatment trial for the
> relapsing form of the disease for two years. Eighty-one
> patients received treatment; 78 who received placebo served
> as controls.
>
> Researchers took MRI scans of all patients to determine
> hypointensity and brain atrophy at baseline and at two
> years. Results showed that hypointensity at baseline was
> linked to brain atrophy over that time period in controls,
> but not in the treatment group. Hypointensity remained
> unchanged in the treatment group, but brain atrophy was
> significantly less.
>
> "These findings suggest that interferon may disrupt the
> relationship between baseline T2H (hypointensity) and
> atrophy over time," Bermel said, noting that there may be
> several explanations for the finding.
>
> "Interferon beta-1a is known to lower the levels of
> inflammatory cytokines in the blood of patients with MS.
> When the body is in a state without inflammation, as it is
> normally, its cells, including neurons, can better
> regulate their contents and byproducts, including iron. In
> untreated MS, which is characterized by brain
> inflammation, iron may be allowed to build up to toxic
> levels in certain brain structures, causing toxic chemical
> reactions and death of nerve cells, leading to what we see
> as brain atrophy on MRI scans.
>
> "Also, interferon is known to help restore the body's
> natural blood- brain barrier, which would keep toxic iron
> from seeping into the cells," Bermel said. "This study shows
> for the first time that interferon treatment may result in
> less brain atrophy in MS through a cascade of events that
> interferes with the pathologic iron deposition."
>
> Additional authors on the study from Buffalo were: Srinivas
> R. Puli,
> M.D., former research associate in the BNAC; Andrew J.
> Fabiano, third-year medical student doing research in
> the BNAC; Bianca Weinstock-Guttman, M.D., assistant
> professor of neurology; Frederick E. Munschauer, M.D.,
> professor and chair of the Department of Neurology, and
> Rohit Bakshi, M.D., associate professor of neurology and
> director of the BNAC.
>
> Elizabeth Fisher, Ph.D., and Richard A. Rudick, M.D., from
> the Cleveland Clinic, performed measurements of whole brain
> atrophy. Jack H. Simon,
> M.D., Ph.D., from the University of Colorado, performed
> additional analysis.
>
> The research was funded by a grant from Alpha Omega Alpha
> and a scholarship from the American Academy of Neurology to
> Bermel and by a grant to Bakshi from the National Institutes
> of Health.
>
> Who loves ya. Tom
>
> Jesus Was A Vegetarian!http://jesuswasavegetarian.7h.com
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > On Wed, 12 Mar 2008 19:08:34 -0700 (PDT),
> > "ironjust...@aol.com"
>
> > <ironjust...@aol.com> wrote:
> > >Who loves ya. Tom
>
> > Tom, the only person you love is yourself. Now go away.-
> > Hide quoted tex=
t -
>
> - Show quoted text -

[Mr-Natural]

On Mar 12, 9:16 pm, Joan Carter <spamf...@sentex.ca> wrote:
> On Wed, 12 Mar 2008 19:08:34 -0700 (PDT),
> "ironjust...@aol.com"
>
> <ironjust...@aol.com> wrote:
> >Who loves ya. Tom
>
> Tom, the only person you love is yourself. Now go away.

I second that motion.

Go away mad. But, can ironjustice the self-absorbed nut-job
please go away!

[Dci]

"Mr-Natural-Health"
<john-h-gohde@naturalhealthperspective.com> wrote in message
news:d6393b81-5d58-43cb-afb3-70514983d1de@n77g2000hse.googleg-
roups.com...
> On Mar 12, 9:16 pm, Joan Carter <spamf...@sentex.ca> wrote:
>> On Wed, 12 Mar 2008 19:08:34 -0700 (PDT),
>> "ironjust...@aol.com"
>>
>> <ironjust...@aol.com> wrote:
>> >Who loves ya. Tom
>>
>> Tom, the only person you love is yourself. Now go away.
>
> I second that motion.
>
> Go away mad. But, can ironjustice the self-absorbed nut-job
> please go away!

I used the kill-file for Tom. It works!

Donn

[Ironjustic]

On Mar 12, 7:08=A0pm, "ironjust...@aol.com"
<ironjust...@aol.com> wrote: would my free bisphosphonate
work .. ? <<

"TRK-530 ia novel bisphosphonate derivative inhibited IL-1"

Original Paper

Inhibitory Effects of TRK-530 on Rat Adjuvant Arthritis
Masahiko Tanahashi, Yuriko Funaba, Masatoshi Itoh, Norio
Kawabe, Teruo Nakadate-Matsushita

Basic Research Laboratories, Toray Industries, Inc., Kamakura,
Kanagawa, Japan

Address of Corresponding Author

Pharmacology 1998;56:242-251 (DOI: 10.1159/000028204)

Abstract

TRK-530 is a novel bisphosphonate derivative. We examined the
anti-inflammatory effects of TRK-530 on adjuvant arthritis
(AA) rats. When TRK-530 at a dose of 2.5 mg/kg was
administered for 2 weeks to AA rats, it inhibited destructive
changes in arthritic joints such as paw edema, bone loss and
joint degeneration. TRK-530 also inhibited splenomegaly and
suppressed the increase in serum sialic acid which is measured
as a systemic parameter of inflammation. To clarify the
inhibitory mechanism of TRK-530, interleukin-1 (IL-1)- like
activities of resident peritoneal macrophages in AA rats given
TRK-530 were compared with those of control rats. We found
that TRK-530 inhibited IL-1-like activity induced by bacterial
lipopolysaccharide 6 weeks after administration when the
IL-1-like activities of control rats were still at high
levels. These findings suggest that TRK-530 exerts
anti-inflammatory activities in AA rats.

--------------------------------------------------------------
---------------=
----

Key Words

TRK-530 Bisphosphonate Adjuvant arthritis Interleukin-1

--------------------------------------------------------------
---------------=
----
Author Contacts

Masahiko Tanahashi Basic Research Laboratories, Toray
Industries, Inc. 1111 Tebiro, Kamakura, Kanagawa 248 (Japan)
Tel. +81 467 32 2111, Fax +81 467 31 1437 E-Mail
tanahash@blab.toray.co.jp

--------------------------------------------------------------
---------------=
----

Article Information

Received: Received: February 14, 1997 Accepted: November 15,
1997 =A9 2008 S. Karger AG, Basel

Who loves ya. Tom

Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com

Man Is A Herbivore! http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING http://tinyurl.com/zk9fk

> On Mar 12, 1:03=A0pm, "ironjust...@aol.com"
> <ironjust...@aol.com> wrote:In these, CPPD crystals form and
> are deposited in the cartilage matrix (chondrocalcinosis)
> and induce inflammatory and/or destructive =A0mechanisms. <<
>
> One might wonder since .. crystallization inhibitors are
> also called bisphosphonates .. would my free bisphosphonate
> work .. ?
>
> http://tinyurl.com/3yqmcn
>
> Hmmm ..
>
> "Etidronate severely inhibits rates of growth and formation
> of various forms of calcium pyrophosphate crystals"
>
> http://pubs.acs.org/cgi-bin/abstract.cgi/cgdefu/2003/3/i01/-
> abs/cg0255...
>
> Who loves ya. Tom
>
> Jesus Was A Vegetarian!http://jesuswasavegetarian.7h.com
>
> Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
>
>
> > On Mar 12, 8:00=A0am, ironjustice
> > <ironjust...@cashette.com> wrote:Anakinra <<
>
> > What is the significance this disease is treated with
> > Colchicine and when that doesn't work they say Anakinra
> > may? This disease is recommended to be treated by
> > bloodletting.
>
> > "Requires the patient be examined particularly for
> > hemochromatosis"
>
> > =A0Z Rheumatol. 2007 Nov;66(7):573-4, 576-8.Related
> > Articles, Links [Diagnosis and treatment of calcium
> > pyrophosphate crystal-induced arthropathy]
>
> > [Article in German]
>
> > Announ N, Guerne PA.
>
> > Division de Rhumatologie, H=F4pital Universitaire de
> > Gen=E8ve, 26 Avenau=
e
> > de Beau-S=E9jour, 1211, Gen=E8ve, Schweiz.
>
> > Calcium pyrophosphate dihydrate deposition (CPPDD) disease
> > is the term used to describe a group of common and
> > potentially severe metabolic arthropathies. In these, CPPD
> > crystals form and are deposited in the cartilage matrix
> > (chondrocalcinosis) and induce inflammatory and/or
> > destructive mechanisms. Most cases are idiopathic, but
> > hyperparathyroidism, hemochromatosis, hypomagnesemia and
> > hypophosphatemia can promote or cause chondrocalcinosis.
> > Early disease (with onset before the age of 60 years) thus
> > requires that the patient be examined for these metabolic
> > conditions, particularly hemochromatosis. The prevalence
> > of CPPDD disease in the general population increases with
> > age, being 10-15% in the age group 65-75 years and more
> > than 40% in the over-80s. Although frequently
> > asymptomatic, chondrocalcinosis can involve severe acute
> > attacks of inflammatory arthritis (pseudogout) and also
> > various types of chronic arthropathy including
> > pseudorheumatoid arthritis,
> > pseudo-osteoarthritis, and pseudoneuropathic joint
> > disease. CPPD crystals can also be deposited in the
> > bursae, ligaments, and tendons and generate inflammation
> > and/or ruptures. The diagnosis is based on synovial
> > fluid analysis (positively birefringent CPPD crystals
> > visualized by compensated polarized light microscopy)
> > and X- rays (punctate and linear radiodense areas in
> > fibrocartilage and hyaline cartilage). Treatment is
> > primarily symptomatic, since there is no known drug that
> > can prevent progression of the joint destruction).
> > Nonsteroid anti-inflammatory drugs (NSAIDs) and
> > intra-articular or systemic glucocorticoids (amounts
> > must be only small if use is prolonged) are the most
> > useful treatments. Colchicine can be effective in
> > recurring pseudogout, and magnesium can be used
> > prophylactically. In a small uncontrolled series
> > methotrexate was effective and aroused interest; it can
> > be used when other treatments fail.
>
> > Publication Types: English Abstract
>
> > PMID: 17932681 [PubMed - in process]
> > -----------------------------
>
> > From Medscape Rheumatology Ask the Experts about
> > Rheumatoid Arthritis and Related Conditions Gout:
> > Treatment Reaction to Allopurinol -- What Next? Posted
> > 11/08/2007
>
> > Arthur Kavanaugh, MD
>
> > Author Information
>
> > Information from Industry Explore an agent offering
> > persistent pain relief with extended benefits. Learn about
> > around-the-clock treatment with potential to reduce the
> > number of breakthrough pain episodes and a demonstrated
> > improvement in pain-related sleep parameters. Read more
> > =A0Question A rash developed on a patient with gout during
> > treatment with both allopurinol and sulfinpyrazone.
> > Desensitization with allopurinol was not successful. The
> > patient is intolerant of nonsteroidal anti- inflammatory
> > drugs and colchicine. What is the next treatment option,
> > and can anakinra be tried?
>
> > Amir Alvi, MBBS, MRCP
>
> > =A0Response from Arthur Kavanaugh, MD Professor,
> > Department of Rheumatology, University of California,
> > San Diego
>
> > This question addresses treatment options for gout. The
> > case described highlights the unmet clinical need for new
> > gout treatments. In this case, the best available therapy,
> > allopurinol, cannot be tolerated because of toxicity, and
> > even desensitization was not successful. In addition,
> > uricosuric therapy was unsuccessful, as it is in many
> > cases of gout. Unfortunately, other treatment options are
> > relatively limited. To lower uric acid, removing
> > contributing factors such as medications, where possible,
> > can be useful. Alteration in diet can have a beneficial
> > effect, but compliance can be difficult for many patients.
> > Other medications with uric acid-lowering properties, such
> > as losartan and fenofibrate, can be tried if there are no
> > contraindications. A drug currently in late-phase
> > development, febuxostat, is a nonpurine xanthine oxidase
> > inhibitor that has shown promise in clinical trials but
> > has not yet been approved for gout.
>
> > Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly
> > used for the treatment of chronic arthritis. Comorbid
> > conditions commonly found among patients with gout,
> > including hypertension and renal dysfunction, which in
> > some cases contribute to the disease, can limit the use of
> > NSAIDs in patients with gout, however. The questioner also
> > raises the possibility of using anakinra, an interleukin-1
> > (IL-1) inhibitor. There has indeed been a good deal of
> > interest in this approach. There are data to suggest that
> > uric acid crystals may drive inflammation, in part through
> > the 'inflammasome,' an inflammatory intracellular pathway
> > that acts partly through elaboration of IL-1. There is
> > anecdotal evidence suggesting that IL-1 inhibitors may
> > indeed be effective in gouty arthritis, and this approach
> > is currently under study. However, the same caution must
> > be used with anakinra as one would undertake when using it
> > for its approved indication of rheumatoid arthritis.
>
> > Who loves ya. Tom
>
> > Jesus Was A Vegetarian!http://jesuswasavegetarian.7h.com
>
> > Man Is A Herbivore!http://tinyurl.com/a3cc3
>
> > DEAD PEOPLE WALKINGhttp://tinyurl.com/zk9fk
>
> > > This seems to be one of the problems associated with
> > > trauma. Unable to handle the cold.
>
> > > "one minute I was paralyzed and the next I was normal"
>
> > > Source: Dalhousie University =A0 =A0 Released: Tue
> > > 11-Mar-2008, 15:15 =
ET
>
> > > Dermatology Team Finds Treatment for Rare "Life-ruining"
> > > Condition Description
>
> > > Relief is now available for 600 people around the world
> > > who suffer from a rare genetic condition triggered by
> > > exposure to cold. "It's like you're freezing from the
> > > inside out," says Rachel Doherty, who took part in a
> > > clinical trial. In proving the effectiveness of
> > > anakinra, a Dalhousie dermatology team successfully
> > > concluded a 20- year quest to find a treatment for
> > > Familial Cold Autoinflammatory Syndrome (FCAS).
>
> > > Newswise -- Dalhousie Medical School dermatologist Dr.
> > > Barrie Ross and=

> > > his colleagues have successfully ended a 20-year quest
> > > to find a treatment for Familial Cold Autoinflammatory
> > > Syndrome (FCAS). The rare=

> > > condition, triggered by exposure to cold, causes severe
> > > discomfort and=

> > > physical incapacity.
>
> > > Through a clinical trial conducted at Capital Health in
> > > Halifax, Dr. Ross and his colleagues proved the
> > > overwhelming effectiveness of anakinra, a
> > > receptor-blocking medication, to ease the pain and
> > > suffering caused by FCAS. The study results were
> > > published this week in the Journal of Cutaneous Medicine
> > > and Surgery.
>
> > > Dr. Ross, an adjunct professor in the Division of
> > > Dermatology, Department of Medicine at Dalhousie and
> > > Capital Health, had the rare honour of seeing his
> > > quest through from beginning to successful end. In
> > > 1986, the year her mother was diagnosed with kidney
> > > failure which is linked to FCAS, Anne Mallais
> > > visited Dr. Ross. She was on a crusade=

> > > to find a cure for the debilitating condition that
> > > afflicts her and many of her family.
>
> > > "From the time Anne came to see me, it was serendipity,
> > > the advancement of technology and perseverance that led
> > > to the clinical trial and the discovery of a treatment,"
> > > says Dr. Ross.
>
> > > FCAS causes hives, fever, chills, myalgias, headache,
> > > stiffness and swelling, among other symptoms. "It's like
> > > you're freezing from the inside out," says Rachel
> > > Doherty. "Your whole body contracts until you=

> > > warm up, which can take hours or days." Doherty took
> > > over the crusade to find a cure from her sister and
> > > participated in the clinical trial.=

>
> > > Following Mallais' visit, Dr. Ross encouraged a
> > > dermatology resident to research, write and later
> > > publish a paper that detailed the literature on what was
> > > then known as Familial Cold Urticaria. The paper caught
> > > the attention of researchers in Germany. The researchers
> > > later teamed up with Dr. Ross to discover the
> > > chromosomal site for FCAS. Six years after the
> > > discovery, Dr. Ross and a group of UK colleagues
> > > pinpointed the specific receptor responsible for FCAS.
> > > When=

> > > triggered, the tumour necrosis factor (TNF) receptor
> > > starts the symptoms of FCAS.
>
> > > "Once we pinpointed the pathway, we looked at other
> > > inflammatory conditions with a common pathway in search
> > > of potential treatments," explains Dr. Ross. "A tip from
> > > a colleague turned us on to anakinra. It was an approved
> > > therapy for rheumatoid arthritis in Canada which meant
> > > that was safe to use." The next step was
>
> ...
>
> read more =BB- Hide quoted text -
>
> - Show quoted text -