|
Synflex Customer Loyalty Program
Sites:
About Arthritis
Is
there increased risk of osteoporosis for people who have
rheumatic disease?
Is there an increased risk of developing osteoporosis if
a person has rheumatoid arthritis or any of the rheumatic
diseases? If yes, what is responsible for the increased risk
of osteoporosis? Should a person with rheumatic disease be
routinely tested...
Mayo
Clinic Suggests Do's and Don'ts for Arthritis Pain
What is the most effective way to relieve arthritis pain?
There is no quick and easy, one-size fits all answer. Gene
G. Hunder, M.D. from Mayo Clinic offers some recommendations
about what to do and what not to do when...
Vioxx
Recall: The fallout still being felt
The fallout from the Vioxx recall is still being felt. The
recall has impacted the U.S. Food and Drug Administration,
Merck, and arthritis patients and doctors. The FDA is issuing
twice the number of public advisories about drug risks as...
Osteoporosis
Risk Factor Quiz
The more risk factors you have for a specific disease, the
more likely it is you will develop that disease. Awareness
of risk factors may also help with prevention if the factor
is something you can control. Do you have...
Celebrex
- Approved for Ankylosing Spondylitis; Warnings Updated
On Label
Celebrex (celecoxib) has been approved by the U.S. Food and
Drug Administration for relief of the signs and symptoms
associated with ankylosing spondylitis. This latest use of
Celebrex is the sixth approved indication for Celebrex in
the United States. The...
Why
is there an increased risk of infection which occurs
with the TNF blockers?
Why is there an increased risk of infection which occurs
with the TNF blockers (Enbrel, Remicade, and Humira)? What
is the relationship between TNF and infection? Read Dr. Zashin's
answer regarding TNF blockers and risk of infection....
Mirapex
(pramipexole): Fibromyalgia pain relieved by Parkinson's
disease drug
A study of 60 fibromyalgia patients who randomly received
gradually increasing doses of Mirapex (pramipexole), a commonly
prescribed medication for Parkinson's disease, or placebo
showed promising results. According to the report in the
August issue of Arthritis & Rheumatism: 42...
How
To Protect Yourself Against Lyme Disease
Reducing exposure to ticks is your best defense against contracting
Lyme disease. There are several approaches you can use to
prevent and control Lyme disease. Learn how to protect yourself
against Lyme Disease. More information about Lyme Disease.
Take the...
Lower
Mortality: Obese RA Patients or Thin RA Patients?
You may think the answer is obvious, but think again. A team
of researchers from the University of Texas Health Sciences
Center reported that obese and overweight patients with rheumatoid
arthritis had "paradoxically lower death rates than
normal weight or...
Vioxx
- Texas trial continues; first federal Vioxx trial set
for November 28
The court is hearing interesting allegations regarding the
conduct of the maker of Vioxx. Merck has been accused in
the Texas trial of trying to "neutralize"
physicians who didn't view Vioxx favorably. Other testimony
focused on a game of "dodge...
Quiz:
Arthritis Risk Factors
A risk factor increases your likelihood of developing a disease
or condition. Theoretically, the more risk factors you have
the higher the risk of developing that condition. Do you
have any of the risk factors associated with arthritis? Take
the...
Site:
Arthritis Research & Therapy - Latest articles
A functional
variant of Fc? receptor IIIA is associated with rheumatoid arthritis in
individuals who are positive for anti-glucose-6-phosphate isomerase antibodies
Anti-glucose-6-phosphate isomerase (GPI) antibodies are known
to be arthritogenic autoantibodies in K/B×N mice, although
some groups have reported that few healthy humans retain
these antibodies. The expression of Fc? receptors (Fc?Rs)
is genetically regulated and has strong implications for
the development of experimental arthritis. The interaction
between immune complexes and Fc?Rs might therefore be involved
in the pathogenesis of some arthritic conditions. To explore
the relationship between functional polymorphisms in Fc?Rs
(FCGR3A-158V/F and FCGR2A-131H/R) and arthritis in individuals
positive for anti-GPI antibodies, we evaluated these individuals
with respect to FCGR genotype. Genotyping for FCGR3A-158V/F
and FCGR2A-131H/R was performed by PCR amplification of the
polymorphic site, followed by site specific restriction digestion
using the genome of 187 Japanese patients with rheumatoid
arthritis (including 23 who were anti-GPI antibody positive)
and 158 Japanese healthy individuals (including nine who
were anti-GPI antibody positive). We report here on the association
of FCGR3A-158V/F functional polymorphism with anti-GPI antibody
positive status. Eight out of nine healthy individuals who
were positive for anti-GPI antibodies possessed the homozygous,
low affinity genotype FCGR3A-158F (odds ratio = 0.09, 95%
confidence interval 0.01?0.89; P = 0.0199), and probably
were 'protected' from arthritogenic antibodies. Moreover,
among those who were homozygous for the high affinity genotype
FCGR3A-158V/V, there were clear differences in anti-human
and anti-rabbit GPI titres between patients with rheumatoid
arthritis and healthy subjects (P = 0.0027 and P = 0.0015,
respectively). Our findings provide a molecular model of
the genetic regulation of autoantibody-induced arthritis
by allele-specific affinity of the Fc?Rs.
Copper
chelation with tetrathiomolybdate suppresses adjuvant-induced
arthritis and inflammation-associated cachexia in rats
Tetrathiomolybdate (TM), a drug developed for Wilson's disease,
produces an anti-angiogenic and anti-inflammatory effect
by reducing systemic copper levels. TM therapy has proved
effective in inhibiting the growth of tumors in animal tumor
models and in cancer patients. We have hypothesized that
TM may be used for the therapy of rheumatoid arthritis and
have examined the efficacy of TM on adjuvant-induced arthritis
in the rat, which is a model of acute inflammatory arthritis
and inflammatory cachexia. TM delayed the onset of and suppressed
the severity of clinical arthritis on both paw volume and
the arthritis score. Histological examination demonstrated
that TM significantly reduces the synovial hyperplasia and
inflammatory cell invasion in joint tissues. Interestingly,
TM can inhibit the expression of vascular endothelial growth
factor in serum synovial tissues, especially in endothelial
cells and macrophages. Moreover, the extent of pannus formation,
which leads to bone destruction, is correlated with the content
of vascular endothelial growth factor in the serum. There
was no mortality in TM-treated rat abnormalities. TM also
suppressed inflammatory cachexia. We suggest that copper
deficiency induced by TM is a potent approach both to inhibit
the progression of rheumatoid arthritis with minimal adverse
effects and to improve the well-being of rheumatoid arthritis
patients.
Expression
of ADAM15 in rheumatoid synovium: up-regulation by vascular
endothelial growth factor and possible implications for
angiogenesis
ADAMs (a disintegrin and metalloproteinases) comprise a new
gene family of metalloproteinases, and may play roles in
cell-cell interaction, cell migration, signal transduction,
shedding of membrane-anchored proteins and degradation of
extracellular matrix. We screened the mRNA expression of
10 different ADAMs with a putative metalloproteinase motif
in synovial tissues from patients with rheumatoid arthritis
(RA) or osteoarthritis (OA). Reverse transcription PCR and
real-time quantitative PCR analyses indicated that among
the ADAMs, ADAM15 mRNA was more frequently expressed in the
RA samples and its expression level was significantly 3.8-fold
higher in RA than in OA (p < 0.01). In situ hybridization,
immunohistochemistry and immunoblotting demonstrated that
ADAM15 is expressed in active and precursor forms in the
synovial lining cells, endothelial cells of blood vessels
and macrophage-like cells in the sublining layer of RA synovium.
There was a direct correlation between ADAM15 mRNA expression
levels and vascular density in the synovial tissues (r =
0.907, p < 0.001; n = 20). ADAM15 was constitutively expressed
in RA synovial fibroblasts and human umbilical vein endothelial
cells (HUVECs), and the expression level was increased in
HUVECs by treatment with vascular endothelial growth factor
(VEGF)165. On the other hand, ADAM15 expression in RA synovial
fibroblasts was enhanced with VEGF165 only if vascular endothelial
growth factor receptor (VEGFR)-2 expression was induced by
treatment with tumor necrosis factor-?, and the expression
was blocked with SU1498, a specific inhibitor of VEGFR-2.
These data demonstrate that ADAM15 is overexpressed in RA
synovium and its expression is up-regulated by the action
of VEGF165 through VEGFR-2, and suggest the possibility that
ADAM15 is involved in angiogenesis in RA synovium.
| Arthritis | glucosamine | liquid
glucosamine | osteoarthritis | dog
arthritis |pet
arthritis | cat
arthritis |horse
arthritis |canine
arthritis | hip
dysplasia | joint
pain relief | arthritis
pain | 8
tips to ease arthritic pain | usage
instructions | synflex
F.A.Q. |
sales@syn-flex-usa.com
D and D Enterprises
Established in 2004
|
