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Rheumatoid Arthritis
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1. Rheumatoid synovial fluid T cells are sensitive to APO2L/TRAIL.
Match Strength: 10.015

The infiltration and accumulation of T cells in the rheumatoid arthritis (RA) synovial fluid (SF) are hallmarks of disease. We aimed to assess the functional relevance of FasL and of APO2L/TRAIL in the persistence of T cells in the rheumatoid SF. We have analyzed the expression of the activation markers HLA-DR and CD69 and also of the death receptor Fas/CD95 and death ligands FasL or APO2L/TRAIL in CD3+ lymphocytes from SF of 62 RA patients, together with their sensitivity to anti-Fas mAb or to rAPO2L/TRAIL, using as controls T lymphocytes present in SF of 20 patients with traumatic arthritis. ... Read More »
» Published in Clin Immunol. 2007 Jan;122(1):28-40. Epub 2006 Sep 18.

2. NOD2 allele variants in patients with rheumatoid arthritis.
Match Strength: 9.650

Recent reports have proven the importance of genetic factors and inflammation in the pathogenesis of rheumatoid arthritis (RA). In the current study, the frequency of NOD2/CARD15 gene variants (R702W, G908R, and L1007fsinsC) was examined in a group of 243 RA patients and 220 healthy controls. There were no statistically significant differences in distribution of NOD2 variant alleles between RA patients and controls. Moreover, there was no significant association between NOD2 variant alleles and joint erosions, extraarticular manifestations, rheumatoid factor, number of swollen and tender ... Read More »
» Published in Clin Rheumatol. 2006 Sep 15;

3. The initial validation of a Markov model for the economic evaluation of (new) treatments for rheumatoid arthritis.
Match Strength: 9.457

OBJECTIVE: Markov models are increasingly used in economic evaluations of (new) treatments for chronic diseases. In this study we propose a Markov model with health states defined by the disease activity score (DAS) to be used to extrapolate efficacy data from short-term clinical trials in rheumatoid arthritis to longer term cost-effectiveness results. Moreover, we perform an initial validation of this model. METHODS: To test the validity of the model, the expected disease course (according to the model) was first compared with the observed disease course in an inception cohort of newly ... Read More »
» Published in Pharmacoeconomics. 2006;24(10):1011-20.

4. Rheumatoid neutrophilic dermatitis.
Match Strength: 9.388

Rheumatoid neutrophilic dermatitis (RND) is an infrequent cutaneous manifestation of rheumatoid arthritis (RA). This condition is seen in patients who are both positive and negative for a circulating rheumatoid factor. Histologically, it presents with a neutrophilic dermatosis, characterized by a heavy dermal infiltrate of neutrophils with variable degrees of leukocytoclasis but no vasculitis. We describe the case of a young female with seronegative RA who had concomitant lesions of RND over both elbows. Her lesions appeared as nodules, but RND has been reported as papules and plaques, ... Read More »
» Published in Cutis. 2006 Aug;78(2):133-6.

5. Design of a new line in treatment of experimental rheumatoid arthritis by artesunate.
Match Strength: 9.350

This study was aimed to evaluate the therapeutic potency of a new antimalarial drug, artesunate, in an experimental model of rheumatoid arthritis. Collagen-induced arthritis (CIA) was induced in Lewis rats.The intraperitoneally administration of artesunate (ARS) and methotrexate (MTX) were started on day 25 postimmunization and continued until final assessment on day 35. During this period, clinical examination was intermittent. The anticollagen type II antibody (CII Ab) and nitric oxide synthesis were measured. The paws and kness were then removed for histopathology and radiography assay. The ... Read More »
» Published in Immunopharmacol Immunotoxicol. 2006;28(3):397-410.

6. Gene therapy works in animal models of rheumatoid arthritis...so what!
Match Strength: 9.286

Rheumatoid arthritis (RA) is a systemic disease with polyarticular manifestation of chronic inflammation in the knees and small joints of hand and feet. The current systemic anti-tumor necrosis factor (TNF)-alpha therapies with biologics ameliorate disease in 60% to 70% of RA patients. However, biologics must be given systemically in relatively high dosages to achieve constant therapeutic levels in the joints, and side effects have been reported. To this end, local gene delivery can provide an alternative approach to achieve high, long-term expression of biologics, optimizing the therapeutic ... Read More »
» Published in Curr Rheumatol Rep. 2006 Oct;8(5):386-93.

7. Effects of regular exercise on pain, fatigue, and disability in patients with rheumatoid arthritis.
Match Strength: 9.171

Rheumatoid arthritis (RA) is a major health problem in Korea. To explore the effects of regular exercise on pain, fatigue, and disability, a descriptive study was conducted in 435 Korean patients with RA. Exercisers were defined as those who are currently exercising more than 3 times a week, for at least 20 minutes, and for more than 6-consecutive months after being diagnosed with RA. The primary finding was that exercisers had significantly less fatigue and disability compared with nonexercisers. Results suggest that regular exercise has advantages for patients with RA to decrease fatigue and ... Read More »
» Published in Fam Community Health. 2006 Oct-Dec;29(4):320-7.

8. Is measurement of IgM and IgA rheumatoid factors (RF) in juvenile rheumatoid arthritis clinically useful?
Match Strength: 9.102

The prevalence and clinical relevance of IgM and IgA RF detected by ELISA were studied in 91 patients with juvenile rheumatoid arthritis (JRA) and 45 healthy children. IgM and IgA RF were detected, respectively, in 33 and 44% of the patients, compared to 6.7 and 15.6% of the healthy children (p = 0.001 and 0.0006, respectively). The frequency of IgM RF was significantly higher in patients with polyarticular (52%) as compared to systemic onset JRA (21%; p = 0.04). Five out of ninety-one patients and none of the control group were IgM RF positive by the latex test. High levels of IgM RF were ... Read More »
» Published in Rheumatol Int. 2007 Feb;27(4):345-9. Epub 2006 Sep 29.

9. The role of mesenchymal cells in the pathophysiology of inflammatory arthritis.
Match Strength: 9.015

Rheumatoid arthritis (RA) is a chronic inflammatory disorder of the joints that can cause severe disability. While the role of inflammatory cells in the pathogenesis of RA has been well established, the specific contribution of resident cells within the synovial membrane, especially those of mesenchymal origin, has become the object of closer scrutiny only recently. The central position of these cells in the disease process of RA is underlined by their involvement in its main pathophysiological features: inflammation, hyperplasia and joint destruction. In this chapter, we provide a ... Read More »
» Published in Best Pract Res Clin Rheumatol. 2006 Oct;20(5):969-81.

10. Genetic markers of treatment response in rheumatoid arthritis.
Match Strength: 8.532

Rheumatoid arthritis patients exhibit a considerable interindividual variability in response to drug treatment. Although many disease-related and demographic factors have been studied to predict treatment outcome, the effective disease-modifying antirheumatic drug (DMARD) therapy is not yet allocated based on factors that predict efficacy. Individual genetic characteristics are thought to play an important role in treatment response; therefore, current research aims to identify these genetic predictors for clinical response. Pharmacogenetic studies are beginning to provide results, which ... Read More »
» Published in Curr Rheumatol Rep. 2006 Oct;8(5):369-77.

11. Disease-modifying antirheumatic drugs are associated with a reduced risk for cardiovascular disease in patients with rheumatoid arthritis: a case control study.
Match Strength: 8.386

Rheumatoid arthritis (RA) is characterized by inflammation and an increased risk for cardiovascular disease (CVD). This study investigates possible associations between CVD and the use of conventional disease-modifying antirheumatic drugs (DMARDs) in RA. Using a case control design, 613 RA patients (5,649 patient-years) were studied, 72 with CVD and 541 without CVD. Data on RA, CVD and drug treatment were evaluated from time of RA diagnosis up to the first cardiovascular event or the end of the follow-up period. The dataset was categorized according to DMARD use: sulfasalazine (SSZ), ... Read More »
» Published in Arthritis Res Ther. 2006;8(5):R151.

12. Treating very early rheumatoid arthritis.
Match Strength: 8.251

Rheumatoid arthritis (RA) is common and leads to joint damage due to persistent synovitis. The persistence of inflammation is maintained by hyperplastic stromal tissue, which drives the accumulation of leukocytes in the synovium. Aggressive treatment after the first 3-4 months of symptoms, with either disease modifying anti-rheumatic drugs or anti-tumor necrosis factor (TNF)-alpha therapy, reduces the rate of disease progression. However, it rarely switches off disease such that remission can be maintained without the continued need for immunosuppressive therapy. There is increasing evidence ... Read More »
» Published in Best Pract Res Clin Rheumatol. 2006 Oct;20(5):849-63.

13. Recent advances in the genetics of rheumatoid arthritis.
Match Strength: 7.874

Recent progress in defining the role of genetic factors in rheumatoid arthritis (RA) has been remarkable. Anticyclic citrullinated peptide (anti-CCP) antibody-positive disease appears to be immunogenetically distinct from anti-CCP-negative disease, with the former subgroup primarily responsible for association and linkage with the HLA-DRB1 shared epitope (SE). There is preliminary evidence that non-HLA genes contribute differentially to anti-CCP-positive and negative disease. The phenotypic differences evident in anti-CCP-positive and negative disease suggest a need to reclassify RA based on ... Read More »
» Published in Curr Rheumatol Rep. 2006 Oct;8(5):394-400.

14. Analysis of p53 and Bak gene mutations in lymphoproliferative disorders developing in rheumatoid arthritis.
Match Strength: 7.840

PURPOSE: Individuals affected by rheumatoid arthritis (RA) occasionally develop lymphoproliferative disorders (RA-LPD). To study the molecular changes underscoring the RA-LPD, mutations of p53 and Bak gene were analyzed in RA-LPD with (MTX-LPD) or without methotrexate treatment for RA (non-MTX-LPD). METHODS: Histology and immunophenotype were immunohistochemically examined in 32 cases of MTX-LPD and 21 of non-MTX-LPD. Polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP) followed by direct sequencing was employed to detect the mutations of p53 and Bak gene. RESULTS: ... Read More »
» Published in J Cancer Res Clin Oncol. 2007 Feb;133(2):125-33. Epub 2006 Sep 20.

15. Anti-cyclic citrullinated peptide (CCP) antibodies in patients with long-standing rheumatoid arthritis and their relationship with extra-articular manifestations.
Match Strength: 7.814

OBJECTIVES: To evaluate frequency of anti-cyclic citrullinated peptide antibodies (anti-CCP) in long-standing rheumatoid arthritis (LsRA) patients and their relationship with extra-articular manifestations of rheumatoid arthritis (RA), in addition to comparing frequency of anti-CCP antibodies in early RA (ERA) and LsRA group. DESIGN AND METHODS: One hundred and fifteen consecutive RA patients were included in the study as having LsRA because their disease duration was longer than 3 years. Thirty-nine consecutive patients with RA were included in the study as having ERA (<3 years). Also, 64 ... Read More »
» Published in Clin Biochem. 2006 Oct;39(10):961-5. Epub 2006 Jul 13.

16. Prostacyclin antagonism reduces pain and inflammation in rodent models of hyperalgesia and chronic arthritis.
Match Strength: 7.509

The inhibition of prostaglandin (PG) synthesis is at the center of current anti-inflammatory therapies. Because cyclooxygenase-2 (COX-2) inhibitors and nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the formation of multiple PGs, there is currently a strong focus on characterizing the role of the different PGs in the inflammation process and development of arthritis. Evidence to date suggests that both PGE(2) and PGI(2) act as mediators of pain and inflammation. Most of the data indicating a role for PGI(2) in this context have been generated in animal models of acute pain. Herein, we ... Read More »
» Published in J Pharmacol Exp Ther. 2006 Dec;319(3):1043-50. Epub 2006 Sep 14.

17. Cardiovascular disease and risk factors in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis.
Match Strength: 7.509

OBJECTIVE: To compare the prevalence of cardiovascular diseases and their risk factors between patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS) and control subjects. METHODS: Data for patients continuously enrolled in an integrated outcomes database between January 1, 2001, and December 31, 2002, with International Classification of Diseases, 9th Revision codes of 714.x (RA), 696.0 (PsA), or 720.0 (AS) were evaluated in this cross-sectional comparative study. Control groups were established for each patient group (1:4 ratio) by matching on the ... Read More »
» Published in J Rheumatol. 2006 Nov;33(11):2167-72. Epub 2006 Sep 1. Comment in: J Rheumatol. 2006 Nov;33(11):2105-7.

18. Bim deficiency leads to exacerbation and prolongation of joint inflammation in experimental arthritis.
Match Strength: 7.265

OBJECTIVE:: Rheumatoid arthritis (RA) is characterized by hyperplasia of the synovial lining, inflammation, and destruction of cartilage and bone. Since there are only a few detectable cells undergoing apoptosis in the joint, it is possible that a defect in apoptosis may contribute to synovial hyperplasia. This study sought to identify and characterize the direct role of apoptotic regulators in a mouse model of inflammatory arthritis. METHODS: Using a serum transfer model, experimental arthritis was induced in mice lacking the proapoptotic Bcl-2 family genes Bak (Bak-/-), Bax (Bax-/-), or Bim ... Read More »
» Published in Arthritis Rheum. 2006 Oct;54(10):3182-93.

19. CD97 neutralisation increases resistance to collagen-induced arthritis in mice.
Match Strength: 7.197

Synovial tissue of rheumatoid arthritis (RA) patients is characterised by an influx and retention of CD97-positive inflammatory cells. The ligands of CD97, CD55, chondroitin sulfate B, and alpha5beta1 (very late antigen [VLA]-5) are expressed abundantly in the synovial tissue predominantly on fibroblast-like synoviocytes, endothelium, and extracellular matrix. Based upon this expression pattern, we hypothesise CD97 expression to result in accumulation of inflammatory cells in the synovial tissue of RA patients. To determine the therapeutic effect of blocking CD97 in an animal model of RA, ... Read More »
» Published in Arthritis Res Ther. 2006;8(5):R155.

20. Chemokine inhibition in inflammatory arthritis.
Match Strength: 7.062

Synovial inflammation in rheumatoid arthritis (RA) and other arthritides is, in part, dependent on migration of inflammatory cells as well as retention of these cells at the site of inflammation. Chemokines play a critical role in these processes and represent an attractive target for therapeutic intervention. Animal models of RA have shown that it is possible to induce clinical improvement by specifically targeting chemokines or their receptors. Although at present only very limited data exist, initial data suggest that it may be possible to reduce synovial inflammation in patients with RA by ... Read More »
» Published in Best Pract Res Clin Rheumatol. 2006 Oct;20(5):929-39.

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