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Pagina 1 a partire dal 381 risultati
Tobacco and other environmental risk factors in rheumatoid arthritis.
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Many environmental factors have been associated with an increased risk of developing Rheumatoid Arthritis (RA), but so far smoking is the only environmental risk factor that has been extensively studied and widely accepted. Smoking is associated with an increased risk of developing seropositive RA
The effect of snuff (smokeless tobacco) on disease activity and function in rheumatoid arthritis: experiences from the Better Anti-Rheumatic FarmacOTherapy, a longitudinal multicenter study on early rheumatoid arthritis.
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BACKGROUND
It is not known whether snuff (moist smokeless tobacco) affects disease activity in rheumatoid arthritis (RA).
OBJECTIVE
This study aims to study the effect of snuff on disease activity and function in Swedish patients with early RA.
METHODS
Between 1992 and 2005, 2800 adult patients were
Expression of Mycobacterium leprae HSP65 in tobacco and its effectiveness as an oral treatment in adjuvant-induced arthritis.
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Transgenic plants are able to express molecules with antigenic properties. In recent years, this has led the pharmaceutical industry to use plants as alternative systems for the production of recombinant proteins. Plant-produced recombinant proteins can have important applications in therapeutics,
Nicotine-induced differential modulation of autoimmune arthritis in the Lewis rat involves changes in interleukin-17 and anti-cyclic citrullinated peptide antibodies.
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OBJECTIVE
Rheumatoid arthritis (RA) is a debilitating autoimmune disease, and smoking is an important environmental factor in a subset of RA patients. A role of the cholinergic antiinflammatory pathway in autoimmune inflammation is increasingly being realized. Nicotine is a major component of
Second-hand exposure to tobacco smoke and its effect on disease activity in Swedish rheumatoid arthritis patients. Data from BARFOT, a multicenter study of RA.
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OBJECTIVE
We studied the prevalence and effect on disease activity of ever having had second-hand exposure to tobacco smoke in Swedish rheumatoid arthritis (RA) patients who had never smoked.
METHODS
Between 1992 and 2005, 2,800 patients were included in the BARFOT early-RA study in Sweden. Disease
Nicotine inhibits tumor necrosis factor-α induced IL-6 and IL-8 secretion in fibroblast-like synoviocytes from patients with rheumatoid arthritis.
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It was recently demonstrated that the cholinergic anti-inflammatory pathway can modulate host inflammatory responses via cholinergic mediators or via electrical stimulation of the vagus nerve. Here, we investigated whether nicotine, a selective cholinergic agonist, plays any anti-inflammatory role
The swollen joint, the thickened artery, and the smoking gun: tobacco exposure, citrullination and rheumatoid arthritis.
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Autoimmune diseases result from an interplay between susceptibility genes and environmental factors. These interacting etiopathogenetic components converge in a critical step preceding disease, the loss of tolerance to self. In this review, we examine the evidences linking tobacco smoking with the
Quantifying anti-cyclic citrullinated peptide titres: clinical utility and association with tobacco exposure in patients with rheumatoid arthritis.
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OBJECTIVE
To determine the significance of quantitative levels of antibodies to cyclic citrullinated peptides (anti-CCP) in a population of patients with rheumatoid arthritis (RA).
METHODS
A total of 241 consecutive sera from patients with RA sent from a large rheumatology clinic for laboratory
Serum cotinine as a biomarker of tobacco exposure and the association with treatment response in early rheumatoid arthritis.
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OBJECTIVE
Cigarette smoking has emerged as a risk factor for the development of rheumatoid arthritis (RA). Recent studies have suggested that cigarette smoking may lead to lower treatment response rates with methotrexate (MTX) and some biologic agents in RA. Knowledge of whether tobacco exposure
Diagnostic utility of, and influence of tobacco usage and genetic predisposition on, immunoglobulin A, rheumatoid factor and anti-citrullinated peptide auto-antibodies in South African rheumatoid arthritis patients.
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Regulatory effect of nicotine on collagen-induced arthritis and on the induction and function of in vitro-cultured Th17 cells.
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OBJECTIVE
To determine the effect of nicotine stimulation on collagen-induced arthritis (CIA), especially on Th17 cells, and the influence of activated acetylcholine receptor signaling on the induction and function of in vitro-cultured Th17 cells.
METHODS
Mice were divided into control and
[Potential influence of nicotine on inflammation and induction of autoantibodies in rats with adjuvant arthritis].
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The influence of chronic administration of nicotine diluted in the drinking water on the parameters of systemic inflammation and autoimmune processes in rats (August line) with adjuvant-induced arthritis, were studied. The experiments have shown that nicotine acts as an antiphlogistic means (the
Chronically administered nicotine attenuates bradykinin-induced plasma extravasation and aggravates arthritis-induced joint injury in the rat.
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We recently showed that acute administration of nicotine in the rat decreases bradykinin-induced plasma extravasation and that adrenal medullary-derived epinephrine, acting at a beta 2-adrenergic receptor, mediates the nicotine effect. Since agents which decrease bradykinin-induced plasma
Hypothesis: tobacco use is a risk factor in rheumatoid arthritis.
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Rheumatoid arthritis (RA) has been described in 3000-5000 year-old skeletal remains from North America by Rothschild, Turner and DeLuca (1). RA was first described unambiguously in Europeans in 1800 (1). Tobacco was introduced into Europe from the New World in the 1600s, and Rothschild, Turner and
Smoking and nicotine exposure delay development of collagen-induced arthritis in mice.
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BACKGROUND
Recent epidemiologic studies have implicated smoking as an environmental risk factor for the development of rheumatoid arthritis (RA). The aim of the present study is the evaluation of the role of cigarette smoke (CS) in the pathogenesis of collagen-induced arthritis in
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