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arthritis/− nikotyna

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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
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,
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
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
The immunoglobulin A isotypes of anti-cyclic citrullinated peptide antibodies (ACPA) and rheumatoid factor (RF) are associated with disease severity and progression in Caucasian rheumatoid arthritis (RA) patients, as well as with genetic predisposition and tobacco

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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