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Biomedical subjects

R A Turner

Publications and source records attributed to R A Turner.

At least 55 records · Page 3Linked to original sources
PubMed1986

Comparison of diflunisal and aspirin in long-term treatment of patients with rheumatoid arthritis.

A multicenter, open-label clinical trial evaluated the efficacy and tolerability of diflunisal given twice daily and aspirin given four times daily in the long-term treatment of patients with rheumatoid arthritis. Patients who successfully completed a 12-week, double-blind, parallel study comparing diflunisal (500 to 750 mg daily) with aspirin (2.6 to 3.9 gm daily) continued on the same medication in a 40-week, open-label segment of the study. The dosage of diflunisal could be increased to a maximum of 1 gm daily during the open-label phase. Both regimens were effective during the 40-week study. Diflunisal was better tolerated than aspirin as judged by the overall incidence of clinical adverse experiences. Patients treated with diflunisal had significantly fewer adverse experiences involving the digestive system and organs of special sense than did those treated with aspirin.

Adult↗
PubMed1985

Spontaneous and aggregated IgG induced rheumatoid factor producing cells in rheumatoid arthritis.

Seropositive rheumatoid arthritis (RA) patients were found to have high numbers of spontaneously occurring cells making rheumatoid factor (RF) reactive with human IgG as measured by a RF plaque forming cell (RF-PFC) assay. There was a significant positive correlation between the number of RF-PFC and both disease activity measured by the sedimentation rate and RF titer measured by the RA latex test. Aggregated IgG and pokeweed mitogen were equally effective stimulators of RF-PFC in cultures of RA peripheral blood mononuclear leukocytes. The rheumatoid ratio of helper (T4): suppressor (T8) T lymphocytes was also significantly increased over the ratio of normal controls, but this ratio did not correlate with the number of RF-PFC. Aggregated IgG or immune complexes may be responsible for stimulating RA RF-PFC in vivo.

Adult↗
PubMed1985

Rheumatoid arthritis and osteoarthritis synovial fluid effects on primary human endothelial cell cultures.

Since vascular proliferation may be important in the pathogenesis of rheumatoid arthritis (RA) and/or osteoarthritis (OA), this study examined the induction of angiogenesis by these synovial fluids (SF). Four of 11 (36%) RA and 2 of 6 (33%) OA SF caused early morphological changes in human endothelial cell cultures. SF from 7 of 11 (63%) RA and 4 of 8 (50%) OA patients resulted in the late formation of tabular networks morphologically resembling capillaries observed in vivo. Early morphological changes in cultures were associated with a significantly (p less than 0.05) longer duration of disease in patients with RA. Factors present in the SF of RA and OA patients may play a role in the excessive vascularization which often occurs in these arthropathies.

Angiogenesis Inducing Agents↗
PubMed1984

Does hyperuricemia protect from rheumatoid inflammation? A clinical study.

The negative association between gout and rheumatoid arthritis is well accepted. The reason for this mutual exclusion is not clear; a protective immunosuppressive effect of hyperuricemia has been included among possible explanations. To test this hypothesis, we reviewed the charts of 160 rheumatoid arthritis patients on whom clinical information and followup for at least a year were available. We selected those patients with persistent hyperuricemia as defined by serum urate levels averaging above 7.5 mg% for at least 6 months. We found 12 patients fulfilling such criteria, and 11 of these were judged to have quiescent, minimally active, or inactive disease during hyperuricemic periods. In 2 patients, flares of the rheumatoid process coincided with normalization of serum urate levels. We propose that persistent hyperuricemia may protect against or decrease the expression of rheumatoid inflammation.

Arthritis, Rheumatoid↗
PubMed1984

Rheumatoid arthritis and small airways function. Effects of disease activity, smoking, and alpha 1-antitrypsin deficiency.

The sensitive pulmonary function tests of change in maximum expiratory flow (delta Vmax 50) and volume of isoflow were used to determine the effects of rheumatoid arthritis (RA), smoking, and alpha 1-antitrypsin deficiency phenotypes on peripheral airways. Patients were prospectively divided into 4 groups: 14 smokers with RA, 12 nonsmokers with RA, 11 smokers without RA, and 13 nonsmokers without RA. delta Vmax 50 was the most discriminating variable and demonstrated significant small airway obstructive disease in the first 3 groups, with an additive effect in the group of smokers with RA. An increased incidence of the alpha 1-antitrypsin-deficient MS phenotype was seen in the RA smoker group, and this phenotype was associated with severe pulmonary disease.

Arthritis, Rheumatoid↗
PubMed1984

Psychological approaches to the management of arthritis pain.

The present review examines the literature regarding the efficacy of cognitive-behavioral and other self-control interventions in helping arthritis patients reduce their pain and functional disabilities. The evidence indicates that self-control interventions have produced significant and positive changes in the pain and functional disabilities of patients with rheumatoid arthritis and arthritis secondary to hemophilia. However, the literature suffers from deficiencies with regard to the use of small subject samples; inadequate control procedures and follow-up assessments; failure to demonstrate that positive outcomes are related to changes in subjects' covert experiences or control of physiological variables; and reliance upon self-report measures of outcome. The review is followed by a description of a multidisciplinary study of the efficacy of a biofeedback-assisted, cognitive-behavioral group therapy program for rheumatoid arthritis patients that features several methodological improvements relative to previous investigations. The preliminary outcome data show that the cognitive-behavioral intervention is associated with reductions in pain behavior and self-reports of pain and disability. It is concluded that, although the self-control interventions have shown promising results, psychologists must demonstrate positive and reliable outcomes among large numbers of arthritis patients over extended periods of time if the interventions are to be viewed as credible by rheumatologists.

Arthritis↗
PubMed1984

Effects of benoxaprofen on human neutrophil function.

In vitro assays of human neutrophil phagocytosis, adherence, enzyme release, and response to chemotactic factors were utilized to determine the effects of benoxaprofen on these cells. At concentrations of 30 and 300 micrograms/ml benoxaprofen partially inhibited phagocytosis without affecting adherence. High concentrations (300 micrograms/ml) of benoxaprofen, but not aspirin or gold, enhanced the release of the granular enzymes beta-glucuronidase and lysozyme, but not the release of the cytoplasmic enzyme lactic dehydrogenase from both resting and phagocytosing neutrophils. High concentrations (300 micrograms/ml) of benoxaprofen also inhibited the response of neutrophils to chemotactic factors as determined by both the leading front and leukotactic index methods. These unique in vitro effects of this antiinflammatory agent are compatible with recent clinical reports concerning its efficacy and toxicity.

Cell Adhesion↗
PubMed1983

Neutrophil migration in response to chemotactic factors: effects of generation conditions and chemotherapeutic agents.

The effects of various chemotactic factor generation conditions and several chemotherapeutic agents on neutrophil migration were determined using in vitro assay systems designed as models for inflammatory processes occurring in the synovial cavities of patients with rheumatoid arthritis. The microtubule-promoting agent concanavalin A and the microfilament-disrupting agent cytochalasin B were shown in these systems to inhibit neutrophil migration towards zymosan-activated serum-derived chemotactic factors. Neutrophils, immunoglobulin G aggregates, and serum were required for maximum generation of comparable chemotactic factors. Insoluble immunoglobulin G aggregates with or without rheumatoid factor produced more chemotactic factor activity on interaction with neutrophils than soluble immunoglobulin G aggregates. Exposure of neutrophils to supratherapeutic levels of the nonsteroidal antiinflammatory agent aspirin decreased neutrophil response to chemotactic factors while exposure to the slow-acting or immunomodulating agents gold, D-penicillamine, or azathioprine had no effect on this neutrophil function. In vitro systems employing neutrophils, insoluble aggregates, and serum may offer useful means for assaying drug effects on important functional components of the rheumatoid inflammatory process.

Antigen-Antibody Complex↗
PubMed1983

Human rheumatoid factor-producing cell induction by 2-mercaptoethanol: immunomodulation by a simple thiol compound.

Two-mercaptoethanol (2-ME), a simple 2 carbon thiol compound with a wide variety of in vitro and in vivo immunomodulating effects, was evaluated for its usefulness as a molecular probe of human antibody producing cell activation by adding 2-ME to cultures of peripheral blood mononuclear leukocytes from normal human volunteers. Culturing normal human leukocytes with 2-ME induced a significant number of cells producing rheumatoid factor as measured by a hemolytic plaque forming cell (PFC) assay. Dose response studies revealed 5 X 10(-5)M to be the optimum concentration of 2-ME for the induction of rheumatoid factor plaque forming cells (RF-PFC). This concentration of 2-ME also maximally induced PFC making antibodies to sheep red cells coupled to the trinitrophenyl (TNP) hapten demonstrating that 2-ME is a polyclonal inducer of human PFC. The addition of 5 X 10(-5) M 2-ME to cultures containing maximal concentrations of the polyclonal stimulators, pokeweed mitogen and human heat-aggregrated IgG, increased the number of RF-PFC detected in these cultures by approximately 50%, although both lower and higher concentrations of 2-ME suppressed the RF-PFC response. We conclude that 2-ME induces normal human leukocytes to produce rheumatoid factor as part of a polyclonal activation of antibody producing cells. 2-ME also has immunomodulating effects when added to other polyclonal stimulators of antibody producing cells.

Adjuvants, Immunologic↗
PubMed1983

Uric acid effects on in vitro models of rheumatoid inflammatory and autoimmune processes.

A neutrophil monolayer system was used to study the effects of uric acid on neutrophil-aggregate interactions important in rheumatoid inflammation. No effect on immunoglobulin G aggregate phagocytosis was seen, but hyperuricaemic levels of uric acid were associated with an enhancement of phagocytosis-induced release of the azurophilic granular enzyme beta-glucuronidase. A trinitrophenyl-coupled mononuclear leucocyte rheumatoid factor plaque-forming assay was utilised to study uric acid effects on polyclonal activation of immunocompetent cells. Low levels of uric acid enhanced and high levels suppressed this system. Hyperuricaemia may enhance some aspects of rheumatoid inflammation, while uric acid may modulate an important component of rheumatoid autoimmunity.

Arthritis, Rheumatoid↗
PubMed1983

Antirheumatic drug effects on neutrophil response to chemotactic factors: a comparison of analytical techniques.

A recently reported technique employing the leukotactic index which represents all migrating cells in vitro neutrophil chemotaxis systems, was compared to the leading front technique for assaying antirheumatic drug effects on this important neutrophil function. Normal human neutrophils were treated with therapeutic concentrations of aspirin, gold sodium thiomalate, D-penicillamine, and azathioprine. The responses of these cells and of control cells to neutrophil-immune complex-serum-derived chemotactic factors were assayed in Boyden chambers. Significant (P less than 0.05) inhibition was observed by the leading front technique only for D-penicillamine at high concentrations. Significant (P less than 0.01) inhibition was seen with D-penicillamine at therapeutic plasma levels with the leukotactic index technique. Gold sodium thiomalate and aspirin at high concentrations also produced significant (P less than 0.01 and P less than 0.05) inhibition of chemotaxis as assayed by the leukotactic index procedure. Azathioprine had no significant effects when studied with either technique. These results indicate that the leukotactic index may be a more sensitive technique for quantitating neutrophil migration in response to chemotactic factors and may therefore provide useful additional information for determining the effects of antirheumatic drugs on this important neutrophil function.

Aspirin↗
PubMed1981

Rheumatoid factor and monosodium urate crystal-neutrophil interactions in gouty inflammation.

A monolayer system was designed to study the interactions between human neutrophils and monosodium urate crystals important in gouty inflammation. The effects of rheumatoid factor on gouty inflammation were then examined in this system and in patients with acute gouty arthritis. Monosodium urate crystal phagocytosis was apparent at 30 min, and this phagocytosis was accompanied by lysosomal enzyme release and decreased neutrophil adherence to plastic petri dishes. Rheumatoid factor did not affect phagocytosis, adherence, or lactic dehydrogenase release and appeared to variably enhance lysosomal enzyme release. Two of 19 acute gouty patients were found to have low titers of rheumatoid factor and, of these, one exhibited mild disease and the other tophaceous destructive disease.

Adult↗
PubMed1981

Induction of autoantibody-producing cells after the coculture of haptenated and normal human mononuclear leukocytes.

The coculture of normal human peripheral blood mononuclear leukocytes (PBL) and autologous mononuclear leukocytes coupled to the trinitrophenyl (TNP) hapten (TNP-PBL) was found to induce a polyclonal activation of antibody-producing cells. The polyclonal activation of antibody-producing cells was demonstrated by detecting the induction of cells producing antibody to sheep red blood cells using a complement-dependent, direct, hemolytic plaque-forming cell (PFC) assay. A ratio of four normal to one haptenated mononuclear leukocyte was found to be optimal for inducing the polyclonal activation of antibody-producing cell in these cultures. The plaque-forming cells assay in these experiments utilized monolayers of indicator red cells. Further evidence for the polyclonal induction of antibody-producing cells by TNP-PBL was provided by demonstrating PFC on monolayers of not only sheep red blood cells, but also autologous human red cells, bromelain-treated autologous red cells, TNP-coupled human and sheep red cells, and human autologous red cells coupled to human heat-aggregated IgG with chromic chloride. Thus cells secreting antibody to TNP, human red cells, and human IgG were induced. Anti-IgG and anti-human red cell-producing cells were first detected on Day 2 of culture and were still present on Day 9. Mononuclear leukocytes altered by chemical haptenation polyclonally stimulate normal mononuclear leukocytes to become antibody-producing cells. This polyclonal stimulation of antibody-producing cells includes cells producing antibodies to human IgG and human autologous red blood cells suggesting that autoantibody-producing cells are induced.

Animals↗
PubMed1979

Cardiac involvement in rheumatoid arthritis. Followup study.

Initial studies from Bowman Gray School of Medicine showed that 18 of 30 patients with classic rheumatoid arthritis (RA) had cardiac involvement from their disease. These abnormalities were detected by echocardiography and consisted of mitral valve and/or pericardial abnormalities. All patients were followed for 4 years from the initial workup. Mitral valve abnormalities were seen on followup in 63% of the patients who initially showed this abnormality, while pericardial effusion remained in 20%. Pericardial thickening persisted in 6 of 7 patients. None of the patients developed constrictive pericarditis or heart failure. There was no definite correlation between persistence of these abnormalities and other clinical data, but it was noticed that patients who had persistent pericardial effusion and mitral valve abnormalities showed a higher number of involved joints and a higher erythrocyte sedimentation rate. The cardiac abnormalities described in this study have remained clinically insignificant in this population of RA patients.

Arthritis, Rheumatoid↗