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J R Minor

Publications and source records attributed to J R Minor.

34 records · Page 2Linked to original sources
PubMed1991

The AIDS research agenda at the National Institutes of Health.

The foundation, goals, and components of the research strategy developed by the National Institutes of Health to combat AIDS and HIV infection are discussed. The AIDS research agenda, based on systems originally designed to coordinate cancer research, involves a national effort to study various aspects of the disease, disseminate information, and rapidly develop and test drugs and vaccines to treat and prevent AIDS and HIV disease. AIDS research makes up approximately 10% of the total NIH budget of $7.6 billion, and the largest portion of that allocation goes to improving current treatments and developing new agents. Drug discovery efforts are supported by the National Institute of Allergy and Infectious Diseases (NIAID) through the Division of Intramural Research, in which biomedical and clinical research is conducted, and the Division of AIDS, which coordinates extramural research in university-based centers and community programs. By providing educational materials and sponsoring conferences, NIAID also helps to disseminate the results of the research it coordinates. Pharmacists support AIDS research through their involvement with study drug products and their role in protocol development, regulatory affairs, product development, and accumulation and distribution of drug information. Research initiatives sponsored by the federal government combine resources of investigators from government, academia, and the pharmaceutical and biotechnological industries to meet the challenges posed by the AIDS epidemic.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Treatment of Wegener's granulomatosis with intermittent high-dose intravenous cyclophosphamide.

PURPOSE: Concerns regarding the long-term toxicity of daily cyclophosphamide (CP) therapy for the systemic vasculitides have led us to evaluate alternative approaches to treatment in an attempt to achieve comparable efficacy with less toxicity. This study sought to determine the efficacy, toxicity, and immunologic effects of glucocorticoids (GC) and intermittent high-dose intravenous CP ("pulse" CP) in the treatment of 14 patients with Wegener's granulomatosis (WG). PATIENTS AND METHODS: The diagnosis of active WG was supported by a typical clinical presentation and histopathologic findings of vasculitis, granulomatous inflammation, and tissue necrosis. GC treatment was initially provided on a daily basis and later tapered to an alternate-day schedule if vasculitis remained inactive. Pulse CP treatment was initially administered once a month for 6 months. If after 6 months remission had been attained and GC therapy had been discontinued, then pulse CP treatment was given at less frequent intervals thereafter. Treatment and evaluation were provided for participants as inpatients in a clinical research center (National Institutes of Health). RESULTS: Thirteen of 14 patients (93%) initially experienced unequivocal improvement with pulse CP therapy, and seven of 14 (50%) achieved remission within 4 months. However, treatment was associated with significant toxicity in two patients and later relapses in nine patients, so that a total of 79% either failed to achieve sustained remission or were unable to continue therapy. Three of 14 (21%) patients have achieved sustained remissions with the pulse CP protocol and one additional patient (who had a limited exacerbation of WG) continues to receive that therapy after 14 to 22 months (mean 17 months). CONCLUSIONS: The use of pulse CP and GC therapy in 14 patients with WG was associated with a high initial response rate. However, failure to respond initially to treatment, to sustain improvement, or to tolerate continued treatment was noted in 79% of patients within a period of 1 to 22 months. These observations indicate that this particular pulse CP protocol does not achieve a high degree of lasting efficacy.

Adult↗
PubMed1988

Cyclosporin A in severe, treatment-refractory rheumatoid arthritis. A randomized study.

STUDY OBJECTIVE: To assess the efficacy and toxicity of cyclosporin A in patients with severe, treatment-refractory rheumatoid arthritis. DESIGN: Prospective randomized, double-blind 6-month trial. PATIENTS: Thirty-one patients who had classic seropositive rheumatoid arthritis with active synovitis unresponsive to conventional therapy. INTERVENTIONS: Patients were randomly assigned to high-dose (10 mg/kg body weight.d) or low-dose (1 mg/kg.d) cyclosporin A therapy. A reduction in the dose was permitted for adverse side effects. After 6 months of therapy, patients who showed clinically relevant improvement, defined as a 40% or greater reduction in their total joint activity score, were given the option to continue receiving the therapy for an additional 6 months. MEASUREMENTS AND MAIN RESULTS: At 6 months, clinically relevant improvement occurred in 10 of 15 patients (95% CI, 38 to 88) receiving high-dose therapy and in 4 of 16 patients (CI, 7 to 52) receiving low-dose therapy (P = 0.02). Statistically significant improvements in individual measures were shown only in the high-dose group. Improvements were noted in the number of tender joints (-18.8; CI, -24.5 to -13.1) and swollen joints (-12.1; CI, -15.4 to -8.6), as well as in physician's global scores (-1.5; CI, -2.1 to -0.9) and patient's global scores (-1.1; CI, -1.9 to -0.5). Improvement in disease activity was maintained through 12 months in the high-dose group. The clinical responses to cyclosporin A were most evident in patients with depressed in-vitro proliferative responses of peripheral blood mononuclear lymphocytes to soluble recall antigens. Toxicities, such as fatigue, gastrointestinal and neurologic complaints, and hypertrichosis were frequent but often reversible with a reduction in the dose. Nephrotoxicity, with a 20% increase in the serum creatinine level, was seen in 27 of 31 patients (CI, 71 to 97). CONCLUSIONS: Cyclosporin A is an effective therapy for severe, treatment-refractory rheumatoid arthritis. Side effects, particularly nephrotoxicity, are common.

Adult↗
PubMed1985

Histamine secretion induced by N-acetyl cysteine.

The mucolytic drug N-acetyl cysteine has been shown to release histamine from cultured mouse mast cells and from human basophils. At neutral pH the release was moderate and non-cytotoxic. If the acidity of the drug was not neutralized, this histamine release was markedly potentiated, but was then associated with a reduction in the viability of the cells. However, the high level of release could not be reproduced by simply exposing the cells to an acidic medium. The results are discussed in terms of a possible mechanism for the adverse reactions sometimes observed during N-acetyl cysteine therapy.

Acetylcysteine↗