Biomedical subjects
E Shinar
Publications and source records attributed to E Shinar.
Treatment of human ulcers by application of macrophages prepared from a blood unit.
Decubital ulcers contribute to morbidity and mortality in elderly patients. Macrophages play a major role in the process of wound healing. We compared the efficacy of local treatment of decubital ulcers in elderly patients using macrophages prepared from a blood unit, vs. conventional treatments. Patients with decubital ulcers (n = 199) hospitalized during one year in a Geriatric Hospital in Israel, were included in the study. The ulcers of 72 patients (average age 82), who provided informed consent, by themselves or by family, were treated by local injection of macrophages prepared from a blood unit in a closed sterile system. The remaining 127 patients (average age 79) were treated conventionally and served as controls. No exclusion criteria were applied. Only a completely healed ulcer was considered a positive outcome of treatment. In the macrophage-treated group 27% (36 out of 131 ulcers) were healed compared to 6% (15 out of 248) in the control group (p < 0.001). There was also a significantly faster healing in the experimental group (p < 0.02). No side effects were noted. We conclude that Macrophages prepared from a blood unit, in cost-effective, closed, sterile system, are significantly more effective than conventional methods for the treatment of ulcers in elderly patients.
Clostridium septicum bacteremia and diffuse spreading cellulitis of the head and neck in a leukemic patient.
Explore the source record for details and available documents.
The effects of m-AMSA on rat isolated heart.
m-AMSA (4'[9-acridinylamino]methansulphon-m-anisidide) is a new cytoxic agent now under clinical trial. We used the rat isolated perfused heart model in order to investigate the cardiac effects of m-AMSA. The results of the dose-response study indicate that m-AMSA has an acute moderate negative inotropic effect. The 90% effect (25% decrease in developed force compared to the control) was observed at drug concentration of 1.5 micrograms/ml. The refractory period (as measured by stimuli of twice diastolic threshold intensity) increased progressively as the drug concentration was increased (up to 2.5 micrograms/ml). Measurements of the strength-duration and strength-interval relationship showed that m-AMSA induced a significant reduction (P less than 0.005) in excitability and prolongation of refactoriness. We suggest that m-AMSA has a membranal cardiotoxic effect in addition to its known intracellular cytotoxic effect.