. Mebendazole, a broad spectrum anthehnintic was evaluated in 32 patients parasitized with tape worm infestations. Eighteen patients were identified as having Hymenolepis nana and 14 as having Taenia saginata. Seventeen patients in addition, were found to have concomitant nematode infection. Patients were treated with one of the five dosage schedules (100 mg b.d. x 3 days, 100 mg q.i.d. x 3 days, 300 mg b.d. x 1 day, 300 mg b.d. x 3 days and 500 mg b.d. x 1 day). Treatment resulted in the passage of long chains of proglottids of T. saginata and whole worms of H. nana. Assessment of results was made at 15 day intervals for 3 months. The most effective dosage schedule was 300 mg b.d. for 3 days which resulted in curing all the six patients suffering from T. saginata and 7 of the 10 harbouring H. nana.

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. One gram of sodium tolbutamide was administered orally to twenty-five patients with hepatic cirrhosis and five normal subjects and its serial plasma levels were measured both before and after phenobarbital pretreatment. Phenobarbital administration reduced the enhanced half life (t1/2) of tolbutamide in nonsmokers with hepatic cirrhosis but no significant alteration was produced in smokers with hepatic cirrhosis.

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. One gram of sodium tolbutamide was administered orally to twenty-five patients with hepatic cirrhosis and five normal subjects and its serial plasma levels were measured both before and after phenobarbital pretreatment. Phenobarbital administration reduced the enhanced half life (t1/2) of tolbutamide in nonsmokers with hepatic cirrhosis but no significant alteration was produced in smokers with hepatic cirrhosis.

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. Guanethidine when administered as bolus intravenous injection produces sharp and short lived initial fall in blood pressure (phase I), followed by a rise in blood pressure (phase II). These initial changes are followed by a progressive fall in blood pressure (phase III) lasting for several days. In the present study an attempt is made to analyse the mechanism of action of the initial fall in BP (phase I). Our observations indicate that this initial fall in BP seen after intravenous guanethidne administration is partly due to activation of peripheral beta adrenergic receptors and partly due to direct peripheral vasodilatation.

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