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A female breeding alpaca with acute lameness of the left hindleg was diagnosed with a craniodorsal coxofemoral luxation. Repair was achieved using extracapsular stabilisation. Two nylon sutures were passed through a hole drilled in the femoral neck and anchored to the dorsal acetabulum using two screws and two spiked washers. A metal crimp was used to tighten and maintain the sutures. Postoperatively the alpaca was confined to a stall for 4 weeks before being returned to a paddock. At 6 months after surgery the alpaca was free of lameness and was successfully mated.

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Primary shortening of the flexor digitorum profundus tendon to the pollicized index finger was routinely performed during all congenital pollicizations over a 3-year period. Interphalangeal joint flexion of the pollicized digit was observed to begin within weeks after pollicization. The rebalancing of the pollicized long flexor musculotendinous unit has the potential for greater long-term strength.

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The use of regular aspirin as an antithrombotic agent has become prevalent in the elderly population. The belief that operative bleeding complications are more common in those patients taking regular aspirin has commonly led to its withdrawal 5-10 days prior to minor dermatologic plastic surgery. Few studies exist to examine the true effects of aspirin on outcome in these patients. All patients presenting for minor dermatologic plastic surgery in a 6-month period were prospectively studied. Two age-matched cohorts were identified: 52 patients taking regular aspirin, and 119 patients taking no aspirin. The incidence of minor and significant bleeding complications was recorded. There was no significant difference in the incidence of minor, significant or total complications between the two groups (Fisher's Exact test, P = 1.00). It is concluded that it is unnecessary to stop aspirin before minor dermatologic plastic surgery.

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Twenty one species of fishes, collected from the Rio Solimões and a tributary lake in the Amazon Basin near Manaus, showed a wide range of methemoglobin formation 1 hr after a dose of 30 mg/kg of sodium nitrite i.p. Methemoglobin formation in two experimental fishes, Brycon cf. melanopterum and Semaprochilodus insignis, maintained in tanks in our INPA laboratory, was studied in detail. Both fishes survived a dose of 10 mg/kg of nitrite i.p. but usually died within 3 hr of a dose of 30 mg/kg with levels of blood methemoglobin in excess of 80%. Methemoglobin produced in vitro by addition of nitrite to fresh blood was slowly reduced back to hemoglobin over a period of several hours at room temperature. Hemoglobin in hemolysates was auto-oxidized to methemoglobin at pH 6.1 and below but not at 6.9 and above.

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A study was made of the metabolism by the rabbit of adenine administered intravenously at a dose of 35 mg/kg with 100 micronCi of 8-14C-adenine. The infused adenine was removed from the blood in two phases, first by diffusion into the tissues and second by metabolic reactions throughout the body. The adenine equilibrated within a few seconds equally between plasma and red blood cells and between them and kidney, liver, duodenum, lung and heart. Diffusion into skeletal muscle was much slower and into brain slowest. The more gradual disappearance of adenine from blood, and from the rest of the body, with a half-life of about 20 minutes and with complete removal by two hours, was predominantly along three pathways, leading to, after four hours: 1) 74 per cent in adenine nucleotide (mostly AMP, ADP, and (ATP); 2) 12 per cent as unchanged adenine in the urine; and 3) 11 per cent as a mixture in almost equal parts of 8-oxyadenine and 2,8-dioxyadenine in the urine. Conversion of adenine to adenine nucleotide, probably by initial reaction with phosphoribosyl pyrophosphate and adenine-phosphoribosyltransferase, was at widely different rates in the organs with duodenum, kidney, liver, and lung high and heart, red blood cell, skeletal muscle and brain relatively low. Sites of formation of the two oxyadenines, probably by action of xanthine oxidase, were not determined.

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A study was made of the metabolism by a human subject of adenine administered intravenously at a dose of 10 mg/kg with 200 micronCi of 8-14C-adenine to learn how similar and different the results might be from those obtained by a much more extensive study by this Laboratory on the rabbit. A rapid initial disappearance of radioactivity from the blood was followed by a slower loss with a half-life of about an hour. The first was probably due to diffusion into the extravascular fluid and the second to metabolism in the tissues. Fifteen per cent of the radioactivity infused was excreted in the urine during the first three hours as unchanged adenine and another 8 per cent was excreted during the first six hours as a mixture, in almost equal parts, of 8-oxyadenine and 2,8-dioxyadenine. Radioactivity in the urine after the second day, starting at 1.5 per cent of the dose per day and declining steadily to 0.5 per cent at three months, was predominantly in uric acid, reflecting turnover of the adenine which had entered body pools of purine nucleotide. Approximately 2 per cent of the injected radioactivity was incorporated into red blood cell AMP, ADP and ATP, each of which, by the second day, had the same specific radioactivity, which then decayed at a rate of 1.3 per cent per day. The results were remarkably similar to those obtained in a previous study on the rabbit. A variety of clinical observations and tests on blood and urine showed no abnormalities attributable to the infusion with adenine.

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Adenine, 8-oxyadenine, and 2,8-dioxyadenine were analyzed, by Dowex-50 column chromatography, in rabbit urine four hours after IV infusion of the following doses of adenine in mg/kg: 2, 4, 8.75, 17.5, 35, 70, 140 and 210. The average excretion in mole percentage of the dose was: adenine, 11.1; 8-oxyadenine, 6.1; and 2,8-dioxyadenine, 6.2. The percentage of excretion of 8-oxyadenine and of 2,8-dioxyadenine was unrelated to the dose of adenine. At doses of adenine of 35 mg/kg and above more than 80 per cent of the 2,8-dioxyadenine in the urine was in the form of microscopic pale yellow spherical particles. The particulate 2,8-dioxyadenine was found in the kidney in a very small amount at the dose of 70 mg/kg and in much greater quantities at 140 and 210 mg/kg.

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