Effect of acetylsalicylic acid on nitric oxide production in infarcted heart in situ

The effect of Acetylsalicylic Acid (ASA, Aspirin) on the myocardial production of the inducible form of nitric oxide synthase (iNOS) and the oxidation products of nitric oxide (nitrite, NO-2 and nitrate, NO-3: NOx) were studied in the rabbit heart two days after ligation of a branch of the left circumflex coronary artery. ASA was administered intravenously as AspisolR, DL-Lysinmono(acetylsalicylate) which is soluble in water. Animals received a total dose of 250, 375, or 500 mg/kg of ASA in five divided doses intravenously. Significant inhibition of iNOS was noted in the infarcted portion of the myocardium at 375 and 500 mg/kg of ASA. The reduction in myocardial nitric oxide (NO) production was paralleled by a diminution in coronary arterial-venous difference of NOx, demonstrating that ASA inhibition extended also to the oxidation products of NO. ASA is an inhibitor of cyclooxygenase (COX). The inhibition of iNOS by ASA demonstrates the close relationship between COX and iNOS activity in the heart in situ. Whether activity of the infarcted heart is influenced by the diminution in the production of NO by ASA is not known.     

Carcinoma showing thymiclike differentiation (CASTLE tumor)

A 67-year-old woman had had a neck mass for 10 years, which recently increased in size. Sonographic, CT, and MR examinations showed a mass in the carotid and posterior spaces (triangle) extending from below the submandibular gland to the supraclavicular fossa, displacing the common carotid artery and the sternomastoid anteriorly. The mass was solid, noncalcified with lobulated outlines, hypoechoic on sonograms, of soft-tissue density on CT scans, isointense on T1-weighted MR images, hyperintense on T2-weighted MR images, and enhanced mildly after injection of contrast material on CT and MR studies. Histologic examination revealed a carcinoma showing thymiclike differentiation, a rare tumor of the neck and thyroid gland.     

Oral contraceptives, norethindrone and mestranol: effects on tissue levels of minerals

The study involved three levels of dietary zinc (deficient, marginal, and adequate) and four hormonal conditions; namely, no steriods, norethindrone, mestranol, and norethindrone plus mestranol. The steroids were incorporated into diets and fed to 11-wk-old female Sprague-Dawley rats. After 10 wk of treatment, various tissues were excised for mineral assays by atomic-absorption spectrophotometry. Both steroids, reduced weight gain. Mestranol depressed plasma zinc, tibia copper and magnesium, and liver iron, but elevated the zinc levels in liver and erythrocytes, plasma copper, liver magnesium and calcium, and iron content of tibia and heart. In general, the effect was most prominent with adequate zinc but diminished in magnitude with the reduction of zinc intake. In addition, norethindrone increased heart iron and tibia calcium. Mestranol appeared to be the main causative factor and may have induced a possible shift of minerals from one pool to another. As expected, zinc deficiency resulted in the reduction of zinc concentrations of plasma, tibia, kidney, and pancreas, and the elevation of copper, iron, magnesium, and calcium concentrations of various tissues.     

Effect of feeding a milk replacer to early-weaned pigs on growth, body composition, and small intestinal morphology, compared with suckled littermates

Feeding of milk replacer to early-weaned pigs was evaluated in two experiments. In Exp. 1, 18 litters of pigs were either weaned conventionally (d 21), split-weaned and fed milk replacer plus starter diet (d 14 and 21), or weaned and fed milk replacer plus starter diet (d 21). Split weaning combined with feeding a milk replacer increased ADG 22% from d 14 and d 28 compared to conventional weaning (P < .05). Feeding a milk replacer plus starter diet after weaning increased ADG 30% between d 21 and 28 compared to conventional weaning (P < .01). In Experiment 2, four litters of 12 pigs each were divided at d 18 into six heavy and six light pigs and randomized across sow-suckled, milk replacer, or starter diet groups. After 1 wk, pigs fed milk replacer weighed 20% more (P < .001), contained 10% more protein (P < .01) and 17% more fat (P < .05), and had 74% longer villi in the proximal small intestine (P < .001) than suckled pigs. In contrast, pigs fed starter diet weighed 19% less (P < .001), contained 20% less protein and fat (P < .001), and had 28% shorter villi in the proximal small intestine (P < .05) than suckled pigs. Therefore, milk replacer feeding the 1st wk after weaning stimulates pig development, both locally in the small intestine and on a whole-body basis, most likely by an increased energy and nutrient intake. Suckling beyond 18 d postnatally inhibits pigs to reach maximal potential weight gain. In conclusion, milk replacer feeding might be beneficial to reach maximal pig weight gain at weaning.