[Analgesic effect of McN-2783 (Zomepirac sodium) for postextraction pain].
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Biomedical subjects
Publications and source records attributed to R Takagi.
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1. Two phospholipase activities, provisionally designated as phospholipase activity I and phospholipase activity II, were found to be present in the mucosal homogenates of rat small intestine. These phospholipase activities were present in the membraneous particle fraction and were characterized in this study without further purification, using phosphatidylcholine as a substrate. Phospholipase activity I was assayed at pH 5.9 in the absence of deoxycholate, whereas phospholipase activity II was assayed at pH 9.4 in the presence of deoxycholate. Phospholipase activity I was more easily inactivated by heat treatment and trypsin digestion than phospholipase activity II. Both phospholipase activities were inhibited by diisopropyl-fluorophosphate but not by SH-binding reagents. 2. Phospholipase activity I had a pH optimum at 5.9. A sigmoid curve was obtained when the amount of the enzyme preparation was plotted against the phospholipase activity I. The unusually low activity found at low enzyme concentrations was enhanced by addition of the heat-inactivated enzyme preparation to a level where a linear relationship was found between the amount of enzyme and the activity. The effector present in the enzyme preparation was tentatively identified as fatty acid(s). The addition of oleic acid or linoleic acid to the incubation mixture enhanced the phospholipase activity I. At 1 mM levels of these fatty acids the highest activity was obtained when 1.5 mM phosphatidylcholine was used as a substrate. 3. The phospholipase activity II increased on addition of deoxycholate. In the presence of 5 mM deoxycholate, a pH optimum was found at 9.6. It was found that the maximal extent of hydrolysis of phosphatidylcholine in the incubation mixture was dependent on the concentration of deoxycholate. This indicates that deoxycholate facilitates the action of phospholipase activity II, presumably by forming deoxycholate-phosphatidylcholine mixed micelles. Phospholipase activity II was found to deacylate specifically the 2-acyl moiety of phospholipids.
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Invasive pulmonary aspergillosis (IPA) has been recognized as an infectious complication in immunocompromised patients. We present a case of IPA, which occluded the descending aorta and left pulmonary artery and led to death after antileukemic chemotherapy. Contrast-enhanced CT demonstrated thrombi in the great vessels as low attenuation areas. These thrombi became extensive despite intensive antibiotic and antifungal therapy. Microscopic examination revealed that the thrombi contained aspergillus hyphae, and occlusions of both great vessels were induced by direct extension of aspergillus. This case illustrates that IPA can be the cause of great vessel occlusion in immunocompromised patients. We describe the CT and autopsy findings of this case and emphasize the virulence of this fungus.
PURPOSE: To examine whether there is any interaction between non-ionic contrast medium and prostaglandin E1 incorporated in lipid microspheres (Lipo-PGE1) in direct and non-direct mixing. MATERIALS AND METHODS: Iopamidol 300 and 370 mgI/ml, iohexol 300 and 350 mgI/ml, and iopromide 300 and 370 mgI/ml were mixed with Lipo-PGE1. In the direct mixing test, both agents were mixed directly in a tube. The appearance of the mixture, average size of the Lipo-PGE1 particles, and changes in pH were observed. In the non-direct mixing test, both agents were poured one after the other into a narrow luminal glass tube. The appearance of the mixture was observed. Lipo-PGE1 and the contrast agent were discharged sequentially via a catheter placed in 5 L of physiological saline. The appearance of the physiological saline was observed. RESULTS: In the direct mixing test, no interaction was observed between iopamidol, iohexol, or iopromide 300 mgI/ml and Lipo-PGE1. Aggregation and creaming were observed in the mixture of iopromide 370 mgI/ml and Lipo-PGE1, and average particle size increased over time. However, there was no apparent change in pH. In the non-direct mixing test, none of the test contrast agents interacted with Lipo-PGE1. CONCLUSION: The test non-ionic contrast media, even if they interacted with Lipo-PGE1 when mixed directly, did not appear to interact with Lipo-PGE1 when mixed in a non-direct manner, which represents the clinically used prescription in pharmacoangiography.