Coronary artery plaque morphology in stable angina and subsets of unstable angina: an in vivo intracoronary ultrasound study

Little information is available regarding the in vivo composition of angina producing culprit atherosclerotic lesions in various anginal syndromes. In this study we used intracoronary ultrasound to determine the composition of culprit lesions in various subsets of anginal syndromes and correlated this composition with the patient's clinical presentation. One hundred and forty six patients referred for angioplasty or atherectomy were classified as having either chronic stable angina (angina which was clinically unchanged for >2 months), crescendo angina (an accelerating pattern of frequent or prolonged anginal episodes), severe rest angina (abrupt onset of prolonged angina) or post-infarction angina (angina within 2 weeks of acute myocardial infarction). Intracoronary ultrasound imaging of the culprit lesion was performed before intervention. Lesions were classified as soft, mixed fibrous without calcium, mixed fibrous with calcium or calcified. Analysis of the ultrasound images revealed that the majority of culprit lesions were soft in severe rest (71%) and post-infarction angina (73%) whereas, the majority of culprit lesions were mixed fibrous or calcified in chronic stable (69%) and crescendo (53%) angina (X²=22.73, p= 0.007). In addition, the frequency of intralesional calcium in chronic stable or crescendo angina was significantly higher than that in severe rest or stable angina. We conclude that the composition of culprit lesions in various anginal subsets are different. The lesion morphology in crescendo angina frequently resembles that in chronic stable angina; while those in severe rest and post-infarction angina are frequently similar. These findings may have implications for medical or interventional treatment of patients with angina.     

Distribution of dichlorodiphenyltrichloroethane (DDT) and its metabolites in an Indian waterway

This paper reports on the results of systematic analyses carried out to assess the distribution of dichlorodiphenyltrichloroethane (DDT) and its metabolites, o,p′-DDT, p,p′-DDE, and p,p′-DDD in a tropical waterway, the Cochin Estuarine System. Six sampling stations along the system were studied. Analyses were carried out during premonsoon, monsoon, and postmonsoon seasons. ΣDDT concentrations as high as 55.422 μg L^?1 were detected. The predominant DDT metabolite was found to be p,p′-DDE. During the monsoon season, o,p′-DDT was not detected at any of the sampling Stations. Station 1 (riverine) and station 6 (coastal zone barmouth) emerged as DDT-free zones and the analytical results have enabled the identification of DDT “hot spots” in the estuary. © 1994 by John Wiley & Sons, Inc..     

Monocytosis is associated with the onset of leukocyte and viral infiltration of the brain inchickens infected with the very virulent Marek's disease virus strain C 12/130

Marek's disease (MDV) virus is mainly known for the induction of visceral lymphomas and lymphoidinfiltration of peripheral nerves. Recently, additional tropism for the central nervous system has been recognisedas a distinct feature of disease induced by very virulent MDV isolates. During the analysis of changes in theperipheral blood leukocyte subpopulations in chickens infected with either a virulent (HPRS-16) or a veryvirulent (C12/130) strain of MDV, we observed a marked monocytosis in chickens infected with C12/130.Perivascular cuffing in brain and mononuclear cell infiltration into the meninges of chickens infected with C12/130 were associated with the appearance of the monocytosis from 6-10 days post-infection. Our results showthat a peripheral blood monocytosis may be a contributory factor in establishing or accelerating the severity ofmononuclear infiltration into the meninges and perivascular spaces in the brain during infection by very virulentC12/130 strain of MDV.     

Effect of fluoroacetate on the inhibitory action of ketone bodies and fatty acids on renal ammoniagenesis.

Renal cortical slices from acidotic dogs (NH4CL) were incubated at pH 7.0 with L-glutamine (1 and 5 mM) or L-glutamate (5 mM) with or without DL-beta-hydroxyburyrate 1 mM, acetoacetate 0.5 mM, as well as oleate, palmitate, octanoate, and crotonate 0.5 mM and in the presence or absence of fluoroacetate 0.05 mM. Fluoroacetate alone increased glutamine or glutamate uptake and ammoniagenesis whereas gluconeogenesis rose only when glutamine 5 mM or glutamate were used. Alanine production also rose by 30% when glutamine but not glutamate was used as substrate in the presence of fluoroacetate. Efficient blocking of the Krebs cycle at the aconitase level by fluoroacetate was evidenced by the release of citrate in the incubation medium and by a slight but significant decrease in oxygen consumption (10-20%). The marked decrease in glutamine uptake, ammoniagenesis, and gluconeogenesis induced by ketone bodies and fatty acids was completely corrected by addition of fluoroacetate. The present studies demonstrate that ketone bodies and fatty acids inhibit renal ammoniagenesis and gluconeogenesis in vitro through their oxidation in the mitochondria. They also suggest that direct transamination of glutamine into alanine (glutaminase II pathway) may be significant when oxidation of pyruvate is inhibited by fluoroacetate.     

Platinum concentrations in human autopsy tumor samples

Platinum concentrations were determined in autopsy tumor samples obtained from 27 patients who had received cisplatin 40-1,029 mg/m2 from 0 to 240 days antemortem. Liver metastases had significantly higher platinum concentrations than did tumors in other sites (p less than 0.005). Platinum concentrations in liver metastases were similar to platinum concentrations in normal liver. Platinum concentrations in gliomas and brain metastases were similar to platinum concentrations in other extrahepatic tumors. Platinum concentration generally decreased with increasing distance into brain from tumor. By multiple stepwise linear regression analysis, the factors that were independently most closely associated with tumor platinum concentration were time from last cisplatin treatment, cumulative lifetime dose of cisplatin, route of cisplatin administration (intraarterial vs. other), and site of tumor deposit (liver vs. other) (r = 0.69, p less than 0.001). Patients whose tumors had responded to cisplatin-containing regimens had mean tumor platinum concentrations that were higher than the mean tumor platinum concentrations in patients whose tumors had not responded to cisplatin (p less than 0.05).     

Fatal outcome of group-G streptococcal meningitis (a case report)

An adult woman developed meningitis caused by Group-G streptococci. The organism was successfully isolated both from blood and cerebrospinal fluid of the patient. The woman succumbed to infection despite an appropriate antibiotic therapy.