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We measured concentrations of cocaine and its major metabolites (benzoylecgonine, ecgonine methylester, norcocaine, and cocaethylene) in 15 autopsied brain regions of 14 human chronic cocaine users. Only slight differences were observed in concentrations of cocaine and its metabolites amongst the examined brain areas. Although it is likely that some postmortem redistribution of the drug must have occurred, our data are consistent with the possibility that behaviorally relevant doses of cocaine are widely distributed throughout the brain of humans who use the drug on a chronic basis. Consideration should therefore be given to the possible pharmacological and toxicological actions of cocaine in both striatal and extra-striatal brain areas in human users of the drug.

Unexpected deaths related to significant hepatopathology are encountered daily by forensic pathologists. After investigation, a decision will be made regarding whether or not to perform an autopsy. In considering the options available to assess the degree of hepatopathology, a study was undertaken to evaluate the potential role of percutaneous core biopsy of the liver at the time of postmortem examination. Postmortem percutaneous hepatic core biopsy was attempted at the time of external examination in 28 nonconsecutive cases examined at the Office of the Chief Medical Examiner, State of Maryland; hepatic tissue was obtained in 26 cases. In 21 of these cases, hepatic tissue was obtained during subsequent partial or complete autopsy and submitted for histologic correlation. There was complete histologic correlation of tissue obtained via percutaneous biopsy with hepatic tissue obtained by open biopsy in 18 of 20 cases (86%). Significant hepatopathology was identified by core biopsy in 5 of 9 cases (56%) with a history of ethanol abuse and in 8 of 19 cases (42%) with a negative ethanol history. The sensitivity of this technique was 82% and the specificity was 100%. This study has shown that core biopsy of the liver can provide information related to the cause of death in cases with and without a history of alcohol consumption. In cases in which a complete autopsy is deferred because of familial religious objections, infectious disease, or time/budgetary constraints, this modality can be used to obtain diagnostic tissue.

Arrhythmogenic right ventricular cardiomyopathy is emerging as a relatively common cause of exercise-induced sudden death in the young. The diagnostic criteria at autopsy are, however, not fully established, leading to both over-and underdiagnosis. We report a young man and a young woman dying suddenly of right ventricular dysplasia during exercise, in whom the gross autopsy findings in the right ventricle were minimal or even absent. However, the histologic features in both right and left ventricles were typical of the disease, and consisted of fibrofatty infiltrates with typical myocyte degeneration of the right ventricle and subepicardial regions of the left ventricle. These cases illustrate that microscopic findings are diagnostic and may be present in the absence of gross findings. Marked fat replacement is not essential for the diagnosis of right ventricular dysplasia, and the right ventricle should be extensively sampled histologically in all cases of sudden unexpected death, especially those that are exercise related.

ABSTRACT: Five enzymes were measured in 50 liver specimens (18 normal liver, 20 Reye liver, 12 diverse liver disorders other than Reye syndrome). The enzymes were: glutamic dehydrogenase (E.C. 1.4.1.3), monoamine oxidase (E.C. 1.4.3.4), lactate dehydrogenase (E.C. 1.1.1.27), DgIucose- 6-phosphate dehydrogenase (E.C. 1.1.1.49), catalase (E.C. 1.11.1.6). The Reye syndrome group showed significant decreases in glutamic dehydrogenase (56%) and monoamine oxidase (70%) compared to normal control tissue and these changes were not characteristic of the non-Reye liver disorder group as a whole. Neither catalase nor lactate dehydrogenase appeared to be altered significantly in the Reye or in the abnormal control group compared with normal controls. Thus, only the prominent decreases in the mitochondrial enzyme activities appeared to be highly characteristic of Reye syndrome. Paradoxically, the means of the five hepatic enzymes and the admission levels of two serum enzymes indicative of liver damage (alanine and aspartate aminotransferase) were remarkably similar for both survivors and nonsurvivors of Reye syndrome.

Five enzymes were measured in 50 liver specimens (18 normal liver, 20 Reye liver, 12 diverse liver disorders other than Reye syndrome). The enzymes were glutamic dehydrogenase (E.C. 1.4.1.3), monoamine oxidase (E.C. 1.4.3.4), lactate dehydrogenase (E.C. 1.1.1.27), DgIucose- 6-phosphate dehydrogenase (E.C. 1.1.1.49), catalase (E.C. 1.11.1.6). The Reye syndrome group showed significant decreases in glutamic dehydrogenase (56) and monoamine oxidase (70) compared to normal control tissue and these changes were not characteristic of the non-Reye liver disorder group as a whole. Neither catalase nor lactate dehydrogenase appeared to be altered significantly in the Reye or in the abnormal control group compared with normal controls. Thus, only the prominent decreases in the mitochondrial enzyme activities appeared to be highly characteristic of Reye syndrome. Paradoxically, the means of the five hepatic enzymes and the admission levels of two serum enzymes indicative of liver damage (alanine and aspartate aminotransferase) were remarkably similar for both survivors and nonsurvivors of Reye syndrome.

The effect of microstructural refinement on the oxidation behavior of γ + laves Ti-45Al-15Cr and γ + σ Ti-40Al-27Nb was investigated. A fine, uniform γ + laves microstructure in Ti-45Al-15Cr resulted in protective alumina scale formation over most of the sample surface at 800°C and 1000°C in air. In contrast, the oxidation resistance of this same alloy was severely degraded by a coarse γ + laves microstructure. The oxidation behavior of Ti-40Al-27Nb at 1200°C in air was poor. Refinement of the γ + σ microstructure in this alloy was not effective in improving oxidation resistance. The mechanistic reasons for these effects, and the implications for improved oxidation resistance through microstructural refinement are discussed.

The mechanism of sudden cardiac death in patients with mitral valve prolapse is poorly understood. Twenty-four hearts from patients with mitral valve prolapse who suddenly died (mean age 34 +/- 8 years) and 16 trauma control hearts (mean age 30 +/- 7 years) were histologically studied. Dysplasia of the atrioventricular nodal artery was present in 18 of 24 hearts with mitral valve prolapse and four of 16 controls hearts ( p = 0.003). The degree of luminal narrowing, as morphometrically measured, was significantly greater in hearts with mitral valve prolapse ( p = 0.003). The degree of fibrosis in the base of the ventricular septum, as calculated by computerized morphometry, was greater in hearts with mitral valve prolapse ( p = 0.0002) and independent of age, sex, and heart weight ( p = 0.005). We conclude that arterial dysplasia in mitral valve prolapse may contribute to sudden cardiac death mediated by ventricular fibrosis. (AM Heart J 1997;134:282-91.)

Toxicological and pathological findings are described in fatalities involving pentazocine (Talwin®) and tripelennamine (Pyribenzamine®). Procedures using thin-layer chromatography, gas chromatography, ultraviolet spectrophotometry, and spectrophotofluorometry are described, as well as the quantitative analysis of biological specimens of drug abuse and homicide victims. Microscopic findings in lung specimens from drug abuse deaths are also described.

Abstract: A commercial superalloy, PWA 1480, was annealed in hydrogen at 1000 � to 1300 � in order to remove a 10 ppmw sulfur impurity. This treatment was very successful above 1200 �, resulting in residual sulfur contents below 0.1 ppmw. The degree of scale adhesion in subse-quent 1100 � cyclic oxidation tests was inversely related to residual sulfur content. Control of adhesion by desulfurization in the absence of reactive elements supports an adhesion mechanism based on oxide-metal bonding weakened by sulfur segregation. Attempts at sulfur purging and improving adhesion by repeated oxidation/polishing were not successful, in contrast to previous studies on NiCrAl.

The transient oxidation of β-NiAl in air at 800 °C and 1100 °C has been studied using electron microscopy. The oxide scale consists predominatly of metastable Al2O3phases. θ-Al2O3is the major oxide phase within 10.0 hr of oxidation at 800 °C and 0.1 hr at 1100 °C. The scales form epitaxially on (001)βand (012)βspecimens throughout the transient stage, whereas the degree of preferred oxide orientation decreases with oxidation time on (011)βand (111)βspecimens. The orientation relationships reflect the small mismatch between parallel close-packed directions in the metal and in the cation sublattice of the oxides. The correlation of distinctive oxide surface morphologies with internal structural defects indicates the strong tendency of the Al2O3scale to growviashort-circuit diffusion paths.

It is shown that molten salts such as Na2CO3or Na2SO4create two types of pitting attack in SiC: attack at structural discontinuities and formation of larger, crater‐like pits.

In the past, hemlock poisoning was only known for its neurotoxic effects; quite recently non-neurological features, consisting of rhabdomyolysis and acute renal failure, have been also described. Here we report our experience with these clinical findings, which we frequently observe in accidental hemlock poisoning. Between 1972 and 1990 we studied 18 patients: 17 of them were poisoned by conline (an alkaloid of Conium maculatim) in Apulia (Italy), and one by cicutoxin (the active principle of water hemlock) in New Mexico (USA). In the non-rapidly-fatal cases we tested myoglobinuria, serum muscle enzymes, and renal function. In the patients with acute renal failure we performed microscopical examination of kidney specimens; immunohistochemistry was carried out to identify myoglobin and actin in tubules. Coniine was detected in urine, serum, or tissues. Neurological features were present in all of our cases: coniine had a curare-like effect on the neuromuscular junction, whereas cicutoxin was convulsant on the central nervous system. In addition rhabdomyolysis was noted in the 17 subjects poisoned by coniine. Acute renal failure was observed in five patients; it was confirmed by histological evidence of tubular necrosis with intratubular deposition of myoglobin and actin released by rhabdomyolysis. Our cases seem to be the first with histopathologically proven acute tubular necrosis in coniine intoxication. In conclusion, in hemlock poisoning neurotoxic manifestations may be accompanied by rhabdomyolysis and acute tubular necrosis; increased awareness of these clinical features is recommended in order to improve the diagnostic and therapeutic procedure.

Hot corrosion of sintered α‐SiC by thin films of Na2SO4and Na2CO3molten salts at 1000 °C, the type that most likely occurs in a turbine engine, reduces the strengths at 20 °C by as much as 50%.