Acetaldehyde, the end product of oxidative ethanol metabolism, contributes to alcohol-induced disease in the liver, but cannot account for damage in organs such as the pancreas, heart, or brain, where oxidative metabolism is minimal or absent; nor can it account for the varied patterns of organ damage found in chronic alcoholics. Thus other biochemical mediators may be important in the pathogenesis of alcohol-induced organ damage. Many human organs were found to metabolize ethanol through a recently described nonoxidative pathway to form fatty acid ethyl esters. Organs lacking oxidative alcohol metabolism yet frequently damaged by ethanol abuse have high fatty acid ethyl ester synthetic activities and show substantial transient accumulations of fatty acid ethyl esters. Thus nonoxidative ethanol metabolism in addition to the oxidative pathway may be important in the pathophysiology of ethanol-induced disease in humans.
Hantavirus pulmonary syndrome (HPS) is an acute respiratory illness with high mortality. It is caused by a newly described New World hantavirus known as Four Corners virus (FCV). Nearly all cases of HPS have occurred in the western United States. The etiologic agents in those cases have been closely related to each other, based upon comparisons of their genetic sequences. We have molecularly cloned the S genomic segment of a hantavirus (Rl-1) implicated in a case on HPS in the northeastern United States. Nucleotide sequence analysis shows that the Rl-1 virus has many similarities to FCV, but is clearly distinct from the western forms of that virus. These data suggest that HPS can be caused by multiple agents that together form a distinctive evolutionary clade.
The investigation of sudden unexpected death in psychiatric patients and the ensuing litigation has brought to our attention many unusual features important in the evaluation of such deaths. Certain pathophysiologic mechanisms of death, rarely encountered in routine forensic science practice, may be important in determining the cause of death in psychiatric patients, especially in cases where the autopsy is unrevealing. Of particular concern is a tendency in the current literature to implicate phenothiazines as a cause of death when the death investigation and the autopsies are incomplete. Thus, based on our experience and on a review of the current literature, we have set forth factors that the forensic pathologist should consider when faced with a sudden psychiatric death. A case report illustrates these unique aspects of scene investigation and analysis of terminal events and autopsy findings.
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