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The article explores death investigation and certification in the U.S. as of 2021, noting how it is governed by a mishmash of laws and officials including medical examiners (MEs), coroners, justices of the peace, districts, sheriff-coroners and prosecutor-coroners. Other topics discussed include the dual purpose of death certificates as a public health document and sources of health data, and the need for better training of physicians in death certification.

The analysis of biological specimens collected at autopsy for the presence of exogenous insulin(s) is of special interest in select death investigations as they may be suspected in the cause of a death. Technical challenges include the limited stability of insulin, and the forensic requirement of differentiating endogenous insulin from pharmaceutical analogs. A novel method was developed for the detection and quantification of human insulin, Glulisine, Lispro, Aspart, Glargine and Detemir in vitreous fluid. An immunoaffinity extraction procedure is performed followed by separation of the insulin α- and β-chains. Liquid chromatography tandem mass spectrometry analysis of the β-chain allows for the unequivocal identification of each insulin analog. The analytical measurement range for each insulin was 0.5–25 ng/mL. The method was evaluated for accuracy, precision, carryover, interferences and stability. Eight vitreous fluid samples collected from cases where untoward insulin use was suspected were subjected to analysis. Positive results were obtained from three samples, and a detailed case history is provided for one of these cases. Even though insulin instability in postmortem biological fluid remains a challenge, this method allows for a reliable forensic-level analysis in vitreous fluid. [ABSTRACT FROM AUTHOR]

The authors now acknowledge that "over 30%" of the "forensic pathologist" cohort were not forensic pathologists. The authors acknowledged that "over 30%" of survey I recipients i were not board certified forensic pathologists, based on "the relative proportion of nonboarded forensic pathologists from the mailing list" that made up the original cohort of 713 survey recipients. A scientific study on the opinions of forensic pathologists must have the entire study cohort be forensic pathologists. [Extracted from the article]

Their survey was of all board-certified anatomic pathologists, not all board-certified forensic pathologists. The survey, however, was sent to 713 anatomic pathologists, not 713 I forensic i pathologists. Forensic pathologists practice a subspecialty; they not only need to be certified in anatomic pathology but also must successfully complete an additional year of training in an accredited forensic pathology fellowship and then must pass a national examination to become a board-certified forensic pathologist. [Extracted from the article]

Limited animal data suggest that the dopaminergic neurotoxin methamphetamine is not toxic to brain (striatal) cholinergic neurons. However, we previously reported that activity of choline acetyltransferase (ChAT), the cholinergic marker synthetic enzyme, can be very low in brain of some human high-dose methamphetamine users. We measured, by quantitative immunoblotting, concentrations of a second cholinergic marker, the vesicular acetylcholine transporter (VAChT), considered to be a 'stable' marker of cholinergic neurons, in autopsied brain (caudate, hippocampus) of chronic users of methamphetamine and, for comparison, in brain of users of cocaine, heroin, and matched controls. Western blot analyses showed normal levels of VAChT immunoreactivity in hippocampus of all drug user groups, whereas in the dopamine-rich caudate VAChT levels were selectively elevated (+48%) in the methamphetamine group, including the three high-dose methamphetamine users who had severely reduced ChAT activity. To the extent that cholinergic neuron integrity can be inferred from VAChT concentration, our data suggest that methamphetamine does not cause loss of striatal cholinergic neurons, but might damage/downregulate brain ChAT in some high-dose users. However, the finding of increased VAChT levels suggests that brain VAChT concentration might be subject to up- and downregulation as part of a compensatory process to maintain homeostasis of neuronal cholinergic activity. This possibility should be taken into account when utilizing VAChT as a neuroimaging outcome marker for cholinergic neuron number in human studies. Synapse 52:223-232, 2004. Published 2004 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]

Animal data suggest that the widely abused psychostimulant methamphetamine can damage brain dopamine neurones by causing dopamine-dependent oxidative stress; however, the relevance to human methamphetamine users is unclear. We measured levels of key antioxidant defences [reduced (GSH) and oxidized (GSSG) glutathione, six major GSH system enzymes, copper­zinc superoxide dismutase (CuZnSOD), uric acid] that are often altered after exposure to oxidative stress, in autopsied brain of human methamphetamine users and matched controls. Changes in the total (n 1/4 20) meth- amphetamine group were limited to the dopamine-rich caudate (the striatal subdivision with the most severe dopamine loss) in which only activity of CuZnSOD (+ 14%) and GSSG levels (+ 58%) were changed. In the six methamphetamine users with severe (- 72 to ) 97%) caudate dopamine loss, caudate CuZnSOD activity (+ 20%) and uric acid levels (+ 63%) were increased with a trend for decreased () 35%) GSH concentration. Our data suggest that brain levels of many antioxidant systems are preserved in methampheta- mine users and that GSH depletion, commonly observed during severe oxidative stress, might occur only with severe dopamine loss. Increased CuZnSOD and uric acid might reflect compensatory responses to oxidative stress. Future studies are necessary to establish whether these changes are associated with oxidative brain damage in human metham- phetamine users. [ABSTRACT FROM AUTHOR]

Objective: Neuroimaging and genetic studies suggest that individual differences in the brain dopaminergic system contribute to the normal variability of human personality (e.g., social detachment and novelty seeking). The authors studied whether presynaptic dopamine function is also associated with personality traits. Method: Presynaptic dopamine synthesis capacity in the brain was measured with positron emission tomography and [[sup 18]F]fluorodopa in 33 healthy adults, and personality traits were assessed with the Karolinska Scales of Personality. Associations were studied by using a linear regression model controlling for the effects of age and gender on both variables. Results: High scores on two of the anxiety-related personality scales, somatic anxiety and muscular tension, and on one aggressivity-related scale, irritability, were significantly associated with Iow [[sup 18]F]fluorodopa uptake in the caudate. No statistically significant associations were observed between [[sup 18]F]fluorodopa uptake and the detachment scale or scales related to novelty-seeking behavior (impulsiveness and monotony avoidance). Conclusions: The results suggest a role for the dopaminergic system in the regulation of anxiety in healthy subjects. Together with previous studies, they also indicate differential involvement of various components of the dopaminergic system in normai and pathological personality traits. [ABSTRACT FROM AUTHOR]