11 research outputs found
Methadone deaths: a toxicological analysis
Aims—To perform a toxicological analysis of deaths involving methadone and to determine the fatal concentration of methadone in such deaths. Methods—Deaths in which methadone was mentioned in the cause of death were identified. Deaths were divided into those associated with methadone only and deaths in which the cause of death was a combination of methadone and other drugs. Toxicological findings in these deaths were analysed and compared with previously published data. Results—One hundred and eleven cases were analysed. In 55 cases, methadone poisoning was given as the sole cause of death. Fifty victims were adults, age range 17–51 years (median, 23), with five victims under 14 years of age. The mean methadone concentration in the adult deaths was 584 µg/litre (median, 435; range, 84–2700). In 56 cases, age range 15–49 years, (median, 28), death was ascribed to a combination of methadone and other drugs. The mean methadone concentration in these deaths was 576 µg/litre (median, 294; range, 49–2440). In 26 cases, multiple site sampling was performed. This revealed that there could be a 100% discrepancy between methadone concentrations, and other drugs, in samples collected in different sites in the same body. Conclusions—There is an overlap between quoted therapeutic methadone concentrations and methadone concentrations seen in fatalities. However, those dying from methadone poisoning might not be the same as those in a methadone programme. A degree of caution must be exercised in determining a fatal concentration because of the phenomenon of postmortem redistribution. Pathologists and toxicologists need to examine all the available postmortem findings in identifying the cause of death. Key Words: methadone • toxicological analysis • drug overdose • postmortem redistributio
Effect of cigarette smoking, pulmonary inflammation, and lung disease on concentrations of carcinoembryonic antigen in serum and secretions.
Calcium regulation of the secretion of ?-amylase isoenzymes and other proteins from barley aleurone layers
Genomic imprinting: a possible mechanism for the parental origin effect in Huntington's chorea.
Isolation and Characterization of Human Prorenin Secreted from Murine Cells Transformed with a Bovine Papilloma Virus–Preprorenin Expression Vector
Astrocytic and microglial response and histopathological changes in the brain of horses with experimental chronic Trypanosoma evansi infection Resposta astrocĂtica e microglial e alterações histopatolĂłgicas no sistema nervoso central de eqĂĽinos infectados cronicamente com Trypanosoma evansi
This study aimed to characterize astrocytic and microglial response in the central nervous system (CNS) of equines experimentally infected with T. evansi. The experimental group comprised males and females with various degrees of crossbreeding, ages between four and seven years. The animals were inoculated intravenously with 10(6) trypomastigotes of T. evansi originally isolated from a naturally infected dog. All equines inoculated with T. evansi were observed until they presented symptoms of CNS disturbance, characterized by motor incoordination of the pelvic limbs, which occurred 67 days after inoculation (DAI) and 124 DAI. The animals in the control group did not present any clinical symptom and were observed up to the 125th DAI. For this purpose the HE histochemical stain and the avidin biotin peroxidase method was used. Lesions in the CNS of experimentally infected horses were those of a wide spread non suppurative meningoencephalomyelitis.The severity of lesions varied in different parts of the nervous system, reflecting an irregular distribution of inflammatory vascular changes. The infiltration of mononuclear cells was associated with anisomorphic gliosis and reactive microglia was identified. The intensity of the astrocytic response in the CNS of the equines infected by T. evansi characterizes the importance of the performance of these cells in this trypanosomiasis. The characteristic gliosis observed in the animals in this experiment suggests the ability of these cells as mediators of immune response. The parasite, T. evansi, was not identified in the nervous tissues.<br>Este estudo objetivou caracterizar a participação astrocĂtica e microglial no sistema nervoso central (SNC) de eqĂĽinos experimentalmente infectados com T. evansi. O grupo experimental foi formado por machos e fĂŞmeas com vários graus de cruzamentos e idade variando entre quatro e sete anos. Os animais foram inoculados com 10(6) tripomastigotas de T. evansi, originalmente isolada de um cĂŁo infectado naturalmente. Todos os eqĂĽinos inoculados foram observados atĂ© o aparecimento dos sintomas neurolĂłgicos, caracterizados por incoordenação motora dos membros pĂ©lvicos, o qual ocorreu entre 67 e 124 dias apĂłs a inoculação (DPI). Os animais do grupo controle nĂŁo apresentaram sinais clĂnicos e foram observados atĂ© o 125Âş DPI. Para este propĂłsito, foram utilizados os mĂ©todos histoquĂmicos (HE) e imunoistoquĂmicos do complexo avidina-biotina peroxidase (ABC). A lesĂŁo no sistema nervoso central (SNC) dos eqĂĽinos infectados com T. evansi foi caracterizada como meningoencefalomielite nĂŁo supurativa. A gravidade das lesões variou em diferentes segmentos do SNC, refletindo distribuição irregular das alterações vasculares. Infiltrado perivascular e menĂngeo foi associado a gliose anisomĂłrfica e microgliose reativa. A intensidade da resposta astrocĂtica no SNC dos equinos infectados com T. evansi caracteriza a importância da performance destas cĂ©lulas nas tripanossomĂases. A gliose observada nos animais deste experimento sugerem a habilidade destas cĂ©lulas como mediadoras da resposta imune. T. evansi nĂŁo foi identificado no parĂŞnquima do SNC