Research conducted previously has demonstrated that apoptosis significantly influences the chicken quality. While ROS are acknowledged as significant activators of apoptosis, the precise mechanism by which they influence muscle cell apoptosis in the post-mortem remains unclear. In this study, chicken samples were treated with rosemarinic acid and H2O2 to induce varying ROS levels, and the ROS-triggered apoptosis mechanism in chicken muscle cells in post-mortem was analyzed. The TUNEL results revealed that elevated ROS levels in chicken were associated with a greater degree of muscle cell apoptosis. Western-blot results suggested that sarcoplasmic ROS could initiate apoptosis through the mitochondrial pathway by activating the MAPK-JNK signaling pathway. Moreover, TEM and shear force results demonstrated that muscle cell apoptosis initiates myofiber fragmentation and structural damage to sarcomeres, ultimately reducing chicken tenderness. This study enhances our understanding of post-mortem muscle cell apoptosis, providing valuable insights for regulating chicken quality.

A medical examiner (ME) system was introduced to England and Wales in 2019 intended to ensure appropriate notification of cases to HM Coroner (HMC). The aim of the study is to determine and compare: (a) the nature of notifications to HMC for Norfolk from the Norfolk and Norwich University Hospital (NNUH) in 2018 compared with 2022; (b) to determine the outcome of those notifications and (c) to establish patterns of change in the number and nature of such notifications. HMC and ME datasets were interrogated to determine differences between notifications to HMC and outcomes in 2018 compared with 2022. From deaths at NNUH (2018 - n  =  2605; 2022 - n  =  2969), there were significantly fewer HMC notifications in 2022 compared with 2018 (25.3% vs. 17.6%). A decrease in notifications was noted for persons undergoing any \'treatment or procedure of a medical or similar nature\' (24.0% vs. 16.2%) p < 0.0014. An increase in notifications was noted for neglect, including self-neglect (3.3% vs. 12.2%) p < 0.001. Of the coronial outcomes, there were significant increases in the numbers of post-mortem (PM) examinations (29.3% vs. 35.5%) p  =  0.0276 and inquests (26.0% vs. 31.4%) p  =  0.0485). There was a significant decrease in no further action by HMC (5.7 vs. 2.3) p  =  0.0485. The study shows that the introduction of the medical examiner service has resulted in significant change in the nature of HMC notification categories. The notifications appear to be more appropriate, with an increased proportion of inquests and PM examinations and with a reduction in 100 A or \'no further action\' outcomes.

While postmortem (PM) toxicology results provide valuable information towards ascertaining both the cause and manner of death in coronial cases, there are also significant difficulties associated with the interpretation of PM drug levels. Such difficulties are influenced by several pharmacokinetic and pharmacodynamic factors including PM redistribution, diffusion, site-to-site variability in drug levels, different drug properties and metabolism, bacterial activity, genetic polymorphisms, tolerance, resuscitation efforts, underlying conditions, and the toxicity profile of cases (i.e. single- or mixed-drug toxicity). A large body of research has been dedicated for better understanding and even quantifying the influence of these factors on PM drug levels. For example, several investigative matrices have been developed as potential indicators of PM redistribution, but they have limited practical value. Reference tables of clinically relevant therapeutic, toxic, and potentially fatal drug concentrations have also been compiled, but these unfortunately do not provide reliable reference values for PM toxicology. More recent research has focused on developing databases of peripheral PM drug levels for a variety of case-types to increase transferability to real-life cases and improve interpretations. Changes to drug levels after death are inevitable and unavoidable. As such, guidelines and practices will continue to evolve as we further our understanding of such phenomena.

In infantile abusive head injury (AHT), subdural haemorrhage (SDH) is commonly held to result from traumatic damage to bridging veins traversing from the surface of the brain to the dura and dural venous sinuses. However, there are limited published radiological or autopsy demonstrations of ruptured bridging veins and several authors also assert that bridging veins are too large to rupture due to the forces associated with AHT. There have been several studies on the size, locations and numbers of adult bridging veins and there is one small study of infant bridging veins. However, there are no microscopic studies of infant bridging veins and only a select few ultrastructural investigations of adult bridging veins. Hitherto, it has been assumed that bridging veins from infants and younger children will display the same anatomical characteristics as those in adulthood. At 19 neonatal, infant and young child post-mortem examinations, we macroscopically examined and sampled bridging veins for microscopy. We compared the histology of those samples with bridging veins from an older child and two adults. We demonstrate that adult bridging veins are usually surrounded by supportive meningeal tissue that appears to be lacking or minimally present around the bridging veins of younger children. Neonatal, infant and young children\'s veins had a free \'bridging\' section. Neonatal and infant bridging veins had smaller diameter ranges and thinner walls (some only 5-7 µm) than those seen in older children and adults. Bridging vein walls contained both fine strands of elastic fibers and a more pronounced elastic lamina. The presence of an elastic lamina occurred more frequently in the older age groups These anatomical differences between the veins of adults and young children may help to explain apparent increased vulnerability of neonatal/infant bridging veins to the forces associated with a shaking-type traumatic event.

A 6-month-old male intact miniature Australian Shepherd presented for surgical consultation for a previously diagnosed patent ductus arteriosus. Echocardiogram revealed a patent ductus arteriosus and a hyperechoic oscillating lesion within the main pulmonary artery. Blood cultures and eventual post-mortem examination revealed Candida tropicalis endocarditis. This case report highlights a rare case of fungal endocarditis with both echocardiographic and post-mortem findings.

Zolpidem, N,N-dimethyl-2-[6-methyl-2-(4-methylphenyl)imidazo[1,2-a]pyridin-3-yl]acetamide, is a hypnotic agent widely used in clinical practice but is detected in many clinical cases of fatal intoxication and suicide. In forensic toxicology, the precise determination of zolpidem concentration in blood is a must to provide concrete evidence of death by zolpidem poisoning. However, the concentrations of zolpidem in blood at autopsy often differ from those at the estimated time of death. In the present study, we found that zolpidem was degraded by hemoglobin (Hb) via the Fenton reaction at various temperatures. The mechanism underlying zolpidem degradation involved the oxidation of its linker moiety. The MS and MS/MS spectra obtained by liquid chromatography quadrupole-Orbitrap mass spectrometry (LC-Q-Orbitrap-MS) showed the formation of 2-hydroxy-N,N-dimethyl-2-(6-methyl-2-(p-tolyl)imidazo[1,2-a]pyridin-3-yl)acetamide (2-OH ZOL) in Hb/H2O2 solution incubated with zolpidem and in the blood of several individuals who died from ingestion of zolpidem. These results suggest that 2-OH ZOL is the post-mortem product of zolpidem degradation by Hb via the Fenton reaction.

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BACKGROUND: The article is one of the very first autopsy reports worldwide, which associates COVID-19 infection and pulmonary fat embolism.
OBJECTIVE: To point to a crucial connection between a severe acute respiratory syndrome caused by coronavirus 2 (SARS-CoV-2) infection and pulmonary fat embolism as one of the possible major mechanisms of severe COVID-19 symptoms.
METHODS: Lung, brain and kidney tissues examination of 16 full human autopsy cases. All deceased suffered from COVID-19 infection, none of them was admitted to hospital prior to death, immediate causes of death vary. Autopsies accompanied by microbiological examination and histological examination using Oil Red O staining were performed. Consequently, we have implemented a control cohort consisting of 16 deceased with no presence of pulmonary infection and various immediate causes of death.
RESULTS: Of the 16 autopsy cases, 11 (68.8%) were males and 5 (31.3%) females, with overall mean age 68.1 (39-86) years. Causes of death of studied subjects were natural, mostly from respiratory failure (in 12 cases, 75%). Cardiopulmonary resuscitation was performed in 7 cases (43.8%). None of dissected persons had larger signs of body trauma. Pulmonary fat embolism was found in 11 cases (68.8%), which generalised to kidneys in 8 patients (50% of all cases, 72.3% of cases with pulmonary fat embolism) and to brain tissue in 1 case.
CONCLUSIONS: We demonstrated a reasonable relation between a COVID-19 disease and a variously severe fat embolism, severity of which does not directly correlate with body weight. Further investigation or even change of medical treatment needs to be considered in patients with COVID-19.

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Investigating the causes of Sudden cardiac death (SCD) is always difficult; in fact, genetic cardiac conditions associated with SCD could be \"silent\" even during autopsy investigation. In these cases, it is important to exclude other aetiology and assist to ask for genetic investigations. Herein, the purpose of this review is to collect the most-implicated genes in SCD and generate a panel with indications for first line and second line investigations. A systematic review of genetic disorders that may cause SCD in the general population was carried out according to the Preferred Reporting Item for Systematic Review (PRISMA) standards. We subsequently listed the genes that may be tested in the case of sudden cardiac death when the autopsy results are negative or with no evidence of acquired cardiac conditions. To make genetic tests more specific and efficient, it is useful and demanded to corroborate autopsy findings with the molecular investigation as evident in the panel proposed. The genes for first line investigations are HCM, MYBPC3, MYH7, TNNT2, TNNI3, while in case of DCM, the most implicated genes are LMNA and TTN, and in second line for these CDM, ACTN2, TPM1, C1QPB could be investigated. In cases of ACM/ARVC, the molecular investigation includes DSP, DSG2, DSC2, RYR2, PKP2. The channelopathies are associated with the following genes: SCN5A, KCNQ1, KCNH2, KCNE1, RYR2. Our work underlines the importance of genetic tests in forensic medicine and clinical pathology; moreover, it could be helpful not only to assist the pathologists to reach a diagnosis, but also to prevent other cases of SCD in the family of the descendant and to standardise the type of analysis performed in similar cases worldwide.