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Background: Foreign body aspiration (FBA) in childhood is a common and fatal accident. This study aimed to investigate the prevalence and epidemiological characteristics of pediatric patients who have died as a result of foreign body aspiration between 2005-2014 in XXXXXXX/XXXXX. Methods: In this retrospective study, medicolegal reports of pediatric cases who died as a result of foreign body aspiration and were autopsied between 2005 and 2014 and were examined by the xxxxxxx Forensic Medicine Institute. The analysis of the research data was done with the Statistical Package for the Social Sciences Results: A total of 6309 forensic autopsies were performed between the years examined, 0.8% (n=51) of them were child deaths due to foreign body aspiration. The average age of the cases was found to be 2.10 ± 2.90, 90.2% of them are in the 0-4 age range. 60.8% of the cases are male. 82.4% of the aspiration material is vegetative products. In terms of foreign body localization, obstruction was found in both main bronchus distal in 45.1% of the cases. Conclusion: It is thought that increasing the awareness of parents and professional caregivers against foreign body aspiration and having received first aid training may lead to a decrease in the incidence and mortality rates.

To evaluate the histopathological, immunohistochemical, and biochemical effects of liver changes after mancozeb administration.Methods: Rats were divided into groups-the control group (n=7) and the mancozeb group (n=7)-, given 500 mg/kg mancozeb dissolved in corn oil daily for four weeks by an orogastric tube. Caspase-3 and tumor necrosis factor-alpha (TNF-α) primary antibodies were used for immunohistochemical analysis. Results: Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values of the mancozeb group increased significantly than ones of the control group. Venous dilatation, inflammation, hepatocyte degeneration, TNF-α, and caspase-3 expression scores increased significantly in the mancozeb group. In the mancozeb group, intensive caspase-3 expression was observed in hepatocyte cells around the central vein in the center of the liver lobule, and there was an increase in TNF-α expression in the inflammatory cells around the enlarged central vein and Kupffer cells and apoptotic hepatocyte cells. Conclusion: Subacute mancozeb exposure in rats leads to elevated toxicity with impaired liver function, increased inflammation in tissue and increased apoptosis due to cellular damage in the liver, and decreased liver regeneration ability due to congestion and degeneration of blood vessels.

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This study aims to evaluate the changes in brain tissue and blood-brain barrier due to oxidative stress during cadmium (Cd) poisoning by biochemical, histopathological, and immunohistochemical methods. Methods: 170-190 g weighing eight-week-old female Wistar albino rats were divided into two groups (control and experimental), with 7 animals in each group. Experimental group rats were given 2 mg/kg/day powdered cadmium chloride dissolved in water intraperitoneally every day for two weeks. Biochemical, histopathological and immunohistochemical examination was performed. Results: It was seen that brain malondialdehyde (MDA) levels increased significantly, and glutathione (GSH) and catalase activity (CAT) activity levels decreased. In addition to degeneration in some pyramidal cells and glial cells, deformity, and picnosis in the nucleus, dilation of the meninges and cortex vessels, and inflammation around the blood vessels were observed. An increase was found in ionized calcium binding adaptor molecule 1 (IBA-1) expression in microglia cells and degenerative endothelial cells, and increased glial fibrillary acidic protein (GFAP) expression was observed in astrocytes and degenerate neurons. Conclusions: It has been shown that cadmium toxicity may cause microgliosis and astrogliogenesis by inducing cytokine production due to cell degeneration, vascularity, and inflammation in the brain cortex and by affecting microglia, astrocytes cells.