BackgroundSudden bath-related deaths occur frequently in Japan, particularly among elderly people. However, the precise mechanism of bath-related death remains uncertain, and effective prevention strategies have not been established.MethodsCases of bath-related deaths (n = 3289) were selected from all cases handled by the Tokyo Medical Examiner’s Office from 2009 to 2011 (N = 41 336). The ages and occurrence dates were examined, and major autopsy findings, including toxicological analysis, were evaluated for the autopsied cases (n = 550).ResultsMost cases occurred in individuals older than 60 years of age during winter. Analysis of autopsy findings revealed water inhalation signs in many cases (n = 435, 79.1%). Circulatory system diseases constituted more than half of the pathological findings regarding factors that may have contributed significantly to death (n = 300, 54.5%), and cardiac lesions were the most common pathological finding (n = 250, 45.5%). However, approximately one-third of the cases exhibited no remarkable pathological findings (n = 198, 36.0%). A quarter of all cases involved blood ethanol levels that exceeded 0.5 mg/mL (n = 140).ConclusionsThe results suggested that drowning plays an important role in the final process of bath-related death. Circulatory system diseases may be the primary underlying pathology; however, there were variations in the medical histories and pathologies of cases of bath-related death. From a preventive perspective, family members should pay attention to elderly people with circulatory system diseases during bathing, particularly in winter. Additionally, the notion that ill or inebriated individuals should not take baths should be reinforced.
Abstract. Des-Á-carboxy prothrombin (DCP) is an established HCC tumor marker, but the precise mechanism of its production is still unclear. Recently, we demonstrated that cytoskeletal changes during epithelial-to-fibroblastoid conversion (EFC) or epithelial mesenchymal transition (EMT) induced by chemicals plays a critical mechanistic role in DCP production via impairment in vitamin K uptake. Our proposed mechanism of DCP production is consistent with substantial clinical evidence. Supplementary vitamin K2 analogues reduced serum DCP levels in hepatocellular carcinoma (HCC) patients. HCC patients with high serum DCP are associated with vascular invasion, metastasis and tumor recurrence. On the other hand, hypoxia has been reported to induce EMT or cytoskeletal changes. Therefore, we examined whether hypoxia induced DCP production during EFC or EMT in HCC cells. Indeed, hypoxic stimulation induced hepatoma cell lines (HepG2 or PLC/PRF/5 cells) to undergo EFC or EMT and these cells produced DCP. Immunofluorescence study demonstrated that hypoxic stimulation impaired labeled low-density lipoprotein uptake, which was a surrogate for vitamin K uptake. In addition, fine filamentous actin network, which has crucial role for clathrin-mediated endocytosis of vitamin K, was disrupted in DCP producing cells by hypoxic stimulation. Thus, hypoxic stimulation induced HCC cells to produce DCP in the same mechanism as chemicals. Furthermore, immunohistochemical study using surgically resected HCC samples showed that a positive staining of nuclear hypoxia inducible factor (HIF)-1· was more frequently observed in HCC cells with stronger staining intensity of DCP. Importantly, clinical observations that DCP as an HCC tumor marker was more useful in larger tumors, which is likely to be exposed with hypoxia during tumor development, support our results.
Abstract. Des-gamma-carboxy prothrombin (DCP) is a well-established tumor marker for hepatocellular carcinoma (HCC), but the precise mechanism by which HCC cells produce DCP remains unknown. Our preliminary experiments demonstrated that HepG2 cells with chemical induction of epithelial-to-fibroblastoid conversion (EFC) produced DCP through impairment of vitamin K uptake via cytoskeletal rearrangement. Therefore, in this study we further examined this mechanism in vitro and using human HCC samples. Hepatoma cell lines (HepG2 and PLC/PRF/5) were induced EFC or epithelial-mesenchymal transition (EMT) by phorbol 12-myristate 13 acetate (TPA) or transforming growth factor (TGF)-ß1. We analyzed these cells by ELISA, Western blotting and immunofluorescent studies. We also examined DCP production and E-cadherin expression in human surgically resected HCC samples by immunohistochemical studies. Labeled low-density lipoprotein (LDL) uptake (as a surrogate for vitamin K) was significantly impaired in DCP-producing hepatoma cells following induction of EFC or EMT. Further, filamentous actin, which plays a critical role in clathrinmediated endocytosis, was dissociated in DCP-producing cells. Latrunculin A, an actin depolymerizer, induced naïve hepatoma cells to produce DCP with impairment of labeled-LDL uptake. In addition, an E-cadherin neutralizing antibody did not induce DCP production. Finally, immunohistochemical studies demonstrated that DCP production was inversely correlated with the intensity of E-cadherin expression in human HCC cells. In conclusion, cytoskeletal changes during EFC or EMT plays a critical mechanistic role in DCP production via impairments in vitamin K uptake.
SynopsisIn order to reduce the internal stress in a cured epoxy resin, the submicron polymer particles were dispersed therein prior to curing. For this purpose, four kinds of poly(buty1 acrylate)/ poly(methy1 methacrylate) core-shell particles were prepared by seeded emulsion polymerization for methyl methacrylate with poly(buty1 acrylate) seed particles having different particle diameter, and subsequently were powdered by drying at room temperature. It was observed by SEM that poly(buty1 acrylate) particles as core were dispersed in the cured epoxy matrix. Poly(methy1 methacrylate) as shell seems to dissolve in the matrix. The internal stress of cured epoxy resin decreased with the modification of the particles and the tendency was enhanced with a decreasing in the particle diameter.
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