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Cancer‐derived myocardial damage is an important cause of death in cancer patients. However, the development of dietary interventions for treating such damage has not been advanced. Here, we investigated the effect of dietary intervention with lauric acid (LAA) and glucose, which was effective against skeletal muscle sarcopenia in a mouse cachexia model, on myocardial damage. Treatment of H9c2 rat cardiomyoblasts with lauric acid promoted mitochondrial respiration and increased ATP production by Seahorse flux analysis, but did not increase oxidative stress. Glycolysis was also promoted by LAA. In contrast, mitochondrial respiration and ATP production were suppressed, and oxidative stress was increased in an in vitro cachexia model in which cardiomyoblasts were treated with mouse cachexia ascites. Ascites‐treated H9c2 cells with concurrent treatment with LAA and high glucose showed that mitochondrial respiration and glycolysis were promoted more than that of the control, and ATP was restored to the level of the control. Oxidative stress was also reduced by the combined treatment. In the mouse cachexia model, myocardiac atrophy and decreased levels of a marker of muscle maturity, SDS‐soluble MYL1, were observed. When LAA in CE‐2 diet was orally administered alone, no significant rescue was observed in the cancer‐derived myocardial disorder. In contrast, combined oral administration of LAA and glucose recovered myocardial atrophy and MYL1 to levels observed in the control without increase in the cancer weight. Therefore, it is suggested that dietary intervention using a combination of LAA and glucose for cancer cachexia might improve cancer‐derived myocardial damage.  相似文献   
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Journal of Natural Medicines - The root of Angelica acutiloba Kitagawa is an important crude drug in Kampo medicines (traditional Japanese medicine). Chemical evaluation of crude drugs is crucial...  相似文献   
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Mammalian CEP55 (centrosomal protein 55 kDa) is a coiled‐coil protein localized to the centrosome in interphase cells and is required for cytokinesis. A homozygous non‐sense mutation in human CEP55 has been recently identified in perinatal lethal MARCH (multinucleated neurons, anhydramnios, renal dysplasia, cerebellar hypoplasia and hydranencephaly) syndrome. We have isolated zebrafish cep55 mutants defective in head morphology. The zebrafish cep55 gene was expressed in the head including the retina and the pectoral fin at 1 day post‐fertilization (dpf), and extensive cell death was widely observed in the head and tail of the cep55 mutant. In the cep55 mutant, the anterior–posterior distance of the ventral pharyngeal arches was short, and retinal lamination was disorganized. Neural cells, such as islet1‐positive cells and pax2‐positive cells, and fli1b‐positive vascular cells were reduced in the head of the cep55 mutant. Thus, we propose that the zebrafish cep55 mutant is a model organism for human MARCH syndrome.  相似文献   
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We previously characterized the morphological characteristics of malignant pleural mesothelioma (MPM) cells with 9p21 homozygous deletion (HD) using a combination of the virtual microscopy and fluorescence in situ hybridization (FISH). In this study, we investigated whether MPM cells with BRCA1‐associated protein 1 (BAP1) loss show the same morphological characteristics identified in MPM cells with 9p21 HD. MPM cells with either BAP1 loss detected by immunocytochemistry (ICC) or 9p21 HD detected by FISH were identified via virtual microscopy prior to ICC or FISH, followed by analysis and quantification of their morphological characteristics. MPM cells with BAP1 loss or 9p21 HD exhibited significantly more frequent cell‐in‐cell engulfment, multinucleation, and larger multicellular clusters composed of more than 10 cells than reactive mesothelial cells. In conclusion, MPM cells with BAP1 loss or 9p21 HD share similar cytological features, indicating that the same morphological criteria can be used to detect MPM cells harboring such genetic aberrations.  相似文献   
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OBJECTIVES: This study was performed to determine the compositions of commercial temporary restorative resins and to evaluate the leachability of plasticizer and residual monomer from them. METHODS: The chemicals in four commercial temporary restorative resins (Dura Seal, Fit Seal, Plast Seal Quick, and Poly Seal) were detected by GCMS and HPLC. The amounts of plasticizers and residual monomers that leached from cured resin samples immersed in ethanol for 1 h to 14 d were determined by HPLC. RESULTS: Phthalate esters used as plasticizers contained 40-55 wt% either di-n-butyl phthalate (DBP) or butyl phthalyl butyl glycolate. The resin monomer included methyl methacrylate (MMA) or a mixture of MMA and 2-hydroxyethyl methacrylate (HEMA); 1,3-butanediol dimethacrylate was added as a cross-linking agent. Each resin contained 40-60 wt% monomer. The amounts of phthalate esters leached increased with immersion time up to 7 d, reaching 120-190 microg/mg, and did not change subsequently. The residual monomers leached gradually for up to 3d and did not change subsequently. The amount of leached residual monomer (MMA, HEMA) was 20-90 microg/mg after 3d storage. More than 50% of the leachable plasticizers and monomers were eluted from the cured resins within 24 and 3 h, respectively. CONCLUSIONS: The amounts of leached plasticizers and residual monomers were extremely large compared with the concentrations of endocrine disrupters and their potentially genotoxic effects. Therefore, it is very important to evaluate the leachability of these compounds from temporary restorative resins.  相似文献   
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