Evaluation of Lindsley pyroxene thermometer for chondrites

第6回極域科学シンポジウム[OA] 南極隕石11月16日（月）　国立国語研究所 2階 講

Effect of Flowing Water on Sr Sorption Changes of Hydrous Sodium Titanate

Radioactive contaminated water has been generated at the Fukushima Daiichi Nuclear Power station (F1NPS). Hydrous sodium titanate (SrTreat (R)) is able to remove radioactive Strontium (Sr) from this water. Knowing the amount of radioactive nuclides in the used as-received SrTreat (R) is important for effective disposal and deposition of the F1NPS waste. This study investigated changes in the ability of SrTreat (R) to sorb Sr, and to understand the causes of changes in the sorbing. An investigation of the Sr sorption ability of SrTreat (R) is important for calculating the initial radioactive inventory of used SrTreat (R). This study carries out Sr sorption studies with acid-base titrations and X-ray photoelectron spectroscopy (XPS) to characterize the properties. After exposure to simulated treated water for 99 h, the surface structure of the SrTreat (R) was changed, and the percentage of sorbed Sr and the buffer capacity for protons decreased. When the amount of radioactive nuclides contained in the used SrTreat (R) is calculated from the sorption data of the as-received SrTreat (R), the radioactive Sr content will be overestimated with a concomitant increase in the deposition and disposal costs of the used SrTreat (R)

Hepatitis C Virus Infection Increases c-Jun N-Terminal Kinase (JNK) Phosphorylation and Accentuates Hepatocyte Lipoapoptosis

BACKGROUND: Hepatitis C virus (HCV) infection and metabolic diseases including nonalcoholic steatohepatitis (NASH) exhibit a complex interplay. Although free fatty acid-mediated apoptosis is a prominent feature of NASH, the impact of HCV infection on hepatocyte lipotoxicity has remained largely unexplored. The study aimed at identifying whether infection by HCV affected the apoptotic pathway in hepatocytes during fatty acid assault. MATERIAL AND METHODS: OR6 cells, which are derived from human hepatocellular carcinoma Huh-7 cells and harbor a full-length HCV RNA genome replication system, were treated with palmitate. Apoptosis was examined by 4’,6-diamidino-2-phenylindole staining. Activation and expression of JNK, Bim, cIAP-1, and Mcl-1 were examined by immunoblotting. mRNA expression of CHOP, a major player in endoplasmic reticulum stress-mediated apoptosis, was assessed by real-time PCR. RESULTS: Palmitate-induced hepatocyte apoptosis was significantly enhanced in OR6 cells compared to cured cells, in which the HCV genome had been eradicated by treatment with interferon-α. Although basal expression of CHOP mRNA was enhanced in OR6 cells compared to cured cells, it was similarly upregulated in both cell lines following palmitate treatment. Notably, palmitate-induced JNK phosphorylation was accentuated in OR6 cells compared to cured cells. Inhibition of JNK with SP600125 attenuated palmitate-induced apoptosis. Palmitate-mediated upregulation of BH3-only protein Bim, which acts downstream of JNK, was also enhanced in OR6 cells compared to cured cells. In contrast, Mcl-1 and cIAP-1 were equally reduced in OR6 cells and cured cells following palmitate treatment. CONCLUSIONS: These findings suggest that during lipoapoptosis, HCV infection may enhance hepatocyte toxicity by increasing JNK phosphorylation