Study on solidification of immisible alloys (M-10)

Alloying of immiscible alloys under microgravity is of interest in metallurgical processes. Several experiments investigating the alloying of immiscible alloys, such as Al-In, Al-Bi, Zn-Bi, and Zn-Pb, were done in space. Homogeneous distribution of small L2 particles in the matrix, such as an emulsion structure, was expected in the space-solidifed alloys. However, the alloys demonstrated an extremely segregated structure. To date insufficient information was obtained to explain these unexpected results. Our experiment was proposed to clarify the solidification manner of immiscible alloys and to obtain fundamental information concerning structural control of the alloys. In space, density differences between the two liquids separated in immiscible regions can be neglected, so that no sedimentation of L(sub 2) phase will take place. When the growth of the alloys is interrupted and this status is frozen by an adequate rapid cooling procedure, it will provide much information concerning decomposing homogeneous liquid and the interaction between the monotectic growth front morphology and the distribution of L(sub 2) phase. It is anticipated that the results will be useful for elucidating the monotectic solidification manner and it will be instructive to explain the segregated structures obtained in the past space experiments

SOCS1 Is a Suppressor of Liver Fibrosis and Hepatitis-induced Carcinogenesis

Hepatocellular carcinomas (HCCs) mainly develop from liver cirrhosis and severe liver fibrosis that are established with long-lasting inflammation of the liver. Silencing of the suppressor of the cytokine signaling-1 (SOCS1) gene, a negative regulator of cytokine signaling, by DNA methylation has been implicated in development or progress of HCC. However, how SOCS1 contributes to HCC is unknown. We examined SOCS1 gene methylation in >200 patients with chronic liver disease and found that the severity of liver fibrosis is strongly correlated with SOCS1 gene methylation. In murine liver fibrosis models using dimethylnitrosamine, mice with haploinsufficiency of the SOCS1 gene (SOCS1−/+ mice) developed more severe liver fibrosis than did wild-type littermates (SOCS1+/+ mice). Moreover, carcinogen-induced HCC development was also enhanced by heterozygous deletion of the SOCS1 gene. These findings suggest that SOCS1 contributes to protection against hepatic injury and fibrosis, and may also protect against hepatocarcinogenesis