Phase diagram and magnetic properties of Co₂ (Cr_1–xMn_x) Ga Heusler alloys were experimentally established. Single phase was obtainable in the entire composition range, 0 ≤ x ≤ 1.0. Order–disorder phase transition temperature from L2₁ to B2 phase (T_t^L21/B2) and the Curie temperature (T_C) increased with increase of Mn composition, in other words, with increase of number of valence electrons (Z_t). The behavior of T_C is general trend in the Co-based Heuselr alloys that were systematically investigated previously, whereas the concentration dependence of T_t^L21/B2 doesn't follow the Bragg–Williams–Gorsky approximation in Co₂ (Cr_1–xMn_x) Ga alloys. Spontaneous magnetization also increases with increase of Z_t with following the generalized Slater–Pauling rule, suggesting that the half-metal-type electronic structure is comparatively kept in the system.

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Cellular senescence is known to be the state of permanent cell cycle arrest. It is induced by a variety of potentially oncogenic stimuli and has therefore long been believed to suppress tumorigenesis, acting as a guardian of tissue homeostasis. However, recent evidences revealed that senescent cells also promote the secretion of inflammatory cytokines, chemokines, growth factors and matrix remodelling factors. These factors can alter the local tissue environment and contribute to some beneficial effects, such as tissue repair, but also to deleterious effects, such as chronic inflammation and cancer development, depending on the biological context. This newly identified senescence phenotype, termed the senescence-associated secretory phenotype (SASP), can be induced by DNA damage that promotes the senescence cell cycle arrest. These senescence-associated secreted factors are involved in homeostatic disorders, such as cancer. Our recent study focused on obesity-associated pathological conditions, and particularly on the link between obesity and liver cancer. We found that the obesity-induced gut microbial metabolite triggered the senescence and SASP of hepatic stellate cells through enterohepatic circulation that contribute to the formation of tumor-promoting microenvironments. These results suggest the role of the senescence-associated secretome in cancer-associated microenvironments in obesity-associated liver cancer.

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Hedgehog (Hh) signaling pathway has crucial roles in embryonic development, cell maintenance and proliferation, and is also known to contribute to cancer cell growth. To understand Hh signaling more precisely and find a seed of drug for treatment of cancer, Hh inhibitors have been targeted. Our group constructed cell based assay using tetracycline regulated (T-Rex) system for Hh/GLI-mediated transcriptional inhibitors. Naturally occurring Hh inhibitors such as physalins, caldenolides and flavonoid glycosides were isolated by this screening assay.

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Copolymer particles for removal of endotoxins (lipopolysaccharides; LPS) were prepared by suspension copolymerization of γ-cyclodextrin (CyD) and 1, 6-hexamethylenediisocyanate. The LPS-removing activity of the copolymer particles was compared with that of poly (ε-lysine) -Cellufine (cationic adsorbent) by a batch method. LPS-removing activity of the cationic adsorbent was unsatisfactory because both the DNA and the LPS were adsorbed at pH 6.0, ionic strength of μ=0.05-0.8. In contrast, the copolymer particles with γ-CyD cavity (CyD content: 14–20 mol%) could selectively remove LPS from a DNA solution (50 μg/ml, pH 6.0 and μ=0.05–0.2) containing LPS (15 EU/ml). The residual concentration of LPS in the treated DNA solution was below 0.1 EU/ml, and the recovery of DNA was 99%.

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Saliva, contains an abundance of proteins, offers an easy, safe, and non-invasive approach, and then possesses a high potential to investigate the stress. Alpha-amylase and chromogranin A are well known proteins as stress markers in saliva, however, past studies were limited to the effect against acute stress. Little is known about the effect of relaxing treatment after long-term stress. In this report, we examined effects of walking on Seaside therapy. We measured salivary amylase activities, blood pressures, and psychological stress response scale tests of about 40 volunteers. Using saliva samples showing a decrease in the activity of amylase after walking, salivary proteins were resolved using sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). Western-blotting analysis was performed after SDS-PAGE, two major bands of alpha-amylase were shown in any cases. Dot-blotting analysis showed that the amount of the proteins cross-linked with antibody of alpha-amylase was increased in spite of the decrease in the amylase activity. The decrease in the amylase activity could not be caused by the decrease of the secretion to saliva. The activity of the salivary amylase might be controlled by other factors. Now, we examined the further analysis about other factors to elucidate the biomarkers in non-stress.

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SBL was originally isolated from frog (Rana catesbeiana) oocytes as a novel sialic acid-binding lectin (SBL) that displayed strong anti-cancer activity. SBL was later shown to be identical to a ribonuclease from oocytes of the same species. The administration of SBL induced apoptosis in mouse leukemia P388 cells but did not kill umbilical vein endothelial or fibroblast cells derived from normal tissues. The cytotoxicity of SBL was inhibited by desialylation of P388 cells and the co-presence of free bovine submaxillary mucin and heparan sulphate. SBL was observed to be incorporated into cells after attachment to cholesterol-rich microdomains and SBL induced apoptosis through the caspase-3 pathway following activation of caspase-8. Addition of the cholesterol remover, methyl-β-cyclodextrin reduced SBL-induced apoptosis with caspase-3 activity. Mass spectrometric and flow cytometric analyses appeared that both a heat shock cognate protein (Hsc70) and a heat shock protein (Hsp70) on the cell membrane bound to SBL and their inhibitor, quercetin significantly reduced SBL-induced apoptosis. Taken together, these findings suggest that sialyl-glycoconjugates present in cholesterol-rich microdomains form complexes with Hsc70 and/or Hsp70 that act as triggers for SBL to induce apoptosis through a pathway involving the activation of caspase-3 and caspase-8.

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