Enantioselective Synthesis of ß-Quaternary Carbon-Containing Chromanes and 3,4-Dihydropyrans via Cu-Catalyzed Intramolecular C-O Bond Formation.

A copper-catalyzed efficient enantioselective construction of chiral quaternary carbon-containing chromanes and 3,4-dihydropyrans is reported. The desymmetric C-O coupling is enabled by a chiral dimethylcyclohexane-1,2-diamine ligand and provides the desired products in good yields with high enantioselectivities. This method presents a broad substrate scope and is applicable to diversely substituted aryl bromides and alkenyl bromides. The application is demonstrated by a gram-scale synthesis and derivatization of the products toward valuable building blocks.

STAT3 and beta-catenin signaling pathway may affect GSK-3beta expression in hepatocellular carcinoma.

BACKGROUND/AIMS: To study the correlation and significance of beta-catenin, STAT3 and GSK-3beta signaling pathway in hepatocellular carcinoma (HCC). METHODOLOGY: The HCC cell line HepG2 was transfected with small interfering RNA (siRNA) directed against 8-catenin or STAT3. After 72 and 96h, protein was extracted and the protein expression of beta-catenin, STAT3, and GSK-3beta was detected by Western blot analysis. RESULTS: After siRNA directed against beta-catenin was transfected into HepG2 cells, beta-catenin protein expression was decreased at 72 and 96h, GSK-3beta and p-GSK-3beta protein expression increased gradually at 72 and 96h, and STAT3 protein expression showed no change following transfection. After siRNA directed against STAT3 was transfected into HepG2 cells, STAT3 protein expression was decreased at 72 and 96h and beta-catenin, GSK-3beta and p-GSK-3beta protein expression all increased at 72h and decreased at 96 h after transfection. CONCLUSION: In HCC, the beta-catenin signaling pathway may regulate GSK-3beta protein expression and the STAT3 signaling pathway may regulate beta-catenin and GSK-3beta protein expression, thereby playing key roles during HCC genesis and development.

[The role and significance of Wnt/beta-catenin signaling pathway regulating the signaling molecules in hepatocellular carcinoma].

OBJECTIVE: To investigate the role and significance of Wnt/beta-catenin signaling pathway regulating GSK-3beta, STAT3, Smad3 and TERT in hepatocellular carcinoma (HCC). METHODS: The HCC cell line HepG2 was transfected with small interfering RNA (siRNA) directed against beta-catenin. Proteins were extracted and the expressions of beta-catenin, GSK-3beta, p-GSK-3beta, STAT3, Smad3 and TERT were detected by Western blot at 72 h and 96 h respectively after transfection. RESULTS: beta-catenin expression was inhibited at both time points and the expression at 96 h was higher than that at 72 h (t = 4.43, P < 0.05). Interestingly, GSK-3beta and p-GSK-3beta expressions increased gradually at 72 and 96 h (tGSK-3beta= 4.98, tp-GSK-3beta= 29.83, P < 0.05) respectively, and STAT3 expression showed no alteration after transfection (F = 0.49, P > 0.05). Smad3 expression was increased at 72 h (t = 10.67, P < 0.05) and decreased to normal at 96 h (t = 1.26, P < 0.05), while TERT expression decreased at 72 h (t = 4.18, P is less than 0.05) and increased to normal at 96 h (t = 1.26, P > 0.05). CONCLUSIONS: Wnt/beta-catenin signaling pathway is related to the expressions of GSK-3beta, Smad3 and TERT, but perhaps not related to STAT3 protein expression in HCC. It suggested that Wnt/beta-catenin signaling pathway might participate in HCC genesis and development through regulating the above three factors.

[The changes of interdigestive migrating motor complex in rats with acute liver failure].

OBJECTIVE: To observe the changes and characteristics of interdigestive migrating motor complex (MMC) in rat models of acute liver failure. METHODS: 30 rat models with acute liver failure were induced with D-galactosamine and another 30 normal rats were used as controls. The indexes of MMC recorded by multi-channel physiological recorder were compared. RESULTS: No significant differences found between the two groups in antral and duodenal MMC cycles and frequencies of duodenal and jejunal MMC III phase. Compared with normal controls, the MMC II phase in the acute liver failure rats was significantly prolonged (t=-3.97, -3.85, P<0.05), the MMC III duration of antrum and duodenum (u=-4.99, t=4.66, P<0.05) was shorter and the MMC III frequency of antrum (u=-4.73, P<0.05) was faster. In addition, the MMC cycle and MMC III phase of jejunum were significantly prolonged (u=-1.63, t=-4.94, P<0.05) and the MMC III phase duration was significantly shorter in the acute liver failure rats (t=5.10, P<0.05). CONCLUSION: Significantly prolonged MMC II phase characterized by migrating clustered contraction, shortened MMC III phase and extended jejunal MMC cycles were probably the major contributors to the gastrointestinal motility disorders in the rats with acute liver failure.