Lewis Pair Catalyzed Regioselective Polymerization of (E,E)-Alkyl Sorbates for the Synthesis of (AB)n Sequenced Polymers.

In this contribution, Lewis pairs (LPs) composed of N-heterocyclic olefins (NHOs) with different steric hindrance and nucleophilicity as Lewis bases (LBs) and Al-based compounds with comparable acidity but different steric hindrance as Lewis acids (LAs) were applied for 1,4-selective polymerization of (E,E)-methyl sorbate (MS) and (E,E)-ethyl sorbate (ES). The effects of steric hindrance, electron-donating ability, and acidity of LPs on MS and ES polymerization were systematically investigated. High catalytic activity and high initiation efficiency can be achieved, leading to the formation of PMS with 100 % 1,4-selectivity, tunable molecular weight (Mw up to 333 kg mol-1 ), and narrow molecular weight distribution (MWD). Block copolymerization of ES and methyl methacrylate (MMA) was also realized. Meanwhile, this system can be applied to other homologous conjugated diene substrates. Furthermore, simple chemical reactions can efficiently convert PMS to different polymers with strict (AB)n sequence structures, such as poly(sorbic acid), poly(propylene-alt-methyl acrylate), poly(propylene-alt-acrylic acid), poly(propylene-alt-allyl alcohol), and poly(ethylene-alt-2-butylene).

Highly Isoselective Ring-Opening Polymerization of rac-Lactide Using Chiral Binuclear Aluminum Catalyst.

The microstructure can significantly affect the physical and mechanical properties of polymers. Five chiral binuclear aluminum methyl complexes (rac1 to rac5) are synthesized by using chiral binaphthalene diamine ligand and characterized by both 1 H and 13 C NMR spectroscopy. The crystal structures of rac3 and rac5 are also identified by single crystal X-ray diffraction. In the presence of i PrOH initiator, these aluminum complexes catalyze the ring-opening polymerization (ROP) of rac-lactide (rac-LA) in a controlled manner and produce polymers with high to excellent isoselectivity (Pm up to 0.93). Even with a catalyst loading as low as 0.1%, polylactide with a Pm of 0.83 can still be obtained. Kinetic studies reveal the first-order dependence on monomer concentration whereas kinetic resolution polymerization provides the evidence to support that these binuclear aluminum catalysts catalyzed ROP of rac-LA adopts enantiomorphic site control mechanism. Furthermore, this strategy can also be applied to the ROP of both ε-caprolactone and δ-valeroactone.

Molecular mechanism of HEIH and HULC in the proliferation and invasion of hepatoma cells.

OBJECTIVE: To study the expression and molecular mechanism of long noncoding RNAs (lncRNA) including HEIH and HULC in proliferation and invasion of hepatoma cells. METHODS: We detected the expression of HEIH and HULC in hepatocellular carcinoma cell line (MHCC97L and HepG2), as well as in human normal hepatocyte line (cHL-7702) by real-time PCR. Using MTT and transwell, we investigated the effect of HEIH and HULC on proliferation and invasion of hepatoma cells with siRNA and expression plasmid. To explore the molecular mechanism, we use western blot to reveal the role of HEIH and HULC in tumor invasion related gene expression. RESULTS: The expression of HEIH and HULC in hepatocellular carcinoma cell line was significantly increased compared with human normal hepatocyte line (P<0.05). The expression of HULC in HepG2 was higher than that in MHCC97L. The over-expression of HULC could enhance proliferation of MHCC97L and HepG2, however, the over-expression of HEIH could not. The over-expression of HULC and HEIH could promote invasion of MHCC97L and HepG2. Invasion of MHCC97L and HepG2 did not have significant change after down-regulating of HEIH and HULC by siRNA. Over-expression of HULC up-regulated the expression of Snail in HepG2. CONCLUSIONS: The expression of HEIH and HULC increased significantly in hepatocellular carcinoma cell line compared with that in human normal hepatocyte line. HULC could promote proliferation of hepatoma cells. HEIH and HULC play an important role in the invasion of hepatocellular carcinoma cell.