[Role of the IGF-1/PI3K pathway and the molecular mechanism of Fuzhenghuayu therapy in a spontaneous recovery rat model of liver fibrosis].

OBJECTIVE: To determine the role of IGF-1/PI3K pathway and investigate the molecular mechanism of Fuzhenghuayu (FZHY) therapy in a spontaneous recovery rat model of liver fibrosis. METHODS: The liver fibrosis model was induced in male Wistar rats by administering 8 weeks of twice weekly CCL4 intraperitoneal injections without (untreated model) or with once daily FZHY (treated model). Normal, untreated rats served as the control group. At weeks 4, 6 and 8 (fibrosis) and 10, 12 and 14 (spontaneous recovery) after modeling initiation, effects on protein (a-SMA, IGF-1, PI3K) and mRNA (IGF-1, PI3K) expression levels were evaluated by immunohistochemistry and RT-PCR, respectively. Serum markers of liver function (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)) and liver cell damage (alkaline hydrolysis, HYP) were measured. Histology was performed to assess the degree of inflammation and fibrosis (Ishak scoring system). RESULTS: In the untreated model group, progression of liver fibrosis (weeks 4, 6 and 8) was accompanied by gradual increases in inflammation, necrosis, serum ALT and AST, and hepatic expression of a-SMA protein and IGF-1 and PI3K protein and mRNA; however, during the spontaneous recovery period (weeks 10, 12 and 14) the IGF-1 and PI3K protein and mRNA levels rapidly decreased and the HYP level, Ishak score, and a-SMA hepatic expression also decreased. The FZHY-treated model group showed significantly lower fibrosis-related up-regulation of IGF-1 and PI3K protein and mRNA expression, HYP level, Ishak score, and a-SMA hepatic expression at each time point (vs. untreated model group). CONCLUSION: The IGF-1/PI3K pathway may contribute to progression of liver fibrosis. The mechanism by which FZHY prevents liver fibrosis in a rat model may involve blocking of the IGF/PI3K pathway and inhibiting HSC activation.

Method of compensating for pixel migration in volume holographic optical disc (VHOD).

Volume holographic optical disc (VHOD) technology is simpler than the angular multiplexing holographic system. However, disc rotation usually causes pixel migration, thus reducing signal quality. This study proposes a special geometrical arrangement to counteract pixel migration. Using paraxial approximation analysis, an optimal geometrical distance ratio, K, is calculated to compensate for pixel migration and improve image quality during disc rotation. The results of approximation analysis are confirmed by both simulation and experimental results.

Reaching Nearly 100% Quantum Efficiencies in Thin Solid Films of Semiconducting Polymers via Molecular Confinements under Large Segmental Stresses.

Quantum efficiencies remain a critical issue for general applications of semiconducting polymers in optoelectronics and others. In this work, we demonstrate that nearly 100% quantum efficiencies (η's) in thin solid films can be reached when the polymer molecules are mechanically stretched into molecular confinement. We selected three conjugated polymers of varied backbone stiffness and interchain coupling, prepared in both diluted and pristine states. All of the polymers when highly diluted (c = 0.1 wt %) exhibited massive η increases after stretching to very large strains (∼300-500%) via micronecking, with the rigid polyfluorene (PFO) and semirigid MEH-PPV both manifesting η ≈ 90%, while the most flexible yet regioregular polythiophene (P3HT-rr) exhibited a 10-fold increase to ∼21%. In the pristine state, molecular aggregation and interchain coupling curtail development of the molecular confinement, but the large-strain deformation still enhances η's significantly, to ∼90% (PFO) and ∼55% (MEH-PPV) despite no increases for the crystalline P3HT-rr. Moreover, upon substitution by a bulkier side-group to reduce interchain coupling, the pristine films of polythiophene (P3EHT) exhibited a ∼3-fold increase of η after the stretching. The nearly 100% of η's in fully stretched molecules indicates that the in situ self-trapping occurring via sub-picosecond backbone interactions can be mostly responsible for energy dissipations and quite suppressible by segmental stress control. The mechanical confinement effects also indicate the fundamental role of molecular mechanics during stabilization and migration of photoexcited charges.

Downregulation of TIPE2 mRNA expression in peripheral blood mononuclear cells from patients with chronic hepatitis C.

PURPOSE: Hepatitis C virus (HCV) infection causes chronic hepatitis in approximately 80 % of cases. Although it is well recognized that the immune system plays an important role in determining the outcomes of HCV infection, the underlying molecular mechanisms of persistent HCV infection and hepatic injury are incompletely understood. Tumor necrosis factor-α-induced protein 8-like 2 (TNFAIP8L2, TIPE2) is a newly identified negative regulator of innate and adaptive immunity. The goal of the present study is to investigate the potential role of TIPE2 in chronic hepatitis C (CHC) infection. METHODS: We used quantitative real-time reverse transcription polymerase chain reaction to examine the mRNA expression levels of TIPE2, Toll-like receptor (TLR) 2, and TLR4 in peripheral blood mononuclear cells from 60 CHC patients and 30 healthy controls. RESULTS: The TIPE2 mRNA expression was significantly downregulated, whereas that of TLR2 and TLR4 was upregulated in CHC patients compared with healthy controls. TIPE2 mRNA expression levels were negatively correlated with serum ALT, AST, and HCV RNA levels. TIPE2 mRNA expression was also negatively correlated with TLR2 and TLR4 mRNA levels in CHC patients. Moreover, TIPE2 mRNA expression was upregulated, whereas that of TLR2 and TLR4 was downregulated after treatment of patients with interferon-α and ribavirin. CONCLUSIONS: These results indicate that HCV may promote chronic hepatitis by decreasing TIPE2 expression while enhancing TLR signaling.