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Transient electroluminescence (EL) from polymer light emitting diodes is investigated by measurements of the response to short voltage pulses. The carrier mobility is derived from the delay time between the electrical pulse and the onset of EL, μapprox. 3×10[sup -4] cm[sup 2]/V s. Bilayer devices with a polyethylene-dioxythiophene (PEDOT), hole injection layer are also studied. The delay time between the electrical pulse and the onset of EL is independent of the thickness of the injection layer, implying that the conducting PEDOT functions as a part of the electrode. When a dc forward bias is applied to the device, the delay time decreases, probably as a result of the shift of the emission zone towards the anode. The EL turn-on depends on the amplitude of the voltage pulse. The data are modeled by an equivalent circuit with a fixed capacitance connected in parallel with a nonlinear resistance. The solution of the differential equation depends on the exact form of the device’s I–V curve. Two analytical solutions are provided, and an analysis based on space-charge-limited current is presented. By applying a dc forward bias in advance to precharge the space-charge capacitance, the turn-on response time is reduced to 12 ns. The EL decay consists of two components with time constants of 15 ns and 1 μs. The decay does not depend on either the amplitude of the voltage pulse or the prebias. © 2002 American Institute of Physics. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effects of reduced nicotinamide adenine dinucleotide phosphooxidase 4 (NOX4) inhibitors GKT137831 and M2-type macrophages on oxidative stress markers NOX4, nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) in the rat hepatic stellate cell line (HSC-T6). Methods: Rat bone marrow macrophages were extracted and induced using interleukin (IL)-4 to differentiate them into M2 phenotype macrophages. HSC-T6 activation was performed with 5 μg/L transforming growth factor β1 (TGF-β1). The proliferation condition of HSC-T6 cells stimulated by the NOX4 inhibitor GKT137831 at a concentration gradient of 5 to 80 μmol/L after 48 hours was detected using the Cell Counting Kit-8 (CCK-8) assay. The optimal drug concentration was chosen and divided into an HSC co-culture group (the control group) and five experimental groups: the TGF-β1 stimulation group, the TGF-β1 +GKT137831 stimulation group, the M2-type macrophage + HSC co-culture group, the M2-type macrophage +TGF-β1 stimulation group, and the M2-type + TGF-β1 + GKT137831 stimulation group. Reactive oxygen species (ROS) production level was detected in each cell using the DCFH-DA probe method. NOX4, α-smooth muscle actin (α-SMA), Nrf2, and HO-1 levels in each group of HSC cells were detected using the qRT-PCR method and the Western blot method. The t -test was used to compare the two groups. The one-way ANOVA method was used to compare multiple groups. Results: Intracellular ROS increased significantly following TGF-β1 stimulation. ROS relative levels in each cell group were 1.03±0.11, 3.88±0.07, 2.90±0.08, 0.99±0.06, 3.30±0.05, 2.21±0.11, F  = 686.1, P  = 0.001, respectively. The mRNA and protein expressions of NOX4, α-SMA, Nrf2, and HO-1 were significantly increased ( P  < 0.05). After the addition of GKT137831, ROS, and NOX4, α-SMA mRNA and protein expression were comparatively decreased in the TGF-β1 stimulation group ( P  < 0.05), while mRNA and protein expressions of Nrf2 and HO-1 were increased ( P  < 0.05). The expression of ROS and NOX4, as well as α-SMA mRNA and protein, produced by HSC were significantly decreased in the co-culture group compared to the single culture group after TGF-β1 stimulation ( P  < 0.05). After the addition of GKT137831, ROS, NOX4, α-SMA mRNA, and protein expression were further reduced in the co-culture group compared with the single culture group ( P  < 0.05), while the mRNA and protein expression of Nrf2 and HO-1 were further increased ( P  < 0.05). Conclusion: NOX4 inhibitor GKT137831 can reduce RO, NOX4, and α-SMA levels while increasing Nrf2 and HO-1 levels in hepatic stellate cells. After M2-type macrophage co-culture, GKT137831 assists in lowering ROS, NOX4, and α-SMA levels while accelerating Nrf2 and HO-1 levels in hepatic stellate cells, which regulates the balance between oxidative stress and anti-oxidative stress systems, thereby antagonizing the fibrosis process.

Purpose of the study was to determine the prevalence of toxoplasma infection among the pregnant women and their newborn infants in Chengdu and to identify risk factors of acquiring toxoplasma infection. The Maternal and Child Health Hospital was selected by random cluster sampling method in the study. Each pregnant women admitted to the above hospital consecutively and her surviving newborn at birth were included in this survey. History, physical examination and blood specimens were obtained from 1,211 pairs of mother-newborns. ELISA was used to detect toxoplasma IgG and IgM antibodies. Results revealed that sera prevalence of toxoplasma IgG antibodies and IgM antibodies of pregnant women were 39.14% and 4.21% respectively. Seraprevalence of toxoplasma IgM antibodies of newborn infants was 1.07%. Congenital malformation of newborn infants may be associated with congenital toxoplasma infection (P < 0.05, OR = 6.32).