Highly Promoting the Performances of Polymer Light-Emitting Diodes via Control of the Residue of a Polar Solvent on an Emissive Layer.

The polar solvent dimethylformamide (DMF) was used to treat the emissive layer (EML) of polymer light-emitting diodes (PLEDs). The formation of a dipole layer at the EML/cathode interface after DMF treatment was proven, which led to a reduction of the electron-injection barrier. The dipole layer was formed mainly because of the intrinsic polarity of DMF. By control of the residue of DMF on the EML, a maximum enhancement of the peak luminous efficiency from 5.33 ± 0.57 to 12.05 ± 1.2 cd/A was achieved. This study suggests that solvent treatment is a simple and efficient approach to realizing highly efficient PLEDs with a high-work-function metal cathode.

[Effect of myriocin on the expression of cyclinD1 in high glucose-induced hypertrophy mesangial cells].

OBJECTIVE: Myriocin (ISP-1) is a new type of immune inhibitor extracted from cordyceps sinensis. This study was to observe the effects of ISP-1 on the expression of cell cycle regulatory protein D1 (cyclinD1) in high glucose-induced hypertrophy rat glomerular mesangial cells (GMCs). METHODS: Rat GMCs were cultured in vitro and divided into three groups: high glucose (450 mg/dL D-glucose), normal glucose (100 mg/dL D-glucose, control) and ISP-1 (450 mg/dL D-glucose plus 100 µg/mL ISP-1). The protein expression of cyclinD1 was detected by flow cytometry. RESULTS: The expression of cyclinD1 in GMCs in the high glucose group increased significantly in a time-dependent manner compared with that in the control group. ISP-1 treatment significantly inhibited the up-regulated expression of cyclinD1 induced by high concentration glucose, and the expression of cyclinD1 was restored to the level of the control group 48 and 72 hrs after ISP-1 treatment. CONCLUSIONS: High concentration of glucose can up-regulate the expression of cyclinD1 in GMCs. ISP-1 may inhibit the up-regulated expression of cyclinD1, which might contribute to the protective effect of ISP-1 against GMC hypertrophy induced by high glucose.

[Mutation of hepatitis B virus S gene in children with hepatitis B virus-associated glomerulonephritis].

OBJECTIVE: Hepatitis B virus-associated glomerulonephritis (HBV-GN) is an immune complex-mediated glomerulonephritis. The present study was conducted to identify HBV S gene mutation in children with HBV-GN. METHODS: Serum HBV DNA was extracted in 53 children, including 30 with HBV-GN, 5 with HBV-carrying nephrosis (control group 1), and 18 HBV carriers (control group 2). HBV S gene sequence was amplified by polymerase chain reaction (PCR). The PCR products were sequenced directly and compared with AY167097.1, an epidemic HBV strain in China. RESULTS: (1) The adw serotype of HBV was found in all the 30 cases with HBV-GN, 5 cases with HBV-carrying nephrosis and 17 HBV carriers except for 1, in whom adr serotype was identified. (2) HBV genotype B was found in 29 children with HBV-GN, 5 cases with HBV-carrying nephrosis and 17 HBV carriers, genotype E was found in a child with HBV-GN, and genotype C in an HBV carrier. (3) A total of 17 kinds of different single nucleotide change in HBV S gene were identified in 21 of 30 (70%) HBV-GN patients. Among them, 16 of 21 (76.2%) nucleotide mutations resulted in amino acid substitution. It was interesting that most (11/16, 68.8%) amino acid substitutions involved threonine, serine and tyrosine, the potential phosphorylation sites of mitogen-activated protein kinase (MAPK) and protein tyrosine kinase (PTK) in HBV protein. Single nucleotide changes which didn not result in amino acid substitution were found in 2 HBV-carrying nephrosis patients, 2 HBV carriers and 5 cases with HBV-GN. CONCLUSION: Single nucleotide changes in HBV S gene were found in most children with HBV-GN. Most mutations in HBsAg resulted in amino acid substitutions involving threonine, serine and tyrosine, which may play a role in the pathogenesis of HBV-GN.

[Role of mast cells and eosinophil cationic protein in the pathogenesis of Henoch-Schonlein purpura nephritis].

OBJECTIVE: Mast cells and eosinophil have been found to play important roles not only in the development of anaphylactic inflammation but also in the chronic progression of organ reconstruction. But their role in the pathogenesis of Henoch-Schonlein purpura nephritis (HSPN) has not been fully understood. The present study was conducted to observe the serum levels of eosinophil cationic protein (ECP) and renal infiltration of mast cells in HSPN in order to elucidate their role in the development and progression of HSPN in children. METHODS: The serum ECP levels were determined in 46 children with HSPN by fluoro-enzyme immunoassay (FEIA) using the Pharmacia CAP System. The distribution of mast cells infiltration was detected by immuno-enzyme-histological staining of tryptase (a marker for mast cell activation) and their relation with pathological changes was analyzed in 32 children with HSPN. RESULTS: The serum ECP levels were 16.3 +/- 6.5 microg/L in the active stage of HSPN, significantly higher than that in remission stage (3.9 +/- 1.4 microg/L, P < 0.01) and that in control group (3.1 +/- 1.7 microg/L, P < 0.01). The number of mast cells in renal interstitium was 4.4 +/- 2.4 cells/mm2 in normal kidney, and significantly increased to 27.2 +/- 19.2 cells/mm2 in children with HSPN ISKDC grade II (P < 0.01) and 42.1 +/- 16.4 cells/mm2 in grade III (P < 0.05 when compared with grade II), 77.9 +/- 15.0 cells/mm2 in grade IV (P < 0.05 when compared with grade III). CONCLUSION: The serum ECP level could reflect disease activity of HSPN, and mast cell infiltration in kidney correlated significantly with renal histological severity in HSPN. Mast cells and eosinophil may play important roles in the development and progression of HSPN.