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Electrochemical doping properties and morphology changes of electropolymerized poly(N-vinylcarbazole) (PVK) thin films were investigated toward improved hole-injection/transport properties in polymer light emitting diode (PLED) devices. The conjugated network polycarbazole thin films (resulting from a poly(N-carbazole) (PCz) network) were prepared by electrodeposition of PVK and/or N-vinylcarbazole comonomer via precursor route and were investigated in situ by electrochemical-surface plasmon resonance spectroscopy (EC-SPS). Distinct doping-dedoping properties and morphology transitions were observed with different compositions of PVK and Cz. By electrochemical doping of the cross-linked conjugated polycarbazole units, the electrochemical equilibrium potential (E eq), which correlates to Fermi level (E f) or the work function (φ w) of the film, was adjusted in the vicinity of the anode electrode. The conjugated network PCz films were then used as a hole-injection/transport layer in a two layer device. Remarkable enhancement of PLED properties was observed when optimal electrochemical doping was done with the films. Important insight was gained on charge transport phenomena between polymer materials and conducting oxide substrates.

Leukemia inhibitory factor (LIF) is a member of the interleukin-6 family of cytokines, which induces a wide range of responses in a variety of cells. The aim of this study was to investigate whether LIF induces cardiomyocyte hypertrophy and transmits signals through the JAK/STAT (indicating just another kinase/signal transducer and activator of transcription) pathway in primary cultured neonatal rat cardiomyocytes. LIF increased protein content and [3H]phenylalanine uptake in cardiomyocytes in a dose-dependent manner. LIF (10(3) U/mL) induced rapid tyrosine phosphorylation of gp130, JAK1, JAK2, STAT1, and STAT3 but not Tyk2 or STAT2. LIF also induced autokinase activity of JAK1 in a time-dependent manner. Gel shift assays for interferon gamma activation site/interferon-stimulated responsive element and sis-inducible element (SIE) revealed that LIF induced dimerization of STAT1 and STAT3 and formation of sis-inducing factor complexes, which subsequently interacted with SIE in the promoter. Preincubation with anti-STAT1 and anti-STAT3 antibodies inhibited the binding of SIF complexes. In conclusion, LIF induces cardiac hypertrophy and directly stimulates the JAK/STAT pathway in cardiomyocytes.