Communications separating the PPV-rich parts and the pyridine-rich segments. This will be explained in more detail elsewhere.The significant red emission at high voltages is probably associated with the higher efficiency for light emission in pyridine-rich segments. As demonstrated by OnodaI7] the EL efficiency for light emission from PPyV is rather high (7 N 0.5 YO ) and it is further enhanced due to the presence of the junctionsr7 in PPV/PPyV. At the present time, we cannot exclude alternative explanations associated with the formation of exciton or impurity bands in the x-x* forbidden gap of PPV upon substitution of the pyridine moieties in the copolymer. ExperimentalThe 2,6-pyridyl-dimethylene-bis-(tetramethylene sulfonium chloride) monomer was prepared by adding tetrahydrothiophene (THT) (15 ml) to 2,6bis(chloromethy1)-pyridine (5 g) in methanol (150 ml). The reaction mixture was kept at 50°C for 4 days and was then concentrated to gelation. The hissulfonium salt was precipitated by addition of ice cold acetone (250 ml) and was isolated. The 1,4-phenylenedimethylene-bis-(tetramethylene sulfonium chloride) was prepared according to the literature procedure. The copolymerization was typically carried out as follows. A mixture of 20 YO (molar) of 2,6pyridyl-dimethylene-bis-(tetramethylene sulfonium chloride) (1.49 g) and 1,4phenylene dimethylene-bis-(tetramethylene sulfonium chloride) (5.96 g) in water (200 ml) was prepared. Polymerization was initiated under nitrogen at 0-2°C by addition of a stoichiometric quantity of 1 N NaOH in water (21.2 ml) under constant vigorous stirring for 1 h. The mixture was neutralized with 1 N HCl(9.4 ml) corresponding to 54.2 % conversion of the monomers to the copolyelectrolyte. The copolyelectrolyte solution was homogenized and dialyzed (Mw cut-off 12000) at 4°C for ten days.Films for the various measurements were prepared by casting the dialyzed copolyelectrolyte on relevant substrates by spin coating. The polyelectrolyte was then converted to the final copolymer, co(2,6PyV-PV) by heating in vacuum, 10-6torr, at 280°C for 12 h. Film thicknesses were determined by X-ray reflectivity at grazing angle using a 12 kW Rigaku rotating anode and found to be approximately 1000 A. Absorption spectra were measured on a HP 8452 diode array spectrometer. PL spectra were recorded on Perkin Elmer Luminescence Spectrometer LS 50. EL spectra were recorded using an Oriel monochromator and the light intensity was quantified with a photo-multiplier (products from Research Inc. model no. R955).

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It is widely recognized that inflammation plays a critical role in cardiac hypertrophy and heart failure. However, clinical trials targeting cytokines have shown equivocal effects indicating the need for a deeper understanding of the precise role of inflammation and inflammatory cells in heart failure.Leukocytes from human subjects and a rodent model of heart failure were characterized by a marked reduction in expression of KLF2 mRNA. Using a mouse model of Angiotensin II-induced non-ischemic cardiac dysfunction, we showed that neutrophils played an essential role in the pathogenesis and progression of heart failure. Mechanistically, chronic Angiotensin II infusion activated a neutrophil KLF2-NETosis pathway that triggered sporadic thrombosis in small myocardial vessels leading to myocardial hypoxia, cell death, and hypertrophy. Conversely, targeting neutrophils, NETs or thrombosis ameliorated these pathological changes and preserved cardiac dysfunction. KLF2 regulated neutrophil activation in response to Angiotensin II at the molecular level, partly through the crosstalk with HIF1 signaling.Taken together, our data implicate neutrophil-mediated immunothrombotic dysregulation as a critical pathogenic mechanism leading to cardiac hypertrophy and heart failure. This neutrophil KLF2-NETosis-thrombosis mechanism underlying chronic heart failure can be exploited for therapeutic gain by therapies targeting neutrophils, NETosis, or thrombosis.