In this study, we fabricated a polymer light emitting diode (PLED) and investigated its electrical and optical characteristics in order to examine the effects of the PFO [poly(9,9-dioctylfluorene-2-7-diyl) end capped with N,N-bis(4-methylphenyl)-4-aniline] concentrations in the emission layer (EML). The PFO polymer was dissolved in toluene ranging from 0.2 to 1.2 wt%, and then spin-coated. To verify the influence of the TPBI [2,2',2"-(1,3,5-Benzinetriyl)-tris(1-phenyl-1-H-benzimidazole)]electron transport layer, TPBI small molecules were deposited by thermal evaporation. The current density, luminance, wavelength and current efficiency characteristics of the prepared PLED devices with and without TPBI layer at various PFO concentrations were measured and compared. The luminance and current efficiency of the PLED devices without TPBI layer were increased, from 117 to 553 cd/m2 and from 0.015 to 0.110 cd/A, as the PFO concentration increased from 0.2 to 1.0 wt%. For the PLED devices with TPBI layer, the luminance and current efficiency were 1724 cd/m2 and 0.501 cd/A at 1.0 wt% PFO concentration. The CIE color coordinators of the PLED device with TPBI layer at 1.0 wt% PFO concentration showed a more pure blue color compared with the one without TPBI, and the CIE values varied from (x, y) = (0.21, 0.23) to (x, y) = (0.16, 0.11).

Nitric oxide (NO) has been known to inf1uence cell fate through apoptotic or necrotic cell death. Here, we investigated the role of nitric oxide on the growth and viability of immortalized human salivary gland (HSG) cells 띠 vitro. Treatrnent of HSG with a NO donor, S-nitroso-N-acetyl-DL-penκi1lamine (SNAP), significantly diminished the growth rate of HSG in a concentration dependent manner. However, this retardation of cell비ar growth rate was not corresponded to the apoptotic cell death of HSG cells, because there were no characteristic apopto디c features such as condensation of nuclear chromatin, nuclear fragmentation, and the apoptotic peak of propidium iodide (PI)-stained nuclei by flow cytome띠. 까ùs implies that HSG cells are resistant to NO-mediated 다π。to:잉city. 1n SNAP treated HSG cells, cell cycle analysis revealed that the number of G2/M phase increased markedly, according to while the percentage of cells in GO/Gl and S phases was not significantly affected. Otherwise, high concentrations of SNAP increased both P1 and annexin V positive cells. 1nterestingly, preincubation of HSG cells with iron chelator, deferoxamine (DFO), significantly diminished NO cytotoxicity more than when HSG cells are only incubated with SNAP which su잃.ests the role of iron homeostasis in NO-mediated cell death of HSG cells. 1n addi디。n ， treatrnent of HSG cells with SNAP specifically cleaved iron regulatory protein-2 (IRP2) while not affecting 1RP1. Collectively, the mπent results s멍gest that NO has a potential to control HSG cell growth through cell cycle arresting at G2/M phase. 1n addi디on ， intracellular iron homeostasis nùght play an important role in regulating cell survival of HSG cells