RESUMO
Quantum dot light-emitting diodes (QLEDs) have attracted increasing attention due to their excellent electroluminescent properties and compatibility with inkjet printing processes, which show great potential in applications of pixelated displays. However, the relatively low resolution of the inkjet printing technology limits its further development. In this paper, high-resolution QLEDs were successfully fabricated by electrohydrodynamic (EHD) printing. A pixelated quantum dot (QD) emission layer was formed by printing an insulating Teflon mesh on a spin-coated QD layer. The patterned QLEDs show a high resolution of 2540 pixels per inch (PPI), with a maximum external quantum efficiency (EQE) of 20.29% and brightness of 35816 cd/m2. To further demonstrate its potential in full-color display, the fabrication process for the QD layer was changed from spin-coating to EHD printing. The as-printed Teflon effectively blocked direct contact between the hole transport layer and the electron transport layer, thus preventing leakage currents. As a result, the device showed a resolution of 1692 PPI with a maximum EQE of 15.40%. To the best of our knowledge, these results represent the highest resolution and efficiency of pixelated QLEDs using inkjet printing or EHD printing, which demonstrates its huge potential in the application of high-resolution full-color displays.
RESUMO
Perovskite quantum dot light-emitting diodes (QLEDs) with high color purity and wide color gamut have good application prospects in the next generation of display technology. However, colloidal perovskite quantum dots (PQDs) may introduce a large number of defects during the film-forming process, which is not conducive to the luminous efficiency of the device. Meanwhile, the disordered film formation of PQDs will form interfacial defects and reduce the device performance. Here, we report an interface-induced crystallinity enhancement (IICE) strategy to increase the crystallinity of PQDs at the hole transport layer (HTL)/PQD interface. As a result, both the Br- vacancies in the PQD film and the interfacial defects were well passivated and the leakage current was also suppressed. We achieved QLEDs with a maximum external quantum efficiency (EQE) of 16.45% and current efficiency (CE) of 61.77 cd/A, showing improved performance to more than twice that of the control devices. The IICE strategy paves a new way to enhance the crystallinity of PQD films, so as to improve the performance of QLEDs for application in the future display field.
RESUMO
Interactive display devices integrating multiple functions have become a development trend of display technology. The excellent luminescence properties of perovskite quantum dots (PQDs) make it an ideal luminescent material for the next generation of wide-color gamut displays. Here we design and fabricate dual-function light-sensing/displaying light-emitting devices based on PQDs. The devices can display information as an output port, and simultaneously sense outside light signals as an input port and modulate the display information in a non-contact mode. The dual functions were attributed to the device designs: (1) the hole transport layer in the devices also acts as the light-sensing layer to absorb outside light signals; (2) the introduced hole trapping layer interface can trap holes originating from the light-sensing layer, and thus tune the charge transport properties and the light-emitting intensities. The sensing and display behavior of the device can be further modulated by light signals with different time and space information. This fusion of sensing and display functions has broad prospects in non-contact interactive screens and communication ports.
RESUMO
A lighting device with a wide color-tunable range is still a challenge for lighting based on either organic light-emitting diodes (OLEDs) or inorganic LEDs. In this work, we first proposed a novel hybrid device of organic LEDs and inorganic blue GaN LEDs to achieve full white and other colors. Organic LEDs were stacked with green and red emissive layers and connected with blue GaN LEDs in parallel but in opposite polarity voltage. Under the alternate-current (AC) driving, the hybrid structure can be controlled independently by applying timing variable opposite voltages to emit the light from either blue LEDs or the stacked OLEDs for forming mixed colors. The hybrid device can generate white light, varying in a wide range by changing the amplitude and duty ratio (DR) of AC-driving signals, from cold white to standard white and to warm white (3668-11 833 K). When an AC voltage of (4.80 V, -2.45 V) was applied, the device has a high color gamut of 95.24% National Television System Committee (NTSC) and a high color rendering index (R a) of 92.4%. The novel hybrid device with the blue LED and OLED in opposite polarity exhibits potential applications in smart solid-state lighting, display, and light communication.
RESUMO
BACKGROUND INFORMATION: MD-2 is associated with the extracellular domain of TLR4 (Toll-like receptor 4) and augments TLR4-dependent LPS (lipopolysaccharide) responses in vitro. Our previous investigation found that PMA-induced HL-60 cell differentiation to macrophages is associated largely with TLR2 and CD14 and, to a much lesser extent, with TLR4. RESULTS: We studied the MD-2 expression during differentiation of HL-60 cells induced by PMA. The results showed that PMA, but not VitD(3) (1alpha,25-dihydroxy-vitamin D(3)), strongly induces MD-2 gene expression by HL-60 cells in a time- and dose-dependent manner. Treatment with an MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase] inhibitor (PD98059) and a JNK (c-Jun N-terminal kinase) inhibitor (SP600125) suppresses PMA-induced MD-2 gene expression, whereas impairment of p38 function by treatment with the inhibitor SB203580 has no effect on MD-2 mRNA. In order to reveal the possible molecular mechanism for such a regulation of MD-2 gene expression, we cloned and analysed the putative MD-2 gene promoter. Transient transfection of different deletion mutants demonstrated that the region -185/-171 (5'-TCCTTTACAGGAAGT-3') of the MD-2 gene promoter is closely related to gene transcription in response to PMA. Additionally, the transcription factor Elk-1 has been found to bind this specific motif. CONCLUSIONS: These results suggest that ERK and JNK pathways are involved in PMA-mediated MD-2 gene expression during HL-60 cell differentiation, and the activation of the MEK/possible ERK/Elk signal pathway is the mechanism responsible for PMA-induced MD-2 gene expression in differentiated HL-60 cells.
Assuntos
Diferenciação Celular , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Expressão Gênica , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Antígeno 96 de Linfócito/genética , Diferenciação Celular/efeitos dos fármacos , MAP Quinases Reguladas por Sinal Extracelular/antagonistas & inibidores , Expressão Gênica/efeitos dos fármacos , Células HL-60 , Humanos , Proteínas Quinases JNK Ativadas por Mitógeno/antagonistas & inibidores , Antígeno 96 de Linfócito/metabolismo , Regiões Promotoras Genéticas , Inibidores de Proteínas Quinases/farmacologia , Transdução de Sinais , Acetato de Tetradecanoilforbol/farmacologia , Fatores de Transcrição/metabolismo , Proteínas Elk-1 do Domínio ets/metabolismoRESUMO
Human cardiac fibroblasts are protected from oxidative stress triggered by inflammation after myocardial injury (Li, P. F., Dietz, R., and von Harsdorf, R. (1999) FEBS Lett. 448, 206-210) by expressing potent antioxidant defenses such as superoxide dismutases, catalases, glutathione-peroxidases, and peroxiredoxins. Recently the transcription factor FOXO3A has been shown to increase resistance to oxidative stress by up-regulation of mitochondrial superoxide dismutase and peroxisomal catalase (Kops, G. J., Dansen, T. B., Polderman, P. E., Saarloos, I., Wirtz, K. W., Coffer, P. J., Huang, T. T., Bos, J. L., Medema, R. H., and Burgering, B. M. (2002) Nature 419, 316-321; Nemoto, S., and Finkel, T. (2002) Science 295, 2450-2452). We hypothesized that FOXO3A also regulates the expression of Prx III, the mitochondrial peroxiredoxin, in human cardiac fibroblasts. We found that depletion of FOXO3A leads to a dramatic reduction of Prx III mRNA and protein in serum-deprived human cardiac fibroblasts. These data suggest that endogenous FOXO3A is necessary for base-line expression of Prx III. Next, we identified two putative FOXO3A DNA binding sites in Prx III promoter at -267 and -244 nucleotides relative to the start codon. We demonstrated that both sequences are required for binding of endogenous FOXO3A to the Prx III promoter by performing electromobility shift assays and chromatin immunoprecipitation assays. Inhibition of endogenous FOXO3A by insulin growth factor 1 prevented binding of FOXO3A to Prx III promoter. In contrast, overexpression of FOXO3A increased Prx III promoter activity. Furthermore, depletion of Prx III was associated with enhanced apoptosis and oxidative stress after serum deprivation. We conclude that FOXO3A mediates Prx III expression, and this may play a critical role in the resistance to oxidative stress in cardiac fibroblasts.