Highly Efficient All-Solution-Processed Quantum Dot Light-Emitting Diodes Using MoOx Nanoparticle Hole Injection Layer.

This paper presents a study that aims to enhance the performance of quantum dot light-emitting didoes (QLEDs) by employing a solution-processed molybdenum oxide (MoOx) nanoparticle (NP) as a hole injection layer (HIL). The study investigates the impact of varying the concentrations of the MoOx NP layer on device characteristics and delves into the underlying mechanisms that contribute to the observed enhancements. Experimental techniques such as an X-ray diffraction and field-emission transmission electron microscopy were employed to confirm the formation of MoOx NPs during the synthesis process. Ultraviolet photoelectron spectroscopy was employed to analyze the electron structure of the QLEDs. Remarkable enhancements in device performance were achieved for the QLED by employing an 8 mg/mL concentration of MoOx nanoparticles. This configuration attains a maximum luminance of 69,240.7 cd/cm2, a maximum current efficiency of 56.0 cd/A, and a maximum external quantum efficiency (EQE) of 13.2%. The obtained results signify notable progress in comparison to those for QLED without HIL, and studies that utilize the widely used poly(3,4-ethylenedioxythiophene):poly(styrene sulfonate) (PEDOT:PSS) HIL. They exhibit a remarkable enhancements of 59.5% and 26.4% in maximum current efficiency, respectively, as well as significant improvements of 42.7% and 20.0% in maximum EQE, respectively. This study opens up new possibilities for the selection of HIL and the fabrication of solution-processed QLEDs, contributing to the potential commercialization of these devices in the future.

Performance Improvement of Quantum Dot Light-Emitting Diodes Using a ZnMgO Electron Transport Layer with a Core/Shell Structure.

Highly efficient and all-solution processed quantum dot light-emitting diodes (QLEDs) with high performance are demonstrated by employing ZnMgO nanoparticles (NPs) with core/shell structure used as an electron transport layer (ETL). Mg-doping in ZnO NPs exhibits a different electronic structure and degree of electron mobility. A key processing step for synthesizing ZnMgO NPs with core/shell structure is adding Mg in the solution in addition to the remaining Mg and Zn ions after the core formation process. This enhanced Mg content in the shell layer compared with that of the core X-ray photoelectron spectroscopy showed a higher number of oxygen vacancies for the ZnMgO core/shell structure, thereby enhancing the charge balance in the emitting layer and improving device efficiency. The QLED incorporating the as synthesized ZnMgO NP core/shell A exhibited a maximum luminance of 55,137.3 cd/m2, maximum current efficiency of 58.0 cd/A and power efficiency of 23.3 lm/W. The maximum current efficiency and power efficiency of the QLED with ZnMgO NP core/shell A improved by as much as 156.3% and 113.8%, respectively, compared to the QLED with a Zn0.9Mg0.1O NP ETL, thus demonstrating the benefits of ZnMgO NPs with the specified core/shell structure.

Microfluidic model for in vitro acute Toxoplasma gondii infection and transendothelial migration.

The protozoan parasite Toxoplasma gondii (T. gondii) causes one of the most common human zoonotic diseases and infects approximately one-third of the global population. T. gondii infects nearly every cell type and causes severe symptoms in susceptible populations. In previous laboratory animal studies, T. gondii movement and transmission were not analyzed in real time. In a three-dimensional (3D) microfluidic assay, we successfully supported the complex lytic cycle of T. gondii in situ by generating a stable microvasculature. The physiology of the T. gondii-infected microvasculature was monitored in order to investigate the growth, paracellular and transcellular migration, and transmission of T. gondii, as well as the efficacy of T. gondii drugs.

Brain physiome: A concept bridging in vitro 3D brain models and in silico models for predicting drug toxicity in the brain.

In the last few decades, adverse reactions to pharmaceuticals have been evaluated using 2D in vitro models and animal models. However, with increasing computational power, and as the key drivers of cellular behavior have been identified, in silico models have emerged. These models are time-efficient and cost-effective, but the prediction of adverse reactions to unknown drugs using these models requires relevant experimental input. Accordingly, the physiome concept has emerged to bridge experimental datasets with in silico models. The brain physiome describes the systemic interactions of its components, which are organized into a multilevel hierarchy. Because of the limitations in obtaining experimental data corresponding to each physiome component from 2D in vitro models and animal models, 3D in vitro brain models, including brain organoids and brain-on-a-chip, have been developed. In this review, we present the concept of the brain physiome and its hierarchical organization, including cell- and tissue-level organizations. We also summarize recently developed 3D in vitro brain models and link them with the elements of the brain physiome as a guideline for dataset collection. The connection between in vitro 3D brain models and in silico modeling will lead to the establishment of cost-effective and time-efficient in silico models for the prediction of the safety of unknown drugs.

Gamma irradiation exposure for collapsed cell junctions and reduced angiogenesis of 3-D in vitro blood vessels.

During radiotherapy, microenvironments neighboring the tumor are also exposed to gamma irradiation; this results in unexpected side effects. Blood vessels can serve as microenvironments for tumors and they play an important role in providing nutrients to tumors. This is mostly related to tumor progression, metastasis, and relapse after therapy. Many studies have been performed to obtain a better understanding of tumor vasculature after radiotherapy with in vitro models. However, compared to 3-D models, 2-D in vitro endothelial monolayers cannot physiologically reflect in vivo blood vessels. We previously remodeled the extracellular matrix (ECM) hydrogel that enhanced the tight barrier formation of 3-D blood vessels and the vascular endothelial growth factor (VEGF) gradient induced angiogenesis in a microfluidic device. In this study, the blood vessel model is further introduced to understand how gamma irradiation affects the endothelial monolayer. After the gamma irradiation exposure, we observed a collapsed endothelial barrier and a reduced angiogenic potential. Changes in the cell behaviors of the tip and stalk cells were also detected in the angiogenesis model after irradiation, which is difficult to observe in 2-D monolayer models. Therefore, the 3-D in vitro blood vessel model can be used to understand radiation-induced endothelial injuries.

Rosiglitazone protects the pancreatic beta-cell death induced by cyclosporine A.

The pathogenesis of post-transplant diabetes mellitus (PTDM) is thought to be partly related to the direct toxic effect of cyclosporine (CsA) on pancreatic beta-cells and the resultant decrease in insulin synthesis and secretion. Although rosiglitazone (Rosi) is an insulin sensitizer, recent data has shown that Rosi also directly protects against beta-cell dysfunction and death. This study was undertaken to clarify the effects of Rosi on CsA-induced beta-cell dysfunction and death. The deterioration in glucose tolerance caused by CsA administration was significantly improved by cotreatment with Rosi. The relative volume and absolute mass of beta-cells were significantly reduced by CsA, whereas combined treatment with Rosi had protective effects. Induction of beta-cell death and increased expression of endoplasmic reticulum (ER) stress markers (CHOP and spliced XBP-1) by CsA were rescued by Rosi. Thus, Rosi signaling directly modulates the ER stress response, promoting beta-cell adaptation and survival. Rosi might be an appropriate drug for preventing and treating CsA-induced PTDM.