Explore the vast range of titles available.

In this paper, the effects of the combination of solvents on the uniformity of a dried emitting layer and on device performance were studied. Green emitter inks with various solvents were prepared, and it was seen that good film uniformity of printed layers could be obtained with a solvent mixture with different boiling points, which reduced the coffee ring effect on a dried surface. During the inkjet process, the drop injection condition aiming was also controlled for better drop-to-drop spacing and reduction of the line-edge roughness. Printed patterns of a small molecular/polymer hybrid emitting layer, composed of the chlorobenzene-dichlorobenzene solvent mixture, showed significantly reduced roughness of the microscopic surface and improved efficiency of the inkjet device, at levels nearly comparable to those of spin-coated patterns. A suitable hole transport layer (HTL) was also further developed as an interfacial material, prior to the solution processing of the emitter. The cross-linkable HTL was composed of triphenylamine as the cross-linking unit and a fluorene-based compound. At the optimized condition of the solvent formulation, printed droplets within 100 µm× 300 µm pixels formed a uniform stripe without remarkable coffee-ring defects and line-edge surface roughness.

In this study, we investigated the ink formulation of poly(3,4-ethylenedioxythiophene) polystyrene sulfonate (PEDOT:PSS) as the hole injection layer (HIL) in an organic light emitting diode (OLED) structure. Generally, in a PEDOT:PSS solution, water is incorporated in the solution for the solution process. However, the fabrication of thin film which contained the water, main solvent, could not easily form by using printing technology except spin-coating process because of the high surface tension of water. On the other hand, mixing PEDOT:PSS solution and ethanol (EtOH), a dilution solvent, could restrain the non-uniform layer that forms by the high surface tension and low volatility of water. Therefore, we printed a PEDOT:PSS solution with various concentrations of EtOH by using a nozzle printer and obtained a uniform pattern. The line width of PEDOT:PSS diluted with 90% (volume ratio) ehtanol was measured as about 4 mm with good uniformity with a 0.1 mm nozzle. Also, imaging software and a scanning electron microscope (SEM) were used to measure the uniformity of PEDOT:PSS coated on a substrate. Finally, we fabricated a green phosphorescent OLED device with printed-PEDOT:PSS with specific concentrations of EtOH and we achieved a current efficiency of 27 cd/A with uniform quality of luminance in the case of device containing 90% EtOH.

Anti-tuberculosis (AT) medications, including isoniazid (INH), can cause drug-induced liver injury (DILI), but the underlying mechanism remains unclear. In this study, we aimed to identify genetic factors that may increase the susceptibility of individuals to AT-DILI and to examine genetic interactions that may lead to isoniazid (INH)-induced hepatotoxicity. We performed a targeted sequencing analysis of 380 pharmacogenes in a discovery cohort of 112 patients (35 AT-DILI patients and 77 controls) receiving AT treatment for active tuberculosis. Pharmacogenome-wide association analysis was also conducted using 1048 population controls (Korea1K). NAT2 and ATP7B genotypes were analyzed in a replication cohort of 165 patients (37 AT-DILI patients and 128 controls) to validate the effects of both risk genotypes. NAT2 ultraslow acetylators (UAs) were found to have a greater risk of AT-DILI than other genotypes (odds ratio [OR] 5.6 [95% confidence interval; 2.5–13.2], P  = 7.2 × 10 −6 ). The presence of ATP7B gene 832R/R homozygosity (rs1061472) was found to co-occur with NAT2 UA in AT-DILI patients ( P  = 0.017) and to amplify the risk in NAT2 UA (OR 32.5 [4.5–1423], P  = 7.5 × 10 −6 ). In vitro experiments using human liver-derived cell lines (HepG2 and SNU387 cells) revealed toxic synergism between INH and Cu, which were strongly augmented in cells with defective NAT2 and ATP7B activity, leading to increased mitochondrial reactive oxygen species generation, mitochondrial dysfunction, DNA damage, and apoptosis. These findings link the co-occurrence of ATP7B and NAT2 genotypes to the risk of INH-induced hepatotoxicity, providing novel mechanistic insight into individual AT-DILI susceptibility. Yoon et al. showed that individuals who carry NAT2 UAs and ATP7B 832R/R genotypes are at increased risk of developing isoniazid hepatotoxicity, primarily due to the increased synergistic toxicity between isoniazid and copper, which exacerbates mitochondrial dysfunction-related apoptosis. Genetic factors amplify tuberculosis drug-induced liver injury risk Tuberculosis is a major health issue, with the bacterium Mycobacterium tuberculosis causing illness and death globally. A key challenge in treating TB is the liver damage caused by drugs used in treatment, particularly isoniazid, which can lead to severe liver injury. While genetic factors like the NAT2 gene have been linked to this drug-induced liver injury, the exact reasons why some people are more susceptible remain unclear. Researchers found that certain genetic variants, particularly in the NAT2 gene and another gene called ATP7B, were more common in patients who suffered liver injury. In conclusion, the research advances our understanding of how genetics can influence the risk of liver injury from TB drugs. This knowledge could lead to more personalized treatment plans and safer TB management in the future. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.