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The morphology and optical and electrical properties of solution-processed and vacuum-deposited 4,4',4″-tris(carbazol-9-yl)triphenylamine (TCTA):2,2'-(1,3-phenylene)bis[5-(4-tert-butylphenyl)-1,3,4-oxadiazole] (OXD-7) composite films are investigated. All of the films exhibit smooth and pinhole-free morphology, while the evaporated films possess enhanced carrier-transport properties compared to solution-processed ones. The close correlation between the carrier-transport feature and the packing density of the film is established. High-efficiency monochromatic and white phosphorescent hybrid organic-inorganic light-emitting diodes with solution-processed small-molecule emissive layers are reported: the maximum external quantum efficiencies of blue, yellow, and red devices are 18.9, 14.6, and 10.2%, respectively; white devices show a maximum luminance efficiency of 40 cd A(-1) and a power efficiency of 20.8 lm W(-1) at 1000 cd m(-2). The efficiencies of blue, red, and white devices represent significant improvement over previously reported values.

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Background and Aims Ischemia‐reperfusion (I/R) injury is an inevitable complication of liver transplantation (LT) and compromises its prognosis. Glycosyltransferases have been recognized as promising targets for disease therapy, but their roles remain open for study in hepatic I/R (HIR) injury. Here, we aim to demonstrate the exact function and molecular mechanism of a glycosyltransferase, N‐acetylgalactosaminyltransferase‐4 (GALNT4), in HIR injury. Approach and Results By an RNA‐sequencing data‐based correlation analysis, we found a close correlation between GALNT4 expression and HIR‐related molecular events in a murine model. mRNA and protein expression of GALNT4 were markedly up‐regulated upon reperfusion surgery in both clinical samples from subjects who underwent LT and in a mouse model. We found that GALNT4 deficiency significantly exacerbated I/R‐induced liver damage, inflammation, and cell death, whereas GALNT4 overexpression led to the opposite phenotypes. Our in‐depth mechanistic exploration clarified that GALNT4 directly binds to apoptosis signal‐regulating kinase 1 (ASK1) to inhibit its N‐terminal dimerization and subsequent phosphorylation, leading to a robust inactivation of downstream c‐Jun N‐terminal kinase (JNK)/p38 and NF‐κB signaling. Intriguingly, the inhibitory capacity of GALNT4 on ASK1 activation is independent of its glycosyltransferase activity. Conclusions GALNT4 represents a promising therapeutic target for liver I/R injury and improves liver surgery prognosis by inactivating the ASK1‐JNK/p38 signaling pathway.

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