Thermally activated delayed fluorescence (TADF) materials based on the multiple resonance (MR) effect are applied in organic light‐emitting diodes (OLEDs), combining high color purity and efficiency. However, they are not fabricated via solution‐processing, which is an economical approach toward the mass production of OLED displays. Here, a solution‐processable MR‐TADF material (OAB‐ABP‐1), with an extended π‐skeleton and bulky substituents, is designed. OAB‐ABP‐1 is synthesized from commercially available starting materials via a four‐step process involving one‐shot double borylation. OAB‐ABP‐1 presents attractive photophysical properties, a narrow emission band, a high photoluminescence quantum yield, a small energy gap between S1 and T1, and low activation energy for reverse intersystem crossing. These properties are attributed to the alternating localization of the highest occupied and lowest unoccupied molecular orbitals induced by the boron, nitrogen, and oxygen atoms. Furthermore, to facilitate charge recombination, two novel semiconducting polymers with similar ionization potentials to that of OAB‐ABP‐1 are synthesized for use as interlayer and emissive layer materials. A solution‐processed OLED device is fabricated using OAB‐ABP‐1 and the aforementioned polymers; it exhibits pure green electroluminescence with a small full‐width at half‐maximum and a high external quantum efficiency with minimum efficiency roll‐off.

An expanded heterohelicene consisting of three BN 2 -embedded [4]helicene subunits (V-DABNA-Mes) has been synthesized by one-shot triple borylation. The key to success is the excessive use of boron tribromide in an autoclave. Based on the multiple resonance effect of three boron and six nitrogen atoms, V-DABNA-Mes exhibited a narrowband sky-blue thermally activated delayed fluorescence with a full width at half-maximum of 16 nm. The resonating π-extension minimized the singlet−triplet energy gap and enabled rapid reverse intersystem crossing with a rate constant of 4.4 × 10 5 s −1 . The solution-processed organic lightemitting diode device, employed as an emitter, exhibited a narrowband emission at 480 nm with a high external quantum efficiency of 22.9%.

The fabrication of zinc tetraphenyl porphyrin (ZnTPP)–silver nanoparticle (AgP) composite films on indium–tin-oxide (ITO) electrodes were carried out by the electrostatic layer-by-layer adsorption technique. The degree of immobilization of AgPs on the ITO electrodes could be controlled by changing the immersion time into the aqueous colloidal solution of AgPs. Maximum enhancement in the photocurrent action spectra as well as the fluorescence emission spectra was observed when optimum amounts of AgP were deposited onto the ITO electrode for the photocurrent and the fluorescence measurements, respectively. Effect of AgP on the photocurrent and the fluorescence suggested the effects of enhanced electric fields resulting from the localized surface plasmon resonance on the enhancement of photocurrent and fluorescence signals. The effect of AgP on the lifetime of the singlet excited state of ZnTPP (1ZnTPP*) indicated that the lifetime of 1ZnTPP* becomes shorter at an immersion time of 6 h. The results of the fluorescence lifetime suggested that the difference of effects of AgP on the photocurrent and the fluorescence is most likely ascribed by that the energy-transfer from 1ZnTPP* to surface plasmon due to AgP aggregates is competitive with the photoinduced electron-transfer from 1ZnTPP* to O2 in the photocurrent measurements.

In treating bladder cancer, determining the molecular mechanisms of tumor invasion, metastasis, and drug resistance are urgent to improving long-term patient survival. One of the metabolic enzymes, aldo-keto reductase 1C1 (AKR1C1), plays an essential role in cancer invasion/metastasis and chemoresistance. In orthotopic xenograft models of a human bladder cancer cell line, UM-UC-3, metastatic sublines were established from tumors in the liver, lung, and bone. These cells possessed elevated levels of EMT-associated markers, such as Snail, Slug, or CD44, and exhibited enhanced invasion. By microarray analysis, AKR1C1 was found to be up-regulated in metastatic lesions, which was verified in metastatic human bladder cancer specimens. Decreased invasion caused by AKR1C1 knockdown suggests a novel role of AKR1C1 in cancer invasion, which is probably due to the regulation of Rac1, Src, or Akt. An inflammatory cytokine, interleukin-1β, was found to increase AKR1C1 in bladder cancer cell lines. One particular non-steroidal anti-inflammatory drug, flufenamic acid, antagonized AKR1C1 and decreased the cisplatin-resistance and invasion potential of metastatic sublines. These data uncover the crucial role of AKR1C1 in regulating both metastasis and drug resistance; as a result, AKR1C1 should be a potent molecular target in invasive bladder cancer treatment.

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