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Most of acridine based thermally activated delayed fluorescence (TADF) emitters are characterized by advantageous reverse intersystem crossing (RISC) rate (kRISCs) due to the perpendicular orientation of the acridine donor to the acceptor moiety, but suffer from a poor radiation rate (kr) typically in the order of 106 s−1. Herein, two sky blue TADF emitters 3,6‐DMAC‐AD‐Py and 3,6‐SFAC‐AD‐Py were developed by linking acridine (DMAC) and spiro‐fluorene‐acridine (SFAC) donors to 10‐(pyridin‐2‐yl)acridin‐9(10H)‐one (AD‐Py) acceptor. Larger SFAC and electron‐deficient pyridyl groups are deliberately incorporated in 3,6‐SFAC‐AD‐Py since the unique through‐space interaction between them is designed to drive the rotation of inner acridine ring in SFAC for enhancing frontier molecular orbitals overlap while keeping a decent TADF behavior. Thus, the kr of 3,6‐SFAC‐AD‐Py is increased to 1.5 × 107 s−1. Simultaneously, SFAC donors improve spin orbital coupling strength and reduce the energy gaps, generating kRISC of 1.8 × 106 s−1. This is the first acridine donor based TADF emitter realizing kr of 107 s−1 and kRISC of 106 s−1 by a through‐space interaction strategy. 3,6‐SFAC‐AD‐Py enables a highly efficient sky‐blue organic light‐emitting diode with a maximum external quantum efficiency (EQE) of 34.7% and Commission International de I'Eclairage coordinates of (0.19, 0.37). More importantly, the EQE still remained 27.6% and 16.9% at high brightness of 1000 and 10,000 cd m−2. Intramolecular through‐space interaction is designed for the first time in a thermally activated delayed fluorescence emitter to pull the appropriate rotation of the acridine donor to deviate from the perpendicular orientation, which solves the common problem of insufficient FMO overlap to simultaneously enhance the radiation transition and reverse intersystem crossing process and thus lead to a high EQE of 34.7% with quite slow efficiency roll‐off in blue organic light‐emitting diodes.

Background: Retinal leukostasis plays an important role in the pathogenesis of diabetic retinopathy. Objectives: We studied the effects of nipradilol, a topical antiglaucoma αβ-blocker and nitric oxide donor, on the retinal vascular leukocyte adhesion of rats with diabetes. Methods: Diabetes was induced in seven Brown-Norway rats by one intravenous injection (65 mg/kg) of streptozotocin and confirmed by blood glucose levels >350 mg/dl 48 h after the injection. Nipradilol solution was instilled in the right eye and nipradilol-free base solution in the left eye for 3 weeks, after which the retinal microcirculation was evaluated by acridine orange leukocyte digital fluorography using laser scanning ophthalmoscopy. Leukocytes trapped in the retina were counted around the optic disc in a 5-disc-diameter area and compared between the right and the left eye. Results: The mean retinal leukostasis count in the nipradilol-treated eyes (19 ± 15 cells) was significantly lower than in the untreated eyes (49 ± 19 cells; p < 0.0008). The diameter of the retinal artery in the eyes treated with nipradilol significantly increased (111 ± 13.5%) compared with untreated eyes (p < 0.03). Conclusions: Topical nipradilol significantly reduced retinal leukostasis in the retinal microcirculation in diabetic rats and may be a prophylactic agent for early diabetic retinopathy through its nitric oxide donor effects on the microcirculation.