Bupivacaine is frequently used for regional anesthesia and postoperative analgesia. However, an inadvertent intravenous injection can cause severe cardiotoxicity, manifesting as arrhythmia, hypotension, and even cardiac asystole. The mechanism of bupivacaine-mediated cardiotoxicity remains unclear. SK2 knockout mice (SK) and wild-type mice (WT) were divided into four groups, with 12 mice per group. We determined the difference in bupivacaine cardiotoxicity between SK2 knockout and WT mice by measuring the time to the first arrhythmia (Tarrhythmia) and the time to asystole (Tasystole). Secondary indicators of cardiotoxicity were the time from the beginning of bupivacaine infusion to 20% prolongation of the QT interval (TQT) and the time to 20% widening of the QRS complex (TQRS). Tarrhythmia and Tasystole were significantly longer in the SK-bupi group than in the WT-bupi group (both P < 0.05). TQT and TQRS were longer in the SK-bupi group than in the WT-bupi group (all P < 0.05). The time to 25%, 50%, and 75% reduction in HR in the SK-bupi group was significantly longer than in the WT-bupi group (all P < 0.05). Knocking out the SK2 channel can reduce bupivacaine-induced cardiotoxicity in the mouse.

Twenty-four young adults with myopia in both eyes and no anisometropia participated in this study. Observers were instructed to read one A4-sized page of Chinese text at different levels of illuminance and text contrast, while their reading distance, head tilt angle and reading speed were recorded using an electromagnetic motion tracking system. Four illuminances (3, 30, 300 and 600 lx) and two text contrast levels (90% and 45%) were tested in randomised order. Observers tended to shorten their reading distance and increase their head tilt angle when reading at low illuminance. In addition, their reading speed was markedly slower at low illuminance and low contrast. These effects were found for both text contrast conditions but were greater at low contrast. Illuminance and text contrast play a critical role in myope’s reading behaviour. An illuminance of 300 lx or more with high-contrast text allows for good reading posture and rapid reading of Chinese text.

Hypoxic pulmonary hypertension (HPH) is a life‐threatening disease that occurs due to a lack of oxygen in the lungs, leading to an increase in pulmonary vascular resistance, right ventricular failure, and ultimately death. HPH is a multifactorial disorder that involves multiple molecular pathways, making it a challenge for clinicians to identify effective therapies. Pulmonary artery smooth muscle cells (PASMCs) play a crucial role in HPH pathogenesis by proliferating, resisting apoptosis, and promoting vascular remodelling. Curcumin, a natural polyphenolic compound, has shown potential as a therapeutic agent for HPH by reducing pulmonary vascular resistance, inhibiting vascular remodelling, and promoting apoptosis of PASMCs. Regulation of PASMCs could significantly inhibits HPH. However, curcumin has the disadvantages of poor solubility and low bioavailability, and its derivative WZ35 has better biosafety. Here, Cu‐based metal organic frameworks (MOFCu) was fabricated to encapsulate the curcumin analogue WZ35 (MOFCu@WZ35) for the inhibition of PASMCs proliferation. The authors found that the MOFCu@WZ35 could promote the death of PASMCs. Furthermore, the authors believed that this drug delivery system will effectively alleviate the HPH.