Our data demonstrate that MPs generated from VHD patients before and after cardiac surgery contributed to endothelial dysfunction, by uncoupling and inhibiting eNOS. Circulating MPs are potential therapeutic targets for the maintenance of vascular function postoperatively.

Endothelial dysfunction is a key early step in atherosclerosis. 25-Hydroxycholesterol (25-OHC) is found in atherosclerotic lesions. However, whether 25-OHC promotes atherosclerosis is unclear. Here, we hypothesized that 25-OHC, a proinflammatory lipid, can impair endothelial function, which may play an important role in atherosclerosis. Bovine aortic endothelial cells were incubated with 25-OHC. Endothelial cell proliferation, migration, and tube formation were measured. Nitric oxide (NO) production and superoxide anion generation were determined. The expression and phosphorylation of endothelial NO synthase (eNOS) and Akt as well as the association of eNOS and heat shock protein (HSP)90 were detected by immunoblot analysis and immunoprecipitation. Endothelial cell apoptosis was monitored by TUNEL staining and caspase-3 activity, and expression of Bcl-2, Bax, cleaved caspase-9, and cleaved caspase-3 were detected by immunoblot analysis. Finally, aortic rings from Sprague-Dawley rats were isolated and treated with 25-OHC, and endothelium-dependent vasodilation was evaluated. 25-OHC significantly inhibited endothelial cell proliferation, migration, and tube formation. 25-OHC markedly decreased NO production and increased superoxide anion generation. 25-OHC reduced the phosphorylation of Akt and eNOS and the association of eNOS and HSP90. 25-OHC also enhanced endothelial cell apoptosis by decreasing Bcl-2 expression and increasing cleaved caspase-9 and cleaved caspase-3 expressions as well as caspase-3 activity. 25-OHC impaired endothelium-dependent vasodilation. These data demonstrated that 25-OHC could impair endothelial function by uncoupling and inhibiting eNOS activity as well as by inducing endothelial cell apoptosis. Our findings indicate that 25-OHC may play an important role in regulating atherosclerosis.

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Driven by the increasing demand for intelligent wearable electronics, pressure sensors have attracted substantial research interest. However, a pressure sensor that possesses both high sensitivity and wearable comfort for practical application in daily activities is still lacking. Herein, we design a fabric−elastomer hybrid pressure sensor that achieves a balance between sensing performance and comfort. In this well-designed sensor, medical gauze coated with silver nanowires acts as substrate to improve the comfort of the sensor, and an elastomer acts as an active sensing element to enhance the sensitivity of the sensor. The sensor exhibits exciting sensing performance, including a high sensitivity (58 kPa −1 , 0−0.5 kPa), long-term endurance (>27 500 cycles), a faster response speed (<27 ms), and an ultralow limit of detection (2.7 Pa). Additionally, by adopting a prestretchable medical bandage as the substrate, the resulting sensor is insensitive to tensile strain and can accurately detect pressure stimuli under complex conditions. Then, we verify the application of the sensor in different scenarios, such as sensing tiny objects, monitoring human physiological information, and recognizing body motion. Additionally, we integrate a 4 × 4 sensor array for spatial information monitoring to provide a proof of concept for future wearable electronics, especially intelligent medical diagnostic systems.