Stretchable strain sensors with high sensitivity or gauge factor (GF), large stretchability, and long-term durability are highly demanded in human motion detection, artificial intelligence, and electronic skins. Nevertheless, to develop high-sensitive sensors without sacrificing the stretchability cannot be realized using simple device configurations. In this work, an acid-interface engineering (AIE) method was proposed to develop a stretchable strain sensor with high GF and large stretchability. The AIE generates a layer of SiO x at the interface between the carbon nanotube (CNT) film and Ecoflex, playing a key role in enhancing the sensor’s GF. Compared to devices without AIE (GF = 2.4), the ones with AIE are significantly improved. At an AIE time of 10 min, the GF up to 1665.9 is achieved without sacrificing the stretchability (>100%). The AIE-generated cracks are found to modulate the electrical behaviors and enhance the GFs of sensors with AIE through the crack-induced rapid reduction in the electrical conduction pathway, which is manipulated by the CNTs bridging over the cracks. The device with AIE proves its high mechanical durability through a cycling test (>10 000 cycles) at a high strain up to ∼80%, further paving its practical applications in various human motion detections.

Background Aloin exerts considerable protective effects in various disease models, and its effect on hepatic ischemia-reperfusion (HIR) injury remains unknown. This research is aimed at conducting an in-depth investigation of the antioxidant, anti-inflammatory, and antiapoptosis effects of aloin in HIR injury and explain the underlying molecular mechanisms. Methods In vivo, different concentrations of aloin were intraperitoneally injected 1 h before the establishment of the HIR model in male mice. The hepatic function, pathological status, oxidative stress, and inflammatory and apoptosis markers were measured. In vitro, aloin (AL, C21H22O9) or lipopolysaccharide (LPS) was added to a culture of mouse primary hepatocytes before it underwent hypoxia/reoxygenation (H/R), and the apoptosis in the mouse primary hepatocytes was analyzed. Results We found that 20 mg/kg was the optimum concentration of aloin for mitigating I/R-induced liver tissue damage, characterized by decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Aloin pretreatment substantially suppressed the generation of hepatic malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and IL-6 and enhanced the hepatic superoxide dismutase (SOD) activities as well as glutathione (GSH) and IL-10 levels in the liver tissue of I/R mice; this indicated that aloin ameliorated I/R-induced liver damage by reducing the oxidative stress and inflammatory response. Moreover, aloin inhibited hepatocyte apoptosis and inflammatory response that was caused by the upregulated expression of Bcl-2, the downregulated expression of cleaved caspase3(C-caspase3), Bax, Toll-like receptor 4 (TLR4), FADD, MyD88, TRAF6, phosphorylated IKKα/β (p-IKKα/β), and phosphorylated nuclear factor κB p65 (p-NF-κB p65).

Acetaminophen (APAP) is one of the safest and most effective over-the-counter (OTC) analgesics and antipyretics, but excessive doses of which will induce hepatotoxicity with high morbidity and mortality worldwide. Kaempferol...

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