Novel Strain Engineering Combined with a Microscopic Pore Synergistic Modulated Strategy for Designing Lattice Tensile-Strained Porous V2C-MXene for High-Performance Overall Water Splitting.

Transition metal carbon/nitride (MXene) holds immense potential as an innovative electrocatalyst for enhancing the overall water splitting properties. Nevertheless, the re-stacking nature induced by van der Waals force remains a significant challenge. In this work, the lattice tensile-strained porous V2C-MXene (named as TS(24)-P(50)-V2C) is successfully constructed via the rapid spray freezing method and the following hydrothermal treatment. Besides, the influence of lattice strain degree and microscopic pores on the catalytic ability is reviewed and explored systematically. The lattice tensile strain within V2C-MXene could widen the interlayer spacing and accelerate the ion transfer. The microscopic pores could change the ion transmission path and shorten the migration distance. As a consequence, the obtained TS(24)-P(50)-V2C shows extraordinary hydrogen evolution reaction and oxygen evolution reaction activity with the overpotential of 154 and 269 mV, respectively, at the current density of 10 mA/cm2, which is quite remarkable compared to the MXene-based electrocatalysts. Moreover, the overall water splitting device assembled using TS(24)-P(50)-V2C as both anode and cathode demonstrates a low cell voltage requirement of 1.57 V to obtain 10 mA/cm2. Overall, the implementation of this work could offer an exciting avenue to overcome the re-stacking issue of V2C-MXene, affording a high-efficiency electrocatalyst with superior catalytic activity and desirable reaction kinetics.

Correction: TRPC6-dependent Ca2+ signaling mediates airway inflammation in response to oxidative stress via ERK pathway.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

TRPC6-dependent Ca2+ signaling mediates airway inflammation in response to oxidative stress via ERK pathway.

Ozone (O3) plays an extremely important role in airway inflammation by generating reactive oxygen species (ROS) including hydrogen peroxide, then promoting redox actions and causing oxidative stress. Evidences indicate that TRPC6 (canonical transient receptor potential channel 6) is a redox-regulated Ca2+ permeable nonselective cation channel, but its role in the setting of oxidative stress-related airway inflammation remains unknown. Here, we found that both TRPC6-/- mice and mice pretreated with SAR7334, a potent TRPC6 inhibitor, were protected from O3-induced airway inflammatory responses. In vitro, both knockdown of TRPC6 expression with shRNA and TRPC6 blockage markedly attenuated the release of cytokines IL-6 and IL-8 induced by O3 or H2O2 in 16HBE cells (human bronchial epithelial cell line). Treatment with O3 or H2O2 enhanced TRPC6 protein expression in vivo and vitro. We also observed that TRPC6-dependent increase of intracellular Ca2+ concentration ([Ca2+]i) was triggered by H2O2, which consisted of the release from intracellular calcium store and the influx of extracellular Ca2+ and could be further strengthened by 6-h O3 exposure in both 16HBE cells and HBEpiCs (primary human bronchial epithelial cells). Moreover, we confirmed that the activation of MAPK signals (ERK1/2, p38, JNK) was required for the inflammatory response induced by O3 or H2O2 while only the phosphorylation of ERK pathway was diminished in the TRPC6-knockdown situation. These results demonstrate that oxidative stress regulates TRPC6-mediated Ca2+ cascade, which leads to the activation of ERK pathway and inflammation and could become a potential target to treat oxidative stress-associated airway inflammatory diseases.

Comparison of Carotid Atherosclerosis between Patients at High Altitude and Sea Level: A Chinese Atherosclerosis Risk Evaluation Study.

OBJECTIVES: To investigate the differences in characteristics of carotid plaques between patients Xining at high altitude and Jinan at sea level using magnetic resonance (MR) imaging. METHODS: Subjects were recruited from a cross-sectional, observational, multicenter imaging study of CARE-II study. Forty-nine (mean age 63.3 ± 12.0 years, 33 males) and 51 (mean age 64.5 ± 12.0 years, 34 males) patients were recruited from a site located in a high altitude region and a site located near sea level, respectively. All patients underwent multicontrast MR vessel wall imaging for carotid arteries on 3.0 T MR scanner. The carotid plaques features were compared between 2 patient groups. RESULTS: Compared with patients at sea level, those at high altitude had significantly greater lumen area (58.5 ± 17.8 mm2 versus 50.0 ± 19.6 mm2, P = .008), smaller maximum normalized wall index (48.6% ± 14.2% versus 57.8% ± 16.3%, P = .002), and smaller percentage volume of calcium (0.9% versus 5.6%, P < .001) in the symptomatic carotid artery. After adjustment for clinical risk factors including age, sex, systolic blood pressure, LDL-C, and statin use, these differences in plaque morphology and composition remained statistically significant. After further adjustment for normalized wall index as a measure of plaque burden, percentage volume of calcification was still significantly smaller in patients at high altitude area than that in patients at sea level area (P = .047). CONCLUSION: Symptomatic subjects from a high altitude area have lower plaque burden and less calcification in the carotid artery compared to those from an area near sea level.

TRPC6 modulates adhesion of neutrophils to airway epithelial cells via NF-κB activation and ICAM-1 expression with ozone exposure.

Ozone (O3) is a major component of air pollution, which has been associated with airway inflammation characterized by the influx of neutrophils in asthmatic subjects. Canonical transient receptor potential 6 (TRPC6) channel is recently identified as a target of oxidative stress which is involved in airway inflammation. However, the regulatory role of TRPC6 in airway epithelial cells and neutrophils has not yet been illuminated in detail. In this study, we investigated the role of TRPC6 in neutrophil adhesion to airway epithelial cells exposed to O3 in vivo and in vitro approaches. Using transgenic mice, the results showed that TRPC6-deficiency attenuated O3-induced neutrophil recruitment to airway epithelial cells and intercellular adhesion molecule-1 (ICAM-1) expression. In vitro, O3 induced ICAM-1 expression and neutrophil adhesion to 16HBE cells (human airway epithelial cell line) and which were reduced by both TRPC6 silencing short hairpin RNA (shRNA) and TRPC6 inhibitor Larixyl Acetate (LA). We also confirmed that TRPC6-dependent Ca2+ entry and NF-κB activation in 16HBE cells were required for ICAM-1-mediated neutrophil adhesion exposed to O3. In conclusion, this study demonstrated the contribution of TRPC6 to O3-induced neutrophil adhesion to airway epithelial cells via NF-κB activation and ICAM-1 expression, which may provide new potential concepts for preventing and treating air pollutant-related inflammatory lung diseases.