Fully sprayed MXene-based high-performance flexible piezoresistive sensor for image recognition

High-performance flexible pressure sensors provide comprehensive tactile perception and are applied in human activity monitoring,soft robotics,medical treatment,and human-computer interface.However,these flexible pressure sensors require extensive nano-architectural design and complicated manufacturing and are timeconsuming.Herein,a highly sensitive,flexible piezoresistive tactile sensor is designed and fabricated,consisting of three main parts:the randomly distributed microstructure on T-ZnOw/PDMS film as a top substrate,multilayer Ti_(3)C_(2)-MXene film as an intermediate conductive filler,and the few-layer Ti_(3)C_(2)-MXene nanosheetbased interdigital electrodes as the bottom substrate.The MXene-based piezoresistive sensor with randomly distributed microstructure exhibits a high sensitivity over a broad pressure range(less than 10 kPa for 175 kPa^(-1))and possesses an out-standing permanence of up to 5000 cycles.Moreover,a 16-pixel sensor array is designed,and its potential applications in visualizing pressure distribution and an example of tactile feedback are demonstrated.This fully sprayed MXene-based pressure sensor,with high sensitivity and excellent durability,can be widely used in,electronic skin,intelligent robots,and many other emerging technologies.

Canonical transient receptor potential channel 1 aggravates myocardial ischemia-and-reperfusion injury by upregulating reactive oxygen species

The canonical transient receptor potential channel(TRPC)proteins form Ca^(2+)-permeable cation channels that are involved in various heart diseases.However,the roles of specific TRPC proteins in myocardial ischemia/reperfusion(I/R)injury remain poorly understood.We observed that TRPC1 and TRPC6 were highly expressed in the area at risk(AAR)in a coronary artery ligation induced I/R model.Trpc1/mice exhibited improved cardiac function,lower serum Troponin T and serum creatine kinase level,smaller infarct volume,less fibrotic scars,and fewer apoptotic cells after myocardial-I/R than wild-type or Trpc6/mice.Cardiomyocyte-specific knockdown of Trpc1 using adeno-associated virus 9 mitigated myocardial I/R injury.Furthermore,Trpc1 deficiency protected adult mouse ventricular myocytes(AMVMs)and HL-1 cells from death during hypoxia/reoxygenation(H/R)injury.RNA-sequencing-based transcriptome analysis revealed differential expression of genes related to reactive oxygen species(ROS)generation in Trpc1/cardiomyocytes.Among these genes,oxoglutarate dehydrogenase-like(Ogdhl)was markedly downregulated.Moreover,Trpc1 deficiency impaired the calcineurin(CaN)/nuclear factorkappa B(NF-kB)signaling pathway in AMVMs.Suppression of this pathway inhibited Ogdhl upregulation and ROS generation in HL-1 cells under H/R conditions.Chromatin immunoprecipitation assays confirmed NF-kB binding to the Ogdhl promoter.The cardioprotective effect of Trpc1 deficiency was canceled out by overexpression of NF-kB and Ogdhl in cardiomyocytes.In conclusion,our findings reveal that TRPC1 is upregulated in the AAR following myocardial I/R,leading to increased Ca^(2+) influx into associated cardiomyocytes.Subsequently,this upregulates Ogdhl expression through the CaN/NF-kB signaling pathway,ultimately exacerbating ROS production and aggravating myocardial I/R injury.