A new flexible piezoelectric tactile sensor array based on polyvinylidene fluoride (PVDF) film is proposed for measuring three-axis dynamic contact force distribution. The array consists of six tactile units arranged as a 3 × 2 matrix with spacing 8 mm between neighbor units. In each unit, a PVDF film is sandwiched between four square-shaped upper electrodes and one square-shaped lower electrode, forming four piezoelectric capacitors. A truncated pyramid bump is located above the four piezoelectric capacitors to improve force transmission. A three-axis contact force transmitted from the top of the bump will lead to the four piezoelectric capacitors underneath undergoing different charge changes, from which the normal and shear components of the force can be calculated. A series of dynamic tests have been carried out by exerting sinusoidal forces with amplitudes ranging from 0 to 0.5 N in the x-axis, 0 to 0.5 N in the y-axis, and 0 to 1.5 N in the z-axis, separately. The tactile units show good sensitivities with 14.93, 14.92, and 6.62 pC/N in the x-, y-, and z-axes, respectively. They can work with good linearity, relatively low coupling effect, high repeatability, and acceptable frequency response in the range of 5–400 Hz to both normal and shear load. In addition, dynamic three-axis force measurement has been conducted for all of the tactile units. The average errors between the applied and calculated forces are 10.68% ± 6.84%. Furthermore, the sensor array can be easily integrated onto a curved surface, such as robotic and prosthetic hands, due to its excellent flexibility.

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Background and Purpose In non‐small‐cell lung carcinoma (NSCLC) patients, the L858R/T790M mutation of the epithelial growth factor receptor (EGFR) is a major cause of acquired resistance to EGFR‐TKIs treatment that limits their therapeutic efficacy. Identification of drugs that can preferentially kill the NSCLC harbouring L858R/T790M mutation is therefore critical. Here, we have evaluated the effects of ursolic acid, an active component isolated from herbal sources, on erlotinib‐resistant H1975 cells that harbour the L858R/T790M mutation. Experimental Approach Gene expression omnibus (GEO) profiles analyses was applied to detect differentially expressed genes in NSCLC cells harbouring EGFR mutation. AnnexinV‐FITC/PI, TUNEL staining, MTT, wound healing, RT‐PCR, qRT‐PCR, western blots, immunostaining, dual‐luciferase reporters and ChIP‐PCR were utilized to investigate the effects of ursolic acid in vitro and in vivo. Key Results The cancer/testis antigen family 45 member A2 (CT45A2) was highly expressed in H1975 cells. Ectopic expression of CT45A2 in H1975 cells increased cell proliferation and motility in vitro. Silencing the CT45A2 expression strongly attenuated H1975 cells motility and growth. The anti‐cancer effect of ursolic acid was critically dependent on CT45A2 expression in H1975 cells. Ursolic acid suppressed CT45A2 gene transcription mediated by transcriptional factor TCF4 and β‐catenin signalling. Conclusions and Implications CT45A2 is a novel oncogene for NSCLC with an EGFR T790 mutation. Ursolic acid induced apoptosis and inhibited proliferation of H1975 cells by negatively regulating the β‐catenin/TCF4/CT45A2 signalling pathway. Therefore, ursolic acid may be a potential candidate treatment for NSCLC harbouring the EGFR‐L858R/T790M mutation.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively triggers cancer cell death via its association with death receptors on the cell membrane, but exerts negligible side effects on normal cells. However, some non-small-cell lung carcinoma (NSCLC) patients exhibited resistance to TRAIL treatment in clinical trials, and the mechanism varies. In this study, we described for the first time that toosendanin (TSN), a triterpenoid derivative used in Chinese medicine for pain management, could significantly sensitize human primary NSCLC cells or NSCLC cell lines to TRAIL-mediated apoptosis both in vitro and in vivo, while showing low toxicity against human primary cells or tissues. The underlying apoptotic mechanisms involved upregulation of death receptor 5 (DR5) and CCAAT/enhancer binding protein homologous protein, which is related to the endoplasmic reticulum stress response, and is further associated with reactive oxygen species generation and Ca2+ accumulation. Surprisingly, TSN also induced autophagy in NSCLC cells, which recruited membrane DR5, and subsequently antagonized the apoptosis-sensitizing effect of TSN. Taken together, TSN can be used to sensitize tumors and the combination of TRAIL and TSN may represent a useful strategy for NSCLC therapy; moreover, autophagy serves as an important drug resistance mechanism for TSN.