Soft pneumatic bending actuators are commonly used in robotic grasping applications and can be applied for handling both delicate and irregularly shaped objects. Because these soft pneumatic actuators are typically embedded with multiple air chambers inside soft, thin structures, their maximum payloads are usually low compared to rigid designs of similar size. This article presents a soft pneumatic bending actuator design using a topology optimization procedure that can maximize the bending capability and thus increase the allowable payload of soft grippers that consist of multiple pneumatic bending actuators. After an optimum design is obtained, multiple identical actuators are prototyped through a molding process using a silicone rubber material. Both two-fingered and three-fingered soft grippers are developed using the topology-optimized pneumatic bending actuators. Experiments, including a bending angle test, an output force test, and a payload test, are conducted in this study, and the results are compared against the test results of the commercial SRT soft pneumatic actuator. The experimental results show that the bending angle for the developed bending actuator is 111 degrees on average of 10 tests at an input pressure of 50 kPa. The output force is 9.45 N at an input pressure of 80 kPa, while the maximum payloads of the two-fingered and three-fingered grippers are 2.66kg and 5.12kg, respectively.

Glioblastoma multiforme (GBM) is a grade IV, highly malignant brain tumor. Because of the heterogeneity of GBM, a multitarget drug is a rational strategy for GBM treatment. Histone deacetylase inhibitors (HDACis) regulate the expression of numerous genes involved in cell death, apoptosis, and tumorigenesis. We found that the HDAC4/HDAC5 inhibitor LMK235 at 0.5 µM significantly reduced the cell viability and colony formation of patient-derived, temozolomide-resistant GBM P#5 TMZ-R, U-87 MG, and T98G cells. Moreover, LMK235 also significantly increased TUBA acetylation, which is an indicator of HDAC inhibition. Interestingly, LMK235 induced MAP1LC3 robust readout and puncta accumulation but did not enhance PARP1 cleavage or the proportion of annexin V-positive cells, suggesting that LMK235-induced cell death occurred via autophagy activation. Further RNA-seq analysis after LMK235 treatment showed that 597 different expression genes compared to control. After bioinformatic analysis by KEGG and STRING, we focused on 34 genes and validated their mRNA expression by qPCR. Further validation showed that 2 µM LMK235 significantly reduced the mRNA and protein expression of SCNN1A. Cell viability of SCNN1A-silenced cells were reduced, but cells were rescued while treated with an autophagy inhibitor bafilomycin A1. Conclusively, SCNN1A plays a role in LMK235-induced autophagy and cell death in GBM cells.

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