Suchergebnisse

In recent years, low-power wireless sensors with high flexibility, portability and computing capability have been extensively applied in areas such as military, medicine and mechanical equipment condition monitoring. In this paper, a novel symmetrical T-shaped trapezoidal micro piezoelectric energy harvester (STTM-PEH) is proposed to supply energy for wireless sensors monitoring the vibrations of mechanical equipment. Firstly, the finite element model (FEM) of the STTM-PEH is established. Secondly, the modal analysis of the T-shaped trapezoidal piezoelectric cantilever beam is carried out by finite element software and its vibration modes are obtained. Additionally, the structural characteristics of the STTM-PEH and the composition of piezoelectric patches are described. Furthermore, the effects of resistance, acceleration coefficient, substrate materials and structural parameters of the output performance of the STTM-PEH are researched. The results indicate that the output power of the STTM-PEH rises first and then falls with a change in resistance, while the output voltage does not increase as resistance increases to a certain extent. Meanwhile, selecting copper as the piezoelectric material of the T-shaped trapezoidal piezoelectric cantilever beam can generate a higher energy output. Finally, how the structural parameters, including piezoelectric patch thickness, substrate thickness and cantilever head length, affect the output performance of the STTM-PEH is studied, which illustrates that the load range of the STTM-PEH can be appropriately broadened by adjusting the length of the cantilever beam head. This research is valuable for designing a novel high performance piezoelectric energy harvester.

Zichang Zhao,1,2,* Wei Shen,2,* Hanbin Zhu,3,* Lin Lin,4 Gening Jiang,1 Yongzhe Zhu,5 Hongyuan Song,2 Liang Wu1 1Department of Thoracic Surgery, Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China; 2Department of Ophthalmology, Changhai Hospital, Second Military Medical University, Shanghai, China; 3Company 11 of Student Brigade, Second Military Medical University, Shanghai, China; 4Department of Regenerative Medicine, Tongji University School of Medicine, Shanghai, China; 5Department of Microbiology, Second Military Medical University, Shanghai, China *These authors contributed equally to this work Background: Previous preclinical and clinical studies have demonstrated that zoledronate might inhibit neointimal hyperplasia at least partly by inhibiting the proliferation, adhesion and migration of vascular smooth muscle cells (VSMCs). However, whether zoledronate influences fibroblasts' proliferation and activation, which also play a key role in neointimal hyperplasia and vascular remodeling, remains largely unknown. In the present study, the effect of zoledronate on fibroblasts was investigated and the underlying molecular mechanisms were examined.Methods: After treatment with zoledronate, changes in biological behaviors, including the morphology, proliferation, cell-cycle distribution and migration of fibroblasts (NIH3T3 cells), were observed. The expression of α-SMA, TGF-β1 and TGF-β2 and the level of Smad2/3 phosphorylation in cultured fibroblasts were examined by Western blot. In vivo expression of α-SMA and TGF-β1 was assessed by immunohistochemical staining.Results: It was shown that the typical fibroblast cell morphology was altered after zoledronate exposure. Cultured fibroblasts treated with zoledronate displayed dose-dependent inhibition of cell proliferation due to cell-cycle arrest in the S phase. Cell migration activities were also dose dependently suppressed by zoledronate treatment. Expression of α-SMA in cultured fibroblasts was significantly reduced by zoledronate treatment. Further analysis showed decreased expression of TGF-β1 and α-SMA by periadventitial delivery of zoledronate in the rat carotid balloon-injury model. The expression of TGF-β1 and TGF-β2 and the phosphorylation of Smad2/3 in cultured fibroblasts were significantly inhibited by zoledronate treatment.Conclusion: Our findings demonstrated that zoledronate can inhibit the proliferation, migration and activation of fibroblasts via the TGF-β signaling pathway and revealed a novel mechanism of zoledronate action against neointimal hyperplasia. Keywords: zoledronate, fibroblasts, neointimal hyperplasia, TGF-β pathway

Over the past four decades, China's food security and nutritional status have improved significantly witnessed by elimination of hunger and poverty, increased diversity of diets, and reduction in child stunting. However, the Chinese food systems will face even greater challenges in the future. These include constraints of natural resources, climate change, multiple challenges of malnutrition, food safety, and external shocks from volatile international market. Fortunately, the Chinese government has made important commitments in the ""Fourteenth Five-year Plan"" on food and nutrition security, health, the environment and climate change including achieving carbon neutrality by 2060. The purpose of this brief is to review major achievements and their enabling factors, future challenges and government strategies as well as our recommendations to transform Chinese food systems for both human and planetary health. This paper will help to bring voices of emerging economies like China in setting the global food systems agenda, providing useful insights on the transformation of its own food systems as well as those in other countries.

Yongqiang Xiao,1,* Dayuan Xu,1,* Hongyuan Song,2,* Futing Shu,1 Pei Wei,3 Xiaolan Yang,3 Chenjian Zhong,3 Xiaohong Wang,4 Werner EG Müller,4 YongJun Zheng,1 Shichu Xiao,1,* Zhaofan Xia11Department of Burn Surgery, Changhai Hospital, Second Military Medical University, Shanghai, People's Republic of China; 2Department of Ophthalmology, Changhai Hospital, Second Military Medical University, Shanghai 200433, People's Republic of China; 3Department of Burns Surgery, Union Hospital, Fujian Medical University, Fuzhou 350001, People's Republic of China; 4Erc Advanced Investigator Grant Research Group at the Institute for Physiological Chemistry, University Medical Center of the Johannes Gutenberg University, Mainz 55128, Germany*These authors contributed equally to this workBackground: Less apoptosis and excessive growth of fibroblasts contribute to the progression of hypertrophic scar formation. Cuprous oxide nanoparticles (CONPs) could have not only inhibited tumor by inducing apoptosis and inhibiting proliferation of tumor cells, but also promoted wound healing. The objective of this study was to further explore the therapeutic effects of CONPs on hypertrophic scar formation in vivo and in vitro.Methods: In vivo, a rabbit ear scar model was established on New Zealand albino rabbits. Six full-thickness and circular wounds (10 mm diameter) were made to each ear. Following complete re-epithelization observed on postoperative day 14, an intralesional injection of CONPs or 5% glucose solution was conducted to the wounds. The photo and ultrasonography of each wound were taken every week and scars were harvested on day 35 for further histomorphometric analysis. In vitro, the role of CONPs in human hypertrophic scar fibroblasts (HSFs) apoptosis and proliferation were evaluated by Tunnel assay, Annexin V/PI staining, cell cycle analysis, and EdU proliferation assay. The endocytosis of CONPs by fibroblasts were detected through transmission electron microscopy (TEM) and the mitochondrial membrane potential and ROS production were also detected.Results: In vivo, intralesional injections of CONPs could significantly improve the scar appearance and collagen arrangement, and decreased scar elevation index (SEI). In vitro, CONPs could prominently inhibit proliferation and induce apoptosis in HSFs in a concentration-dependent manner. In addition, CONPs could be endocytosed into mitochondria，damage the mitochondrial membrane potential and increase ROS production.Conclusion: CONPs possessed the therapeutic potential in the treatment of hypertrophic scar by inhibiting HSFs proliferation and inducing HSFs apoptosis.Keywords: CONPs, hypertrophic scar, apoptosis, proliferation, mitochondria