A Bidirectional Single-Stage DC/AC Converter for Grid Connected Energy Storage Systems

Jianliang Chen,Xiaozhong Liao,Deshang Sha 전력전자학회 2015 JOURNAL OF POWER ELECTRONICS Vol.15 No.4

In this paper, a unified control strategy using the current space vector modulation (CSVM) technique is proposed and applied to a bidirectional three-phase DC/AC converter. The operation of the converter changes with the direction of the power flow. In the charging mode, it works as a buck type rectifier; and during the discharging mode, it operates as a boost type inverter, which makes it suitable as an interface between high voltage AC grids and low voltage energy storage devices. This topology has the following advantages: high conversion efficiency, high power factor at the grid side, tight control of the charging current and fast transition between the charging and discharging modes. The operating principle of the mode analysis, the gate signal generation, the general control strategy and the transition from a constant current (CC) to a constant voltage (CV) in the charging mode are discussed. The proposed control strategy has been validated by simulations and experimental results obtained with a 1kW laboratory prototype using supercapacitors as an energy storage device.

A Bidirectional Single-Stage DC/AC Converter for Grid Connected Energy Storage Systems

Chen, Jianliang,Liao, Xiaozhong,Sha, Deshang The Korean Institute of Power Electronics 2015 JOURNAL OF POWER ELECTRONICS Vol.15 No.4

In this paper, a unified control strategy using the current space vector modulation (CSVM) technique is proposed and applied to a bidirectional three-phase DC/AC converter. The operation of the converter changes with the direction of the power flow. In the charging mode, it works as a buck type rectifier; and during the discharging mode, it operates as a boost type inverter, which makes it suitable as an interface between high voltage AC grids and low voltage energy storage devices. This topology has the following advantages: high conversion efficiency, high power factor at the grid side, tight control of the charging current and fast transition between the charging and discharging modes. The operating principle of the mode analysis, the gate signal generation, the general control strategy and the transition from a constant current (CC) to a constant voltage (CV) in the charging mode are discussed. The proposed control strategy has been validated by simulations and experimental results obtained with a 1kW laboratory prototype using supercapacitors as an energy storage device.

TGF-β1/IL-11/MEK/ERK signaling mediates senescence-associated pulmonary fibrosis in a stress-induced premature senescence model of Bmi-1 deficiency

Haiyun Chen,Jialong Liang,Xin Gu,Jiawen Zhou,Chunfeng Xie,Xianhui Lv,Rong Wang,Qing Liu,Zhiyuan Mao,Haijian Sun,Guoping Zuo,Dengshun Miao,Jianliang Jin 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

To study whether TGF-β1/IL-11/MEK/ERK (TIME) signaling mediates senescence-associated pulmonary fibrosis (SAPF) in Bmi-1-deficient (Bmi-1−/−) mice and determines the major downstream mediator of Bmi-1 and crosstalk between p16INK4a and reactive oxygen species that regulates SAPF, phenotypes were compared among 7-week-old p16INK4a and Bmi-1 double-knockout, N-acetylcysteine (NAC)-treated Bmi-1−/−, Bmi-1−/−, and wild-type mice. Pulmonary fibroblasts and alveolar type II epithelial (AT2) cells were used for experiments. Human pulmonary tissues were tested for type Ι collagen, α-smooth muscle actin (α-SMA), p16INK4a, p53, p21, and TIME signaling by using enzyme-linked immunosorbent assay (ELISA). Our results demonstrated that Bmi-1 deficiency resulted in a shortened lifespan, ventilatory resistance, poor ventilatory compliance, and SAPF, including cell senescence, DNA damage, a senescence-associated secretory phenotype and collagen overdeposition that was mediated by the upregulation of TIME signaling. The signaling stimulated cell senescence, senescence-related secretion of TGF-β1 and IL-11 and production of collagen 1 by pulmonary fibroblasts and the epithelial-to-mesenchymal transition of AT2 cells. These processes were inhibited by anti-IL-11 or the MEK inhibitor PD98059. NAC treatment prolonged the lifespan and ameliorated pulmonary dysfunction and SAPF by downregulating TIME signaling more than p16INK4a deletion by inhibiting oxidative stress and DNA damage and promoting ubiquitinproteasome degradation of p16INK4a and p53. Cytoplasmic p16INK4a accumulation upregulated MEK/ERK signaling by inhibiting the translocation of pERK1/2 (Thr202/Tyr204) from the cytoplasm to the nucleus in senescent fibroblasts. The accumulation of collagen 1 and α-SMA in human lungs accompanied by cell senescence may be mediated by TIME signaling. Thus, this signaling in aging fibroblasts or AT2 cells could be a therapeutic target for preventing SAPF.

Slab analysis of large cylindrical shell rolling considering mixed friction

Suwen Chen,Hongmin Liu,Yan Peng,Jianliang Sun 대한기계학회 2014 JOURNAL OF MECHANICAL SCIENCE AND TECHNOLOGY Vol.28 No.11

Large cylindrical shell rolling is an advanced plastic-forming technique that has unequal speed and radius of both its upper and lowerrolls. A theoretical model for a large cylindrical shell rolling that is based on the slab method is proposed, in which the non-uniform normaland shear stresses that act on the vertical sides are considered. A mixed friction model of combined Coulomb and sticking friction isused to present interface friction, to improve the accuracy of the proposed model. The rolling pressure, rolling force, and torque as well asfriction stress can be rapidly and easily calculated through the proposed model at different rolling conditions. The predicted rolling forceis consistent with the experimental result. The research results provide valuable guidelines for both the design and optimization of rollingproduct, process, and equipment.

A Wrapper for Extracting Information Records from Forums based on Page Segmentation

Chunshan Li,Jingjing Chen,Dianhui Chu,Ge Song,Haijun Zhang,Yunming Ye,Jianliang Xu 보안공학연구지원센터 2014 International Journal of Database Theory and Appli Vol.7 No.4

MiR-200c-3p inhibits LPS-induced M1 polarization of BV2 cells by targeting RIP2

Zhao Lei,Liu Xiaosong,Yang Jiankai,Wang Xiaoliang,Liu Xiaomeng,Wu Jianliang,Li Chen,Xu Donggang,Hu Yuhua 한국유전학회 2022 Genes & Genomics Vol.44 No.4

Background: Microglia are important immune cells, which can be induced by lipopolysaccharide (LPS) into M1 phenotype that express pro-inflammatory cytokines. Some studies have shown that microRNAs play critical roles in microglial activation. Objective: This study was designed to investigate the role of miR-200c-3p in regulating inflammatory responses of LPS-treated BV2 cells. Methods: The expression of miR-200c-3p in BV2 cells was detected by real-time PCR. Receptor-interacting protein 2 (RIP2) was predicted as a target gene of miR-200c-3p. Their relationship was verified by dual-luciferase reporter assay. The function of miR-200c-3p and RIP2 in microglial polarization and NF-κB signaling was further evaluated. Results: LPS treatment reduced miR-200c-3p expression in a dose-dependent and time-dependent manner in BV2 cells. LPS treatment increased the expression of M1 phenotype markers inducible nitric oxide synthase (iNOS) and major histocompatibility complex class (MHC)-II, promoted the release of pro-inflammatory cytokines interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α, and enhanced the nuclear translocation and phosphorylation of nuclear factor-kappaB (NF-κB) p65. Reversely, miR-200c-3p mimics down-regulated the levels of these inflammatory factors. Furthermore, RIP2 was identified to be a direct target of miR-200c-3p. RIP2 knockdown had a similar effect to miR-200c-3p mimics. Overexpression of RIP2 eliminated the inhibitory effect of miR-200c-3p on LPS-induced M1 polarization and NF-κB activation in BV2 cells. Conclusions: MiR-200c-3p mimics suppressed LPS-induced microglial M1 polarization and NF-κB activation by targeting RIP2. MiR-200c-3p/RIP2 might be a potential therapeutic target for the treatment of neuroinflammation-associated diseases.