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| 1 | Endometrial membrane organoids from human embryonic stem cell combined with the 3D Matrigel for endometrium regeneration in asherman syndrome显示文摘Asherman’s syndrome(AS),a leading cause of uterine infertility worldwide,is characterized by scarring of the uterine surfaces lacking endometrial epithelial cells,which prevents endometrial regeneration.Current research on cell therapy for AS focuses on mesenchymal and adult stem cells from the endometrium.However,insufficient number,lack of purity,and rapid senescence of endometrial epithelial progenitor cells(EEPCs)during experimental processes restrict their use in cell therapies.In this study,we induced human embryonic stem cells-9(H9-ESC)into EEPCs by optimizing the induction factors from the definitive endoderm.EEPCs,which act as endometrial epithelial cells,accompanied by human endometrial stromal cells provide a niche environment for the development of endometrial membrane organoids(EMOs)in an in vitro 3D culture model.To investigate the function of EMOs,we transplanted tissue-engineered constructs with EMOs into an in vivo rat AS model.The implantation of EMOs into the damaged endometrium facilitates endometrial regeneration and angiogenesis.Implanting EMOs developed from human embryonic stem cells into the endometrium might prove useful for“endometrial re-engineering”in the treatment of Asherman’s syndrome. | Xiuxiu Jiang Xingmiao Li Xiangwei Fei Jiajie Shen Jianhua Chen Meijun Guo Yangyang Li | 2021 | Bioactive Materials2021，6，11： | 11 |
| 2 | RUAP:Random Rearrangement Block Matrix-Based Ultra-Lightweight RFID Authentication Protocol for End-Edge-Cloud Collaborative Environment显示文摘Cloud computing provides powerful processing capabilities for large-scale intelligent Internet of things(IoT)terminals.However,the massive realtime data processing requirements challenge the existing cloud computing model.The edge server is closer to the data source.The end-edge-cloud collaboration offloads the cloud computing tasks to the edge environment,which solves the shortcomings of the cloud in resource storage,computing performance,and energy consumption.IoT terminals and sensors have caused security and privacy challenges due to resource constraints and exponential growth.As the key technology of IoT,Radio-Frequency Identification(RFID)authentication protocol tremendously strengthens privacy protection and improves IoT security.However,it inevitably increases system overhead while improving security,which is a major blow to low-cost RFID tags.The existing RFID authentication protocols are difficult to balance overhead and security.This paper designs an ultra-lightweight encryption function and proposes an RFID authentication scheme based on this function for the end-edge-cloud collaborative environment.The BAN logic proof and protocol verification tools AVISPA formally verify the protocol’s security.We use VIVADO to implement the encryption function and tag’s overhead on the FPGA platform.Performance evaluation indicates that the proposed protocol balances low computing costs and high-security requirements. | Yu Luo Kai Fan Xingmiao Wang Hui Li Yintang Yang | 2022 | China Communications2022，19，7： | 0 |
| 3 | Japanese Encephalitis Virus NS2B-3 Protein Complex Promotes Cell Apoptosis and Viral Particle Release by Down-Regulating the Expression of AXL显示文摘Japanese encephalitis virus(JEV) is a flavivirus transmitted by mosquitoes that causes severe encephalitis in humans and animals. It has been suggested that AXL, a transmembrane protein, can promote the replication of various flaviviruses,such as dengue(DENV), Zika(ZIKV), and West Nile(WNV) viruses. However, the effect of AXL on JEV infection has not yet been determined. In the present study, we demonstrate that AXL is down-regulated after JEV infection in the late stage. JEV NS2B-3 protein specifically interacted with AXL, and promoted AXL degradation through the ubiquitin–proteasome pathway. AXL-degradation increased cell apoptosis by disrupting phosphatidylinositol 3-kinase(PI3 K)/Akt signal transduction. In addition, the degradation of AXL promoted JEV release to supernatant, whereas the virus in the cell lysates decreased. The supplementation of AXL ligand Gas6 inhibited the JEV-mediated degradation of AXL. Altogether,we discover a new function of NS2B-3 during the process of JEV replication, and provide a new insight into the interactions between JEV and cell hosts. | Shengda Xie Zhenjie Liang Xingmiao Yang Junhui Pan Du Yu Tongtong Li Ruibing Cao | 2021 | Virologica Sinica2021，36，6： | 0 |
| 4 | CPAL, as a New Mediator of Cardiomyocyte Metabolic Alterations and Pyroptosis, Regulates Myocardial Infarction Injury in Mice显示文摘Myocardial infarction (MI), the most serious of the ischemic heart diseases, is accompanied by myocardial metabolic disorders and the loss of cardiomyocytes. Increasing evidence has shown that long noncoding RNAs (lncRNAs) are involved in various pathological conditions such as cancer and cardiovascular diseases (CVDs), and are emerging as a novel biomarker for these disorders. This study aims to investigate the regulatory role and mechanisms of lncRNAs in myocardial remodeling in the setting of MI. We find that post-infarcted hearts exhibit a reduction of adenosine triphosphate (ATP) and an alteration of the glucose and lipid metabolism genes cluster of differentiation 36 (CD36), hexokinase 1 (HK1), and clucose transporter 4 (GLUT4), accompanied by cardiomyocyte pyroptosis. We then identify a previously unknown conserved lncRNA, AK009126 (cardiomyocyte pyroptosis-associated lncRNA, CPAL), which is remarkably upregulated in the myocardial border zone of MI mice. Importantly, the adeno-associated virus 9 (AAV9)-mediated silencing of endogenous CPAL by its short hairpin RNA (shRNA) partially abrogates myocardial metabolic alterations and cardiomyocyte pyroptosis during MI in mice. Mechanistically, CPAL is shown to bind directly to nuclear factor kappa B (NFκB) and to act as an activator of NFκB to induce NFκB phosphorylation in cardiomyocytes. We also find that CPAL upregulates caspase-1 expression at the transcriptional level and consequently promotes the release of interleukin (IL)-18 and IL-1β from cardiomyocytes. Collectively, our findings reveal the conserved lncRNA CPAL as a new regulator of cardiac metabolic abnormalities and cardiomyocyte pyroptosis in the setting of MI and suggest CPAL as a new therapeutic target to protect cardiomyocytes against ischemic injury in infarcted hearts. | Jiamin Li Hongru Xue Ning Xu Liling Gong Ming Li Sijia Li Di Huang Qingwei Zhang Pengyu Li Qingsui Li Hang Yu Yining Liu Yadong Xue Haixin Chen Jiali Liu Wanyu Zhang Mingbin Liu Siyu Chang Xianzhi Lang Xingmiao Zhao Weijie Du Benzhi Cai Ning Wang Baofeng Yang | 2023 | Engineering2023，，1： | 0 |
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