255 results on '"Xiao-Mei Yang"'
Search Results
2. Vortex-Induced Vibration Performance Analysis of Long-Span Sea-Crossing Bridges Using Unsupervised Clustering
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Tao Chen, Yi-Lun Wu, Xiao-Mei Yang, and Shu-Han Yang
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sea-crossing bridge ,vortex-induced vibration ,clustering ,performance analysis ,correlation ,Naval architecture. Shipbuilding. Marine engineering ,VM1-989 ,Oceanography ,GC1-1581 - Abstract
Vortex-induced vibration is a type of wind-induced vibration occurring frequently in large-span sea-crossing bridges under relatively low wind speeds, posing a threat to the structural fatigue performance and driving comfort. Identifying the instantaneous occurrence moments of vortex-induced vibration is a prerequisite for establishing a data-driven prediction model for vortex-induced vibration, and it is of great significance for the monitoring and early warning of vortex-induced vibration performance in bridges. To automatically detect the occurrence moments of vortex-induced vibration and establish a correlation model between vortex-induced vibration amplitude and environmental factors, this study proposes a fuzzy C-means clustering-based classification method. In order to detect the occurrence moments of vortex-induced vibration more finely, only short-term or even instantaneous structural vibration indicators were selected and transformed for distribution as clustering features. The entire detection process could be carried out unsupervised, reducing the manual cost of obtaining vortex-induced vibration information from massive monitoring data. Finally, actual vortex-induced vibration test data from a certain overseas bridge was utilized to verify the feasibility of this method. Based on the classification results, the correlation between vortex-induced vibration amplitude and environmental variables was determined, providing valuable guidance for predicting vortex-induced vibration amplitudes.
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- 2024
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3. An Adaptive Chirp Mode Decomposition-Based Method for Modal Identification of Time-Varying Structures
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Xiao-Jun Yao, Yu-Chun Lv, Xiao-Mei Yang, Feng-Yang Wang, and Yong-Xiang Zheng
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modal identification ,adaptive chirp mode decomposition ,time-varying structure ,instantaneous frequency ,time–frequency distribution ,Mathematics ,QA1-939 - Abstract
Modal parameters are inherent characteristics of civil structures. Due to the effect of environmental factors and ambient loads, the physical and modal characteristics of a structure tend to change over time. Therefore, the effective identification of time-varying modal parameters has become an essential topic. In this study, an instantaneous modal identification method based on an adaptive chirp mode decomposition (ACMD) technique was proposed. The ACMD technique is highly adaptable and can accurately estimate the instantaneous frequencies of a structure. However, it is important to highlight that an initial frequency value must be selected beforehand in ACMD. If the initial frequency is set incorrectly, the resulting instantaneous frequencies may lack accuracy. To address the aforementioned problem, the Welch power spectrum was initially developed to extract a high-resolution time–frequency distribution from the measured signals. Subsequently, the time–frequency ridge was identified based on the maximum energy position in the time–frequency distribution plot, with the frequencies associated with the time–frequency ridge serving as the initial frequencies. Based on the initial frequencies, the measured signals with multiple degrees of freedom could be decomposed into individual time-varying components with a single degree of freedom. Following that, the instantaneous frequencies of each time-varying component could be calculated directly. Subsequently, a sliding window principal component analysis (PCA) method was introduced to derive instantaneous mode shapes. Finally, vibration data collected under various operational scenarios were used to validate the proposed method. The results demonstrated the effective identification of time-varying modal parameters in real-world civil structures, without missing modes.
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- 2024
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4. Nanobody-based bispecific T-cell engager (Nb-BiTE): a new platform for enhanced T-cell immunotherapy
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Xiao-mei Yang, Xuan-dong Lin, Wei Shi, Shen-xia Xie, Xia-ning Huang, Shi-hua Yin, Xiao-bing Jiang, Bruce D. Hammock, Zhi Ping Xu, and Xiao-ling Lu
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Medicine ,Biology (General) ,QH301-705.5 - Published
- 2023
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5. TRPV4 enhances the synthesis of fatty acids to drive the progression of ovarian cancer through the calcium-mTORC1/SREBP1 signaling pathway
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Lan Lin, Xiao Li, Ai-Jia Wu, Jia-bin Xiu, Yu-Zheng Gan, Xiao-mei Yang, and Zhi-Hong Ai
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Biological sciences ,Molecular biology ,Cancer ,Science - Abstract
Summary: Transient receptor potential vanilloid 4 (TRPV4) is a nonselective cation channel activated by various stimuli, such as heat. A recent study reported that high expression of TRPV4 predicted a poor prognosis in ovarian cancer patients. This study demonstrated that TRPV4 was highly expressed in ovarian cancer and had the ability to promote proliferation and migration. Through RNA-seq and related experiments, we confirmed that the oncogenic pathway of TRPV4 in ovarian cancer may be related to the fatty acid synthesis. By correlation analysis and RNA-seq, we demonstrated that SREBP1 and mTORC1 were inseparably related to that. Therefore, we used inhibitors to perform experiments. Calcium fluorescent probe experiments suggest that the change of calcium content in ovarian cancer cells was related to the downstream mTORC1 signaling pathway and fatty acid synthesis. These results confirmed that TRPV4 affected the fatty acid synthesis through the calcium-mTOR/SREBP1 signaling pathway, thereby promoting ovarian cancer progression.
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- 2023
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6. Disulfiram inhibits liver fibrosis in rats by suppressing hepatic stellate cell activation and viability
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Xiao-Mei Yang, Zheng Wu, Xiaoqi Wang, Yaoqi Zhou, Lei Zhu, Dongxue Li, Hui-Zhen Nie, Ya-Hui Wang, Jun Li, and Xueyun Ma
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Disulfiram ,Liver fibrosis ,Hepatic stellate cell ,Co-culture ,Therapeutics. Pharmacology ,RM1-950 ,Toxicology. Poisons ,RA1190-1270 - Abstract
Abstract Background Liver fibrosis is a wound-healing response to chronic injury, featuring with excess accumulation of extracellular matrix secreted by the activated hepatic stellate cells (HSC). Disulfiram (DSF), also known as Antabuse, has been used for the treatment of alcohol addiction and substance abuse. Recently, overwhelming studies had revealed anti-cancer effects of DSF in multiple cancers, including liver cancer. But the actual effects of DSF on liver fibrosis and liver function remain unknown. Methods In this study, we evaluated the effects of low-dose DSF in CCl4- and Bile Duct Ligation (BDL)—induced hepatic fibrosis rat models. Cell proliferation was detected by using the Cell-Light™ EdU Apollo®567 Cell Tracking Kit. Cell apoptosis was analyzed using a TdT-mediated dUTP nick end labeling (TUNEL) kit, viability was measured with Cell Counting Kit-8(CCK8). Relative mRNA expression of pro-fibrogenic was assessed using quantitative RT-PCR. The degree of liver fibrosis, activated HSCs, were separately evaluated through Sirius Red-staining, immunohistochemistry and immunofluorescence. Serum alanine aminotransferase (ALT) and asparagine aminotransferase (AST) activities were detected with ALT and AST detecting kits using an automated analyzer. Results Liver fibrosis was distinctly attenuated while liver functions were moderately ameliorated in the DSF-treated group. Activation and proliferation of primary rat HSCs isolated from rat livers were significantly suppressed by low-dose DSF. DSF also inhibited the viability of in vitro cultured rat or human HSC cells dose-dependently but had no repressive role on human immortalized hepatocyte THLE-2 cells. Interestingly, upon DSF treatment, the viability of LX-2 cells co-cultured with THLE-2 was significantly inhibited, while that of THLE-2 co-cultured with LX-2 was increased. Further study indicated that HSCs apoptosis was increased in DSF/CCl4-treated liver samples. These data indicated that DSF has potent anti-fibrosis effects and protective effects toward hepatocytes and could possibly be repurposed as an anti-fibrosis drug in the clinic. Conclusions DSF attenuated ECM remodeling through suppressing the transformation of quiet HSCs into proliferative, fibrogenic myofibroblasts in hepatic fibrosis rat models. DSF provides a novel approach for the treatment of liver fibrosis.
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- 2022
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7. Activation of GDNF-ERK-Runx1 signaling contributes to P2X3R gene transcription and bone cancer pain
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Zhu-Lin Yuan, Xiao-Dan Liu, Zi-Xian Zhang, Song Li, Yue Tian, Ke Xi, Jie Cai, Xiao-Mei Yang, Min Liu, and Guo-Gang Xing
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Physiology ,Molecular physiology ,Molecular biology ,Molecular medicine ,Science - Abstract
Summary: Bone cancer pain is a common symptom in cancer patients with bone metastases and its underlying mechanisms remain unknown. Here, we report that Runx1 directly upregulates the transcriptional activity of P2X3 receptor (P2X3R) gene promoter in PC12 cells. Knocking down Runx1 in dorsal root ganglion (DRG) neurons suppresses the functional upregulation of P2X3R, attenuates neuronal hyperexcitability and pain hypersensitivity in tumor-bearing rats, whereas overexpressing Runx1 promotes P2X3R gene transcription in DRG neurons, induces neuronal hyperexcitability and pain hypersensitivity in naïve rats. Activation of GDNF-GFRα1-Ret-ERK signaling is required for Runx1-mediated P2X3R gene transcription in DRG neurons, and contributes to neuronal hyperexcitability and pain hypersensitivity in tumor-bearing rats. These findings indicate that the Runx1-mediated P2X3R gene transcription resulted from activation of GDNF-GFRα1-Ret-ERK signaling contributes to the sensitization of DRG neurons and pathogenesis of bone cancer pain. Our findings identify a potentially targetable mechanism that may cause bone metastasis-associated pain in cancer patients.
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- 2022
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8. The essential roles of M ps 1 in spermatogenesis and fertility in mice
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Qiang Fang, Xue-Lin Chen, Lei Zhang, Ya-Bin Li, Tian-Zeng Sun, Chen-Xin Yang, Jian-Feng Chang, Xiao-Mei Yang, and Feng Sun
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Cytology ,QH573-671 - Abstract
Abstract Monopolar spindle 1 (MPS1), which plays a critical role in somatic mitosis, has also been revealed to be essential for meiosis I in oocytes. Spermatogenesis is an important process involving successive mitosis and meiosis, but the function of MPS1 in spermatogenesis remains unclear. Here, we generated Mps1 conditional knockout mice and found that Ddx4-cre-driven loss of Mps1 in male mice resulted in depletion of undifferentiated spermatogonial cells and subsequently of differentiated spermatogonia and spermatocytes. In addition, Stra8-cre-driven ablation of Mps1 in male mice led to germ cell loss and fertility reduction. Spermatocytes lacking M ps 1 have blocked at the zygotene-to-pachytene transition in the prophase of meiosis I, which may be due to decreased H2B ubiquitination level mediated by MDM2. And the expression of many meiotic genes was decreased, while that of apoptotic genes was increased. Moreover, we also detected increased apoptosis in spermatocytes with Mps1 knockout, which may have been the reason why germ cells were lost. Taken together, our findings indicate that MPS1 is required for mitosis of gonocytes and spermatogonia, differentiation of undifferentiated spermatogonia, and progression of meiosis I in spermatocytes.
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- 2021
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9. miR-1249-5p regulates the osteogenic differentiation of ADSCs by targeting PDX1
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Xiao-Mei Yang, Ya-Qi Song, Liang Li, Dong-Ming Liu, and Guang-Dong Chen
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miR-1249-5p ,Adipose derived stem cells ,Osteogenic Differentiation ,PDX1 ,Orthopedic surgery ,RD701-811 ,Diseases of the musculoskeletal system ,RC925-935 - Abstract
Abstract Background Osteoporosis (OP) is an age-related systemic bone disease. MicroRNAs (miRNAs) are involved in the regulation of osteogenic differentiation. The purpose of this study was to explore the role and mechanism of miR-1249-5p for promoting osteogenic differentiation of adipose-derived stem cells (ADSCs). Methods GSE74209 dataset was retrieved from NCBI Gene Expression Omnibus (GEO) database and performed bioinformatic analyses. OP tissue and healthy control tissues were obtained and used for RT-PCR analyses. ADSCs were incubated with miR-1249-5p mimic, inhibitor and corresponding negative control (NC), alkaline phosphatase (ALP) staining, and Alizarin Red Staining (ARS) were then performed to assess the role of miR-1249-5p for osteogenesis of ADSCs. Targetscan online website and dual-luciferase reporter assay were performed to verify that the 3′-UTR of PDX1 mRNA is a direct target of miR-1249-5p. RT-PCR and western blot were also performed to identify the mechanism of miR-1249-5p for osteogenesis of ADSCs. Results A total of 170 differentially expressed miRNAs were selected, among which, 75 miRNAs were downregulated and 95 miRNAs were upregulated. Moreover, miR-1249-5p was decreased in OP patients, while showed a gradual increase with the extension of induction time. miR-1249-5p mimic significantly increased osteogenic differentiation capacity and p-PI3K and p-Akt protein levels. Luciferase activity in ADSCs co-transfected of miR-1249-5p mimic with PDX1-WT reporter plasmids was remarkably decreased, but there was no obvious change in miR-1249-5p mimic with PDX1-MUT reporter plasmids co-transfection group. Overexpression PDX1 could partially reverse the promotion effects of miR-1249-5p on osteogenesis of ADSCs. Conclusion In conclusion, miR-1249-5p promotes osteogenic differentiation of ADSCs by targeting PDX1 through the PI3K/Akt signaling pathway.
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- 2021
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10. Determination of the Interaction and Pharmacological Modulation of MCHR1 Signaling by the C-Terminus of MRAP2 Protein
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Meng Wang, Yue Zhai, Xiaowei Lei, Jing Xu, Bopei Jiang, Zhe Kuang, Cong Zhang, Shangyun Liu, Shan Bian, Xiao-Mei Yang, Tao Zan, Li-Na Jin, Qingfeng Li, and Chao Zhang
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MRAP2 ,GPCR ,melanin-concentrating hormone ,pharmacological regulation ,MCHR1 ,Diseases of the endocrine glands. Clinical endocrinology ,RC648-665 - Abstract
Melanin concentrating hormone (MCH), an orexigenic neuropeptide, is primarily secreted by the hypothalamus and acts on its receptor, the melanin-concentrating hormone receptor 1 (MCHR1), to regulate appetite and energy homeostasis. The Melanocortin Receptor Accessory Protein 2 (MRAP2), a small single transmembrane protein broadly expressed in multiple tissues, has been defined as a vital endocrine modulator of five melanocortin receptors (MC1R–MC5R) and several other GPCRs in the regulation of central neuronal activities and peripheral energy balance. Here, we demonstrated the interaction between MRAP2 and MCHR1 by immunoprecipitation and bimolecular fluorescent assay and found that MRAP2 could inhibit MCHR1 signaling in vitro. A series of functional truncations of different regions further identified that the C-terminal domains of MRAP2 protein were required for the pharmacological modulation of intracellular Ca2+ coupled cascades and membrane transport. These findings elucidated the broad regulatory profile of MRAP2 protein in the central nervous system and may provide implications for the modulation of central MCHR1 function in vivo.
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- 2022
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11. Transcranial Magnetic Stimulation Alleviates Levodopa-Induced Dyskinesia in Parkinson's Disease and the Related Mechanisms: A Mini-Review
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Yi Wu, Xue-bing Cao, Wei-qi Zeng, Heng Zhai, Xiao-qian Zhang, Xiao-man Yang, Chi Cheng, Jia-ling Wang, Xiao-mei Yang, and Yan Xu
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transcranial magnetic stimulation ,Parkinson's disease ,dyskinesia ,mechanism ,treatment ,Neurology. Diseases of the nervous system ,RC346-429 - Abstract
After long-term use of levodopa, Parkinson's patients almost inevitably develop dyskinesia, a kind of drug side effect manifesting as uncontrollable choreic movements and dystonia, which could be crippling yet have limited therapeutic options. Transcranial magnetic stimulation is the most widely studied non-invasive neuromodulation technology to treat levodopa-induced dyskinesia. Many studies have shown that transcranial magnetic stimulation has beneficial effects on levodopa-induced dyskinesia and is patient-tolerable, barely with reported adverse effects. Changes in brain connectivity, neuroplasticity, neurotransmitter, neurorestoration, and blood flow modulation could play crucial roles in the efficacy of transcranial magnetic stimulation for levodopa-induced dyskinesia. The appearance of new modes and application for emerging targets are possible solutions for transcranial magnetic stimulation to achieve sustained efficacy. Since the sample size in all available studies is small, more randomized double-blind controlled studies are needed to elucidate the specific treatment mechanisms and optimize treatment parameters.
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- 2021
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12. Modal Identification of Structures by Eliminating the Effect of the High Ocean Wind
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Chun-Xu Qu, Chang-Chong Liu, Xiao-Mei Yang, Hui-Juan Liu, Hong-Nan Li, and Yu-Feng Zhang
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modal identification ,offshore structures ,bridges ,wind excitation ,structural health monitoring ,Naval architecture. Shipbuilding. Marine engineering ,VM1-989 ,Oceanography ,GC1-1581 - Abstract
Tropical cyclone is a rapidly rotating storm system with severe excitation such as high wind. This severe excitation may change the performance of structures, such as bridges, wharves and wind turbine structures. It is very necessary to monitor this important change. Modal parameters are the ones to reflect the structural instinct behavior. However, many identification methods assume that the excitation is white noise, which is not the truth during high ocean wind excitation. Therefore, the modal identification method to deal with severe ocean wind excitation should be investigated. This paper proposes an innovative method to eliminate the effect of high ocean wind on modal identification. The formulation to generate an impulse response is described, where the effect of high wind is pointed. Then the elimination method is derived using the wind velocity spectrum and correlation function. After the wind field is simulated, the wind velocities and spectra at all accelerometer positions are obtained. The real impulse response form is obtained. Then, modal identification using the real impulse response is performed. Finally, a practical cable-stayed bridge is employed and modal identification is performed. The results show that the identified modes can reflect structural real behavior.
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- 2022
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13. GPAA1 promotes gastric cancer progression via upregulation of GPI-anchored protein and enhancement of ERBB signalling pathway
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Xiao-Xin Zhang, Bo Ni, Qing Li, Li-Peng Hu, Shu-Heng Jiang, Rong-Kun Li, Guang-Ang Tian, Li-Li Zhu, Jun Li, Xue-Li Zhang, Yan-Li Zhang, Xiao-Mei Yang, Qin Yang, Ya-Hui Wang, Chun-Chao Zhu, and Zhi-Gang Zhang
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Gastric cancer ,GPAA1 ,GPI-anchored proteins ,EGFR ,ERBB2 ,Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Abstract Background Gastric cancer is one of the deadliest malignant tumours, with a high incidence in China, and is regulated by aberrantly overexpressed oncogenes. However, existing therapies are insufficient to meet patients’ needs; thus, the identification of additional therapeutic targets and exploration of the underlying mechanism are urgently needed. GPAA1 is the subunit of the GPI transamidase that transfers the GPI anchor to proteins within the ER. The functional impacts of increased expression levels of GPAA1 in human cancers are not well understood. Methods Data mining was performed to determine the pattern of GPAA1 expression and the reason for its overexpression in tumour and adjacent normal tissues. In vitro and in vivo experiments evaluating proliferation and metastasis were performed using cells with stable deletion or overexpression of GPAA1. A tissue microarray established by the Ren Ji Hospital was utilized to analyse the expression profile of GPAA1 and its correlation with prognosis. Western blotting, an in situ proximity ligation assay, and co-immunoprecipitation (co-IP) were performed to reveal the mechanism of GPAA1 in gastric cancer. Results GPAA1 was a markedly upregulated oncogene in gastric cancer due to chromosomal amplification. GPAA1 overexpression was confirmed in specimens from the Ren Ji cohort and was associated with ERBB2 expression, predicting unsatisfactory patient outcomes. Aberrantly upregulated GPAA1 dramatically contributed to cancer growth and metastasis in in vitro and in vivo studies. Mechanistically, GPAA1 enhanced the levels of metastasis-associated GPI-anchored proteins to increase tumour metastasis and intensified lipid raft formation, which consequently promoted the interaction between EGFR and ERBB2 as well as downstream pro-proliferative signalling. Conclusions GPAA1 facilitates the expression of cancer-related GPI-anchored proteins and supplies a more robust platform—the lipid raft—to promote EGFR-ERBB2 dimerization, which further contributes to tumour growth and metastasis and to cancer progression. GPAA1 could be a promising diagnostic biomarker and therapeutic target for gastric cancer.
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- 2019
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14. Reliability of three-dimensional color flow Doppler and two-dimensional pulse wave Doppler transthoracic echocardiography for estimating cardiac output after cardiac surgery
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Guang-wei Hao, Yang Liu, Guo-guang Ma, Jun-yi Hou, Du-ming Zhu, Lan Liu, Ying Zhang, Hua Liu, Ya-min Zhuang, Zhe Luo, Guo-wei Tu, Xiao-mei Yang, and Hai-yan Chen
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Three-dimensional color flow doppler ,Two-dimensional pulse wave doppler ,Cardiac output ,Cardiac surgery ,Diseases of the circulatory (Cardiovascular) system ,RC666-701 - Abstract
Abstract Background Three-dimensional color flow Doppler (3DCF) is a new convenient technique for cardiac output (CO) measurement. However, to date, no one has evaluated the accuracy of 3DCF echocardiography for CO measurement after cardiac surgery. Therefore, this single-center, prospective study was designed to evaluate the reliability of three-dimensional color flow and two-dimensional pulse wave Doppler (2D-PWD) transthoracic echocardiography for estimating cardiac output after cardiac surgery. Methods Post-cardiac surgical patients with a good acoustic window and a low dose or no dose of vasoactive drugs (norepinephrine
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- 2019
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15. Targeting cancer stem cell signature gene SMOC-2 Overcomes chemoresistance and inhibits cell proliferation of endometrial carcinomaResearch in context
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Huan Lu, Dan-dan Ju, Guang-dong Yang, Lin-yan Zhu, Xiao-mei Yang, Jun Li, Wei-wei Song, Jin-hao Wang, Can-can Zhang, Zhi-gang Zhang, and Rong Zhang
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Medicine ,Medicine (General) ,R5-920 - Abstract
Background: Endometrial cancer is one of the most common gynecological malignancies and has exhibited an increasing incidence rate in recent years. Cancer stem cells (CSCs), which are responsible for tumor growth and chemoresistance, have been confirmed in endometrial cancer. However, it is still challenging to identify endometrial cancer stem cells to then target for therapy. Methods: Flow cytometry was used to identify the endometrial cancer stem cells. Sphere formation assay, western blotting, qRT-PCR assay, cell viability assay, xenograft assay and immunohistochemistry staining analysis were utilized to evaluate the effect of SPARC-related modular calcium binding 2 (SMOC-2) on the cells proliferation and drug resistance. Cell viability assay, qRT-PCR assay, immunofluorescence staining, Co-IP assay and luciferase reporter gene assay were performed to explore the possible molecular mechanism by which SMOC-2 activates WNT/β-catenin pathway. Findings: We found the expression of SPARC-related modular calcium binding 2 (SMOC-2), a member of SPARC family, was higher in endometrial CSCs than that in non-CSCs. SMOC-2 was also more highly expressed in spheres than in monolayer cultures. The silencing of SMOC-2 suppressed cell sphere ability; reduced the expression of the stemness-associated genes SOX2, OCT4 and NANOG; and enhanced chemosensitivity in endometrial cancer cells. By co-culture IP assay, we demonstrated that SMOC-2 directly interacted with WNT receptors (Fzd6 and LRP6), enhanced ligand-receptor interaction with canonical WNT ligands (Wnt3a and Wnt10b), and finally, activated the WNT/β-catenin pathway in endometrial cancer. SMOC-2 expression was closely correlated with CSC markers CD133 and CD44 expression in endometrial cancer tissue. Interpretation: Taken together, we conclude that SMOC-2 might be a novel endometrial cancer stem cell signature gene and therapeutic target for endometrial cancer. Fund: National Natural Science Foundation of China, Scientific and Technological Innovation Act Program of Shanghai Science and Technology Commission, Scientific and Technological Innovation Act Program of Fengxian Science and Technology Commission, Natural Science Foundation of Shanghai. Keywords: SMOC-2, Endometrial carcinoma, Cancer stem cells, Chemoresistance, WNT/β-catenin pathway
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- 2019
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16. STK3 Suppresses Ovarian Cancer Progression by Activating NF-κB Signaling to Recruit CD8+ T-Cells
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Xiangyu Wang, Fengmian Wang, Zhi-Gang Zhang, Xiao-Mei Yang, and Rong Zhang
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Immunologic diseases. Allergy ,RC581-607 - Abstract
Serine/threonine protein kinase-3 (STK3) is a critical molecule of the Hippo pathway but little is known about its biological functions in the ovarian cancer development. We demonstrated the roles of STK3 in ovarian cancer. Existing databases were used to study the expression profile of STK3. STK3 was significantly downregulated in OC patients, and the low STK3 expression was correlated with a poor prognosis. In vitro cell proliferation, apoptosis, and migration assays, and in vivo subcutaneous xenograft tumor models were used to determine the roles of STK3. The overexpression of STK3 significantly inhibited cell proliferation, apoptosis, and migration of ovarian cancer cells in vitro and tumor growth in vivo. Bisulfite sequencing PCR analysis was performed to validate the methylation of STK3 in ovarian cancer. RNA sequencing and gene set enrichment analysis (GSEA) were used to compare the transcriptome changes in the STK3 overexpression ovarian cancer and control cells. The signaling pathway was analyzed by western blotting. STK3 promoted the migration of CD8+ T-cells by activating nuclear transcription factor κB (NF-κB) signaling. STK3 is a potential predictor of OC. It plays an important role in suppressing tumor growth of ovarian cancer and in chemotaxis of CD8+ T-cells.
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- 2020
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17. Internal jugular vein variability predicts fluid responsiveness in cardiac surgical patients with mechanical ventilation
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Guo-guang Ma, Guang-wei Hao, Xiao-mei Yang, Du-ming Zhu, Lan Liu, Hua Liu, Guo-wei Tu, and Zhe Luo
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Internal jugular veins ,Inferior vena cava ,Stroke volume variation ,Fluid responsiveness ,Cardiac surgery ,Medical emergencies. Critical care. Intensive care. First aid ,RC86-88.9 - Abstract
Abstract Background To evaluate the efficacy of using internal jugular vein variability (IJVV) as an index of fluid responsiveness in mechanically ventilated patients after cardiac surgery. Methods Seventy patients were assessed after cardiac surgery. Hemodynamic data coupled with ultrasound evaluation of IJVV and inferior vena cava variability (IVCV) were collected and calculated at baseline, after a passive leg raising (PLR) test and after a 500-ml fluid challenge. Patients were divided into volume responders (increase in stroke volume ≥ 15%) and non-responders (increase in stroke volume
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- 2018
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18. Squid ink polysaccharide prevents autophagy and oxidative stress affected by cyclophosphamide in Leydig cells of mice: a pilot study
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Yi-Peng Gu, Xiao-Mei Yang, Zhen-Hua Duan, Jiang-Hua Shang, Ping Luo, Wei Xiao, Da-Yan Zhang, and Hua-Zhong Liu
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Autophagy ,Cyclophosphamide ,Leydig cells ,Oxidative stress ,Squid ink polysaccharide ,Medicine - Abstract
Objective(s): The aim of this study was to explore the effects of Squid ink polysaccharide (SIP) on prevention of autophagy and oxidative stress induced by cyclophosphamide (CP) in Leydig cells of mice. Materials and Methods: Examination of reproductive organ exponents, abnormal sperm rate, activities of superoxide dismutase (SOD), catalase (CAT), contents of malondialdehyde (MDA), and histological structure were performed to detect the optimal dose of SIP against oxidative stress damage in vivo, and autophagy-associated protein LC3 and Beclin-1 were examined by immunofluorescence, and their expression was detected by Western blot analysis. Leydig cells ultrastructural changes were observed by transmission fluorescent microscope. Results: SIP significantly inhibited sperm aberration, histological structure and injury of seminiferous tubules caused by CP, as well as the antioxidant activity of SOD and CAT were increased; contents of MDA were decreased. The optimal dose of SIP for prevention of oxidative stress injury by CP was 80 mg/kg. In addition, LC3 and Beclin-1 fluorescent granules were much less in the Leydig cell layer after treatment via SIP compared with the CP-treated group, and the expression levels of LC3 and Beclin-1 were also decreased. Furthermore, characteristics of cell autophagy such as mitochondrial swelling, autophagic vacuoles, and chromatin pyknosis were observed in CP-treated Leydig cells, but SIP could effectively weaken injury of Leydig cell ultrastructure by CP. Conclusion: SIP, as an antioxidant, prevents the cytoskeleton damage through up-regulation antioxidant capacity and inhibition autophagy caused by CP.
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- 2017
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19. A comparison of early versus late initiation of renal replacement therapy for acute kidney injury in critically ill patients: an updated systematic review and meta-analysis of randomized controlled trials
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Xiao-mei Yang, Guo-wei Tu, Ji-li Zheng, Bo Shen, Guo-guang Ma, Guang-wei Hao, Jian Gao, and Zhe Luo
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Renal replacement therapy ,Timing ,Acute kidney injury ,Diseases of the genitourinary system. Urology ,RC870-923 - Abstract
Abstract Background To investigate the impact of timing the initiation of renal replacement therapy (RRT) on clinical outcomes in critically ill patients with acute kidney injury (AKI), focusing on the randomized controlled trials (RCTs) in this field. Methods The PubMed, EMBASE and Cochrane databases were searched between January 1, 1985, and June 30, 2016, to identify randomized trials that assessed the timing of initiation of RRT in patients with AKI. Results Nine RCTs, with a total of 1636 patients, were enrolled in this meta-analysis. A pooled analysis of the studies indicated no mortality benefit with “early” RRT, with an RR of 0.98 (95% CI 0.78 to 1.23, P = 0.84). There was no significant difference in intensive care unit (ICU) length of stay (LOS) or hospital LOS between the early and late RRT groups for survivors or nonsurvivors. Pooled analysis also demonstrated no significant change in renal function recovery (RR 1.02, 95% CI 0.88 to 1.19, I2 = 59%), RRT dependence (RR 0.76, 95% CI 0.42 to 1.37, I2 = 0%), duration of RRT (Mean difference 1.43, 95% CI -1.75 to 4.61, I2 = 78%), renal recovery time (Mean difference 0.73, 95% CI -2.09 to 3.56, I2 = 70%) or mechanical ventilation time (Mean difference − 0.95, 95% CI -3.54 to 1.64, I2 = 64%) between the early and late RRT groups. We found no significant differences in complications between the groups. Conclusions Our meta-analysis revealed that the “early” initiation of RRT in critically ill patients did not result in reduced mortality. Pooled analysis of secondary outcomes also showed no significant difference between the early and late RRT groups. More well-designed and large-scale trials are expected to confirm the result of this meta-analysis.
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- 2017
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20. Early Kinetics of Procalcitonin in Predicting Surgical Outcomes in Type A Aortic Dissection Patients
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Hua Liu, Zhe Luo, Lan Liu, Xiao-Mei Yang, Ya-Min Zhuang, Ying Zhang, Guo-Wei Tu, Guo-Guang Ma, Guang-Wei Hao, Jian-Feng Luo, Ji-Li Zheng, and Chun-Sheng Wang
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Perioperative Period ,Procalcitonin ,Sensitivity ,Specificity ,Type A Aortic Dissection ,Medicine - Abstract
Background: In cardiac surgery, elevation of procalcitonin (PCT) could be observed postoperatively in the absence of any evidence of infection and also seems to be a prognostic marker. PCT levels measured in patients undergoing Type A aortic dissection (TAAD) were used to determine prognostic values for complications and surgical outcomes. Methods: Measurements of PCT, C-reactive protein (CRP), and leukocyte count were observed in TAAD surgery patients (n = 251; average age: 49.02 ± 12.83 years; 78.5% male) at presurgery (T0) and 24 h (T1), 48 h (T2), and 7 days (T3) postsurgery. PCT clearance (PCTc) on days 2 and 7 was calculated: (PCTday1− PCTday2/day7)/PCTday1 × 100%. Endotracheal intubation duration, length of stay (LOS) in the Intensive Care Unit (ICU)/hospital, and complications were recorded. Results: PCT peaked 24 h postsurgery (median 2.73 ng/ml) before decreasing. Correlation existed between PCT levels at T1 and duration of cardiopulmonary bypass (P = 0.001, r = 0.278). Serum PCT concentrations were significantly higher in nonsurvivor and multiple organ dysfunction syndrome groups on all postoperative days. PCT levels at T1 correlated with length of time of ventilation support and ICU/hospital LOS. Comparing PCT values of survivors versus nonsurvivors, a PCT cutoff level of 5.86 ng/ml at T2 had high sensitivity (70.6%) and specificity (74.3%) in predicting in-hospital death. PCTc-day 2 and 7 were significantly higher in survivor compared with nonsurvivor patients (38% vs. 8%, P= 0.012, 83% vs. −39%, P< 0.001). A PCTc-day 7 cutoff point of 48.7% predicted survival with high sensitivity (77.8%) and specificity (81.8%). Conclusions: PCT level and PCTc after TAAD surgery might serve as early prognostic markers to predict postoperative outcome. PCT measurement may help identify high-risk patients.
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- 2017
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21. Integrin α9 Suppresses Hepatocellular Carcinoma Metastasis by Rho GTPase Signaling
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Yan-Li Zhang, Xin Xing, Li-Bo Cai, Lei Zhu, Xiao-Mei Yang, Ya-Hui Wang, Qin Yang, Hui-Zhen Nie, Zhi-Gang Zhang, Jun Li, and Xue-Li Zhang
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Immunologic diseases. Allergy ,RC581-607 - Abstract
Integrin subunit alpha 9 (ITGA9) mediates cell-cell and cell-matrix adhesion, cell migration, and invasion through binding different kinds of extracellular matrix (ECM) components. However, its potential role and underlying molecular mechanisms remain unclear in hepatocellular carcinoma (HCC). Here, we found that ITGA9 expression was obviously decreased in patients with HCC, which was negatively correlated with HCC growth and metastasis. ITGA9 overexpression significantly inhibited cell proliferation and migration in vitro as well as tumor growth and metastasis in vivo. Our data demonstrated that the inhibitory effect of ITGA9 on HCC cell motility was associated with reduced phosphorylation of focal adhesion kinase (FAK) and c-Src tyrosine kinase (Src), disrupted focal adhesion reorganization, and decreased Rac1 and RhoA activity. Our data suggest ITGA9, as a suppressor of HCC, prevents tumor cell migration and invasiveness through FAK/Src-Rac1/RhoA signaling.
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- 2018
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22. Exemestane Attenuates Hepatic Fibrosis in Rats by Inhibiting Activation of Hepatic Stellate Cells and Promoting the Secretion of Interleukin 10
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Ya-Hui Wang, Rong-Kun Li, Ying Fu, Jun Li, Xiao-Mei Yang, Yan-Li Zhang, Lei Zhu, Qin Yang, Jian-Ren Gu, Xin Xing, and Zhi-Gang Zhang
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Immunologic diseases. Allergy ,RC581-607 - Abstract
Exemestane (EXE) is an irreversible steroidal aromatase inhibitor mainly used as an adjuvant endocrine therapy for postmenopausal women suffering from breast cancer. Besides inhibiting aromatase activity, EXE has multiple biological functions, such as antiproliferation, anti-inflammatory, and antioxidant activities which are all involved in hepatic fibrosis. Therefore, we investigated the role of EXE during the progress of hepatic fibrosis. The effect of EXE on liver injury and fibrosis were assessed in two hepatic fibrosis rat models, which were induced by either carbon tetrachloride (CCl4) or bile duct ligation (BDL). The influence of EXE treatment on activation and proliferation of primary rat hepatic stellate cells (HSCs) was observed in vitro. The results showed that EXE attenuated the liver fibrosis by decreasing the collagen deposition and α-SMA expression in vivo and inhibited the activation and proliferation of primary rat HSCs in vitro. Additionally, EXE promoted the secretion of antifibrotic and anti-inflammatory cytokine IL-10 in vivo and in HSC-T6 culture media. In conclusion, our findings reveal a new function of EXE on hepatic fibrosis and prompted its latent application in liver fibrotic-related disease.
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- 2017
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23. A Wideband Antenna with Circular and Rectangular Shaped Slots for Mobile Phone Applications
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Wei-Hua Zong, Xiao-Mei Yang, Xia Xiao, Shan-Dong Li, Xiang-Yang Wei, Zhe-Jun Jin, and Xiao-Yun Qu
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Electrical engineering. Electronics. Nuclear engineering ,TK1-9971 ,Cellular telephone services industry. Wireless telephone industry ,HE9713-9715 - Abstract
A wideband slot antenna for mobile phone applications is proposed. The antenna has two slots with open ends etched on the opposite edges of the ground plane. The main slot, of total length of 59 mm, is composed of a rectangle connected to a circle having radius of 5 mm. Another slot, having a rectangular shape with width of 2.8 mm and length of 26 mm, is employed to enhance the antenna bandwidth. The slots are fed by means of a rectangular monopole connected to a circular patch joined to a bent 50 Ω microstrip transmission line forming two right angles. To obtain a wideband impedance matching, the upper edge of the monopole and a part of the feeding line evolve along the top edge of the two slots. To reduce the antenna size, the upper part of the board above the slot (just 3 mm from the slot) is folded vertically to the ground plane. The measured bandwidth of the antenna is 0.698–1.10 GHz and 1.64–2.83 GHz covering LTE700/2300/2500, GSM850/900/1800/1900, and UMTS bands.
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- 2016
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24. CTHRC1 Acts as a Prognostic Factor and Promotes Invasiveness of Gastrointestinal Stromal Tumors by Activating Wnt/PCP-Rho Signaling
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Ming-Ze Ma, Chun Zhuang, Xiao-Mei Yang, Zi-Zhen Zhang, Hong Ma, Wen-Ming Zhang, Haiyan You, Wenxin Qin, Jianren Gu, Shengli Yang, Hui Cao, and Zhi-Gang Zhang
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Neoplasms. Tumors. Oncology. Including cancer and carcinogens ,RC254-282 - Abstract
Gastrointestinal stromal tumors (GISTs) are the major gastrointestinal mesenchymal tumors with a variable malignancy ranging from a curable disorder to highly malignant sarcomas. Metastasis and recurrence are the main causes of death in GIST patients. To further explore the mechanism of metastasis and to more accurately estimate the recurrence risk of GISTs after surgery, the clinical significance and functional role of collagen triple helix repeat containing-1 (CTHRC1) in GIST were investigated. We found that CTHRC1 expression was gradually elevated as the risk grade of NIH classification increased, and was closely correlated with disease-free survival and overall survival in 412 GIST patients. In vitro experiments showed that recombinant CTHRC1 protein promoted the migration and invasion capacities of primary GIST cells. A luciferase reporter assay and pull down assay demonstrated that recombinant CTHRC1 protein activated noncanonical Wnt/PCP-Rho signaling but inhibited canonical Wnt signaling. The pro-motility effect of CTHRC1 on GIST cells was reversed by using a Wnt5a neutralizing antibody and inhibitors of Rac1 or ROCK. Taken together, these data indicate that CTHRC1 may serve as a new predictor of recurrence risk and prognosis in post-operative GIST patients and may play an important role in facilitating GIST progression. Furthermore, CTHRC1 promotes GIST cell migration and invasion by activating Wnt/PCP-Rho signaling, suggesting that the CTHRC1-Wnt/PCP-Rho axis may be a new therapeutic target for interventions against GIST invasion and metastasis.
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- 2014
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25. A Discretized Tikhonov Regularization Method for a Fractional Backward Heat Conduction Problem
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Zhi-Liang Deng and Xiao-Mei Yang
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Mathematics ,QA1-939 - Abstract
We propose a numerical reconstruction method for solving a time-fractional backward heat conduction problem. Based on the idea of reproducing kernel approximation, we reconstruct the unknown initial heat distribution from a finite set of scattered measurements of transient temperature at a fixed final time. The standard Tikhonov regularization technique using the norm of reproducing the kernel Hilbert space as the penalty term is adopted to provide a stable solution when the measurement data contains noise. Numerical results indicate that the proposed method is efficient.
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- 2014
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26. A Point Source Identification Problem for a Time Fractional Diffusion Equation
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Xiao-Mei Yang and Zhi-Liang Deng
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Physics ,QC1-999 - Abstract
An inverse source identification problem for a time fractional diffusion equation is discussed. The unknown heat source is supposed to be space dependent only. Based on the use of Green’s function, an effective numerical algorithm is developed to recover both the intensities and locations of unknown point sources from final measurements. Numerical results indicate that the proposed method is efficient and accurate.
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- 2013
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27. Lumican Accelerates Wound Healing by Enhancing α2β1 Integrin-Mediated Fibroblast Contractility.
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Xiao-Jin Liu, Fan-Zhi Kong, Ya-Hui Wang, Jiang-Hong Zheng, Wei-Dong Wan, Chen-Liang Deng, Guang-Yu Mao, Jun Li, Xiao-Mei Yang, Yan-Li Zhang, Xue-Li Zhang, Song-Lin Yang, and Zhi-Gang Zhang
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Medicine ,Science - Abstract
Lumican is a dermatan sulfate proteoglycan highly expressed in connective tissue and has the ability to regulate collagen fibril assembly. Previous studies have shown that lumican is involved in wound healing, but the precise effects of lumican on reepithelialization and wound contraction, the two pivotal aspects of skin wound healing, have not been investigated. Here we explored the roles of lumican in fibroblast contractility, a main aspect of skin wound healing, by adopting mice skin wound healing model and the corresponding in vitro cellular experiments. Our results showed that lumican can promote skin wound healing by facilitating wound fibroblast activation and contraction but not by promoting keratinocyte proliferation and migration. Silencing of integrin α2 completely abolished the pro-contractility of lumican, indicating lumican enhances fibroblast contractility via integrin α2. Our study for the first time demonstrated that lumican can affect fibroblast's mechanical property, which is pivotal for many important pathological processes, such as wound healing, fibrosis, and tumor development, suggesting that lumican might have a potential to be used to modulate these processes.
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- 2013
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28. The sortase A substrates FnbpA, FnbpB, ClfA and ClfB antagonize colony spreading of Staphylococcus aureus.
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Eleni Tsompanidou, Emma L Denham, Mark J J B Sibbald, Xiao-Mei Yang, Jolien Seinen, Alexander W Friedrich, Girbe Buist, and Jan Maarten van Dijl
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Medicine ,Science - Abstract
Staphylococcus aureus is an important human pathogen that is renowned both for its rapid transmission within hospitals and the community, and for the formation of antibiotic resistant biofilms on medical implants. Recently, it was shown that S. aureus is able to spread over wet surfaces. This motility phenomenon is promoted by the surfactant properties of secreted phenol-soluble modulins (PSMs), which are also known to inhibit biofilm formation. The aim of the present studies was to determine whether any cell surface-associated S. aureus proteins have an impact on colony spreading. To this end, we analyzed the spreading capabilities of strains lacking non-essential components of the protein export and sorting machinery. Interestingly, our analyses reveal that the absence of sortase A (SrtA) causes a hyper-spreading phenotype. SrtA is responsible for covalent anchoring of various proteins to the staphylococcal cell wall. Accordingly, we show that the hyper-spreading phenotype of srtA mutant cells is an indirect effect that relates to the sortase substrates FnbpA, FnbpB, ClfA and ClfB. These surface-exposed staphylococcal proteins are known to promote biofilm formation, and cell-cell interactions. The hyper-spreading phenotype of srtA mutant staphylococcal cells was subsequently validated in Staphylococcus epidermidis. We conclude that cell wall-associated factors that promote a sessile lifestyle of S. aureus and S. epidermidis antagonize the colony spreading motility of these bacteria.
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- 2012
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29. Acoustic characterization of hydrate formation and decomposition in clay-bearing sediments.
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Yi-Jian Zhu, Xiao-Mei Yang, Xing Huang, Hao Li, Xiao-Hui Wang, Yi-Fei Sun, Peng Xiao, Chang-Yu Sun, and Guang-Jin Chen
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GAS hydrates , *METHANE hydrates , *SEDIMENTS , *ILLITE , *CLAY , *VELOCITY - Abstract
Understanding the acoustic characteristics of hydrates in various sediments is crucial for hydrate resource detection and safe and efficient exploitation, as hydrate occurrence patterns vary greatly in different sediments. In this work, sediments with different bentonite contents, water saturations, and types were prepared to investigate the characteristics of P-wave velocity (reflecting the magnitude of hydrate saturation in the sediment) and amplitude (reflecting the degree of hydrate-sediment cementation) during hydrate formation and depressurization. During hydrate formation, the P-wave velocity and amplitude have similar trends. As clay content increases, the P-wave velocity increase rates quickened. On the other hand, the increased rate of P-wave velocity slows down with the increase of water saturation in the clay-bearing sediments. Comparing various types of sediment shows that the water absorption and swelling of bentonite reduce the pore space, speeding up the cementation of the hydrate with the sediment and increasing P-wave velocity at a faster rate. Correspondence between P-wave velocity and hydrate saturation is strongly related to sediment type, clay content, and water saturation. The rapidly decreasing amplitude in the early stage of hydrate depressurization indicates that hydrate in clay-bearing sediments is weakly cemented to the sediments, which is prone to stratigraphic instability. The findings of this study offer guidance for hydrate resource assessments in clay-bearing sediments as well as geologic risk estimations during hydrate mining. [ABSTRACT FROM AUTHOR]
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- 2024
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30. Bayesian approach for limited-aperture inverse acoustic scattering with total variation prior.
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Xiao-Mei Yang, Zhi-Liang Deng, and Ailin Qian
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- 2022
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31. Bayesian inverse problems using homotopy.
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Xiao-Mei Yang and Zhi-Liang Deng
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- 2022
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32. CSMD3Deficiency Leads to Motor Impairments and Autism-Like Behaviors via Dysfunction of Cerebellar Purkinje Cells in Mice
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Ke Xi, Si-Qing Cai, Hui-Fang Yan, Yue Tian, Jie Cai, Xiao-Mei Yang, Jing-Min Wang, and Guo-Gang Xing
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General Neuroscience - Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with highly heritable heterogeneity. Mutations of CUB and sushi multiple domains 3 (CSMD3) gene have been reported in individuals with ASD. However, the underlying mechanisms of CSMD3 for the onset of ASD remain unexplored. Here, using maleCSMD3knock-out (CSMD3−/−) mice, we found that genetic deletion ofCSMD3produced core autistic-like symptoms (social interaction deficits, restricted interests, and repetitive and stereotyped behaviors) and motor dysfunction in mice, indicating that theCSMD3gene can be considered as a candidate for ASD. Moreover, we discovered that the ablation ofCSMD3in mice led to abnormal cerebellar Purkinje cell (PC) morphology in Crus I/II lobules, including aberrant developmental dendritogenesis and spinogenesis of PCs. Furthermore, combiningin vivofiber photometry calcium imaging andex vivoelectrophysiological recordings, we showed that theCSMD3−/−mice exhibited an increased neuronal activity (calcium fluorescence signals) in PCs of Crus I/II lobules in response to movement activity, as well as an enhanced intrinsic excitability of PCs and an increase of excitatory rather than inhibitory synaptic input to the PCs, and an impaired long-term depression at the parallel fiber–PC synapse. These results suggest that CSMD3 plays an important role in the development of cerebellar PCs. Loss of CSMD3 causes abnormal PC morphology and dysfunction in the cerebellum, which may underlie the pathogenesis of motor deficits and core autistic-like symptoms inCSMD3−/−mice. Our findings provide novel insight into the pathophysiological mechanisms by whichCSMD3mutations cause impairments in cerebellar function that may contribute to ASD.SIGNIFICANCE STATEMENTAutism spectrum disorder (ASD) is a neurodevelopmental disorder with highly heritable heterogeneity. Advances in genomic analysis have contributed to numerous candidate genes for the risk of ASD. Recently, a novel giant geneCSMD3encoding a protein with CUB and sushi multiple domains (CSMDs) has been identified as a candidate gene for ASD. However, the underlying mechanisms ofCSMD3for the onset of ASD remain largely unknown. Here, we unravel that loss ofCSMD3results in abnormal morphology, increased intrinsic excitabilities, and impaired synaptic plasticity in cerebellar PCs, subsequently leading to motor deficits and ASD-like behaviors in mice. These results provide novel insight into the pathophysiological mechanisms by whichCSMD3mutations cause impairments in cerebellar function that may contribute to ASD.
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- 2023
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33. CCBE1 promotes mitochondrial fusion by inhibiting the TGFβ-DRP1 axis to prevent the progression of hepatocellular carcinoma
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Guang-Ang Tian, Wen-Ting Xu, Xue-Li Zhang, Yao-Qi Zhou, Yue Sun, Li-Peng Hu, Shu-Heng Jiang, Hui-Zhen Nie, Zhi-Gang Zhang, Lei Zhu, Jun Li, Xiao-Mei Yang, and Lin-Li Yao
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Molecular Biology - Published
- 2023
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34. Fully automated modal tracking for long-span high-speed railway bridges
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Xiao-Mei Yang, Hongnan Li, Ting-Hua Yi, Chun-Xu Qu, and Hua Liu
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Building and Construction ,Civil and Structural Engineering - Abstract
Modal parameters are inherent structural characteristics that are valuable for model updating, condition assessment, and early warning of bridges. Operational modal tracking technology has been a popular research topic in bridge structural health monitoring (SHM) because of its output-only advantage; that is, only the vibration responses of the bridge are necessary for modal identification. The real-time objective of bridge SHM requires operational modal tracking to be fully automated. Because the loads acting on long-span high-speed railway bridges are various, the modal identification methods should be changed according to the excitation characteristics; otherwise, the results may be incorrect. However, there is no unified framework for simultaneously tracking the modal evolution of a bridge under different excitations. In this study, modal tracking strategies based on ambient loads, train loads and immediately a train moving past the bridge were developed to identify the operational modal parameters of the bridge. In addition, a unified tracking framework was established to automatically switch among the three-stage modal-tracking strategies, which utilizes the real-time positioning of the axle loads. Furthermore, the computational efficiency of the tracking strategies and the obstacles of operational modal analysis were analyzed to provide a reference for mode-based SHM of bridges, and the essential parameters in the tracking algorithms were suggested. The three-stage modal-tracking methods were validated through long-term monitoring data of a long-span high-speed railway bridge. The results indicated that the best tracking results were generated from free-vibration data, while the modal-tracking under ambient loads had best timeliness.
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- 2022
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35. Transglutaminases are oncogenic biomarkers in human cancers and therapeutic targeting of TGM2 blocks chemoresistance and macrophage infiltration in pancreatic cancer
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Shan Zhang, Hong-Fei Yao, Hui Li, Tong Su, Shu-Heng Jiang, Hao Wang, Zhi-Gang Zhang, Fang-Yuan Dong, Qin yang, and Xiao-Mei Yang
- Subjects
Cancer Research ,Oncology ,Molecular Medicine ,General Medicine - Abstract
Backgroud: Transglutaminases (TGs) are multifunctional enzymes with transglutaminase cross-linking, atypical GTPase/ATPase and kinase activity. Here, an integrated comprehensive analysis shows the genomic, transcriptomic and immunological landscapes of the TGs varies among different cancers. Methods Gene expression pattern and immune cell infiltration in pan-cancer were obtained from The Cancer Genome Atlas (TCGA) databases and Gene Set Enrichment Analysis (GSEA) datasets. Western blotting, immunofluorescence, ELISA, and orthotopic xenograft model were performed to validate our database-derived results. Results The overall expression of TGs (designated as TG score) is significantly upregulated in multiple cancers and related to worse patient survial. The expression of the TG family can be regulated by multiple mechanisms at the genetic, epigenetic and transcriptional levels. Transcriptionfactors crucial for epithelial to mesenchymal transition (EMT) are commonly correlated with TG score in many cancer types. Importantly, TGM2 expression displays a close connection with the chemoresistances of a wide range of chemodrugs. TGM2, F13A1 and overall TG score are positively correlated with the infiltration of immune cells in all cancer types tested. Functional and clinical verification reveals that higher TGM2 expression is linked with worse patient survival, increased IC50 value of gemcitabine, and abundant tumor-infiltrating macrophages in pancreatic cancer. Mechanistically, increased C-C motif chemokine ligand 2 (CCL2) release affored by TGM2 contributes to macrophage infiltration with tumor microenvironment. Conclusions These results reveal the relevances and molecular networks of TG genes in human cancers, highlighting the significance of TGM2 in pancreatic cancer which may provide some promising directions for immunotherapy and dealing with chemoresistance.
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- 2023
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36. Polydopamine surface functionalized submicron ZnO for broadening the processing window of 3D printable PLA composites
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Xiao-Mei Yang, Guang-Zhong Yin, Olga Zafra Amorós, María Arroyo Hernández, Jimena de la Vega, and José Manuel Torralba
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PDA ,Ingeniería Mecánica ,Materiales ,Polymers and Plastics ,Surface functionalization ,Organic Chemistry ,Materials Chemistry ,ZnO ,PLA ,PLA · Surface functionalization · ZnO · 3D printing · PDA ,3D printing ,Química ,Ingeniería Industrial - Abstract
The “catalytic degradation” of metal oxides limits the wide application of PLA when PLA needs to be modified by adding metal oxides to achieve desired properties. Zinc oxide (ZnO) is a common and widely used agent as it can be used for many properties, such as antioxidant, antibacterial, etc. However, detrimental effects often exist on the properties of polymers after introducing the ZnO, due to the catalytic degradation. In this study, we used polydopamine (PDA) to construct ZnO@PDA core-shell submicron particles via the self-polymerization of dopamine (DA) in alkaline solution, aimed to produce a surface functionalization that would be used to control the rate of degradation of PLA by ZnO during thermal processing, and promote the preservation of mechanical properties. PLA with different contents of ZnO and ZnO@PDA were prepared by a simple melt extrusion method. The degradation behavior, mechanical properties and antibacterial activity of ZnO/PLA and ZnO@PDA/PLA were investigated. It was found that the incorporation of ZnO@PDA in PLA at different contents exhibits a dramatic control over the degradation rate when compared to that of the ZnO/PLA with the same filler content. Notably, the T5% and T50% of 3%-ZnO@PDA/PLA increased by 36.4 oC and 31.9 oC. GPC results showed the molecular weight of 3%-ZnO@PDA/PLA was only reduced by 15.8% after thermal processing. In addition, 3%-ZnO@PDA/PLA can be 3D-printed smoothly. That is to say, the introduction of ZnO@PDA can increase the processing window of PLA/ZnO composites, providing the possibility for materials that need to be included in civil application. Accordingly, ZnO@PDA/PLA samples showed higher tensile strength and elongation at break than that of corresponding ZnO/PLA samples. Regarding the antibacterial behavior, the ZnO@PDA/PLA have more bacterial growth disability effect against Gram(+) bacteria than that of pure PLA. This publication is funded through the project "MAMAP - Materials and models against pandemics" (REACT-EU resources of the Madrid Operational Program 2014-2020, in the action line of R+D+i projects in response to COVID-19). Project funded by the Community of Madrid and by the European Regional Development Fund of the European Union "A way to make Europe". Financed as part of the Union's response to the COVID-19 pandemic, through the agreement signed between the Community of Madrid (Regional Ministry of Education, Universities, Science, and Spokesperson) and the IMDEA Materials Foundation for the direct granting of a grant of 1.937.000.00 euros to fund research activities on SARS-COV 2 and the COVID-19 disease funded with REACT-EU resources from the European Regional Development Fund.
- Published
- 2023
37. Data from SPON2 Promotes M1-like Macrophage Recruitment and Inhibits Hepatocellular Carcinoma Metastasis by Distinct Integrin–Rho GTPase–Hippo Pathways
- Author
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Zhi-Gang Zhang, Qiang Xia, Su-Jae Lee, Ho-Young Lee, Li-Peng Hu, Guang-Ang Tian, Shu-Heng Jiang, Ming-Xuan Feng, Xue-Li Zhang, Hui-Zhen Nie, Lei Zhu, Qin Yang, Ya-Hui Wang, Jun Li, Fang Fang, Xiao-Mei Yang, Qing Li, and Yan-Li Zhang
- Abstract
Tumor-associated macrophages (TAM) represent key regulators of the complex interplay between cancer and the immune microenvironment. Matricellular protein SPON2 is essential for recruiting lymphocytes and initiating immune responses. Recent studies have shown that SPON2 has complicated roles in cell migration and tumor progression. Here we report that, in the tumor microenvironment of hepatocellular carcinoma (HCC), SPON2 not only promotes infiltration of M1-like macrophages but also inhibits tumor metastasis. SPON2-α4β1 integrin signaling activated RhoA and Rac1, increased F-actin reorganization, and promoted M1-like macrophage recruitment. F-Actin accumulation also activated the Hippo pathway by suppressing LATS1 phosphorylation, promoting YAP nuclear translocation, and initiating downstream gene expression. However, SPON2-α5β1 integrin signaling inactivated RhoA and prevented F-actin assembly, thereby inhibiting HCC cell migration; the Hippo pathway was not noticeably involved in SPON2-mediated HCC cell migration. In HCC patients, SPON2 levels correlated positively with prognosis. Overall, our findings provide evidence that SPON2 is a critical factor in mediating the immune response against tumor cell growth and migration in HCC.Significance: Matricellular protein SPON2 acts as an HCC suppressor and utilizes distinct signaling events to perform dual functions in HCC microenvironment.Graphical Abstract: http://cancerres.aacrjournals.org/content/canres/78/9/2305/F1.large.jpg. Cancer Res; 78(9); 2305–17. ©2018 AACR.
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- 2023
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38. Supplementary Data from Targeting Purinergic Receptor P2Y2 Prevents the Growth of Pancreatic Ductal Adenocarcinoma by Inhibiting Cancer Cell Glycolysis
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Zhi-Gang Zhang, Yong-Wei Sun, Gary Guishan Xiao, Jun Li, Ya-Hui Wang, Xiao-Mei Yang, Qin Yang, Yan-Li Zhang, Xiao-Yan Cao, Guang-Ang Tian, Yong-Sheng Jiang, Yan-Miao Huo, Ming-Wei Yang, Li-Li Zhu, Qing Li, Ling-Ye Tao, Shu-Heng Jiang, Xiao-Xin Zhang, and Li-Peng Hu
- Abstract
Supplymentary data figure 1-8 and table 1-2
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- 2023
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39. Data from Targeting Purinergic Receptor P2Y2 Prevents the Growth of Pancreatic Ductal Adenocarcinoma by Inhibiting Cancer Cell Glycolysis
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Zhi-Gang Zhang, Yong-Wei Sun, Gary Guishan Xiao, Jun Li, Ya-Hui Wang, Xiao-Mei Yang, Qin Yang, Yan-Li Zhang, Xiao-Yan Cao, Guang-Ang Tian, Yong-Sheng Jiang, Yan-Miao Huo, Ming-Wei Yang, Li-Li Zhu, Qing Li, Ling-Ye Tao, Shu-Heng Jiang, Xiao-Xin Zhang, and Li-Peng Hu
- Abstract
Purpose:Extensive research has reported that the tumor microenvironment components play crucial roles in tumor progression. Thus, blocking the supports of tumor microenvironment is a promising approach to prevent cancer progression. We aimed to determine whether blocking extracellular ATP–P2RY2 axis could be a potential therapeutic approach for PDAC treatment.Experimental Design:Expression of P2RY2 was determined in 264 human PDAC samples and correlated to patient survival. P2RY2 was inhibited in human PDAC cell lines by antagonist and shRNA, respectively, and cell viability, clonogenicity, and glycolysis were determined. RNA sequencing of PDAC cell line was applied to reveal underlying molecular mechanisms. Multiple PDAC mouse models were used to assess the effects of the P2RY2 inhibition on PDAC progression.Results:P2RY2 was upregulated and associated with poor prognosis in PDAC. Activated P2RY2 by increased extracellular ATP in tumor microenvironment promoted PDAC growth and glycolysis. Further studies showed that the agonist-activated P2RY2 triggered PI3K/AKT–mTOR signaling by crosstalk with PDGFR mediated by Yes1, resulting in elevated expression of c-Myc and HIF1α, which subsequently enhanced cancer cell glycolysis. Genetic and pharmacologic inhibition of P2RY2 impaired tumor cell growth in subcutaneous and orthotopic xenograft model, as well as delayed tumor progression in inflammation-driven PDAC model. In addition, synergy was observed when AR-C118925XX, the selective antagonist of P2RY2 receptor, and gemcitabine were combined, resulting in prolonged survival of xenografted PDAC mice.Conclusions:These findings reveal the roles of the P2RY2 in PDAC metabolic reprogramming, suggesting that P2RY2 might be a potential metabolic therapeutic target for PDAC.
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- 2023
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40. Supplementary Figures S1-8 from SPON2 Promotes M1-like Macrophage Recruitment and Inhibits Hepatocellular Carcinoma Metastasis by Distinct Integrin–Rho GTPase–Hippo Pathways
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Zhi-Gang Zhang, Qiang Xia, Su-Jae Lee, Ho-Young Lee, Li-Peng Hu, Guang-Ang Tian, Shu-Heng Jiang, Ming-Xuan Feng, Xue-Li Zhang, Hui-Zhen Nie, Lei Zhu, Qin Yang, Ya-Hui Wang, Jun Li, Fang Fang, Xiao-Mei Yang, Qing Li, and Yan-Li Zhang
- Abstract
Supplementary figures of expression of SPON2, integrin subunit, LATS1 and YAP, effect of SPON2 on M2-like TAM infiltration, co-location of SPON2 and integrin α4/α5, influence of RhoA T19N/Q63L and Rac1 T17N mutants on active RhoA and Rac1, effect of chemokines on primed THP-1 cell migration
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- 2023
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41. Supplementary materials and methods from SPON2 Promotes M1-like Macrophage Recruitment and Inhibits Hepatocellular Carcinoma Metastasis by Distinct Integrin–Rho GTPase–Hippo Pathways
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Zhi-Gang Zhang, Qiang Xia, Su-Jae Lee, Ho-Young Lee, Li-Peng Hu, Guang-Ang Tian, Shu-Heng Jiang, Ming-Xuan Feng, Xue-Li Zhang, Hui-Zhen Nie, Lei Zhu, Qin Yang, Ya-Hui Wang, Jun Li, Fang Fang, Xiao-Mei Yang, Qing Li, and Yan-Li Zhang
- Abstract
Supplementary materials and methods of isolation of hMC, immunohistochemical and H&E staining, 3D spheroid analysis, PLA, q-PCR, lentivirus production and cell transduction, siRNA, production of rSPON2, ELISA assay and chemokine assay
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- 2023
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42. Ssri Antidepressant Citalopram Reverses the Warburg Effect and Elicits Anti-Tumor Immunity by Targeting Glut1 and C5ar1
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Fangyuan Dong, Kang He, Shan Zhang, Kaiyuan Song, Jun Li, Mingxuan Feng, Xiao-Mei Yang, Xueli Zhang, Hao Wang, Hui Li, Xiao-Cao Miao, Li-Peng Hu, Rong-Kun Li, Lin-Tai Da, Xu Wang, Zhijun Bao, Zhi-gang Zhang, and Shuheng Jiang
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- 2023
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43. Effect of p18 on endothelial barrier function by mediating vascular endothelial Rab11a-VE-cadherin recycling
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Xu-Ting Zhi, Bo-Wen Xu, Xiao-Mei Yang, Zhi-Qiang Cheng, and Zhi-Bo Yan
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endocrine system ,Gene knockdown ,endocrine system diseases ,Chemistry ,Organic Chemistry ,Inflammation ,General Medicine ,Cadherins ,Endocytosis ,Applied Microbiology and Biotechnology ,Biochemistry ,Analytical Chemistry ,Cell biology ,Adherens junction ,Antigens, CD ,In vivo ,medicine ,Gene silencing ,medicine.symptom ,VE-cadherin ,Molecular Biology ,RAB11A ,Biotechnology - Abstract
Endothelial barrier integrity requires recycling of VE-cadherin to adherens junctions. Both p18 and Rab11a play significant roles in VE-cadherin recycling. However, the underlying mechanism and the role of p18 in activating Rab11a have yet to be elucidated. Performing in vitro and in vivo experiments, we showed that p18 protein bound to VE-cadherin before Rab11a through its VE-cadherin-binding domain (aa 1-39). Transendothelial resistance showed that overexpression of p18 promoted the circulation of VE-cadherin to adherens junctions and the recovery of the endothelial barrier. Silencing of p18 caused endothelial barrier dysfunction and prevented Rab11a-positive recycling endosome accumulation in the perinuclear recycling compartments. Furthermore, p18 knockdown in pulmonary microvessels markedly increased vascular leakage in mice challenged with lipopolysaccharide and cecal ligation puncture. This study showed that p18 regulated the pulmonary endothelial barrier function in vitro and in vivo by regulating the binding of Rab11a to VE-cadherin and the activation of Rab11a.
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- 2021
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44. Performance Warning of Bridges under Train Actions through Equivalent Frequency Response Functions
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Xiao-Mei Yang, Ting-Hua Yi, Chun-Xu Qu, Hong-Nan Li, and Hua Liu
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Building and Construction ,Civil and Structural Engineering - Published
- 2022
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45. Overexpression of ARHGAP30 suppresses growth of cervical cancer cells by downregulating ribosome biogenesis
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Yincheng Teng, Zhihong Ai, Xiao-Mei Yang, Lan Lin, Xiao Li, Wei Xu, Xiaolu Zhu, Aijia Wu, and Qinyang Xu
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Cancer Research ,GTPase-activating protein ,Carcinogenesis ,cervical cancer ,Immunoprecipitation ,ARHGAP30 ,Down-Regulation ,Mice, Nude ,Uterine Cervical Neoplasms ,ribosome biogenesis ,Ribosome biogenesis ,ubiquitination ,Mass Spectrometry ,HeLa ,Mice ,chemistry.chemical_compound ,nucleolin ,Cell Line, Tumor ,Protein biosynthesis ,Animals ,Humans ,Tumor Stem Cell Assay ,Cell Proliferation ,Mice, Inbred BALB C ,biology ,Cell growth ,GTPase-Activating Proteins ,RNA-Binding Proteins ,Original Articles ,General Medicine ,Phosphoproteins ,biology.organism_classification ,Neoplasm Proteins ,Cell biology ,Oncology ,chemistry ,RNA, Ribosomal ,Puromycin ,Protein Biosynthesis ,Female ,Original Article ,Ribosomes ,Nucleolin ,Cell Nucleolus ,HeLa Cells - Abstract
We aimed to identify whether Rho GTPase activating proteins (RhoGAPs) were downregulated in cervical cancers and might be targeted to reduce the growth of cervical cancer using the GEO database and immunohistochemical analysis to identified changes in transcription and protein levels. We analyzed their proliferation, clone formation ability, and their growth as subcutaneous tumors in mice. To detect ARHGAP30 localization in cells, immunofluorescence assays were conducted. Mass spectrometry combined with immunoprecipitation experiments were used to identify binding proteins. Protein interactions were validated with co‐immunoprecipitation assays. Western‐blot and q‐PCR were applied to analyze candidate binding proteins that were associated with ribosome biogenesis. Puromycin incorporation assay was used to detect the global protein synthesis rate. We identified that ARHGAP30 was the only downregulated RhoGAP and was related to the survival of cervical cancer patients. Overexpression of ARHGAP30 in cervical cancer cells inhibited cell proliferation and migration. ARHGAP30 immunoprecipitated proteins were enriched in the ribosome biogenesis process. ARHGAP30 was located in the nucleous and interacted with nucleolin (NCL). Overexpression of ARHGAP30 inhibited rRNA synthesis and global protein synthesis. ARHGAP30 overexpression induced the ubiquitination of NCL and decreased its protein level in Hela cells. The function of ARHGAP30 on cervical cancer cell ribosome biogenesis and proliferation was independent of its RhoGAP activity as assessed with a RhoGAP‐deficient plasmid of ARHGAP30R55A. Overall, the findings revealed that ARHGAP30 was frequently downregulated and associated with shorter survival of cervical cancer patients. ARHGAP30 may suppress growth of cervical cancer by reducing ribosome biogenesis and protein synthesis through promoting ubiquitination of NCL., ARHGAP30 suppressed growth of cervical cancer by reducing ribosome biogenesis and protein synthesis through promoting ubiquitination of nucleolin.
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- 2021
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46. Two lanthanide coordination polymers: treatment activity on the endometrial carcinoma by inhibiting the VEGF signaling pathway
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Xiao-Mei Yang, Yan Zhang, Hui Xue, and Cui-Lan Gong
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Inorganic Chemistry ,Physical and Theoretical Chemistry - Published
- 2021
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47. Contribution of AMPA Receptor-Mediated LTD in LA/BLA-CeA Pathway to Comorbid Aversive and Depressive Symptoms in Neuropathic Pain
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Jing-Gui Song, Xiao-Mei Yang, Ling-Yu Kong, You Wan, Jie Cai, Jiang-Ping Liu, Xi-Yuan Han, Guo-Gang Xing, Ke Xi, Si-Qing Cai, Hong Jiang, and Ling-Yu Liu
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Male ,Patch-Clamp Techniques ,Dendritic spine ,Conditioning, Classical ,Emotions ,Genetic Vectors ,Comorbidity ,AMPA receptor ,Anxiety ,Amygdala ,Rats, Sprague-Dawley ,Synapse ,Food Preferences ,Neuroplasticity ,Avoidance Learning ,Animals ,Medicine ,Single-Blind Method ,Receptors, AMPA ,Ligation ,Research Articles ,Swimming ,Sensitization ,Basolateral Nuclear Complex ,Depression ,business.industry ,Long-Term Synaptic Depression ,General Neuroscience ,Central Amygdaloid Nucleus ,Lentivirus ,Chronic pain ,Excitatory Postsynaptic Potentials ,medicine.disease ,Endocytosis ,Rats ,Spinal Nerves ,medicine.anatomical_structure ,Hyperalgesia ,Rotarod Performance Test ,Neuropathic pain ,Exploratory Behavior ,Neuralgia ,Peptides ,business ,Neuroscience - Abstract
Comorbid anxiety and depressive symptoms in chronic pain are a common health problem, but the underlying mechanisms remain unclear. Previously, we have demonstrated that sensitization of the CeA neurons via decreased GABAergic inhibition contributes to anxiety-like behaviors in neuropathic pain rats. In this study, by using male Sprague Dawley rats, we reported that the CeA plays a key role in processing both sensory and negative emotional-affective components of neuropathic pain. Bilateral electrolytic lesions of CeA, but not lateral/basolateral nucleus of the amygdala (LA/BLA), abrogated both pain hypersensitivity and aversive and depressive symptoms of neuropathic rats induced by spinal nerve ligation (SNL). Moreover, SNL rats showed structural and functional neuroplasticity manifested as reduced dendritic spines on the CeA neurons and enhanced LTD at the LA/BLA-CeA synapse. Disruption of GluA2-containing AMPAR trafficking and endocytosis from synapses using synthetic peptides, either pep2-EVKI or Tat-GluA2((3Y)), restored the enhanced LTD at the LA/BLA-CeA synapse, and alleviated the mechanical allodynia and comorbid aversive and depressive symptoms in neuropathic rats, indicating that the endocytosis of GluA2-containing AMPARs from synapses is probably involved in the LTD at the LA/BLA-CeA synapse and the comorbid aversive and depressive symptoms in neuropathic pain in SNL-operated rats. These data provide a novel mechanism for elucidating comorbid aversive and depressive symptoms in neuropathic pain and highlight that structural and functional neuroplasticity in the amygdala may be important as a promising therapeutic target for comorbid negative emotional-affective disorders in chronic pain. SIGNIFICANCE STATEMENT Several studies have demonstrated the high comorbidity of negative affective disorders in patients with chronic pain. Understanding the affective aspects related to chronic pain may facilitate the development of novel therapies for more effective management. Here, we unravel that the CeA plays a key role in processing both sensory and negative emotional-affective components of neuropathic pain, and LTD at the amygdaloid LA/BLA-CeA synapse mediated by GluA2-containing AMPAR endocytosis underlies the comorbid aversive and depressive symptoms in neuropathic pain. This study provides a novel mechanism for elucidating comorbid aversive and depressive symptoms in neuropathic pain and highlights that structural and functional neuroplasticity in the amygdala may be important as a promising therapeutic target for comorbid negative emotional-affective disorders in chronic pain.
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- 2021
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48. Dobutamine-sparing strategy in managing patients with impaired ejection fraction undergoing coronary artery bypass grafting: less is more?
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Xiao-Mei Yang, Ying Zhang, Guo-Wei Tu, Zhe Luo, Jing-Chao Luo, Kanhua Yin, Ming-Hao Luo, and Xiao-Ming Lin
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Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,Ejection fraction ,Bypass grafting ,business.industry ,medicine.anatomical_structure ,Internal medicine ,medicine ,Cardiology ,Dobutamine ,business ,Letter to the Editor ,medicine.drug ,Artery - Published
- 2021
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49. Recent advances in flame retardant and mechanical properties of polylactic acid: A review
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Xiao-Mei Yang, Shuang Qiu, Abdulmalik Yusuf, Jun Sun, Zhongjie Zhai, Junhuan Zhao, and Guang-Zhong Yin
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Structural Biology ,General Medicine ,Molecular Biology ,Biochemistry - Published
- 2023
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50. The short isoform of PRLR suppresses the pentose phosphate pathway and nucleotide synthesis through the NEK9-Hippo axis in pancreatic cancer
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Xiao-Mei Yang, Yan-Li Zhang, Jun Li, Yi-Fan Zhang, Shu-Heng Jiang, Qing Li, Zhigang Zhang, Lei Zhu, Ya-Hui Wang, Gary Guishan Xiao, Pei-Qi Huang, Li-Peng Hu, Huizhen Nie, Yanqiu Yu, Jianguang Ji, Qin Yang, and Yong-Wei Sun
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0301 basic medicine ,Medicine (miscellaneous) ,Pentose Phosphate Pathway ,Mice ,0302 clinical medicine ,NIMA-Related Kinases ,Protein Isoforms ,pancreas ,Precision Medicine ,Pharmacology, Toxicology and Pharmaceutics (miscellaneous) ,TEAD1 ,Nucleotides ,Nuclear Proteins ,TEA Domain Transcription Factors ,isoform ,Prognosis ,DNA-Binding Proteins ,Hippo signaling ,030220 oncology & carcinogenesis ,Heterografts ,Transketolase ,Carcinoma, Pancreatic Ductal ,Signal Transduction ,Research Paper ,Receptors, Prolactin ,hormone ,Down-Regulation ,Mice, Transgenic ,Biology ,Pentose phosphate pathway ,Glucosephosphate Dehydrogenase ,Protein Serine-Threonine Kinases ,03 medical and health sciences ,Pancreatic cancer ,Cell Line, Tumor ,medicine ,Animals ,Humans ,Hippo Signaling Pathway ,RNA, Messenger ,Transcription factor ,Cell Proliferation ,Hippo signaling pathway ,Prolactin receptor ,medicine.disease ,biosynthesis ,Mice, Mutant Strains ,Pancreatic Neoplasms ,030104 developmental biology ,Cancer research ,Chromatin immunoprecipitation ,metabolism ,Transcription Factors - Abstract
Prolactin binding to the prolactin receptor exerts pleiotropic biological effects in vertebrates. The prolactin receptor (PRLR) has multiple isoforms due to alternative splicing. The biological roles and related signaling of the long isoform (PRLR-LF) have been fully elucidated. However, little is known about the short isoform (PRLR-SF), particularly in cancer development and metabolic reprogramming, a core hallmark of cancer. Here, we reveal the role and underlying mechanism of PRLR-SF in pancreatic ductal adenocarcinoma (PDAC). Methods: A human PDAC tissue array was used to investigate the clinical relevance of PRLR in PDAC. The in vivo implications of PRLR-SF in PDAC were examined in a subcutaneous xenograft model and an orthotopic xenograft model. Immunohistochemistry was performed on tumor tissue obtained from genetically engineered KPC (KrasG12D/+; Trp53R172H/+; Pdx1-Cre) mice with spontaneous tumors. 13C-labeled metabolite measures, LC-MS, EdU incorporation assays and seahorse analyses were used to identify the effects of PRLR-SF on the pentose phosphate pathway and glycolysis. We identified the molecular mechanisms by immunofluorescence, coimmunoprecipitation, proximity ligation assays, chromatin immunoprecipitation and promoter luciferase activity. Public databases (TCGA, GEO and GTEx) were used to analyze the expression and survival correlations of the related genes. Results: We demonstrated that PRLR-SF is predominantly expressed in spontaneously forming pancreatic tumors of genetically engineered KPC mice and human PDAC cell lines. PRLR-SF inhibits the proliferation of PDAC cells (AsPC-1 and BxPC-3) in vitro and tumor growth in vivo. We showed that PRLR-SF reduces the expression of genes in the pentose phosphate pathway (PPP) and nucleotide biosynthesis by activating Hippo signaling. TEAD1, a downstream transcription factor of Hippo signaling, directly regulates the expression of G6PD and TKT, which are PPP rate-limiting enzymes. Moreover, NEK9 directly interacts with PRLR-SF and is the intermediator between PRLR and the Hippo pathway. The PRLR expression level is negatively correlated with overall survival and TNM stage in PDAC patients. Additionally, pregnancy and lactation increase the ratio of PRLR-SF:PRLR-LF in the pancreas of wild-type mice and subcutaneous PDAC xenograft tumors. Conclusion: Our characterization of the relationship between PRLR-SF signaling, the NEK9-Hippo pathway, PPP and nucleotide synthesis explains a mechanism for the correlation between PRLR-SF and metabolic reprogramming in PDAC progression. Strategies to alter this pathway might be developed for the treatment or prevention of pancreatic cancer.
- Published
- 2021
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