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FOXO3 mutation predicting gefitinib-induced hepatotoxicity in NsCLC patients through regulation of autophagy

Acta Pharmaceutica sinica B 2022年第9期12卷 3639-3649页

作者： shaoxing Guan Xi Chen Youhao Chen Guohui Wan Qibiao su Heng Liang Yunpeng Yang Wenfeng Fang Yan Huang Hongyun Zhao Wei Zhuang shu Liu Fei Wang Wei Feng Xiaoxu Zhang Min Huang Xueding Wang Li Zhang Laboratory of Drug Metabolism and Pharmacokinetics School of Pharmaceutical SciencesSun Yat-sen UniversityGuangzhou 510060China state Key Laboratory of Oncology in south China Collaborative Innovation Center for Cancer MedicineSun Yat-sen University Cancer CenterGuangzhou 510060China College of Health science Guangdong Pharmaceutical UniversityGuangzhou 510006China sun Yat-sen Memorial hospital Sun Yat-sen UniversityGuangzhou 510080China Ersha Department of Pharmacy the Second Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhou 510105China

Hepatotoxicity is a common side effect for patients treated with gefitinib,but the related pathogenesis is unclear and lacks effective predictor and management strategies.A multi-omics approach integrating pharmacometabolomics,pharmacokinetics and pharmacogenomics was employed in non-small cell lung cancer patients to identify the effective predictor for gefitinib-induced hepatotoxicity and explore optional therapy ***,we found that patients with rs4946935 AA,located in Forkhead Box O3(FOXO3)which is a well-known autophagic regulator,had a higher risk of hepatotoxicity than those with the GA or GG variant(OR=18.020,95%CI=2.473 to 459.1784,P=0.018)in a gefitinib-concentration dependent ***,functional experiments identified that rs4946935_A impaired the expression of FOXO3 by inhibiting the promotor activity,increasing the threshold of autophagy initiation and inhibiting the autophagic activity which contributed to gefitinib-induced liver *** contrast,erlotinib-induced liver injury was independent on the variant and expression levels of *** study reveals that FOXO3 mutation,leading to autophagic imbalance,plays important role in gefitinib-induced hepatotoxicity,especially for patients with high concentration of *** conclusion,FOXO3 mutation is an effective predictor and erlotinib might be an appropriately and well-tolerated treatment option for patients carrying rs4946935 AA.

关键词： Gefitinib Hepatotoxicity Pharmacometabolomic Pharmacokinetics Pharmacogenomics FOXO3 Autophagy

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Fatigue‑Resistant and Hysteresis‑Free Composite Fibers with a Heterogeneous Hierarchical structure

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Advanced Fiber Materials 2023年第5期5卷 1643-1656页

作者： siming Li Junwei Xu Yan Mu Peng Wang Heng Zhu Binhong Liu Zhe Chen Zilong Han shaoxing Qu Eye Center of the second Affiliated hospital State Key Laboratory of Fluid Power&Mechatronic SystemKey Laboratory of Soft Machines and Smart Devices of Zhejiang ProvinceCenter for X‑Mechanicsand Department of Engineering MechanicsZhejiang UniversityHangzhou 310027China

Fatigue-resistant and hysteresis-free composite fibers hold great promise for the next generation of wearable electronic *** this study,a novel approach for the fabrication of composite fibers with outstanding elasticity and mechanical stability is *** design incorporates a heterogeneous hierarchical structure(HHs),which mimics the structure of arteries,to achieve enhanced fatigue resistance and hysteresis-free *** composite fibers,Ecoflex-polyacrylamide fibers(EPFs),are created through the combination of heterogeneous elastomers and strong interfacial *** results show that the EPFs exhibit exceptional fatigue resistance,being able to withstand up to 10,000 load–unload cycles at strains of 300%without any noticeable changes in their mechanical *** potential applications of these EPFs are demonstrated through their use as strain sensors for monitoring human motion in both air and water,as well as in energyharvesting e-textiles.

关键词： Heterogeneous hierarchical structure Composite fibers Fatigue resistance Hysteresis free Wearable electronic devices

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Nephron-sparing surgery for small renal cell carcinoma

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Journal of Nanjing Medical University 2009年第3期23卷 207-211页

作者： Yongsheng Li shaoxing Zhu Weizhong Cai shiping Chen Qiyong Li Department of Urology Affiliated Union Hospital of Fujian Medical University Fuzhou 350001 China

Objective：To investigate the method and effect of nephron-sparing surgery in the treatment of small renal cell carcinoma. Methods： From August 1 997 to October 2008, 48 cases of small renal cell carcinomas were confirmed by surgery and pathology, and reviewed retrospectively. Of the 48 cases, there was 1 patient with bilateral tumors, 8 with solitary kidney tumors, 1 with unilateral tumor and a damaged contralateral kidney, and 38 with unilateral tumors and a normal contralateral kidney; 9 underwent tumor enucleation and the remaining patients received partial nephrectomy. Results：There were no local tumor recurrences and/or tumor metastasis at a mean followup of 60 months. Conclusion： Confirming conclusions from other centers, we have found that nephron-sparing surgery is an effective treatment for small renal cell carcinomas.

关键词： small renal cell carcinoma nephron-sparing surgery kidney neoplasms

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Genome of staphylococcus xylosus and Comparison with *** and ***

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Journal of Genetics and Genomics 2014年第7期41卷 413-416页

作者： Xiaojuan Tan Lin Liu shili Liu Dongting Yang Yikun Liu shuang Yang Aiqun Jia Nan Qin school of Environmental and Biological Engineering Nanjing University of Science and Technology state Key Laboratory for Diagnosis and Treatment of Infectious Disease The First Affiliated HospitalZhejiang University NGs sequencing Department Beijing Genomics Institute (BGI) Institute of Pathogen Microbiology School of MedicineShandong University

staphylococci are Gram-positive, AT-rich cocci, and often stick together in grape-like clusters. The genus can be classified into two groups based on their ability to produce coagulase, an enzyme that causes clotting of blood plasma （Otto, 2004）. Coagulase-positive staphylococci include staphylococcus aureus, a common pathogen of community-acquired and nosocomial infections （smith et al., 2009）.

关键词： In NJ

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Generation of a Hutchinson-Gilford progeria syndrome monkey model by base editing

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Protein & Cell 2020年第11期11卷 809-824页

作者： Fang Wang Weiqi Zhang Qiaoyan Yang Yu Kang Yanling Fan Jingkuan Wei Zunpeng Liu shaoxing Dai Hao Li Zifan Li Lizhu Xu Chu Chu Jing Qu Chenyang si Weizhi Ji Guang-Hui Liu Chengzu Long Yuyu Niu Yunnan Key Laboratory of Primate Biomedical Research Institute of Primate Translational MedicineKunming University of Science and TechnologyKunming 650500China Faculty of Life science and Technology Kunming University of Science and TechnologyKunming 650500China Institute for stem Cell and Regeneration Chinese Academy of ScienceBeijing 100101China CAs Key Laboratory of Genomic and Precision Medicine Beijing Institute of GenomicsChinese Academy of SciencesBeijing 100101China China National Center for Bioinformation Beijing 100101China University of Chinese Academy of sciences Beijing 100049China The Leon H Charney Division of Cardiology New York University School of MedicineNew YorkNY 10016USA state Key Laboratory of stem Cell and Reproductive Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China state Key Laboratory of Membrane Biology Institute of ZoologyChinese Academy of SciencesBeijing 100101China Advanced Innovation Center for Human Brain Protection and National Clinical Research Center for Geriatric DisordersXuanwu Hospital Capital Medical UniversityBeijing 100053China Department of Neuroscience and Physiology New York University School of MedicineNew YorkNY 10016USA Department of Neurology New York University School of MedicineNew YorkNY 10016USA

Many human genetic diseases,including Hutchinson-Gilford progeria syndrome(HGPs),are caused by single point *** is a rare disorder that causes premature aging and is usually caused by a de novo point mutation in the LMNA *** editors(BEs)composed of a cytidine deaminase fused to CRIsPR/Cas9 nickase are highly efficient at inducing C to T base conversions in a programmable manner and can be used to generate animal disease models with single amino-acid ***,we generated the first HGPs monkey model by delivering a BE mRNA and guide RNA(gRNA)targeting the LMNA gene via microinjection into monkey *** out of six newborn monkeys carried the mutation specifically at the target *** monkeys expressed the toxic form of lamin A,progerin,and recapitulated the typical HGPs phenotypes including growth retardation,bone alterations,and vascular ***,this monkey model genetically and clinically mimics HGPs in humans,demonstrating that the BE system can efficiently and accurately generate patient-specific disease models in non-human primates.

关键词： base editing non-human primate HGPs

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