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Interpolation on Weak Martingale Hardy Space

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Acta Mathematica Sinica,English Series 2009年第8期25卷 1297-1304页

作者： Yong JIAO Wei CHEN pei de liu School of Mathematical Science and Computing Technology Central South University Changsha 410081 P. R. China School of Mathematics and Statistics Wuhan University Wuhan 430072 P. R. China

By the weak atomic decompositions of weak martingale Hardy spaces, we investigate the interpolation spaces between weak martingale Hardy spaces and martingale Hardy spaces.

关键词： interpolation martingale weak atomic decomposition

Interpolation theorems on weighted Lorentz martingale spaces

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Science China Mathematics 2007年第9期50卷 1217-1226页

作者： Yong JIAO Li-ping FAN pei-de liu School of Mathematics and Statistics Wuhan University Wuhan 430072China

In this paper several interpolation theorems on martingale Lorentz spaces are *** proofs are based on the atomic decompositions of martingale Hardy spaces over weighted measure *** the interpolation theorems,we obtain... 详细信息

关键词： Lorentz martingale space interpolation theorem atomic decomposition weighted inequality 60G42 60G46

Capturing the opportunities to initiate an in-depth integration of traditional Chinese medicine and western medicine

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Frontiers of Medicine 2014年第3期8卷 268-271页

作者： Jia-Hua Qu Bing liu Zhu-Qin Zhang de-pei liu State Key Laboratory of Medical Molecular Biology Department of Biochemistry and Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences and Peking Union Medical College Beijing 100005 China

Medicine is mainly categorized into traditional Chinese medicine （TCM） from the east and western medicine from the west. The abundant practical experiences and classical medical theories in ancient China show that TCM not only studies the diagnosis, therapy, and prognosis of diseases but also focuses on prevention before disease onset and rehabilitation after therapy. These factors are characterized by the application of treatment methods, including prescription, acupuncture, and moxibustion. By comparison, western medicine utilizes modern instruments and standardized index analytical tools to evaluate diseases and perform quantitative and qualitative research in biological mor- phology and local positioning of life and disease. Therefore, TCM and western medicine are two different medical systems with respective advantages.

关键词： Capturing opportunities initiate in-depth integration

Mouse macrophage specific knockout of SIRT1 influences macrophage polarization and promotes angiotensin Ⅱ-induced abdominal aortic aneurysm formation

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Journal of Genetics and Genomics 2018年第1期45卷 25-32页

作者： Zhuqin Zhang Jing Xu Yue liu Tingting Wang Jianfei pei Liqin Cheng delong Hao Xiang Zhao Hou-Zao Chen de-pei liu State Key Laboratory of Medical Molecular Biology Department of Biochemistry and Molecular Biology Institute of Basic Medical Sciences Chinese Academy of Medical Sciences Peking Union Medical College No.5 Dong Dan San Tiao Beijing 100005 China

Abdominal aortic aneurysm （AAA） is a vascular degenerative disease. Macrophage polarization and the balance between classically activated macrophages （M1） and alternatively activated macrophages （M2） are crucial for AAA pathogenesis. The present study aims to investigate the roles of macrophage SIRTI in AAA formation and macrophage polarization. We found that in mouse peritoneal macrophages, SIRT1 expression was decreased after M1 stimulation, but was enhanced after M2 stimulation. Results from SIRT1flox/flox mice and macrophage specific SIRT1 knockout mice with treatment of angiotensin II （Ang 11） for 4 weeks showed that macropbage specific deficiency of SIRT1 increased the incidence of AAA and exacerbated the severity, including more severe aneurysm types, enlarged diameter of the aneurysm and increased degradation of elastin. In mouse aortas, SIRT1 deficiency increased the pro- inflammatory M1 molecule inducible nitric oxide synthase （iNOS）, and decreased M2 molecules such as arginase 1 （Argl） and mannose receptor （MR）. Furthermore, in peritoneal macrophages, SIRT1 deficiency increased the expression of M1 inflammatory molecules, but decreased the expression of M2 molecules. Overexpression of SIRT1 had the opposite effects. Thus, macrophage specific knockout of SIRT1 influences macrophage polarization and accelerates Ang II-induced AAA formation.

关键词： SIRT1 Inflammation Macrophage polarization Abdominal aortic aneurysm

Human paraoxonase gene cluster overexpression alleviates angiotensin II-induced cardiac hypertrophy in mice

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Science China(Life Sciences) 2016年第11期59卷 1115-1122页

作者： Jian-Fei pei Yun-Fei Yan Xiaoqiang Tang Yang Zhang Shen-Shen Cui Zhu-Qin Zhang Hou-Zao Chen de-pei liu State Key Laboratory of Medical Molecular Biology Department of Biochemistry and Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences & Peking Union Medical College

Cardiac hypertrophy is the strongest predictor of the development of heart failure, and anti-hypertrophic treatment holds the key to improving the clinical syndrome and increasing the survival rates for heart failure. The paraoxonase(PON) gene cluster(PC) protects against atherosclerosis and coronary artery diseases. However, the role of PC in the heart is largely unknown. To evaluate the roles of PC in cardiac hypertrophy, transgenic mice carrying the intact human PON1, PON2, and PON3 genes and their flanking sequences were studied. We demonstrated that the PC transgene(PC-Tg) protected mice from cardiac hypertrophy induced by Ang II; these mice had reduced heart weight/body weight ratios, decreased left ventricular wall thicknesses and increased fractional shortening compared with wild-type(WT) control. The same protective tendency was also observed with an Apoe^(-/-)background. Mechanically, PC-Tg normalized the disequilibrium of matrix metalloproteinases(MMPs)/tissue inhibitors of MMPs(TIMPs) in hypertrophic hearts, which might contribute to the protective role of PC-Tg in cardiac fibrosis and, thus, protect against cardiac remodeling. Taken together, our results identify a novel anti-hypertrophic role for the PON gene cluster, suggesting a possible strategy for the treatment of cardiac hypertrophy through elevating the levels of the PON gene family.

关键词： cardiac hypertrophy fibrosis paraoxonase gene cluster angiotensin II

Lysine-specific demethylase 1 Represses THP-1 Monocyte-to-macrophage Differentiation

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Chinese Medical Sciences Journal 2013年第2期28卷 82-87页

作者： Rui-feng Yang Guo-wei Zhao Shu-ting Liang Hou-zao Chen de-pei liu National Laboratory of Medical Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences & Peking Union Medical College

Objective To investigate the role of lysine-specific demethylase 1 （LSD1） in the process of THP-1 monocyte-to-macrophage differentiation. Methods Quantitative reverse transcription-polymerase chain reaction （qRT-PCR） and Western blotting were performed to analyze the expression of LSD1 and interleukin-6 （IL-6） in THP-1 monocytes and THP-l-derived macrophages. Chromatin immunoprecipitation （ChiP） assay was applied to detect the occupancy of LSD1 and H3K4 methylation at IL-6 promoter during THP-1 monocyte-to-macrophage differentiation. IL-6 mRNA level and H3K4 methylation at IL-6 promoter were analyzed using qRT-PCR and ChiP assay in LSD 1 -knockdown THP- 1 cells treated with 12-O-tetradecanoylphorbol- 13-acetate （TPA） for 0 4, 8, 12, and 24 hours. Fluorescence activated flow cytometry was performed to reveal the percentage of macrophages differentiated from THP- 1 monocytes. Results The expression of LSD1 reduced during THP-1 monocyte-to-macrophage differentiation （P〈0.01）. LSD1 occupancy decreased and H3K4 methylation increased at IL-6 promoter during the differentiation. With knockdown of LSD1, H3K4 methylation at IL-6 promoter was found increased after TPA treatment at different times points （all P〈0.05, except 24 hours）. The percentage of macrophages increased significantly in theTHP-I cells with LSD1 knockdown （P〈0.05）. Conclusions LSD1 is repressed during the monocyte-to-macrophage differentiation of THP-1 cells. Suppression of LSD 1-mediated H3K4 demethylation may be required for THP-1 monocyte-to-macrophage differentiation.

关键词： lysine-specific demethylase 1 interleukin-6 H3K4 methylation monocyte-to-macrophage differentiation

Proteomic and phosphoproteomic profiling of COVID-19-associated lung and liver injury:a report based on rhesus macaques

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Signal Transduction and Targeted Therapy 2022年第2期7卷 375-378页

作者： Jiang-Feng liu Ya-Nan Zhou Shuai-Yao Lu Ye-Hong Yang Song-Feng Wu de-pei liu Xiao-Zhong Peng Jun-Tao Yang State Key Laboratory of Medical Molecular Biology Department of Biochemistry and Molecular BiologyInstitute of Basic Medical Sciences Chinese Academy of Medical SciencesSchool of Basic Medicine Peking Union Medical CollegeBeijing 100005China National Kunming High-level Biosafety Primate Research Center Institute of Medical BiologyChinese Academy of Medical Sciences and Peking Union Medical CollegeYunnanChina State Key Laboratory of Medical Molecular Biology Department of Biochemistry and Molecular BiologyMedical Primate Research CenterNeuroscience CenterInstitute of Basic Medical Sciences Chinese Academy of Medical SciencesSchool of Basic Medicine Peking Union Medical CollegeBeijingChina State Key Laboratory of Proteomics Beijing Proteome Research CenterNational Center for Protein Sciences(Beijing)Research Unit of Proteomics&Research and Development of New Drug of Chinese Academy of Medical SciencesInstitute of LifeomicsBeijing 102206China

dear Editor,The ongoing COVID-19 pandemic,caused by severe acute respiratory syndrome conronavirus 2(SARS-CoV-2),has led to over 209,201,939 confirmed cases and 4,390,467 deaths all over the world as of 19 August 2021(https://***/).Novel therapeutic agents and vaccines are desperately needed and mechanism exploration is *** clinical tissues are preferred samples for molecular and mechanism study,COVID-19 clinical tissues are rare and mostly come from autopsies of end-stage patients.1,2 Animal models,especially nonhuman primate models,are therefore constructed for SARS-CoV-2-associated research.

关键词： clinical acute respiratory

Up-regulation of Fas Ligand Expression by Sirtuin 1 in both Flow-restricted Vessels and Serum-stimulated Vascular Smooth Muscle Cells

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Chinese Medical Sciences Journal 2013年第2期28卷 65-71页

作者： Li Li Peng Gao Hou-zao Chen Zhu-qin Zhang Ting-ting Xu Yu-yan Jia Hui-na Zhang Guan-hua Du de-pei liu Beijing Key Laboratory of Drug Target and Screening Research Institute of Materia MedicaChinese Academy of Medical Sciences & Peking Union Medical College National Laboratory of Medical Molecular Biology Institute of Basic Medical SciencesChinese Academy of Medical Sciences & Peking Union Medical College

Objective To study the role of sirtuin 1 （SIRT1） in Fas ligand （FasL） expression regulation during vascular lesion formation and to elucidate the potential mechanisms. Methods SIRT1 and FasL protein levels were detected by Western blotting in either mouse arteries extract or the whole rat aortic vascular smooth muscle cell （VSMC） lysate. Smooth muscle cell （SMC）-specific human SIRT1 transgenic （Tg） C57BL/6 mice and their littermate wild-type （WT） controls underwent complete carotid artery ligation （ligation groups） or the ligation-excluded operation （sham groups）. The carotid arteries were collected 1 day after operation. Reverse transcription-polymerase chain reaction was performed to detect the mRNA levels of SIRT1 and FasL. Luciferase reporter assays were performed to detect the effect of WT-SIRT1, a dominant-negative form of SIRT1 （SIRT1H363Y）, and GATA-6 on the promoter activity of FasL. Flow cytometry assay was applied to measure the hypodiploid DNA content of VSMC so as to monitor cellular apoptosis. Results SIRTI was expressed in both rat aortic VSMCs and mouse arteries. Forced SIRT1 expression increased FasL expression both in injured mouse carotid arteries 1 day after ligation （P〈0.001） and VSMCs treated with serum （P〈0.05 at the transcriptional level, P〈0.001 at the protein level）. No notable apoptosis was observed. Furthermore, transcription factor GATA-6 increased the promoter activity of FasL （P〈0.001）. The induction of FasL promoter activity by GATA-6 was enhanced by WT-SIRT1 （P〈0.001）, while SIRT1H363Y significantly relieved the enhancing effect of WT-SIRT1 on GATA-6 （P〈0.001）. Conclusions Overexpression of SIRT1 up-regulates FasL expression in both flow-restricted mouse carotid arteries and serum-stimulated VSMCs. The transcription factor GATA-6 participates in the transcriptional regulation of FasL expression by SIRT 1.

关键词： sirtuinl Fas ligand GATA-6 vascular smooth muscle cell

SIRT1 promotes myeloid leukemogenesis through derepression of HOXA cluster genes

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SIRT1 promotes myeloid leukemogenesis through derepression o...