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| 1 | 2018 Chinese Pediatric Cardiology Society(CPCS) guideline for diagnosis and treatment of syncope in children and adolescents显示文摘Syncope belongs to the transient loss of consciousness(TLOC), characterized by a rapid onset, short duration, and spontaneous complete recovery. It is common in children and adolescents, accounting for 1% to 2% of emergency department visits.Recurrent syncope can seriously affect children's physical and mental health, learning ability and quality of life and sometimes cardiac syncope even poses a risk of sudden death. The present guideline for the diagnosis and treatment of syncope in children and adolescents was developed for guiding a better clinical management of pediatric syncope. Based on the globally recent development and the evidence-based data in China, 2018 Chinese Pediatric Cardiology Society(CPCS) guideline for diagnosis and treatment of syncope in children and adolescents was jointly prepared by the Pediatric Cardiology Society, Chinese Pediatric Society, Chinese Medical Association(CMA)/Committee on Pediatric Syncope, Pediatricians Branch, Chinese Medical Doctor Association(CMDA)/Committee on Pediatric Cardiology, Chinese College of Cardiovascular Physicians, Chinese Medical Doctor Association(CMDA)/Pediatric Cardiology Society, Beijing Pediatric Society, Beijing Medical Association(BMA). The present guideline includes the underlying diseases of syncope in children and adolescents, the diagnostic procedures, methodology and clinical significance of standing test and headup tilt test, the clinical diagnosis vasovagal syncope, postural orthostatic tachycardia syndrome, orthostatic hypotension and orthostatic hypertension, and the treatment of syncope as well as follow-up. | Cheng Wang Yaqi Li Ying Liao Hong Tian Min Huang Xiangyu Dong Lin Shi Jinghui Sun Hongfang Jin Junbao Du Jindou An Jie Chen Mingwu Chen Qi Chen Sun Chen Yonghong Chen Zhi Chen Adolphus Kai-tung Chau Junbao Du Zhongdong Du Junkai Duan Hongyu Duan Xiangyu Dong Lin Feng Lijun Fu Fangqi Gong Yonghao Gui Ling Han Zhenhui Han Bing He Zhixu He Xiufen Hu Yimin Hua Guoying Huang Min Huang Ping Huang Yujuan Huang Hongfang Jin Mei Jin Bo Li Fen Li Tao Li Xiaohui Li Xiaoyan Liu Yan Li Haitao Lv Tiewei Lv Zipu Li Luyi Ma Silin Pan Yusheng Pang Hua Peng Yuming Qin Jie Shen Lin Shi Kun Sun Jinghui Sun Hong Tian Jie Tian Cheng Wang Hong Wang Lei Wang Jinju Wang Wendi Wang Yuli Wang Rongzhou Wu Tianhe Xia Yanyan Xiao Chunhong Xie Yanlin Xing Zhenyu Xiong Baoyuan Xu Yi Xu Hui Yan Shiwei Yang Qijian Yi Xia Yu Xianyi Yu Yue Yuan Hongyan Zhang Huili Zhang Li Zhang Qingyou Zhang Xi Zhang Yanmin Zhang Zhiwei Zhang Cuifen Zhao Bin Zhou Hua Zhu | 2018 | Science Bulletin2018，63，23： | 54 |
| 2 | Blockade of Tim-3 Pathway Ameliorates Interferon-γ Production from Hepatic CD8^+ T Cells in a Mouse Model of Hepatitis B Virus Infection显示文摘T cell immunoglobulin-and mucin-domain-containing molecule-3(Tim-3) has been reported to participate in the pathogenesis of inflammatory diseases. However,whether Tim-3 is involved in hepatitis B virus(HBV) infection remains unknown. Here,we studied the expression and function of Tim-3 in a hydrodynamics-based mouse model of HBV infection. A significant increase of Tim-3 expression on hepatic T lymphocytes,especially on CD8+ T cells,was demonstrated in HBV model mice from day 7 to day 18. After Tim-3 knockdown by specific shRNAs,significantly increased IFN-γ production from hepatic CD8+ T cells in HBV model mice was observed. Very interestingly,we found Tim-3 expression on CD8+ T cells was higher in HBV model mice with higher serum anti-HBs production. Moreover,Tim-3 knockdown influenced anti-HBs production in vivo. Collectively,our data suggested that Tim-3 might act as a potent regulator of antiviral T-cell responses in HBV infection. | Ying Ju Nan Hou Xiaoning Zhang Di Zhao Ying Liu Jinjin Wang Fang Luan Wei Shi Faliang Zhu Wensheng Sun Lining Zhang Chengjiang Gao Lifen Gao Xiaohong Liang Chunhong Ma | 2009 | Cellular & Molecular Immunology2009，6，1： | 19 |
| 3 | Increased expression of human T-cell immunoglobulin-and mucin-domain-containing molecule-4 in peripheral blood mononuclear cells from patients with system lupus erythematosus显示文摘全身的豺狼座 erythematosus (SLE ) 是 prototypic 自体免疫的疾病。天生、适应的免疫合作地贡献 SLE 的发展。介绍抗原的房间(APC ) 被建议了连接天生、适应的免疫。T 房间 immunoglobulin-domain-containing 和 mucin-domain-containing molecule-4 (Tim-4;另外作为 Timd4 知道) ,首先在 APC 的表面上表示了,是 TIM 家庭,的一个成员作为免疫系统的潜在的管理者收到了许多注意的分子的一个最近描述的组。在这研究,我们使用了量的即时反向的抄写聚合酶链反应从 SLE 病人在外部血 mononuclear 房间( PBMC )检验 Tim-4 的 mRNA 表示并且进一步在 PBMC 和浆液肿瘤坏死因素( TNF )分析了在 Tim-4 和 Tim-1 (为 Tim-4 的潜在的 ligand )的表示之间的关联-伪层次。结果证明在 PBMC 的那个 Tim-4 mRNA 表达式比在健康控制在 SLE 病人是显著地更高的,特别在疾病的活跃阶段的那些病人。而且, Tim-4 mRNA 层次密切在 SLE 病人然而并非在控制组在 PBMC 并且与浆液 TNF- 伪层次与 Tim-1 mRNA 层次被相关。一起拿,这些结果证明 Tim-4 可以涉及 SLE 的致病。 | Peiqing Zhao Liyun Xu Piming Wang Xiaohong Liang Jianni Qi Peng Liu Chun Guo Lining Zhang Chunhong Ma Lifen Gao | 2010 | Cellular & Molecular Immunology2010，7，2： | 11 |
| 4 | Increased Tim-3 expression alleviates liver injury by regulating macrophage activation in MCD-induced NASH mice显示文摘As an immune checkpoint,Tim-3 plays roles in the regulation of both adaptive and innate immune cells including macrophages and is greatly involved in chronic liver diseases.However,the precise roles of Tim-3 in nonalcoholic steatohepatitis(NASH)remain unstated.In the current study,we analyzed Tim-3 expression on different subpopulations of liver macrophages and further investigated the potential roles of Tim-3 on hepatic macrophages in methionine and choline-deficient diet(MCD)-induced NASH mice.The results of flow cytometry demonstrated the significantly increased expression of Tim-3 on all detected liver macrophage subsets in MCD mice,including F4/80^(+)CD11b^(+),F4/80^(+)CD68^(+),and F4/80^(+)CD169^(+)macrophages.Remarkably,Tim-3 knockout(KO)significantly accelerated MCD-induced liver steatosis,displaying higher serum ALT,larger hepatic vacuolation,more liver lipid deposition,and more severe liver fibrosis.Moreover,compared with wild-type C57BL/6 mice,Tim-3 KO MCD mice demonstrated an enhanced expression of NOX2,NLRP3,and caspase-1 p20 together with increased generation of IL-1βand IL-18 in livers.In vitro studies demonstrated that Tim-3 negatively regulated the production of reactive oxygen species(ROS)and related downstream pro-inflammatory cytokine secretion of IL-1βand IL-18 in macrophages.Exogenous administration of N-Acetyl-L-cysteine(NAC),a small molecular inhibitor of ROS,remarkably suppressed caspase-1 p20 expression and IL-1βand IL-18 production in livers of Tim-3 KO mice,thus significantly reducing the severity of steatohepatitis induced by MCD.In conclusion,Tim-3 is a promising protector in MCD-induced steatohepatitis by controlling ROS and the associated pro-inflammatory cytokine production in macrophages. | Xianhong Du Zhuanchang Wu Yong Xu Yuan Liu Wen Liu Tixiao Wang Chunyang Li Cuijuan Zhang Fan Yi Lifen Gao Xiaohong Liang Chunhong Ma | 2019 | Cellular & Molecular Immunology2019，16，11： | 9 |
| 5 | Irinotecan plus S-1 versus S-1 in patients with previously treated recurrent or metastatic esophageal cancer(ESWN 01):a prospective randomized,multicenter,open-labeled phase 3 trial显示文摘Background:The benefit of systemic treatments in esophageal squamous cell carcinoma(ESCC)which has pro-gressed after chemotherapy is still uncertain and optimal regimens based on randomized trials have not yet been established.We aimed to compare the efficacy of irinotecan plus S-1 with S-1 monotherapy in recurrent or metastatic ESCC patients who had resistance to platinum-or taxane-based chemotherapy.Methods:We conducted a prospective randomized,multicenter,open-label,phase 3 trial in 15 centers across China.Eligible patients were adults with histologically confirmed recurrent or metastatic ESCC,and were randomly assigned(ratio,1:1)to receive either irinotecan plus S-1(intravenous infusion of irinotecan[160 mg/m2]on day 1 and oral S-1[80-120 mg]on days 1-10,repeated every 14 days)or oral S-1 monotherapy(80-120 mg/day on days 1-14,repeated every 21 days)using a central computerized minimization procedure.The primary endpoint was progression-free survival(PFS).Results:Between December 23,2014 and July 25,2016,we screened 148 patients and randomly assigned 123 patients to receive either irinotecan plus S-1 regimen(n=61)or S-1 monotherapy(n=62).After a median follow-up of 29.2 months(95%confidence interval[CI]17.5-40.9 months),the median PFS was significantly longer in the irinotecan plus S-1 group than in the S-1 monotherapy group(3.8 months[95%CI 2.9-4.3 months]vs.1.7 months[95%CI 1.4-2.7 months],hazard ratio=0.58,95%CI 0.38-0.86,P=0.006).The objective response rates were 24.6%in the irinotecan plus S-1 group and 9.7%in the S-1 monotherapy group(P=0.002).The patients in the irinotecan plus S-1 group presented with increased rates of grade 3-4 leukopenia(16.4%vs.0%),neutropenia(14.8%vs.1.6%),and nausea(4.9%vs.0%).No significant difference in grade 3-4 diarrhea and no treatment-related deaths were observed in both groups.Conclusions: The combination of irinotecan with S-1 was similarly tolerable but significantly prolonged PFS compared to S-1 monotherapy as a second- or third-line treatment in patients with recurrent or metastatic ESCC. | Jing Huang Binghe Xu Ying Liu Junxing Huang Ping Lu Yi Ba Lin Wu Yuxian Bai Shu Zhang Jifeng Feng Ying Cheng Jie Li Lu Wen Xianglin Yuan Changwu Ma Chunhong Hu Qingxia Fan Xi Wang | 2019 | Cancer Communications2019，39，1： | 8 |
| 6 | Hepatitis B virus X protein modulates the apoptosis of hepatoma cell line induced by TRAIL显示文摘The purpose of this study is to observe the effects of HBx on the apoptosis of hepatoma cells induced by TNF-related apoptosis-inducing ligand (TRAIL) and to study prelimi- nary molecular mechanisms for its effects. In order to set up a model in vitro, BEL7402-HBx cell line, stably expressing HBx mRNA, was established by stable transfection of pcDNA-HBx, which contains HBx gene, into hepatoma cell line BEL7402. Control cell line BEL7402-cDNA3, stably transfected with pcDNA3, was set up simultaneously as a control. Trypan blue exclusion test, caspase 3 activity detection and TUNEL assay were performed to detect the apoptosis of BEL7402, BEL7402-cDNA3, BEL7402-HBx induced by TRAIL. The expression of TRAIL recep- tors in three groups was analyzed by Flow cytometry. In addition, phosphorothioated antisense oligonucleotide against the translation initial region of HBx gene (PS-asODNs/HBx) was used to block the expression of HBx in HepG2.2.15 cells and to further confirm the effects of HBx on TRAIL-induced apoptosis. Trypan blue exclusion test indicated that TRAIL had a dose-dependent cytotoxicity on BEL7402, BEL7402-cDNA3 and BEL7402-HBx cells. Under treatment of the same concentration of TRAIL, BEL7402-HBx had a higher apoptosis rate and a higher level of Caspase 3 activation than BEL7402 and BEL7402-cDNA3. TUENL assay showed that the apoptosis rate of BEL7402-HBx induced by 10 μg/L TRAIL was 41.4%±7.2%, signifi- cantly higher than that of BEL7402 and BEL7402-cDNA3 cells. Blockade of HBx expression in Hep G2.2.15 cells partly inhibited the apoptosis induced by TRAIL. The introduction or blockade of HBx did not change the expression pattern of TRAIL receptors. The present study firstly con- firms the effects of HBx on TRAIL- induced apoptosis from two different points and it is not re- lated with the expression level of TRAIL receptors. This would be useful to further clarify the roles of imbalanced apoptosis in pathogenesis of Hepatitis B and related hepatocellular carcinoma. | LIANG Xiaohong 1 , SUN Wensheng 1 , GAO Lifen 1 , MA Chunhong 1 , HAN Lihui 1 & CHEN Youhai 2 1. Institute of Immunology, Medical School of Shandong University, Jinan 250012, China 2. Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia PA19104, USA | 2005 | Science China(Life Sciences)2005，48，3： | 7 |
| 7 | Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small-cell lung cancer (OPTIMAL, CTONG-0802): a multicentre, open-label, randomised, phase 3 study显示文摘 | Caicun Zhou Yi-Long Wu Gongyan Chen Jifeng Feng Xiao-Qing Liu Changli Wang Shucai Zhang Jie Wang Songwen Zhou Shengxiang Ren Shun Lu Li Zhang Chengping Hu Chunhong Hu Yi Luo Lei Chen Ming Ye Jianan Huang Xiuyi Zhi Yiping Zhang Qingyu Xiu Jun Ma Li Zhang C | 2011 | Lancet Oncology2011，，8： | 7 |
| 8 | Anti-PD-L1/TGF-BR fusion protein (SHR-1701) overcomes disrupted lymphocyte recovery-induced resistance to PD-1/PD-L1 inhibitors in lung cancer显示文摘Background:Second-generation programmed cell death-protein 1/pro-grammed death-ligand 1(PD-1/PD-L1)inhibitors,such as bintrafusp alfa(M7824),SHR-1701,and YM101,have been developed to simultaneously block PD-1/PD-L1 and transforming growth factor-beta/transforming growth factor-beta receptor(TGF-P/TGF-βR).Consequently,it is necessary to identify predictive factors of lung cancer patients who are not only resistant to PD-1/PD-LI inhibitors but also sensitive to bifunctional drugs.The purpose of this study was to search for such predictors.Methods:Multivariable Cox regression was used to study the association between the clinical outcome of treatment with PD-1/PD-L1 inhibitors and lym-phocyte recovery after lymphopenia in lung cancer patients.Murine CMT167 lung cancer cells were engineered to express the firefly luciferase gene and implanted orthotopically in the lung of syngeneic mice.Bioluminescence imag-ing,flow cytometry,and immunohistochemistry were employed to detrmine response to immunotherapy and function of tumor-infiltrating immune cells.Results:For lung cancer patients treated with anti-PD-1/PD-LI antibodies,poor lymphocyte recovery was associated with a shorter progression-free survival(PFS;P<0.001),an accumulation of regulatory T cells(Tregs),and an elimi-nation of CD8+T cells in the peripheral blood.Levels of CD8+T cells and Treg cells were also imbalanced in the tumors and peripheral immune organs of mice with poor lymphocyte recovery after chemotherapy.Moreover,these mice failed to respond to anti-PD-1 antibodies but remained sensitive to the anti-PD-LI/TGF-βR fusion protein(SHR-1701).Consistently,SHR-1701 but not anti-PD-1 antibod-ies,markedly enhanced IFN-γproduction and Ki-67 expression in peripheral CD8+T cells from patients with impaired lymphocyte recovery.Conclusions:Lung cancer patients with poor lymphocyte recovery and suffer-ing from persistent lymphopenia after previous chemotherapy are resistant to anti-PD-1/PD-L1 antibodies but might be sensitive to second-generation agents such as SHR-1701. | Bo Cheng Kaikai Ding Pengxiang Chen Jianxiong Ji Tao Luo Xiaofan Guo Wei Qiu Chunhong Ma Xue Meng Jian Wang Jinming Yu Yuan Liu | 2022 | Cancer Communications2022，42，1： | 5 |
| 9 | Automatic Change Detection from SAR Images Based on Fuzzy Entropy Principle显示文摘 | PAN Chunhong PRINET Veronique YANG Qing MA Songde | 2007 | Chinese Journal of Electronics2007，16，1： | 4 |
| 10 | Hepatitis B virus evades immune recognition via RNA adenosine deaminase ADAR1-mediated viral RNA editing in hepatocytes显示文摘HBV is considered as a“stealth”virus that does not invoke interferon(IFN)responses;however,the mechanisms by which HBV bypasses innate immune recognition are poorly understood.In this study,we identified adenosine deaminases acting on RNA 1(ADAR1),which is a key factor in HBV evasion from IFN responses in hepatocytes.Mechanically,ADAR1 interacted with HBV RNAs and deaminated adenosine(A)to generate inosine(I),which disrupted host immune recognition and thus promoted HBV replication.Loss of ADAR1 or its deficient deaminase activity promoted IFN responses and inhibited HBV replication in hepatocytes,and blocking the IFN signaling pathways released the inhibition of HBV replication caused by ADAR1 deficiency.Notably,the HBV X protein(HBx)transcriptionally promoted ADAR1 expression to increase the threshold required to trigger intrinsic immune activation,which in turn enhanced HBV escape from immune recognition,leading to persistent infection.Supplementation with 8-azaadenosine,an ADAR1 inhibitor,efficiently enhanced liver immune activation to promote HBV clearance in vivo and in vitro.Taken together,our results delineate a molecular mechanism by which HBx promotes ADAR1-derived HBV immune escape and suggest a targeted therapeutic intervention for HBV infection. | Liyuan Wang Yang Sun Xiaojia Song Zehua Wang Yankun Zhang Ying Zhao Xueqi Peng Xiaodong Zhang Chunyang Li Chengjiang Gao Nailin Li Lifen Gao Xiaohong Liang Zhuanchang Wu Chunhong Ma | 2021 | Cellular & Molecular Immunology2021，18，8： | 2 |
| 11 | OTUD5 promotes innate antiviral and antitumor immunity through deubiquitinating and stabilizing STING显示文摘Stimulator of interferon genes(STING)is an adaptor protein that is critical for effective innate antiviral and antitumor immunity.The activity of STING is heavily regulated by protein ubiquitination,which is fine-tuned by both E3 ubiquitin ligases and deubiquitinases.Here,we report that the deubiquitinase OTUD5 interacts with STING,cleaves its K48-linked polyubiquitin chains,and promotes its stability.Consistently,knockout of OTUD5 resulted in faster turnover of STING and subsequently impaired type I IFN signaling following cytosolic DNA stimulation.More importantly,Lyz2-Cre Otud5^(fl/Y) mice and CD11-Cre Otud5^(fl/Y) mice showed more susceptibility to herpes simplex virus type 1(HSV-1)infection and faster development of melanomas than their corresponding control littermates,indicating that OTUD5 is indispensable for STING-mediated antiviral and antitumor immunity.Our data suggest that OTUD5 is a novel checkpoint in the cGAS-STING cytosolic DNA sensing pathway. | Yunyun Guo Fei Jiang Lingli Kong Haifeng Wu Honghai Zhang Xiaorong Chen Jian Zhao Baoshan Cai Yanqi Li Chunhong Ma Fan Yi Lei Zhang Bingyu Liu Yi Zheng Lingqiang Zhang Chengjiang Gao | 2021 | Cellular & Molecular Immunology2021，18，8： | 2 |
| 12 | Direct conversion of mouse astrocytes into neural progenitor cells and specific lineages of neurons显示文摘Background:Cell replacement therapy has been envisioned as a promising treatment for neurodegenerative diseases.Due to the ethical concerns of ESCs-derived neural progenitor cells(NPCs)and tumorigenic potential of iPSCs,reprogramming of somatic cells directly into multipotent NPCs has emerged as a preferred approach for cell transplantation.Methods:Mouse astrocytes were reprogrammed into NPCs by the overexpression of transcription factors(TFs)Foxg1,Sox2,and Brn2.The generation of subtypes of neurons was directed by the force expression of cell-type specific TFs Lhx8 or Foxa2/Lmx1a.Results:Astrocyte-derived induced NPCs(AiNPCs)share high similarities,including the expression of NPC-specific genes,DNA methylation patterns,the ability to proliferate and differentiate,with the wild type NPCs.The AiNPCs are committed to the forebrain identity and predominantly differentiated into glutamatergic and GABAergic neuronal subtypes.Interestingly,additional overexpression of TFs Lhx8 and Foxa2/Lmx1a in AiNPCs promoted cholinergic and dopaminergic neuronal differentiation,respectively.Conclusions:Our studies suggest that astrocytes can be converted into AiNPCs and lineage-committed AiNPCs can acquire differentiation potential of other lineages through forced expression of specific TFs.Understanding the impact of the TF sets on the reprogramming and differentiation into specific lineages of neurons will provide valuable strategies for astrocyte-based cell therapy in neurodegenerative diseases. | Kangmu Ma Xiaobei Deng Xiaohuan Xia Zhaohuan Fan Xinrui Qi Yongxiang Wang Yuju Li Yizhao Ma Qiang Chen Hui Peng Jianqing Ding Chunhong Li Yunlong Huang Changhai Tian Jialin C.Zheng | 2018 | Translational Neurodegeneration2018，7，1： | 2 |
| 13 | CUL4B facilitates HBV replication by promoting HBx stabilization显示文摘Objective:Hepatitis B virus(HBV)infection is a major public health problem worldwide.However,the regulatory mechanisms underlying HBV replication remain unclear.Cullin 4 B-RING ubiquitin E3 ligase(CRL4 B)is involved in regulating diverse physiological and pathophysiological processes.In our study,we aimed to explain the role of CUL4 B in HBV infection.Methods:Cul4 b transgenic mice or conditional knockout mice,as well as liver cell lines with CUL4 B overexpression or knockdown,were used to assess the role of CUL4 B in HBV replication.Immunoprecipitation assays and immunofluorescence staining were performed to study the interaction between CUL4 B and HBx.Cycloheximide chase assays and in vivo ubiquitination assays were performed to evaluate the half-life and the ubiquitination status of HBx.Results:The hydrodynamics-based hepatitis B model in Cul4 b transgenic or conditional knockout mice indicated that CUL4 B promoted HBV replication(P<0.05).Moreover,the overexpression or knockdown system in human liver cell lines validated that CUL4 B increased HBV replication in an HBx-dependent manner.Importantly,immunoprecipitation assays and immunofluorescence staining showed an interaction between CUL4 B and HBx.Furthermore,CUL4 B upregulated HBx protein levels by inhibiting HBx ubiquitination and proteasomal degradation(P<0.05).Finally,a positive correlation between CUL4 B expression and HBV pg RNA level was observed in liver tissues from HBV-positive patients and HBV transgenic mice.Conclusions:CUL4 B enhances HBV replication by interacting with HBx and disrupting its ubiquitin-dependent proteasomal degradation.CUL4 B may therefore be a potential target for anti-HBV therapy. | Haixia Shan Bo Wang Xiaodong Zhang Hui Song Xi Li Yongxin Zou Baichun Jiang Huili Hu Hao Dou Changshun Shao Lifen Gao Chunhong Ma Xiaoyun Yang Xiaohong Liang Yaoqin Gong | 2022 | Cancer Biology & Medicine2022，19，1： | 2 |
| 14 | CUL4B negatively regulates Toll-like receptor-triggered proinflammatory responses by repressing Pten transcription显示文摘Toll-like receptors (TLRs) play critical roles in innate immunity and inflammation. The molecular mechanisms by which TLR signaling is fine-tuned remain to be completely elucidated. Cullin 4B (CUL4B), which assembles the CUL4B-RING E3 ligase complex (CRL4B), has been shown to regulate diverse developmental and physiological processes by catalyzing monoubiquitination for histone modification or polyubiquitination for proteasomal degradation. Here, we identified the role of CUL4B as an intrinsic negative regulator of the TLR-triggered inflammatory response. Deletion of CUL4B in macrophages increased the production of proinflammatory cytokines and decreased anti-inflammatory cytokine IL-10 production in response to pathogens that activate TLR3, TLR4, or TLR2. Myeloid cell-specific Cul4b knockout mice were more susceptible to septic shock when challenged with lipopolysaccharide, polyinosinic-polycytidylic acid or Salmonella typhimurium infection. We further demonstrated that enhanced TLR-induced inflammatory responses in the absence of CUL4B were mediated by increased GSK3β activity. Suppression of GSK3β activity efficiently blocked the TLR-triggered increase in proinflammatory cytokine production and attenuated TLR-triggered death in Cul4b mutant mice. Mechanistically, CUL4B was found to negatively regulate TLR-triggered signaling by epigenetically repressing the transcription of Pten, thus maintaining the anti-inflammatory PI3K-AKT-GSK3β pathway. The upregulation of PTEN caused by CUL4B deletion led to uncontrolled GSK3β activity and excessive inflammatory immune responses. Thus, our findings indicate that CUL4B functions to restrict TLR-triggered inflammatory responses through regulating the AKT-GSK3β pathway. | Yu Song Peishan Li Liping Qin Zhiliang Xu Baichun Jiang Chunhong Ma Changshun Shao Yaoqin Gong | 2021 | Cellular & Molecular Immunology2021，18，2： | 2 |
| 15 | Biocompatible Nanocomplexes for Molecular Targeted MRI Contrast Agent显示文摘 | Zhijin Chen Dexin Yu Shaojie Wang Na Zhang Chunhong Ma Zaijun Lu | 2009 | Nanoscale Research Letters2009，，7： | 1 |
| 16 | Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small-cell lung cancer (OPTIMAL, CTONG-0802): a multicentre, open-label, randomised, phase 3 study显示文摘 | Caicun Zhou Yi-Long Wu Gongyan Chen Jifeng Feng Xiao-Qing Liu Changli Wang Shucai Zhang Jie Wang Songwen Zhou Shengxiang Ren Shun Lu Li Zhang Chengping Hu Chunhong Hu Yi Luo Lei Chen Ming Ye Jianan Huang Xiuyi Zhi Yiping Zhang Qingyu Xiu Jun Ma Li Zhang C | 2011 | Lancet Oncology2011，，8： | 1 |
| 17 | Erlotinib versus chemotherapy as first-line treatment for patients with advanced EGFR mutation-positive non-small-cell lung cancer (OPTIMAL, CTONG-0802): a multicentre, open-label, randomised, phase 3 study显示文摘 | Caicun Zhou Yi-Long Wu Gongyan Chen Jifeng Feng Xiao-Qing Liu Changli Wang Shucai Zhang Jie Wang Songwen Zhou Shengxiang Ren Shun Lu Li Zhang Chengping Hu Chunhong Hu Yi Luo Lei Chen Ming Ye Jianan Huang Xiuyi Zhi Yiping Zhang Qingyu Xiu Jun Ma Li Zhang C | 2011 | Lancet Oncology2011，，8： | 1 |
| 18 | USP3 deubiquitinates and stabilizes the adapter protein ASC to regulate inflammasome activation显示文摘Inflammasomes are essential components of the innate immune system and its defense against infections,whereas the dysregulation of inflammasome activation has a detrimental effect on human health.The activation of inflammasomes is subjected to tight regulation to maintain immune homeostasis,yet the underlying mechanism remains elusive.Here,we identify USP3 as a direct deubiquitinating enzyme(DUB)for ASC,the central adapter mediating the assembly and activation of most inflammasomes.USP3 removes the K48-linked ubiquitination on ASC and strengthens its stability by blocking proteasomal degradation.Additionally,USP3 promotes inflammasome activation,and this function was confirmed in mouse models of aluminum(Alum)-induced peritonitis,F.novicida infection and flagellin-induced pneumonia in vivo.Our work unveils that USP3 functions as a key regulator of ASC ubiquitination and maintains the physiological role of ASC in mediating inflammasome activation,and we propose a new mechanism by which the ubiquitination of ASC regulates inflammasome activation. | Wanxin Zhuang Lei Zhang Yi Zheng Bingyu Liu Chunhong Ma Wei Zhao Suxia Liu Feng Liu Chengjiang Gao | 2022 | Cellular & Molecular Immunology2022，19，10： | 1 |
| 19 | Zhx2 and Zbtb20: Novel regulators of postnatal alpha-fetoprotein repression and their potential role in gene reactivation during liver cancer显示文摘 | Martha L. Peterson Chunhong Ma Brett T. Spear | 2011 | Seminars in Cancer Biology2011，，1： | 1 |
| 20 | SAR image de-speckling based on modified frost filter显示文摘 | Zhang Zhaohui Pan Chunhong Ma Songde | 2005 | Journal of Image and Graphics2005，10，4： | 1 |
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