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| 1 | Anti-inflammatory mechanisms of the novel cytokine interleukin-38 in allergic asthma显示文摘We elucidated the anti-inflammatory mechanisms of IL-38 in allergic asthma.Human bronchial epithelial cells and eosinophils were cocultured upon stimulation with the viral RLR ligand poly(I:C)/LyoVec or infection-related cytokine TNF-αto induce expression of cytokines/chemokines/adhesion molecules.House dust mite(HDM)-induced allergic asthma and humanized allergic asthma NOD/SCID murine models were established to assess anti-inflammatory mechanisms in vivo.IL-38 significantly inhibited induced proinflammatory IL-6,IL-1β,CCL5,and CXCL10 production,and antiviral interferon-βand intercellular adhesion molecule-1 expression in the coculture system.Mass cytometry and RNA-sequencing analysis revealed that IL-38 could antagonize the activation of the intracellular STAT1,STAT3,p38 MAPK,ERK1/2,and NF-κB pathways,and upregulate the expression of the host defense-related gene POU2AF1 and anti-allergic response gene RGS13.Intraperitoneal injection of IL-38 into HDM-induced allergic asthma mice could ameliorate airway hyperreactivity by decreasing the accumulation of eosinophils in the lungs and inhibiting the expression of the Th2-related cytokines IL-4,IL-5,and IL-13 in the bronchoalveolar lavage fluid(BALF)and lung homogenates.Histological examination indicated lung inflammation was alleviated by reductions in cell infiltration and goblet cell hyperplasia,together with reduced Th2,Th17,and innate lymphoid type 2 cell numbers but increased proportions of regulatory T cells in the lungs,spleen,and lymph nodes.IL-38 administration suppressed airway hyperreactivity and asthma-related IL-4 and IL-5 expression in humanized mice,together with significantly decreased CCR3^(+) eosinophil numbers in the BALF and lungs,and a reduced percentage of human CD4^(+)CRTH2^(+)Th2 cells in the lungs and mediastinal lymph nodes.Together,our results demonstrated the anti-inflammatory mechanisms of IL-38 and provided a basis for the development of a regulatory cytokine-based treatment for allergic asthma. | Xiaoyu Sun Tianheng Hou Edwin Cheung Tiffany Nga-Teng Iu Victor Wai-Hou Tam Ida Miu-Ting Chu Miranda Sin-Man Tsang Paul Kay-Sheung Chan Christopher Wai-Kei Lam Chun-Kwok Wong | 2020 | Cellular & Molecular Immunology2020，17，6： | 22 |
| 2 | NOD2 和 TLR2 ligands 由在遗传性过敏症的像皮炎的皮肤发炎与真皮的成纤维细胞交往触发 basophils 和嗜曙红血球的激活显示文摘有遗传性过敏症的皮炎(广告) 的病人的皮肤由葡萄球菌 aureus 为殖民有唯一的倾向(S。aureus ) ,它贡献发炎和广告的冷酷的预后。尽管位于 S 下面的机制。不清楚的、最近的研究在在 S 调整煽动性的回答为模式识别受体发现了一个枢轴的角色的广告遗体的导致 aureus 的恶化。aureus 感染。在现在的学习,我们使用了像广告的皮肤发炎的一个典型老鼠模型并且发现了那 S。联系 aureus 的核苷酸绑定 oligomerization 包含域的蛋白质 2 (NOD2 ) 并且像使用费的受体 2 (TLR2 ) ligands 加重了像广告的症状,它进一步被败坏由在里面 basophils 和嗜曙红血球的 vivo 扩大。随后的组织学的分析表明真皮的成纤维细胞在像广告的皮肤损害是弥漫的。有 basophils 和嗜曙红血球的人的真皮的成纤维细胞的合作文化在真皮的成纤维细胞上导致了对 NOD2/TLR2 ligands 和细胞间的粘附 molecule-1 的提高的表示的精力旺盛的 cytokine/chemokine 回答。Basophils 和嗜曙红血球为在合作文化的广告相关的 cytokine/chemokine 表示主要负责。直接细胞间的接触为在 basophils 和真皮的成纤维细胞之间的串音是必要的,当可溶的调停人是足够的调停时嗜曙红血球成纤维细胞相互作用。而且,细胞内部的 p38 激活 mitogen 的蛋白质 kinase,细胞外的调整信号的 kinase,和表明小径的原子 factor-kappa B 为在广告相关的发炎的 basophils,嗜曙红血球,和真皮的成纤维细胞的 NOD2/TLR2 调停 ligand 的激活是必要的。这研究通过天生的有免疫力的房间的激活提供广告的 NOD2/TLR2-mediated 恶化的证据因此使一条新奇机械学的小径由清楚些哪个 S。aureus 贡献广告的 pathophysiology。 | Delong Jiao Chun-Kwok Wong Huai-Na Qiu Jie Dong Zhe Cai Man Chu Kam-Lun Hon Miranda Sin-Man Tsang Christopher Wai-Kei Lam | 2016 | Cellular & Molecular Immunology2016，13，4： | 8 |
| 3 | Over-expression of fibroblast growth factor receptor 3 in human hepatocellular carcinoma显示文摘AIM: To describe the significant over-expression of fibroblast growth factor receptor 3 (FGFR3), which is a signal transduction and cell proliferation related gene in hepatocellular carcinoma (HCC).METHODS: Following DNA microarray, Northern blot and quantitative real-time PCR were employed to confirm FGFR3 expression difference in HCC tissues and surrounding non-neoplastic liver tissue. FGFR3 expression levels were further determined by immunohistochemical study in 43 cases of HCC.RESULTS: Northern blot results showed the significant over-expression of FGFR3 in HCC tissues, which was consistent with that from DNA microarray. Quantitative real-time PCR demonstrated that the mean ratio of FGFR3 mRNA to glyceraldehyde-3-phosphate dehydrogenase (GADPH) mRNA in HCC tissue was 0.250, whereas the ratio in non-neoplastic liver tissue was 0.014. Statistical analyses of 43 cases of HCC revealed that HCC scored higher than the matched non-neoplastic liver tissues.Examination of clinicopathological features revealed a strong correlation of over-expression of FGFR3 with poor tumor differentiation and high nuclear grade.CONCLUSION: Over-expression of FGFR3 may play an important role in liver carcinogenesis. FGFR3 may be an ideal candidate as a molecular marker in the diagnosis of HCC and a potential therapeutic target. | Wei-Hua Qiu Bing-Sen Zhou Peiguo G. Chu Wen-Gang Chen Christopher Chung Jennifer Shih Paul Hwu Christopher Yeh Richard Lopez Yun Yen | 2005 | World Journal of Gastroenterology2005，11，34： | 8 |
| 4 | Meteorin-β/Meteorin like/IL-41 attenuates airway inflammation in house dust mite-induced allergic asthma显示文摘We sought to examine the regulatory effect of Meteorin-β(Metrnβ)/Meteorin like(Metrnl)/IL-41 on lung inflammation in allergic asthma.We found that Metrnβwas elevated significantly in asthmatic patients and in mice with allergic asthma induced by house dust mite(HDM)extract.Upon exposure to HDM,Metrnβwas secreted predominantly by airway epithelial cells and inflammatory cells,including macrophages and eosinophils.The increased Metrnβeffectively blocked the development of airway hyperreactivity(AHR)and decreased inflammatory cell airway infiltration and type 2 cytokine production,which was associated with downregulated DC-mediated adaptive immune responses.Moreover,Metrnβimpaired the maturation and function of bone marrow-derived dendritic cells in vitro.Asthmatic mice adoptively transferred with dendritic cells isolated from Metrnβ-treated allergic mice displayed decreased AHR,airway inflammation,and lung injury.Metrnβalso displayed anti-inflammatory properties in immunodeficient SCID mice with allergic asthma and in in vitro 3D ALI airway models.Moreover,blockade of Metrnβby anti-Metrnβantibody treatment promoted the development of allergic asthma.These results revealed the unappreciated protective roles of Metrnβin alleviating DC-mediated Th2 inflammation in allergic asthma,providing the novel treatment strategy of therapeutic targeting of Metrnβin allergic asthma. | Xun Gao Ting-Fan Leung Gary Wing-Kin Wong Wing-Hung Ko Mengyun Cai Ellie Jiayi He Ida Miu-Ting Chu Miranda Sin-Man Tsang Ben Chung-Lap Chan Jiawei Ling Xiao Fan Liwei Lu Christopher Wai-Kei Lam Chun-Kwok Wong | 2022 | Cellular & Molecular Immunology2022，19，2： | 5 |
| 5 | Characteristics of Clostridium difficile infection in patients hospitalized with myelodysplastic syndrome or acute myelogenous leukemia显示文摘AIM To evaluate factors associated with Clostridium difficile infection (CDI) and outcomes of CDI in the myelodysplastic syndrome(MDS) and acute myeloid leukemia (AML) population.METHODS After IRB approval,all MDS/AML patients hospitalized at the University of Maryland Greenebaum Comprehensive Cancer Center between August 2011 and December 2013 were identified.Medical charts were reviewed for demographics,clinical information,development of CDI,complications of CDI,and mortality.Patients with CDI,defined as having a positive stool PCR done for clinical suspicion of CDI,were compared to those without CDI in order to identify predictors of disease.A t-test was used for comparison of continuous variables and chisquare or Fisher's exact tests were used for categorical variables,as appropriate.RESULTS Two hundred and twenty-three patients (60.1% male,mean age 61.3 years,13% MDS,87% AML) had 594 unique hospitalizations during the study period.Thirtyfour patients (15.2%) were diagnosed with CDI.Factors significantly associated with CDI included lower albumin at time of hospitalization (P < 0.0001),prior diagnosis of CDI (P < 0.0001),receipt of cytarabine-based chemotherapy (P = 0.015),total days of neutropenia (P = 0.014),and total days of hospitalization (P = 0.005).Gender (P = 0.10),age (P = 0.77),proton-pump inhibitor use (P = 0.73),receipt of antibiotics (P = 0.66),and receipt of DNA hypomethylating agent-based chemotherapy (P = 0.92) were not significantly associated with CDI.CONCLUSION CDI is common in the MDS/AML population.Factors significantly associated with CDI in this population include low albumin,prior CDI,use of cytarabine-based chemotherapy,and prolonged neutropenia.In this study,we have identified a subset of patients in which prophylaxis studies could be targeted. | Kamini Shah Bryan F Curtin Christopher Chu Daniel Hwang Mark H Flasar Erik von Rosenvinge | 2017 | World Journal of Clinical Oncology2017，8，5： | 3 |
| 6 | Comprehensive functional annotation of susceptibility variants identifies genetic heterogeneity between lung adenocarcinoma and squamous cell carcinoma显示文摘Although genome-wide association studies have identified more than eighty genetic variants associated with non-small cell lung cancer(NSCLC)risk,biological mechanisms of these variants remain largely unknown.By integrating a large-scale genotype data of 15581 lung adenocarcinoma(AD)cases,8350 squamous cell carcinoma(SqCC)cases,and 27355 controls,as well as multiple transcriptome and epigenomic databases,we conducted histology-specific meta-analyses and functional annotations of both reported and novel susceptibility variants.We identified 3064 credible risk variants for NSCLC,which were overrepresented in enhancer-like and promoter-like histone modification peaks as well as DNase I hypersensitive sites.Transcription factor enrichment analysis revealed that USF1 was AD-specific while CREB1 was SqCC-specific.Functional annotation and genebased analysis implicated 894 target genes,including 274 specifics for AD and 123 for SqCC,which were overrepresented in somatic driver genes(ER=1.95,P=0.005).Pathway enrichment analysis and Gene-Set Enrichment Analysis revealed that AD genes were primarily involved in immune-related pathways,while SqCC genes were homologous recombination deficiency related.Our results illustrate the molecular basis of both wellstudied and new susceptibility loci of NSCLC,providing not only novel insights into the genetic heterogeneity between AD and SqCC but also a set of plausible gene targets for post-GWAS functional experiments. | Na Qin Yuancheng Li Cheng Wang Meng Zhu Juncheng Dai Tongtong Hong Demetrius Albanes Stephen Lam Adonina Tardon Chu Chen Gary Goodman Stig EBojesen Maria Teresa Landi Mattias Johansson Angela Risch H-Erich Wichmann Heike Bickeboller Gadi Rennert Susanne Arnold Paul Brennan John KField Sanjay Shete Loic Le Marchand Olle Melander Hans Brunnstrom Geoffrey Liu Rayjean JHung Angeline Andrew Lambertus AKiemeney Shan Zienolddiny Kjell Grankvist Mikael Johansson Neil Caporaso Penella Woll Philip Lazarus Matthew BSchabath Melinda CAldrich Victoria LStevens Guangfu Jin David CChristiani Zhibin Hu Christopher IAmos Hongxia Ma Hongbing Shen | 2021 | Frontiers of Medicine2021，15，2： | 3 |
| 7 | Halofuginone suppresses T cell proliferation by blocking proline uptake and inducing cell apoptosis显示文摘 | Tony L.H. Chu Qiunong Guan Christopher Y.C. Nguan Caigan Du | 2013 | International Immunopharmacology2013，，4： | 2 |
| 8 | Dynamic glial response and crosstalk in demyelination-remyelination and neurodegeneration processes显示文摘Multiple sclerosis is an autoimmune disease in which the immune system attacks the myelin sheath in the central nervous system.It is characterized by blood-brain barrier dysfunction throughout the course of multiple sclerosis, followed by the entry of immune cells and activation of local microglia and astrocytes.Glial cells(microglia, astrocytes, and oligodendrocyte lineage cells) are known as the important mediators of neuroinflammation, all of which play major roles in the pathogenesis of multiple sclerosis.Network communications between glial cells affect the activities of oligodendrocyte lineage cells and influence the demyelination-remyelination process.A finely balanced glial response may create a favorable lesion environment for efficient remyelination and neuroregeneration.This review focuses on glial response and neurodegeneration based on the findings from multiple sclerosis and major rodent demyelination models.In particular, glial interaction and molecular crosstalk are discussed to provide insights into the potential cell-and molecule-specific therapeutic targets to improve remyelination and neuroregeneration. | Tianci Chu Lisa B.E.Shields Wenxin Zeng Yi Ping Zhang Yuanyi Wang Gregory N.Barnes Christopher B.Shields Jun Cai | 2021 | Neural Regeneration Research2021，16，7： | 2 |
| 9 | Increasing rates of cardiac device infections among medicare beneficiaries: 1990–1999显示文摘 | Christopher H Cabell Paul A Heidenreich Vivian H Chu Christopher M Moore Martin E Stryjewski G.Ralph Corey Vance G Fowler | 2004 | American Heart Journal2004，，4： | 1 |
| 10 | Dynamic Hepatitis C Virus Genotypic and Phenotypic Changes in Patients Treated With the Protease Inhibitor Telaprevir显示文摘 | Christoph Sarrazin Tara L. Kieffer Doug Bartels Brian Hanzelka Ute Müh Martin Welker Dennis Wincheringer Yi Zhou Hui–May Chu Chao Lin Christine Weegink Henk Reesink Stefan Zeuzem Ann D. Kwong | 2007 | Gastroenterology2007，，5： | 1 |
| 11 | Hierarchical modeling identifies novel lung cancer susceptibility variants in inflammation pathways among 10,140 cases and 11,012 controls显示文摘 | Darren R. Brenner Paul Brennan Paolo Boffetta Christopher I. Amos Margaret R. Spitz Chu Chen Gary Goodman Joachim Heinrich Heike Bickeb?ller Albert Rosenberger Angela Risch Thomas Muley John R. McLaughlin Simone Benhamou Christine Bouchardy Juan Pablo Lew | 2013 | Human Genetics2013，，： | 1 |
| 12 | SPQD14090400000528显示文摘 | Gerhard Glenn S Chu Xin Wood G Craig Gerhard Genevieve M Benotti Peter Petrick Anthony T Gabrielsen Jon Strodel William E Still Christopher D Argyropoulos George | 2013 | Human Heredity (-)2013，，2： | 1 |
| 13 | Phase I trial of a multi-epitope-pulsed dendritic cell vaccine for patients with newly diagnosed glioblastoma显示文摘 | Surasak Phuphanich Christopher J. Wheeler Jeremy D. Rudnick Mia Mazer HongQian Wang Miriam A. Nu?o Jaime E. Richardson Xuemo Fan Jianfei Ji Ray M. Chu James G. Bender Elma S. Hawkins Chirag G. Patil Keith L. Black John S. Yu | 2013 | Cancer Immunology, Immunotherapy2013，，： | 1 |
| 14 | SPQD14090400000528显示文摘 | Gerhard Glenn S Chu Xin Wood G Craig Gerhard Genevieve M Benotti Peter Petrick Anthony T Gabrielsen Jon Strodel William E Still Christopher D Argyropoulos George | 2013 | Human Heredity . 2013 (2-4)2013，，2： | 1 |
| 15 | Pressure gradient evolution in the near-Earth magnetotail at the arrival of BBFs显示文摘Using in situ observations from THEMIS A, D and E during the 2008–2011 tail season, we present a statistical study of the evolution of pressure gradients in the near-Earth tail during bursty bulk flow(BBF) convection.We identified 138 substorm BBFs and 2,197 non-substorm BBFs for this study. We found that both the pressure and the BZcomponent of the magnetic field were enhanced at the arrival of BBFs at the spacecraft locations. We suggest that the increase of BZduring non-substorm BBFs is associated with flux pile-up. However, the much stronger enhancement of BZduring substorm BBFs implies the occurrence of magnetic field dipolarization which is caused by both the flux pile-up process and near-Earth current disruption. Furthermore, a bow-wave-like high pressure appears to be formed at the arrival of substorm BBFs,which is responsible for the formation of region-1-sense FACs. The azimuthal pressure gradient associated with the arrival of substorm BBFs lasts for about 5 min. The enhanced pressure gradient associated with the bow waveis caused by the braking and diversion of the Earthward flow in the inner plasma sheet. The results from this statistical study suggest that the braking and azimuthal diversion of BBFs may commonly create azimuthal pressure gradients, which are related to the formation of the FAC of the substorm current wedge. | Zhonghua Yao Zuyin Pu Aimin Du Vassilis Angelopoulos Christopher J.Owen Jiang Liu Xiangning Chu Xin Cao Suiyan Fu Qiugang Zong Yuan Wang | 2014 | Chinese Science Bulletin2014，59，34： | 1 |
| 16 | Multiple Recurrent De Novo CNVs, Including Duplications of the 7q11.23 Williams Syndrome Region, Are Strongly Associated with Autism显示文摘 | Stephan J. Sanders A. Gulhan Ercan-Sencicek Vanessa Hus Rui Luo Michael T. Murtha Daniel Moreno-De-Luca Su H. Chu Michael P. Moreau Abha R. Gupta Susanne A. Thomson Christopher E. Mason Kaya Bilguvar Patricia B.S. Celestino-Soper Murim Choi Emily L. Crawf | 2011 | Neuron2011，，5： | 1 |
| 17 | Dynamic Hepatitis C Virus Genotypic and Phenotypic Changes in Patients Treated With the Protease Inhibitor Telaprevir显示文摘 | Christoph Sarrazin Tara L. Kieffer Doug Bartels Brian Hanzelka Ute Müh Martin Welker Dennis Wincheringer Yi Zhou Hui–May Chu Chao Lin Christine Weegink Henk Reesink Stefan Zeuzem Ann D. Kwong | 2007 | Gastroenterology2007，，5： | 1 |
| 18 | Per ceptions of the organizational context and psychological con tract breach:Assessing competing perspectives 显示文摘 | Christopher CR Chu Hsiang Chang Russell EJ | 2009 | Behavior and Human Decision Processes2009，2，108： | 1 |
| 19 | Estrogen-related genes and their contribution to racial differences in breast cancer risk显示文摘 | Kerryn Reding Chu Chen Kimberly Lowe David Doody Christopher Carlson Christina Chen John Houck Linda Weiss Polly Marchbanks Leslie Bernstein Robert Spirtas Jill McDonald Brian Strom Ronald Burkman Michael Simon Jonathan Liff Janet Daling Kathleen Malone | 2012 | Cancer Causes & Control2012，，5： | 1 |
| 20 | Kindlin-2 loss in condylar chondrocytes causes spontaneous osteoarthritic lesions in the temporomandibular joint in mice显示文摘The progressive destruction of condylar cartilage is a hallmark of the temporomandibular joint(TMJ) osteoarthritis(OA);however, its mechanism is incompletely understood. Here, we show that Kindlin-2, a key focal adhesion protein, is strongly detected in cells of mandibular condylar cartilage in mice. We find that genetic ablation of Kindlin-2 in aggrecan-expressing condylar chondrocytes induces multiple spontaneous osteoarthritic lesions, including progressive cartilage loss and deformation, surface fissures, and ectopic cartilage and bone formation in TMJ. Kindlin-2 loss significantly downregulates the expression of aggrecan, Col2a1 and Proteoglycan 4(Prg4), all anabolic extracellular matrix proteins, and promotes catabolic metabolism in TMJ cartilage by inducing expression of Runx2and Mmp13 in condylar chondrocytes. Kindlin-2 loss decreases TMJ chondrocyte proliferation in condylar cartilages. Furthermore,Kindlin-2 loss promotes the release of cytochrome c as well as caspase 3 activation, and accelerates chondrocyte apoptosis in vitro and TMJ. Collectively, these findings reveal a crucial role of Kindlin-2 in condylar chondrocytes to maintain TMJ homeostasis. | Yumei Lai Wei Zheng Minghao Qu Christopher C.Xiao Sheng Chen Qing Yao Weiyuan Gong Chu Tao Qinnan Yan Peijun Zhang Xiaohao Wu Guozhi Xiao | 2022 | International Journal of Oral Science2022，14，3： | 0 |
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