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| 1 | 面向21世纪的卒中新定义:美国心脏病学会和美国卒中学会声明显示文摘尽管脑血管病有着全球性影响且对其病理生理学的认识有了很多进步,但是'卒中'这一术语在临床实践、临床研究或公共卫生评估中的定义却不一致。传统的定义依据于临床,却没有考虑到科学技术的进步。美国心脏协会(AHA)和美国卒中协会(ASA)卒中分会组织了写作小组,为21世纪卒中新定义撰写专家共识性声明。中枢神经系统(CNS)梗死,指由缺血所导致的脑、脊髓或视网膜的细胞死亡,是基于持续性损害的神经病理学、神经影像学和(或)临床证据。CNS梗死表现为一个临床谱:缺血性卒中特指伴有明显症状的CNS梗死,而静息性梗死根据定义指未引起已知的症状的梗死。卒中也还包括脑出血和蛛网膜下腔出血。新定义的卒中结合了临床和组织学标准,可被用于实践、研究和公共卫生评估。 | 俞羚 董荃 宋叶平 江静雯 李卉 刘亮贤 苏爱萍 李焰生 Sacco RL Kasner SE Broderick JP Caplan LR Connors JJ Culebras A Elkind MS George MG Hamdan AD Higashida RT Hoh BL Janis LS Kase CS Kleindorfer DO Lee JM Moseley ME Peterson ED Turan TN Valderrama AL Vinters HV | 2013 | 神经病学与神经康复学杂志2013，10，2： | 188 |
| 2 | Methylation-dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeutics显示文摘交往受体的蛋白质 kinase-3 (RIP3 或 RIPK3 ) 是执行 “ 的细胞的机械的必要部分; programmed”或 “ regulated”坏死。这里,我们证明那规划坏死响应许多化学疗法的代理人被激活并且贡献导致化疗的房间死亡。然而,我们证明那 RIP3 表情经常在化学疗法的死亡期间由于它的 transcriptional 开始地点, MLKL 的这样 RIP3 依赖的激活和下游地规划的坏死附近的 genomic methylation 是在癌症房间的 silenced 大部分被镇压。不过,有 hypomethylating 代理人的治疗恢复 RIP3 表示,并且从而以一种 RIP3 依赖的方式把敏感提升到 chemotherapeutics。RIP3 表示在 85% 乳癌病人与正常织物相比在肿瘤被减少,建议那 RIP3 缺乏断然在肿瘤生长 / 发展期间被选择。因为 hypomethylating 代理人在病人是相当容忍得好的,我们建议病人们可以从收到 hypomethylating 代理人与常规 chemotherapeutics 在治疗以前导致 RIP3 表示有益于的那 RIP3 缺乏的癌症。 | Gi-Bang Koo Michael J Morgan Da-Gyum Lee Woo-Jung Kim Jung-Ho Yoon Ja Seung Koo Seung I1 Kim Soo Jung Kim Mi Kwon Son Soon Still Hong Jean M Mulcahy Levy Daniel A Pollyea Craig T Jordan Pearlly Yan David Frankhouser Deedra Nicolet Kati Maharry Guido Marcucci Kyeong Sook Choi Hyeseong Cho ndrew Thorbum You-Sun Kim | 2015 | Cell Research2015，25，6： | 20 |
| 3 | 鲁豫皖三省麻疹监测试点项目效果评价显示文摘为了评价鲁、豫、皖三省麻疹监测合作项目的实施效果 ,综合三省项目进展报告、世界卫生组织现场评估报告、法定传染病报告系统、急性弛缓性麻痹病例监测系统和项目省开展的专项研究进行了分析。结果显示 :项目省麻疹疫苗强化免疫的效果不同 ;除有免疫史记录的病例比例 <80 %外 ,其它麻疹监测系统的关键指标都有明显提高 ;常规免疫接种率的报告质量提高不明显 ,漏报和报告表格过于复杂是重要的影响因素 ;实施风疹控制后 ,风疹的平均感染年龄从 1999年的 9 8岁 ,提高至 2 0 0 3年的 13 9岁。 | 左树岩 许青 郭万申 唐继海 夏伟 梁晓峰 lisa A Lee | 2004 | 中国计划免疫2004，10，5： | 18 |
| 4 | Coordinated peak expression of MMP-26 and TIMP-4 in preinvasive human prostate tumor显示文摘因为早察觉和治疗为病人的医药管理是批评的,为早前列腺癌症诊断的新奇简历标记的鉴定是高度重要的。在基础房间层和地下室膜的连续性的混乱为高级职业人员静电干扰 intraepithelial 瘤形成(HGPIN ) 的前进是必要的到在人的前列腺的侵略腺癌。涉及变换到侵略显型的分子是强烈审查的题目。我们以前报导了矩阵 metalloproteinase-26 (MMP-26 ) 经由地下室膜蛋白质并且由激活 MMP-9 的酶原形式的劈开支持人的前列腺癌症房间的侵略。而且,我们发现了 metalloproteinases-4 (TIMP-4 ) 的那个织物禁止者是大多数有势力 MMP-26 的内长的禁止者。这里,我们更高示威(p<0.0001 ) 在 HGPIN 和癌症的 MMP-26 和 TIMP-4 表示,与非肿瘤的 acini 相比。他们的表示层次在 HGPIN 是最高的,但是在一样的纸巾在侵略癌症(为各个的 p<0.001 ) 衰退。连续前列腺癌症织物节染色的 Immunohistochemical 建议 MMP-26 和 TIMP-4 的 colocalization。现在的学习显示 MMP-26 和 TIMP-4 可以在 HGPIN 的变换期间起一个不可分的作用到侵略癌症并且可以也为早前列腺癌症诊断用作标记。房间研究(2006 ) 16:750-758。做 i:10.1038/sj .cr.7310089;出版联机 2006 年 8 月 29 日。 | Seakwoo Lee Kevin K Desai Kenneth A Iczkowski Robert G Newcomer Kevin J WU Yun-Ge Zhao Winston W Tan Mark D Roycik Qing-Xiang Amy Sang | 2006 | Cell Research2006，16，9： | 18 |
| 5 | Endoscopy and polyps-diagnostic and therapeutic advances in management显示文摘Despite multiple efforts aimed at early detection through screening, colon cancer remains the third leading cause of cancer-related deaths in the United States, with an estimated 51000 deaths during 2013 alone. The goal remains to identify and remove benign neoplastic polyps prior to becoming invasive cancers. Polypoid lesions of the colon vary widely from hyperplastic, hamartomatous and inflammatory to neoplastic adenomatous growths. Although these lesions are all benign, they are common, with up to one-quarter of patients over 60 years old will develop pre-malignant adenomatous polyps. Colonoscopy is the most effective screening tool to detect polyps and colon cancer, although several studies have demonstrated missed polyp rates from 6%-29%, largely due to variations in polyp size. This number can be as high as 40%, even with advanced (> 1 cm) adenomas. Other factors including sub-optimal bowel preparation, experience of the endoscopist, and patient anatomical variations all affect the detection rate. Additional challenges in decision-making exist when dealing with more advanced, and typically larger, polyps that have traditionally required formal resection. In this brief review, we will explore the recent advances in polyp detection and therapeutic options. | Scott R Steele Eric K Johnson Bradley Champagne Brad Davis Sang Lee David Rivadeneira Howard Ross Dana A Hayden Justin A Maykel | 2013 | World Journal of Gastroenterology2013，19，27： | 16 |
| 6 | Fabrication of 3D Printed PCL/PEG Polyblend Scaffold Using Rapid Prototyping System for Bone Tissue Engineering Application显示文摘 | Su A Park Sang Jin Lee Ji Min Seok Jun Hee Lee Wan Doo Kim Il Keun Kwon | 2018 | Journal of Bionic Engineering2018，15，3： | 15 |
| 7 | Management of distal humeral coronal shear fractures显示文摘Coronal shear fractures of the distal humerus are rare,complex fractures that can be technically challenging to manage. They usually result from a low-energy fall and direct compression of the distal humerus by the radial head in a hyper-extended or semi-flexed elbow or from spontaneous reduction of a posterolateral subluxation or dislocation. Due to the small number of soft tissue attachments at this site, almost all of these fractures are displaced. The incidence of distal humeral coronal shear fractures is higher among women because of the higher rate of osteoporosis in women and the difference in carrying angle between men and women. Distal humeral coronal shear fractures may occur in isolation, may be part of a complex elbow injury, or may be associated with injuries proximal or distal to the elbow. An associated lateral collateral ligament injury is seen in up to 40% and an associated radial head fracture is seen in up to 30% of these fractures. Given the complex nature of distal humeral coronal shear fractures, there is preference for operative management. Operative fixation leads to stable anatomic reduction, restores articular congruity, and allows initiation of early range-of-motion movements in the majority of cases. Several surgical exposure and fixation techniques are available to reconstruct the articular surface fol owing distal humeral coronal shear fractures. The lateral extensile approach and fixation with countersunk headless compression screws placed in an anterior-to-posterior fashion are commonly used. We have found a two-incision approach(direct anterior and lateral) that results in less soft tissue dissection and better outcomes than the lateral extensile approach in our experience. Stiffness, pain, articular incongruity, arthritis, and ulnohumeral instability may result if reduction is non-anatomic or if fixation fails. | Shahram S Yari Nathan L Bowers Miguel A Craig Lee M Reichel | 2015 | World Journal of Clinical Cases2015，3，5： | 15 |
| 8 | The wonders of BMP9:From mesenchymal stem cell differentiation,angiogenesis,neurogenesis,tumorigenesis,and metabolism to regenerative medicine显示文摘Although bone morphogenetic proteins(BMPs)initially showed effective induction of ectopic bone growth in muscle,it has since been determined that these proteins,as members of the TGF-b superfamily,play a diverse and critical array of biological roles.These roles include regulating skeletal and bone formation,angiogenesis,and development and homeostasis of multiple organ systems.Disruptions of the members of the TGF-b/BMP superfamily result in severe skeletal and extra-skeletal irregularities,suggesting high therapeutic potential from understanding this family of BMP proteins.Although it was once one of the least characterized BMPs,BMP9 has revealed itself to have the highest osteogenic potential across numerous experiments both in vitro and in vivo,with recent studies suggesting that the exceptional potency of BMP9 may result from unique signaling pathways that differentiate it from other BMPs.The effectiveness of BMP9 in inducing bone formation was recently revealed in promising experiments that demonstrated efficacy in the repair of critical sized cranial defects as well as compatibility with bone-inducing bio-implants,revealing the great translational promise of BMP9.Furthermore,emerging evidence indicates that,besides its osteogenic activity,BMP9 exerts a broad range of biological functions,including stem cell differentiation,angiogenesis,neurogenesis,tumorigenesis,and metabolism.This review aims to summarize our current understanding of BMP9 across biology and the body. | Sami Mostafa Mikhail Pakvasa Elam Coalson Allen Zhu Alex Alverdy Hector Castillo Jiaming Fan Alex Li Yixiao Feng Di Wu Elliott Bishop Scott Du Mia Spezia Alissa Li Ofir Hagag Alison Deng Winny Liu Mingyang Li Sherwin S·Ho Aravind Athiviraham Michael J·Lee Jennifer Moriatis Wolf Guillermo A·Ameer Hue H·Luu Rex C·Haydon Jason Strelzow Kelly Hynes Tong-Chuan He Russell R·Reid | 2019 | Genes & Diseases2019，6，3： | 15 |
| 9 | 肌萎缩性侧索硬化蛋白激活小胶质细胞NLRP3炎性小体显示文摘小胶质细胞NLRP3炎性小体激活正在成为神经退行性变过程中神经炎症的关键因素。诸如β-淀粉样蛋白和α-突触核蛋白之类的致病性蛋白质聚集体触发小胶质NLRP3激活,从而导致半胱天冬酶-1激活和IL-1β的分泌。在小鼠肌萎缩性侧索硬化症(ALS)的SOD1G93A模型中,半胱天冬酶-1和IL-1β均促进疾病进展,提示小胶质NLRP3在该进程中发挥作用。然而先前的研究表明,SOD1G93A小鼠小胶质细胞不表达NLRP3,SOD1G93A蛋白在小胶质细胞中产生独立于NLRP3的IL-1β。本研究论证了使用Nlrp3-GFP基因敲入小鼠,在SOD1G93A小鼠中小胶质细胞表达NLRP3。本研究显示聚集和可溶性SOD1G93A均可激活小鼠原代小胶质细胞中的炎性小体,导致半胱天冬酶-1和IL-1β裂解,ASC斑点形成以及呈剂量和时间依赖性的IL-1β分泌。重要的是,SOD1G93A无法从缺乏Nlrp3的小胶质细胞或者用特异性NLRP3抑制剂MCC950预处理的小胶质细胞中诱导IL-1β分泌,从而证实NLRP3是介导SOD1诱导的小胶质细胞IL-1β分泌的关键炎症小体复合物。在TDP-43Q331K ALS小鼠模型中也观察到小胶质NLRP3上调,TDP-43野生型和突变蛋白亦可以NLRP3依赖性的方式激活小胶质炎性小体。从机制上讲,本研究确定了活性氧簇和ATP的生成是SOD1G93A介导的NLRP3激活所需的关键事件。总之,本研究的数据表明ALS小胶质细胞表达NLRP3,而病理ALS蛋白激活小胶质NLRP3炎性小体。因此,NLRP3抑制可能是阻止小胶质细胞神经炎症和ALS疾病进展的潜在治疗方法。 | Vandana Deora John D Lee Eduardo AAlbornoz Luke McAlary Cyril J Jagaraj Avril A B Robertson Julie D Atkin Matthew A Cooper Kate Schroder Justin J Yerbury Richard Gordon Trent MWoodruff 杜一星(编译) | 2020 | 神经损伤与功能重建2020，15，9： | 13 |
| 10 | Calcium signaling and T-type calcium channels in cancer cell cycling显示文摘Regulation of intracellular calcium is an important signaling mechanism for cell proliferation in both normal and cancerous cells. In normal epithelial cells, free calcium concentration is essential for cells to enter and accomplish the S phase and the M phase of the cell cycle. In contrast, cancerous cells can pass these phases of the cell cycle with much lower cytoplasmic free calcium concentrations, indicating an alternative mechanism has developed for fulfilling the intracellular calcium requirement for an increased rate of DNA synthesis and mitosis of fast replicating cancerous cells. The detailed mechanism underlying the altered calcium loading pathway remains unclear; however, there is a growing body of evidence that suggests the T-type Ca2+ channel is abnormally expressed in cancerous cells and that blockade of these channels may reduce cell proliferation in addition to inducing apoptosis. Recent studies also show that the expression of T-type Ca2+ channels in breast cancer cells is proliferation state dependent, i.e. the channels are expressed at higher levels during the fast-replication period, and once the cells are in a non-proliferation state, expression of this channel isminimal. Therefore, selectively blocking calcium entry into cancerous cells may be a valuable approach for preventing tumor growth. Since T-type Ca2+ channels are not expressed in epithelial cells, selective T-type Ca2+ channel blockers may be useful in the treatment of certain types of cancers. | James T Taylor Xiang-Bin Zeng Jonathan E Pottle Kevin Lee Alun R Wang Stephenie G Yi lennifer A S Scruggs Suresh S Sikka Ming Li | 2008 | World Journal of Gastroenterology2008，14，32： | 12 |
| 11 | 豫鲁皖三省小学新生预防接种状况评估显示文摘为了解中国小学新生的预防接种状况 ,在豫鲁皖三省 ,按照便利原则抽取小学新生进行了描述性研究。共调查小学 18所 ,其中农村小学 8所、城市小学 10所 ;小学新生 2 2 35人 ,其中城市小学 14 12人 ,农村小学 82 4人。有预防接种证 12 84人 ,预防接种证持有率为 5 7 4 %。无预防接种证但在当地接种点查找到预防接种记录的 5 87人 ,占 2 6 3%。因此有预防接种记录的共 1871人 ,占 83 7%。在所有小学新生中完成口服脊髓灰质炎疫苗 (OPV)全程免疫的占 6 2 9% ,完成卡介苗 (BCG)免疫的占 81 9% ,完成麻疹疫苗 (MV)全程免疫的占 5 5 2 % ,完成乙型肝炎疫苗 (HepB)全程免疫的占 6 7 3% ,完成百白破联合疫苗 (DPT)全程免疫的占 70 3% ,接种白破联合疫苗 (TD)的占 32 7% ;也即缺种或漏种OPV、BCG、MV、HepB、DPT、TD儿童的比例依次为 :37 1%、18 1%、4 4 8%、32 7%、2 9 7%、6 7 3%。调查发现 ,城市小学新生预防接种证持有率、各种疫苗全程免疫接种率均高于农村小学 ;在城市小学新生中流动儿童预防接种证持有率、各种疫苗全程免疫接种率低于整体水平。如果在入学时严格查验预防接种情况 ,并对缺种或漏种的新生进行补种 ,可有效提高小学新生的接种率。对婴儿时未免疫的贫穷地区儿童、计划外出生儿童。 | 盛利 Lisa A Lee 左树岩 郭万申 余文周 许青 冯子健 | 2003 | 中国计划免疫2003，9，5： | 11 |
| 12 | Is endoscopic ultrasound examination necessary in the management of esophageal cancer?显示文摘Despite substantial efforts at early diagnosis, accurate staging and advanced treatments, esophageal cancer(EC) continues to be an ominous disease worldwide. Risk factors for esophageal carcinomas include obesity, gastroesophageal reflux disease, hard-alcohol use and tobacco smoking. Five-year survival rates have improved from 5% to 20% since the 1970 s, the result of advances in diagnostic staging and treatment. As the most sensitive test for locoregional staging of EC, endoscopic ultrasound(EUS) influences the development of an optimal oncologic treatment plan for a significant minority of patients with early cancers, which appropriately balances the risks and benefits of surgery, chemotherapy and radiation. EUS is costly, and may not be available at all centers. Thus, the yield of EUS needs to be thoughtfully considered for each patient. Localized intramucosal cancers occasionally require endoscopic resection(ER) for histologic staging or treatment; EUS evaluation may detect suspicious lymph nodes prior to exposing the patient to the risks of ER. Although positron emission tomography(PET) has been increasingly utilized in staging EC, it may be unnecessary for clinical staging of early, localized EC and carries the risk of false-positive metastasis(over staging). In EC patients with evidence of advanced disease, EUS or PET may be used to define the radiotherapy field. Multimodality staging with EUS, crosssectional imaging and histopathologic analysis of ER, remains the standard-of-care in the evaluation of early esophageal cancers. Herein, published data regarding use of EUS for intramucosal, local, regional and metastatic esophageal cancers are reviewed. An algorithm to illustrate the current use of EUS at The University of Texas MD Anderson Cancer Center is presented. | Tomas DaVee Jaffer A Ajani Jeffrey H Lee | 2017 | World Journal of Gastroenterology2017，23，5： | 11 |
| 13 | Gastro-intestinal toxicity of chemotherapeutics in colorectal cancer:The role of inflammation显示文摘Chemotherapy-induced diarrhea(CID)is a common and often severe side effect experienced by colorectal cancer(CRC)patients during their treatment.As chemotherapy regimens evolve to include more efficacious agents,CID is increasingly becoming a major cause of dose limiting toxicity and merits further investigation.Inflammation is a key factor behind gastrointestinal(GI)toxicity of chemotherapy.Different chemotherapeutic agents activate a diverse range of pro-inflammatory pathways culminating in distinct histopathological changes in the small intestine and colonic mucosa.Here we review the current understanding of the mechanisms behind GI toxicity and the mucositis associated with systemic treatment of CRC.Insights into the inflammatory response activated during this process gained from various models of GI toxicity are discussed.The inflammatory processes contributing to the GI toxicity of chemotherapeutic agents are increasingly being recognised as having an important role in the development of anti-tumor immunity,thus conferring added benefit against tumor recurrence and improving patient survival.We review the basic mechanisms involved in the promotion of immunogenic cell death and its relevance in the treatment of colorectal cancer.Finally,the impact of CID on patient outcomes and therapeutic strategies to prevent or minimise the effect of GI toxicity and mucositis are discussed. | Chun Seng Lee Elizabeth J Ryan Glen A Doherty | 2014 | World Journal of Gastroenterology2014，20，14： | 10 |
| 14 | Colonoscopy-induced ischemic colitis in patients without risk factors显示文摘Ischemic colitis is the most common form of intestinal ischemia.It is a condition that is commonly seen in the elderly and among individuals with risk factors for ischemia.Common predisposing conditions for ischemic colitis are major vascular occlusion,small vessel disorder,shock,some medications,colonic obstructions and hematologic disorders.Ischemic colitis following colonoscopy is rare.Here,we report two cases of ischemic colitis after a routine screening colonoscopy in patients without risk factors for ischemia. | Sang Ok Lee Sae Hee Kim Sung Hee Jung Chan Woong Park Min Ji Lee Jin A Lee Hyun Cheol Koo Anna Kim Hyun-Young Han Dong-Wook Kang | 2014 | World Journal of Gastroenterology2014，20，13： | 9 |
| 15 | Mechanosignaling activation of TGFβmaintains intervertebral disc homeostasis显示文摘Intervertebral disc(IVD) degeneration is the leading cause of disability with no disease-modifying treatment.IVD degeneration is associated with instable mechanical loading in the spine, but little is known about how mechanical stress regulates nucleus notochordal(NC) cells to maintain IVD homeostasis. Here we report that mechanical stress can result in excessive integrin α_vβ_6-mediated activation of transforming growth factor beta(TGFβ), decreased NC cell vacuoles, and increased matrix proteoglycan production, and results in degenerative disc disease(DDD). Knockout of TGFβ type II receptor(TβRII) or integrin α_v in the NC cells inhibited functional activity of postnatal NC cells and also resulted in DDD under mechanical loading.Administration of RGD peptide, TGFβ, and α_vβ_6-neutralizing antibodies attenuated IVD degeneration. Thus,integrin-mediated activation of TGFβ plays a critical role in mechanical signaling transduction to regulate IVD cell function and homeostasis. Manipulation of this signaling pathway may be a potential therapeutic target to modify DDD. | Qin Bian Lei Ma Amit Jain Janet L Crane Khaled Kebaish Mei Wan Zhengdong Zhang X Edward Guo Paul D Sponseller Cheryle A Seguin Lee H Riley Yongjun Wang Xu Cao | 2017 | Bone Research2017，5，1： | 9 |
| 16 | Genomic change in hepatitis B virus associated with development of hepatocellular carcinoma显示文摘AIM: To determine the genomic changes in hepatitis B virus(HBV) and evaluate their role in the development of hepatocellular carcinoma(HCC) in patients chronically infected with genotype C HBV.METHODS: Two hundred and forty chronic hepatitis B(CHB) patients were subjected and followed for a median of 105 mo. HCC was diagnosed in accordance with AASLD guidelines. The whole X, S, basal core promoter(BCP), and precore regions of HBV were sequenced using the direct sequencing method.RESULTS: All of the subjects were infected with genotype C HBV. Out of 240 CHB patients, 25(10%) had C1653 T and 33(14%) had T1753 V mutation in X region; 157(65%) had A1762T/G1764 A mutations in BCP region, 50(21%) had G1896 A mutation in precore region and 67(28%) had pre-S deletions. HCC occurred in 6 patients(3%). The prevalence of T1753 V mutation was significantly higher in patients who developed HCC than in those without HCC. The cumulative occurrence rates of HCC were 5% and 19% at 10 and 15 years, respectively, in patients with T1753 V mutant, which were significantly higher than 1% and 1% in those with wild type HBV(P < 0.001).CONCLUSION: The presence of T1753 V mutation in HBV X-gene significantly increases the risk of HCC development in patients chronically infected with genotype C HBV. | Danbi Lee Heather Lyu Young-Hwa Chung Jeong A Kim Priya Mathews Elizabeth Jaffee Lei Zheng Eunsil Yu Young Joo Lee Soo Hyung Ryu | 2016 | World Journal of Gastroenterology2016，22，23： | 9 |
| 17 | CD69 expression on airway eosinophils and airway inflammation in a murine model of asthma显示文摘Background Asthma is a chronic airway disease with inflammation characterized by physiological changes (airway hyper-responsiveness, AHR) and pathological changes (inflammatory cells infiltration and mucus production). Eosinophils play a key role in the allergic inflammation. But the causative relationship between eosinophils and airway inflammation is hard to prove. One of the reasons is lack of activation marker of murine eosinophils. We investigated the expression of CD69 on murine eosinophils in vitro, the relationship between the expression of CD69 on eosinophils from peripheral blood and bronchoalveolar lavage fluid and on airway inflammation in asthmatic mice. Methods Eosinophils from peripheral blood of IL-5 transgenic mice (NJ.1638) were purified. Mice were divided into five groups: wild type mice sensitized and challenged with saline (WS group), wild type mice sensitized and challenged with ovalbumin (WO group), IL-5-/- mice sensitized and challenged with saline and transferred with purified eosinophils (ISE group), IL-5-/- mice sensitized and challenged with OVA and transferred with purified eosinophils (IOE group), IL-5-/- mice sensitized and challenged with OVA and transferred with purified eosinophils, pretreated with anti CD4 monoclonal antibody (IOE+antiCD4mAb group). IL-5-/- mice were sensitized with OVA at day 0 and day 14, then challenged with OVA aerosol. On days 24, 25, 26 and 27 purified eosinophils were transferred intratracheally to IL-5-/- mice. On day 28, blood and BALF were collected and CD69 expression on eosinophils measured by flowcytometry. Results Purified eosinophils did not express CD69. But eosinophils cultured with PMA+MA, IFN-γ, IL-5 or GM-CSF expressed CD69 strongly. Eosinophils from blood of WO, WS group did not express CD69 at all. The numbers of eosinophils in BALF of WO group, IOE group, ISE group and IOE+antiCD4mAb group were significantly higher than in mice of WS group which did not have eosinophils at all. CD69 expression on eosinophils in BALF of IOE and WO groups was strong. Eosinophils in BALF of ISE and IOE+antiCDmAb groups did not express CD69. The mucus production result was similar to CD69 expression. There were eosinophils infiltration in lung slides of all groups except WS group. Conclusion Activation in airway of eosinophils could directly lead to airway inflammation. | WANG Hui-ying SHEN Hua-hao James J Lee Nancy A Lee | 2006 | Chinese Medical Journal2006，，23： | 8 |
| 18 | High level of preoperative carbohydrate antigen 19-9 is a poor survival predictor in gastric cancer显示文摘AIM:To assess the clinical significance and the prognostic value of preoperative serum carbohydrate antigen 19-9(CA 19-9)level in gastric cancer.METHODS:Between January 2005 and December2006,1960 patients underwent surgery for histologically confirmed gastric cancer.Of these,163 patients had elevated serum levels of CA 19-9 preoperatively,and1628 patients had normal serum levels of CA 19-9 preoperatively.For this study,325 patients were selected from the group of 1628 patients by age,sex,and cancer stage to serve as controls.Statistically significant differences in survival rates were calculated using the log-rank test.A P value less than 0.05 was considered statistically significant and was determined using SAS software.RESULTS:The baseline characteristics showed some differences between the two groups with regard to histology.Overall survival(OS)in the elevated and nonelevated group was 37.90 and 68.67 mo,respectively(P<0.001).N stage(P=0.001)was a significant predictor of disease-free survival by multivariate analysis.Also,N stage(P<0.001),and the presence of peritoneal metastasis(P<0.001)remained independent factors in predicting OS by multivariate analysis.Additionally,preoperative serum CA 19-9 levels were significantly associated with OS in univariate(P=0.009)and multivariate(P=0.021)analyses.CONCLUSION:Serum CA 19-9 can be considered an independent prognostic factor in predicting OS in patients anticipating surgery for gastric cancer. | A Ra Choi Jun Chul Park Jie-Hyun Kim Sung Kwan Shin Sang Kil Lee Yong Chan Lee Jae Bock Chung | 2013 | World Journal of Gastroenterology2013，19，32： | 8 |
| 19 | Cardiotrophin 1 stimulates beneficial myogenic and vascular remodeling of the heart显示文摘出生后的心通过 hypertrophic 生长适应应力和超载,可能病理学或有益的一个过程(生理的肥大) 。生理的肥大改进心脏的性能在健康并且 diseased 个人,然而,宣传这有利改编的机制仍然保持糟糕定义。我们识别 cytokine cardiotrophin (CT1 ) 1 作为能够包括导致的导出 cardiomyocyte 的 angiogenic 信号的心肌层,和刺激的短暂、可逆的肥大概括心的生理的生长的特色的一个因素增加了由脉管形成。CT1 的能力从 caspase 激活的调停 CK2 的制止发源导致生理的肥大,阻止到无限制的病理学的生长的转变。外长的 CT1 蛋白质交货稀释了病理并且在正确的心失败的一个严格的模型恢复了可收缩的功能,建议为这难处理的心脏病的一种新奇处理选择。 | Mohammad Abdul-Ghani Colin Suen Baohua Jiang Yupu Deng Jonathan J Weldrick Charis Putinski Steve Brunette Pasan Femando Tom T Lee Peter Flynn Frans H H Leenen Patrick G Burgon Duncan J Stewar Lynn A Megeney | 2017 | Cell Research2017，27，10： | 8 |
| 20 | Neuroimaging the brain-gut axis in patients with irritable bowel syndrome显示文摘AIM:To summarize and synthesize current literature on neuroimaging the brain-gut axis in patients with irritable bowel syndrome(IBS).METHODS:A database search for relevant literature was conducted using Pub Med,Scopus and Embase in February 2015.Date filters were applied from the year2009 and onward,and studies were limited to those written in the English language and those performed upon human subjects.The initial search yielded 797articles,out of which 38 were pulled for full text review and 27 were included for study analysis.Investigations were reviewed to determine study design,methodology and results,and data points were placed in tabular format to facilitate analysis of study findings across disparate investigations.RESULTS:Analysis of study data resulted in the abstraction of four key themes:Neurohormonal differences,anatomic measurements of brain structure and connectivity,differences in functional responsiveness of the brain during rectal distention,and confounding/correlating patient factors.Studies in this review noted alterations of glutamate in the left hippocampus(HIPP),commonalities across IBS subjects in terms of brain oscillation patterns,cortical thickness/gray matter volume differences,and neuroanatomical regions withincreased activation in patients with IBS:Anterio cingulate cortex,mid cingulate cortex,amygdala anterior insula,posterior insula and prefrontal cortex.A striking finding among interventions was the substantia influence that patient variables(e.g.,sex,psychologica and disease related factors)had upon the identification of neuroanatomical differences in structure and con nectivity.CONCLUSION:The field of neuroimaging can provide insight into underlying physiological differences that distinguish patients with IBS from a healthy population. | Kristen R Weaver Lee Anne B Sherwin Brian Walitt Gail D'Eramo Melkus Wendy A Henderson | 2016 | World Journal of Gastrointestinal Pharmacology and Therapeutics2016，7，2： | 8 |
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