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A meta-analysis of soluble suppression of tumorigenicity 2 （sST2） and clinical outcomes in pulmonary hypertension

Journal of Geriatric Cardiology 2017年第12期14卷 766-771页

作者： King Sum Luk christina ip Meng-Qi GONG Sunny Hei WONG William KK Wu Mei DONG Guang-Ping LI Ka Pang Chan Yi-Mei DU Tong LIU Martin CS Wong David Shu Cheong Hui Gary Tse Department of Medicine and Therapeutics Faculty of Medicine Chinese University ofHong Kong Hong Kong China Li Ka Shing Institute of Health Sciences Faculty of Medicine Chinese University ofHong Kong Hong Kong China Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease Department of Cardiology Tianjin Institute of Cardiology Second Hospital of Tianjin Medical University Tianjin China Department of Anaesthesia and Intensive Care State Key Laboratory of Digestive Disease LKS Institute of Health Sciences The Chinese University of Hong Kong Hong Kong China The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine Department of Cardiology Qilu Hospital Shandong University Jinan China Research Center of Ion Channelopathy Institute of Cardiology Union Hospital Tongii Medical College Huazhong University of Science and Technology Wuhan China JC School of Public Health and Primary Care The Chinese University ofHong Kong Hong Kong China State Key Laboratory of Digestive Disease LKS Institute of Health Sciences Chinese University ofHong Kong Hong Kong China

Suppression of Tumorigenicity 2 （ST2） is a member of the interleukin （IL）-1 receptor family The ST2 receptor exists in two isoforms - ST2 ligand （ST2L） and soluble ST2 （sST2）.ST2L is a membrane receptor and sST2 is a trun- cated receptor which is soluble in the blood, allowing it to be detected in serum. IL-33 is a member of the IL-1 family of ligand and is the fimctional ligand of ST2L receptor. It binds to the ST2L, thereby mediating its immune function.

关键词： Mortality Poor outcomes Pulmonary hypertension Soluble suppression of tumorigenicity 2 SST2

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Beta-7 integrin controls enterocyte migration in the small intestine

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World Journal of Gastroenterology 2015年第6期21卷 1759-1764页

作者： Elke Kaemmerer Paula Kuhn Ursula Schneider Thomas Clahsen Min Kyung Jeon christina Klaus Julia Andruszkow Michael Hrer Sabine Ernst Angela Schippers Norbert Wagner Nikolaus Gassler Institute of Pathology RWTH Aachen University Department of Pediatrics RWTH Aachen University Department of Medical Statistics RWTH Aachen University

AIM:To hypothesize that beta-7 integrin affects cellularmigration of both,lymphocytes and ***:The nucleoside analog Brd U was ip injected in beta-7-deficient mice(C57BL/6-Itgbtmlcgn/J)of male gender and age-matched male C57BL/J J mice(wild type)4,20,or 40 h before *** total small intestine was isolated,dissected,and used for morphometrical *** U-positive epithelial cells were numbered in at least 15 hemi-crypts per duodenum,jejunum,and ileum of each *** outer most Brd U-positive cell(cellmax)was determined per hemi-crypt,numerically documented,and statistically ***:Integrins containing the beta-7-chain were exclusively expressed on *** the small intestinal mucosa of beta-7 integrin-deficient mice the number of intraepithelial lymphocytes was drastically ***,the Peyer’s patches of beta-7integrin-deficient mice appeared *** beta-7integrin-deficient mice the location of cellmax was found in a higher position than it was the case for the *** difference was already detected at 4 h after Brd U application,but significantly increased with time(40 h after Brd U injection)in all small intestinal segments investigated,i.e.,duodenum,jejunum,and *** of small intestinal enterocytes was different between the experimental groups measured by cellmax ***:The E-cadherin beta-7 integrin pathway probably controls migration of enterocytes within the small intestinal surface lining epithelial layer.

关键词： Barrier function Cell migration Inflammatory bowel

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DAC2004成为迄今为止规模最大的EDA工具展会

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今日电子 2004年第8期 30-34页

作者： christina Nickolas

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