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Role of autophagy in the pathogenesis of inflammatory bowel disease

World Journal of Gastroenterology 2017年第11期23卷 1944-1953页

作者： Tomoya Iida Kei Onodera hiroshi nakase Department of Gastroenterology and Hepatology Sapporo Medical University School of MedicineHokkaido 060-8556Japan

Inflammatory bowel disease(IBD) results from a complex series of interactions between susceptibility genes, the environment, and the immune ***, some studies provided strong evidence that the process of autophagy affects several aspects of mucosal immune responses. Autophagy is a cellular stress response that plays key roles in physiological processes, such as innate and adaptive immunity, adaptation to starvation, degradation of aberrant proteins or organelles, antimicrobial defense, and protein secretion. Dysfunctional autophagy is recognized as a contributing factor in many chronic inflammatory diseases, including IBD. Autophagy plays multiple roles in IBD pathogenesis by altering processes that include intracellular bacterial killing, antimicrobial peptide secretion by Paneth cells, goblet cell function, proinflammatory cytokine production by macrophages, antigen presentation by dendritic cells, and the endoplasmic reticulum stress response in enterocytes. Recent studies have identified susceptibility genes involved in autophagy, such as NOD2, ATG16L1, and IRGM, and active research is ongoing all over the world. The aim of this review is a systematic appraisal of the current literature to provide a better understanding of the role of autophagy in the pathogenesis of IBD. Understanding these mechanisms will bring about new strategies for the treatment and prevention of IBD.

关键词： Autophagy Inflammatory bowel disease Genome-wide association study Ulcerative colitis Crohn’s disease

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Heparin bridge therapy and post-polypectomy bleeding

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World Journal of Gastroenterology 2016年第45期22卷 10009-10014页

作者： Toshiyuki Kubo Kentaro Yamashita Kei Onodera Tomoya Iida Yoshiaki Arimura Masanori Nojima hiroshi nakase Department of Gastroenterology and Hepatology Sapporo Medical University Department of Gastroenterology Otaru City General Hospital Center for Translational Research the Institute of Medical Science the University of Tokyo

AIM To identify risk factors for post-polypectomy bleeding(PPB), focusing on antithrombotic agents. METHODS This was a case-control study based on medical records at a single center. PPB was defined as bleeding that occurred 6 h to 10 d after colonoscopic polypectomy and required endoscopic hemostasis. As risk factors for PPB, patient-related factors including anticoagulants, antiplatelets and heparin bridge therapy as well as polyp- and procedure-related factors were evaluated. All colonoscopic hot polypectomies, endoscopic mucosal resections and endoscopic submucosal dissections performed between January 2011 and December 2014 were reviewed. RESULTS PPB occurred in 29(3.7%) of 788 polypectomies performed during the study period. Antiplatelet or anticoagulant agents were prescribed for 210(26.6%)patients and were ceased before polypectomy except for aspirin and cilostazol in 19 cases. Bridging therapy using intravenous unfractionated heparin was adopted for 73 patients. The univariate analysis revealed that anticoagulants, heparin bridge, and anticoagulants plus heparin bridge were significantly associated with PPB(P < 0.0001) whereas antiplatelets and antiplatelets plus heparin were not. None of the other factors including age, gender, location, size, shape, number of resected polyps, prophylactic clipping and resection method were correlated with PPB. The multivariate analysis demonstrated that anticoagulants and anticoagulants plus heparin bridge therapy were significant risk factors for PPB(P < 0.0001). Of the 29 PPB cases, 4 required transfusions and none required surgery. A thromboembolic event occurred in a patient who took anticoagulant. CONCLUSION Patients taking anticoagulants have an increased risk of PPB, even if the anticoagulants are interrupted before polypectomy. Heparin-bridge therapy might be responsible for the increased PPB in patients taking anticoagulants.

关键词： Post-polypectomy 流血肝磷脂桥治疗结肠的 polypectomy 抗凝剂 Antiplatelets 内视镜的外科

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Insulin-like growth factor-1, IGF binding protein-3, and the risk of esophageal cancer in a nested case-control study

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World Journal of Gastroenterology 2017年第19期23卷 3488-3495页

作者： Yasushi Adachi Masanori Nojima Mitsuru Mori Kentaro Yamashita Hiro-o Yamano hiroshi nakase Takao Endo Kenji Wakai Kiyomi Sakata Akiko Tamakoshi Division of Gastroenterology Department of Internal MedicineSapporo Shirakaba-dai Hospital Department of Gastroenterology Sapporo Medical University The Institute of Medical Science Hospital The University of Tokyo Department of Public Health Sapporo Medical UniversitySchool of Medicine Department of Preventive Medicine Nagoya UniversityGraduate School of Medicine Department of Hygiene and Preventive Medicine Iwate Medical University School of Medicine Department of Public Health Hokkaido University School of Medicine

AIM To assess the relationship between serum levels of insulin-like growth factor-1(IGF1)/IGF-binding protein-3(IGFBP3)and the risk of esophageal *** We assessed the relationship between the serum levels of these molecules and the risk of esophageal cancer in a prospective,nested case-control study of participants from the Japan Collaborative Cohort Study.A baseline survey was conducted from 1988 to *** the 110585 enrolled participants,35%donated blood *** who had been diagnosed with esophageal cancer were considered cases for nested case-control studies.A conditional logistic model was used to estimate odds ratios for the incidence of esophageal cancer associated with serum IGF1 and IGFBP3 *** Thirty-one cases and 86 controls were eligible for the present *** molar ratio of IGF1/IGFBP3,which represents the free and active form of IGF1,was not correlated with the risk of esophageal carcinoma.A higher molar difference between IGFBP3and IGF1,which estimates the free form of IGFBP3,was associated with a decreased risk of esophageal carcinoma(P=0.0146),and people in the highest tertile had the lowest risk(OR=0.107,95%CI:0.017-0.669).After adjustment for body mass index,tobacco use,and alcohol intake,the molar difference of IGFBP3-IGF1 was inversely correlated with the risk of esophageal carcinoma(P=0.0150).CONCLUSION The free form of IGFBP3,which is estimated by this molar difference,may be inversely associated with esophageal cancer incidence.

关键词：食道的癌症像胰岛素的生长因素像胰岛素的生长因素绑定蛋白质嵌套的盒子控制学习机会比率

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Packet SS-CDMA Modem with Carrier Frequency Offset Compensation

Packet SS-CDMA Modem with Carrier Frequency Offset Compensat...

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IEEE第14届国际个人无线移动通信大会

作者： Atsuyoshi Yamaguchi Jun Takagi hiroshi Oguma Seong-Kweon Kim Suguru Kameda Hiroyuki nakase Yoji Isota Kazuo Tsubouchi Research Institute of Electrical Communication Tohoku University Katahira 2-1-1 Aoba-ku Sendai 980-8577 Japan Research Institute of Electrical Communication Tohoku University Katahira 2-1-1 Aoba-ku Sendai 980-8577 Japan Visiting researcher from Industrial Technology Institute Miyagi Prefectural GovernmentJapan. Research Institute of Electrical Communication Tohoku University Katahira 2-1-1 Aoba-ku Sendai 980-8577 Japan Research Institute of Electrical Communication Tohoku University Katahira 2-1-1 Aoba-ku Sendai 980-8577 Japan Research Institute of Electrical Communication Tohoku University Katahira 2-1-1 Aoba-ku Sendai 980-8577 Japan Research Institute of Electrical Communication Tohoku University Katahira 2-1-1 Aoba-ku Sendai 980-8577 Japan Research Institute of Electrical Communication Tohoku University Katahira 2-1-1 Aoba-ku Sendai 980-8577 Japan

We have proposed new carrier frequency offset compensation algorithm for packet spread-spectrum code- division multiple-access (SS-CDMA) system. For evaluation of carrier frequency offset, 11-chip

关键词： Packet SS-CDMA Carrier frequency offset Downlink

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