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| 1 | Effects of adacolumn selective leukocytapheresis on plasma cytokines during active disease in patients with active ulcerative colitis显示文摘瞄准:调查在临床的活动索引的 ulcerative (UC )( 蔡) 和 IL-1ra, IL-10, IL-6 和 IL-18 的传播层次之间的关系。方法:IL-1ra, IL-10, IL-6 和 IL-18 的血层次与活跃 UC 在 31 个病人被测量,吝啬的蔡是 11.1,从 5-25 ;并且是的 12 个健康个人控制。病人们与 Adacolumn 被给粒细胞和单核白血球 adsorptive 词首字母的脱落(GMA ) 。忍受 FcgammaR 并且补充受体的白细胞被吸附到列 leucocytapheresis 搬运人。每个病人能在 8 wk 上收到多达 11 个 GMA 会议。结果:我们发现了在蔡和 IL-10 之间的强壮的关联(r = 0.827, P <
0.001 ) , IL-6 (r = 0.785, P <
0.001 ) 并且 IL-18 (r = 0.791, P <
0.001 ) 。IL-1ra 没与蔡一起被相关。后面的 GMA 治疗, 31 个病人中的 24 个完成了宽恕,所有 4 cytokines 的层次掉在健康控制里到层次。进一步, IL-1ra 和 IL-10 的血层次在从遵守了搬运人的白细胞建议版本的 60 min 在列流出和流入增加了。 | Hiroyuki Hanai Takayuki Iida Masami Yamada Yoshihiko Sato Ken Takeuchi Tatsuo Tanaka Kenji Kondo Masataka Kikuyama Yasuhiko Maruyama Yasushi Iwaoka Akiko Nakamura Kazuhisa Hirayama Abby R Saniabadi Fumitoshi Watanabe | 2006 | World Journal of Gastroenterology2006，12，21： | 8 |
| 2 | Association between Diabetes Mellitus and Oral Health Status in Japanese Adults显示文摘Aim The objective of this study was to analyze the oral health among Japanese adults, with and without diabetes mellitus. Methodology The subjects were 518 community residents aged 20 to 91 years in Japan, who participated in the 'Akita health and nutrition survey' and the 'Akita dental disease survey', conducted in 2006. The surveys comprised a self-administered questionnaire, along with medical and dental examinations. Results Using the community periodontal index (CPI), the mean numbers of sextants presenting codes 0, 1 and 2 were significantly lower in diabetics than non-diabetics among the 59 years or younger age group. Although the mean numbers of sextants with codes 0, 1 and 2 among the 60 to 69 years age group were lower, and sextants with a code X among the 59 years or younger age group were higher in diabetics than non-diabetics, no statistically significant differences were detected. The tendency of lower mean numbers of natural teeth and functional tooth units in diabetics than non-diabetics was observed, however no differences were statistically significant. Conclusion The outcome of periodontal disease seemed to be influenced by the diabetic state to some degree, but a clear association between diabetes and oral health status was not found. | Masayuki Ueno Susumu Takeuchi Akiko Oshiro Kayoko Shinada Satoko Ohara Yoko Kawaguchi | 2010 | International Journal of Oral Science2010，2，2： | 6 |
| 3 | Involvement of the TAGE-RAGE system in non-alcoholic steatohepatitis: Novel treatment strategies显示文摘Non-alcoholic fatty liver disease(NAFLD)is a major cause of liver disease around the world.It includes a spectrum of conditions from simple steatosis to non-alcoholic steatohepatitis(NASH)and can lead to fibrosis,cirrhosis,liver failure,and/or hepatocellular carcinoma.NAFLD is also associated with other medical conditions such as obesity,diabetes mellitus(DM),metabolic syn-drome,hypertension,insulin resistance,hyperlipidemia,and cardiovascular disease(CVD).In diabetes,chronic hyperglycemia contributes to the development of both macro-and microvascular conditions through a variety of metabolic pathways.Thus,it can cause a variety of metabolic and hemodynamic conditions,including upregulated advanced glycation end-products(AGEs)synthesis.In our previous study,the most abundant type of toxic AGEs(TAGE);i.e.,glyceraldehyde-derived AGEs,were found to make a significant contribution to the pathogenesis of DM-induced angiopathy.Furthermore,accumulating evidence suggests that the binding of TAGE with their receptor(RAGE)induces oxidative damage,promotes inflammation,and causes changes in intracellular signaling and the expression levels of certain genes in various cell populations including hepatocytes and hepatic stellate cells.All of these effects could facilitate the pathogenesis of hypertension,cancer,diabetic vascular complications,CVD,dementia,and NASH.Thus,inhibiting TAGE synthesis,preventing TAGE from binding to RAGE,and downregulating RAGE expression and/or the expression of associated effector molecules all have potential as therapeutic strategies against NASH.Here,we examine the contributions of RAGE and TAGE to various conditions and novel treatments that target them in order to prevent the development and/or progression of NASH. | Masayoshi Takeuchi Jun-ichi Takino Akiko Sakasai-Sakai Takanobu Takata Tadashi Ueda Mikihiro Tsutsumi Hideyuki Hyogo Sho-ichi Yamagishi | 2014 | World Journal of Hepatology2014，6，12： | 5 |
| 4 | Contribution of the toxic advanced glycation end-productsreceptor axis in nonalcoholic steatohepatitis-related hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC) is one of the most common malignancies worldwide. The main etiologies of HCC are hepatitis B virus and hepatitis C virus(HCV), and non-hepatitis B/non-hepatitis C HCC(NBNCHCC) has also been identified as an etiological factor. Although the incidence of HCV-related HCC in Japan has decreased slightly in recent years, that of NBNC-HCC has increased. The onset mechanism of NBNC-HCC, which has various etiologies, remains unclear; however, nonalcoholic steatohepatitis(NASH), a severe form of nonalcoholic fatty liver disease, is known to be an important risk factor for NBNC-HCC. Among the different advanced glycation end-products(AGEs) formed by the Maillard reaction, glyceraldehyde-derived AGEs, the predominant components of toxic AGEs(TAGE), have been associated with NASH and NBNC-HCC, including NASH-related HCC. Furthermore, the expression of the receptor for AGEs(RAGE) has been correlated with the malignant progression of HCC. Therefore, TAGE induce oxidative stress by binding with RAGE may, in turn, lead to adverse effects, such as fibrosis and malignant transformation, in hepatic stellate cells and tumor cells during NASH or NASH-related HCC progression. The aim of this review was to examine the contribution of the TAGE-RAGE axis in NASH-related HCC. | Jun-ichi Takino Kentaro Nagamine Takamitsu Hori Akiko Sakasai-Sakai Masayoshi Takeuchi | 2015 | World Journal of Hepatology2015，7，23： | 4 |
| 5 | Cross-regulation of the Nanog and Cdx2 promoters显示文摘在哺乳动物的胚胎,内部房间团(ICM ) 的分离和 trophectoderm (TE ) 的第一种房间命运选择,,被抄写因素, Oct4 和 Cdx2 的互相对抗的效果调整 pluripotency 因素, Nanog,是必要的指定 epiblast。我们分析了 Nanog 和 Cdx2 的倡导者,并且发现了这二个抄写因素同样相互地被调整。用有有条件的 TE 区别的一根胚胎的干细胞线,我们证明 Nanog overexpression 压制 TE 标记的 upregulation,当时 Nanog 击倒的 upregulates TE 标记的表示。我们推进 Nanog 和 Cdx2 绑在并且镇压的表演对方的倡导者。而 Nanog 大美人在 ICM 导致可检测的 Cdx2 表示,我们不管多么不观察胚囊开发的公开混乱,显示 Nanog 起到在 ICM 和 TE 的分离的 Oct4 的一个谄媚的作用。 | Lingyi Chen Akiko Yabuuchi Sarah Eminli Ayumu Takeuchi Chi-Wei Lu Konrad Hochedlinger George Q Daley | 2009 | Cell Research2009，19，9： | 3 |
| 6 | Tenascin-C is upregulated in the skin lesions of patients with atopic dermatitis显示文摘 | Kaoru Ogawa Mikito Ito Kaori Takeuchi Akiko Nakada Masayuki Heishi Hajime Suto Kouichi Mitsuishi Yuji Sugita Hideoki Ogawa Chisei Ra | 2005 | Journal of Dermatological Science2005，，： | 1 |
| 7 | Preparation of dense LiFePO4/C composite positive electrodes using spark-plasma-sintering process显示文摘 | Tomonari Takeuchi Mitsuharu Tabuchi Akiko Nakashima | 2005 | Journal of Power Sources2005，146，12： | 1 |
| 8 | Development of CZTS-based thin film solar cells显示文摘 | Hironori Katagiri Kazuo Jimbo Win Shwe Maw Koichiro Oishi Makoto Yamazaki Hideaki Araki Akiko Takeuchi | 2008 | Thin Solid Films2008，，7： | 1 |
| 9 | Preparation of dense LiFePO4/C composite positive electrodes using spark-plasma-sintering process显示文摘 | Tomonari Takeuchi Mitsuharu Tabuchi Akiko Nakashima | 2005 | Journal of Power Sources2005，46，： | 1 |
| 10 | Imperfection - senstive overall buckling of single - layer latticed domes 显示文摘 | Seishi Yamada Akiko Takeuchi Yoshiyuki Tada | 2001 | Journal of Engineering Mechanics2001，，4： | 1 |
| 11 | Upregulation of Nitric Oxide Production in Vascular Endothelial Cells by All-trans Retinoic Acid Through the Phosphoinositide 3-Kinase/Akt Pathway显示文摘 | Akira Uruno Akira Sugawara Hiroshi Kanatsuka Hiroyuki Kagechika Akiko Saito Kazunori Sato Masataka Kudo Kazuhisa Takeuchi Sadayoshi Ito | 2005 | Circulation2005，，5： | 1 |
| 12 | Preparation of dense LiFePO4/C composite positive electrodes using spark - plasma - sintering process 显示文摘 | Tomonari Takeuchi Mitsuharu Tabuchi Akiko Nakashi- ma | 2005 | Journal of Power Sources2005，46，： | 1 |
| 13 | Generation of glyceraldehyde-derived advanced glycation end-products in pancreatic cancer cells and the potential of tumor promotion显示文摘AIM To determine the possibility that diabetes mellitus promotes pancreatic ductal adenocarcinoma via glyceraldehyde(GA)-derived advanced glycation-end products(GA-AGEs).METHODS PANC-1,a human pancreatic cancer cell line,was treated with 1-4 mmol/L GA for 24 h. The cell viability and intracellular GA-AGEs were measured by WST-8 assay and slot blotting. Moreover,immunostaining of PANC-1 cells with an anti-GA-AGE antibody was performed. Western blotting(WB) was used to analyze the molecular weight of GA-AGEs. Heat shock proteins 90α,90β,70,27 and cleaved caspase-3 were analyzed by WB. In addition,PANC-1 cells were treated with GA-AGEs-bovine serum albumin(GA-AGEs-BSA),as a model of extracellular GA-AGEs,and proliferation of PANC-1 cells was measured.RESULTS In PANC-1 cells,GA induced the production of GA-AGEs and cell death in a dose-dependent manner. PANC-1 cell viability was approximately 40% with a 2 mmol/L GA treatment and decreased to almost 0% with a 4 mmol/L GA treatment(each significant difference was P < 0.01). Cells treated with 2 and 4 mmol/L GA produced 6.4 and 21.2 μg/mg protein of GA-AGEs,respectively(P <0.05 and P < 0.01). The dose-dependent production of some high-molecular-weight(HMW) complexes of HSP90β,HSP70,and HSP27 was observed following administration of GA. We considered HMW complexes to be dimers and trimers with GA-AGEs-mediated aggregation. Cleaved caspase-3 could not be detected with WB. Furthermore,10 and 20 μg/m L GA-AGEs-BSA was 27% and 34% greater than that of control cells,respectively(P < 0.05 and P < 0.01).CONCLUSION Although intracellular GA-AGEs induce pancreatic cancer cell death,their secretion and release may promote the proliferation of other pancreatic cancer cells. | takanobu takata tadashi ueda akiko sakasai-sakai masayoshi takeuchi | 2017 | World Journal of Gastroenterology2017，23，27： | 0 |
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