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| 1 | 在不影响人足细胞(前)肾素受体信号下,阿利吉仑能抑制细胞内血管紧张素Ⅱ水平显示文摘 | Sakoda M Ichihara A Kurauchi-Mito A Narita T Kinou-chi K Murohashi-Bokuda K Saleem MA Nishiyama A Suzuki F Itoh H 黄晓斌 | 2010 | 中华高血压杂志2010，18，7： | 18 |
| 2 | Induction of Pluripotent Stem Cells from Adult Human Fibroblasts by Defined Factors显示文摘 | Kazutoshi Takahashi Koji Tanabe Mari Ohnuki Megumi Narita Tomoko Ichisaka Kiichiro Tomoda Shinya Yamanaka | 2007 | Cell2007，，5： | 11 |
| 3 | Excessive portal flow causes graft failure in extremely small-for-size liver transplantation in pigs显示文摘AIM: To evaluate the effects of a portocaval shunt on the decrease of excessive portal flow for the prevention of sinusoidal microcirculatory injury in extremely smallfor-size liver transplantation in pigs.METHODS: The right lateral lobe of pigs, i.e. the 25%of the liver, was transplanted orthotopically. The pigs were divided into two groups: graft without portocaval shunt (n = 11) and graft with portocaval shunt (n=11).Survival rate, portal flow, hepatic arterial flow, and histological findings were investigated.RESULTS: In the group without portocaval shunt, all pigs except one died of liver dysfunction within 24 h after transplantation. In the group with portocaval shunt,eight pigs survived for more than 4 d. The portal flow volumes before and after transplantation in the group without portocaval shunt were 118.2±26.9 mL/min/100 g liver tissue and 270.5±72.9 mL/min/100 g liver tissue,respectively. On the other hand, in the group with portocaval shunt, those volumes were 124.2±27.8 mL/min/100 g liver tissue and 42.7±32.3 mL/min/100 g liver tissue, respectively (P<0.01). As for histological findings in the group without portocaval shunt, destruction of the sinusoidal lining and bleeding in the peri-portal areas were observed after reperfusion, but these findings were not recognized in the group with portocaval shunt.CONCLUSION: These results suggest that excessive portal flow is attributed to post transplant liver dysfunction after extreme small-for-size liver transplantation caused by sinusoidal microcirculatory injury. | Hong-Sheng Wang Nobuhiro Ohkohchi Yoshitaka Enomoto Masahiro Usuda Shigehito Miyagi Takeshi Asakura Hiroo Masuoka Takashi Aiso Keisuke Fukushima Tomohiro Narita Hideyuki Yamaya Atsushi Nakamura Satoshi Sekiguchi Naoki Kawagishi Akira Sato Susumu Satomi | 2005 | World Journal of Gastroenterology2005，11，44： | 8 |
| 4 | Axonal remodeling in the corticospinal tract after stroke: how does rehabilitative training modulate it?显示文摘Stroke causes long-term disability, and rehabilitative training is commonly used to improve the consecutive functional recovery. Following brain damage, surviving neurons undergo morphological alterations to reconstruct the remaining neural network. In the motor system, such neural network remodeling is observed as a motor map reorganization. Because of its significant correlation with functional recovery, motor map reorganization has been regarded as a key phenomenon for functional recovery after stroke. Although the mechanism underlying motor map reorganization remains unclear, increasing evidence has shown a critical role for axonal remodeling in the corticospinal tract. In this study, we review previous studies investigating axonal remodeling in the corticospinal tract after stroke and discuss which mechanisms may underlie the stimulatory effect of rehabilitative training. Axonal remodeling in the corticospinal tract can be classified into three types based on the location and the original targets of corticospinal neurons, and it seems that all the surviving corticospinal neurons in both ipsilesional and contralesional hemisphere can participate in axonal remodeling and motor map reorganization. Through axonal remodeling, corticospinal neurons alter their output selectivity from a single to multiple areas to compensate for the lost function. The remodeling of the corticospinal axon is influenced by the extent of tissue destruction and promoted by various therapeutic interventions, including rehabilitative training. Although the precise molecular mechanism underlying rehabilitation-promoted axonal remodeling remains elusive, previous data suggest that rehabilitative training promotes axonal remodeling by upregulating growth-promoting and downregulating growth-inhibiting signals. | Naohiko Okabe Kazuhiko Narita Osamu Miyamoto | 2017 | Neural Regeneration Research2017，12，2： | 8 |
| 5 | Induction of Pluripotent Stem Cells from Adult Human Fibroblasts by Defined Factors显示文摘 | Kazutoshi Takahashi Koji Tanabe Mari Ohnuki Megumi Narita Tomoko Ichisaka Kiichiro Tomoda Shinya Yamanaka | 2007 | Cell2007，，5： | 7 |
| 6 | Bisphenol A in combination with TNF-a selectively induces Th2 cell-promoting dendritic cells in vitro with an estrogen-like activity显示文摘Bisphenol A(BPA)is a monomer used in manufacturing a wide range of chemical products,including epoxy resins and polycarbonate.BPA,an important endocrine disrupting chemical that exerts estrogen-like activities,is detectable at nanomolar levels in human serum worldwide.The pregnancy associated doses of 17b-estradiol(E2)plus tumor-necrosis factor-a(TNF-a)induce distorted maturation of human dendritic cells(DCs)that result in an increased capacity to induce T helper(Th)2 responses.The current study demonstrated that the presence of BPA during DC maturation influences the function of human DCs,thereby polarizing the subsequent Th response.In the presence of TNF-a,BPA treatment enhanced the expression of CC chemokine ligand 1(CCL1)in DCs.In addition,DCs exposed to BPA/TNF-a produced higher levels of IL-10 relative to those of IL-12p70 on CD40 ligation,and preferentially induced Th2 deviation.BPA exerts the same effect with E2 at the same dose(0.01–0.1 mM)with regard to DC-mediated Th2 polarization.These findings imply that DCs exposed to BPA will provide one of the initial signals driving the development and perpetuation of Th2-dominated immune response in allergic reactions. | Hongchuan Guo Tianyi Liu Yasushi Uemura Shunchang Jiao Deqing Wang Zilin Lin Yayoi Narita Motoharu Suzuki Narumi Hirosawa Yasuko Ichihara Osamu Ishihara Hirosato Kikuchi Yasushi Sakamoto Satoru Senju Qiuhang Zhang Feng Ling | 2010 | Cellular & Molecular Immunology2010，7，3： | 6 |
| 7 | 熔融沉积法制备纤维素纳米纤维增强聚乳酸基复合材料的拉伸性能显示文摘生物可降解聚合物可以在保持结构力学性能的同时可以实现碳中性,是石油基聚合物的潜在替代品。在这些聚合物中,聚乳酸(Polylactic acid,PLA)因其良好的力学性能、生物相容性和热塑性而特别有发展前景。本文利用机械脱脂纤维素纳米纤维(Cellulose nanofiber,CNF)来提高聚乳酸的力学性能,该纤维具有显著的力学性能和生物降解性。熔融沉积建模(Fused deposition modeling,FDM)是热塑性聚合物的三维打印方法之一,可以降低制造成本。本研究采用FDM法制备了机械脱脂CNF增强PLA基复合材料,并在两个打印方向(0°/90°和+45°/-45°)上研究了它们的拉伸性能,梳理了机械制备CNF增强PLA基复合材料的印刷方向与拉伸行为之间的关系。此外,利用扫描电镜研究了机械脱脂CNF增强PLA基复合材料的显微组织和断口。 | KURITA Hiroki BERNARD Chrystelle LAVROVSKY Agathe NARITA Fumio | 2021 | Transactions of Nanjing University of Aeronautics and Astronautics2021，38，1： | 5 |
| 8 | Pathogenesis of extrapulmonary manifestations of Mycoplasma pneumoniae infection with special reference to pneumonia显示文摘 | Mitsuo Narita | 2010 | Journal of Infection and Chemotherapy2010，，3： | 3 |
| 9 | Summary of Environmental Impact Assessment for Mining Seafloor Massive Sulfides in Japan显示文摘 | Teruyoshi Narita Junya Oshika Nobuyuki Okamoto Tetsuhiko Toyohara Tetsuya Miwa | 2015 | Journal of Shipping and Ocean Engineering2015，5，3： | 3 |
| 10 | Is branched-chain amino acid nutritional supplementation beneficial or detrimental in heart failure?显示文摘Sarcopenia or cachexia is often complicated in heart failure.Nutritional support,particularly branched-chain amino acid(BCAA)supplementation,is a candidate treatment for improving sarcopenia or cachexia in elderly patients.However,the efficacy of BCAA supplementation in patients with heart failure has not been established,and the issue is comparatively more complex.Indeed,there are conflicting reports on the efficacy of BCAA supplementation.The evidence for including BCAA supplementation in treating patients with heart failure was reviewed,and the complexity of the issue was discussed. | Koichi Narita Eisuke Amiya | 2021 | World Journal of Cardiology2021，13，6： | 3 |
| 11 | 家庭血压的季节性变化及其与靶器官损害的关系:日本晨峰-家庭血压研究显示文摘已有研究报道,冬季家庭血压的季节性变化很大,但家庭血压的季节性差异及其与靶器官损害(target organ damage, TOD)的关系仍不清楚。方法:该横断面研究采用日本晨峰-家庭血压(Japan morning surge-home blood pressure, J-HOP)研究的数据,以评估家庭血压的季节差异、隐蔽性高血压(诊室血压<140/90和家庭血压≥135/85 mm Hg。 | Narita K Hoshide S Fujiwara T Kanegae H Kariol K | 2021 | 中华高血压杂志2021，29，5： | 2 |
| 12 | Pretreatment AKR1B10 expression predicts the risk of hepatocellular carcinoma development after hepatitis C virus eradication显示文摘AIM To clarify the association between aldo-keto reductase family 1 member B10(AKR1B10) expression and hepatocarcinogenesis after hepatitis C virus eradication.METHODS In this study,we enrolled 303 chronic hepatitis C patients who had achieved sustained virological response(SVR) through interferon-based antiviral therapy. Pretreatment AKR1B10 expression in the liver was immunohistochemically assessed and quantified as a percentage of positive staining area by using image-analysis software. A multivariate Cox analysis was used to estimate the hazard ratios(HRs) of AKR1B10 expression for hepatocellular carcinoma(HCC) development after achieving SVR. The cumulative incidences of HCC development were evaluated using Kaplan-Meier analysis and the log-rank test.RESULTS Of the 303 chronic hepatitis C patients,153(50.5%) showed scarce hepatic AKR1B10 expression,quantified as 0%,which was similar to the expression in control normal liver tissues. However,the remaining 150 patients(49.5%) exhibited various degrees of AKR1B10 expression in the liver,with a maximal AKR1B10 expression of 73%. During the median follow-up time of 3.6 years(range 1.0-10.0 years),8/303 patients developed HCC. Multivariate analysis revealed that only high AKR1B10 expression(≥ 8%) was an independent risk factor for HCC development(HR = 15.4,95%CI: 1. 8- 1 3 2. 5,P = 0. 0 1 2). T h e 5- y e a r c u m u l a t i v e incidences of HCC development were 13.7% and 0.5% in patients with high and low AKR1B10 expression,respectively(P < 0.001). During the follow-up period after viral eradication,patients expressing high levels of AKR1B10 expressed markedly higher levels of alanine aminotransferase and α-fetoprotein than did patients exhibiting low AKR1B10 expression.CONCLUSION Chronic hepatitis C patients expressing high levels of hepatic AKR1B10 had an increased risk of HCC development even after SVR. | Ayato Murata Takuya Genda Takafumi Ichida Nozomi Amano Sho Sato Hironori Tsuzura Shunsuke Sato Yutaka Narita Yoshio Kanemitsu Yuji Shimada Katsuharu Hirano Katsuyori Iijima Ryo Wada Akihito Nagahara Sumio Watanabe | 2016 | World Journal of Gastroenterology2016，22，33： | 2 |
| 13 | Mesenchymal stem cells for treatment of aortic aneurysms显示文摘An aortic aneurysm(AA) is a silent but life-threatening disease that involves rupture. It occurs mainly in aging and severe atherosclerotic damage of the aortic wall. Even though surgical intervention is effective to prevent rupture, surgery for the thoracic and thoraco-abdom-inal aorta is an invasive procedure with high mortality and morbidity. Therefore, an alternative strategy for treatment of AA is required. Recently, the molecular pathology of AA has been clarified. AA is caused by an imbalance between the synthesis and degradation of extracellular matrices in the aortic wall. Chronic inflam-mation enhances the degradation of matrices directly and indirectly, making control of the chronic inflamma-tion crucial for aneurysmal development. Meanwhile, mesenchymal stem cells(MSCs) are known to be ob-tained from an adult population and to differentiate into various types of cells. In addition, MSCs have not only the potential anti-inflammatory and immunosuppres-sive properties but also can be recruited into damagedtissue. MSCs have been widely used as a source for celltherapy to treat various diseases involving graft-versus-host disease, stroke, myocardial infarction, and chronicinflammatory disease such as Crohn's disease clinically.Therefore, administration of MSCs might be availableto treat AA using anti-inflammatory and immnosup-pressive properties. This review provides a summary ofseveral studies on 'Cell Therapy for Aortic Aneurysm'including our recent data, and we also discuss the pos-sibility of this kind of treatment. | Aika Yamawaki-Ogata Ryotaro Hashizume Xian-Ming Fu Akihiko Usui Yuji Narita | 2014 | World Journal of Stem Cells2014，6，3： | 2 |
| 14 | JNK contributes to temozolomide resistance of stem-like glioblastomacells via regulation of MGMT expression显示文摘 | Masashi Okada Atsushi Sato Keita Shibuya Eriko Watanabe Shizuka Seino Shuhei Suzuki Manabu Seino Yoshitaka Narita Soichiro Shibui Takamasa Kayama Chifumi Kitanaka | 2014 | International Journal of Oncology2014，，2： | 2 |
| 15 | Differentiating a large abdominal cystic lymphangioma from multicystic mesothelioma: report of a case显示文摘 | Hiroshi Nagata Yutaka Yonemura Emel Canbay Haruaki Ishibashi Makoto Narita Makio Mike Nobuyasu Kano | 2014 | Surgery Today2014，，7： | 2 |
| 16 | 高脂饮食诱导的巨噬细胞抑制因子-1通过激活肿瘤间质细胞产生促肿瘤细胞因子促进前列腺癌的进展显示文摘背景与目的 最近研究表明高脂饮食(high-fat diet,HFD)和/或HFD诱导的肥胖可影响前列腺癌(prostate cancer,PCa)的进展,但HFD在PCa微环境中的作用尚不清楚。本研究旨在阐明HFD环境下PCa进展的分子机制,描述以巨噬细胞抑制因子-1(macrophage inhibitory cytokine-1,MIC-1)活性为主的肿瘤间质微环境的特征。方法 我们利用HFD或正常饮食的PC-3M-luc-C6 PCa小鼠模型,研究了HFD对PCa间质微环境和MIC-1信号活性的影响。我们分离了原发PCa患者来源的前列腺周围脂肪细胞,并研究了其对前列腺间质成纤维细胞活性及其分泌细胞因子的影响。进一步研究了MIC-1信号的表达模式及其对人PCa间质活性和肿瘤进展的影响。结果 在PC-3M-luc-C6 PCa小鼠模型中,HFD通过上调前列腺间质成纤维的MIC-1信号通路活性,增加了白介素(interleukin,IL)-8和IL-6的分泌,促进了PCa细胞的生长和侵袭。另外,前列腺周围脂肪细胞通过增加脂肪分解和游离脂肪酸的释放,直接促进了PC-3细胞产生MIC-1和前列腺间质成纤维细胞分泌IL-8。前列腺癌患者血清MIC-1水平增高与人PCa间质活性、高血清IL-8、IL-6水平、脂肪酶高活性、PCa患者疾病进展及高体重指数具有显著相关性。胶质细胞源性神经营养因子受体α(glial-derived neurotrophic factor receptor α-like,GFL)是MIC-1的特异性受体,在PCa细胞和癌周间质成纤维细胞中都出现高表达,雄激素去势治疗和化疗都降低了其表达水平。结论 HFD通过增加游离脂肪酸水平,在代谢水平上调了MIC-1信号活性,从而激活了PCa间质微环境,这可能是HFD和/或脂肪诱导的PCa进展的关键机制。 | Mingguo Huang Shintaro Narita Atsushi Koizumi Taketoshi Nara Kazuyuki Numakura Shigeru Satoh Hiroshi Nanjo Tomonori Habuchi | 2022 | 癌症2022，41，2： | 2 |
| 17 | Etiology and prognostic significance of severe uremic pruritus in chronic hemodialysis patients显示文摘 | Narita I Alchi B Omori K | 2006 | Kidney Int2006，69，： | 1 |
| 18 | Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy显示文摘 | Mofii T Fujita H Narita T | 2003 | J Diab Compl2003，17，1： | 1 |
| 19 | Formation and atomic structures of BnNn (n=24-60) clusters studied by mass spectrometry,high-resolution electron microscopy and molecular orbital calculations显示文摘 | Atsushi Nishiwaki Ichihito Narita | 2004 | Physics B 20042004，，： | 1 |
| 20 | Cancer cells expressing Toll-like receptors and the tumor microenvironment显示文摘 | SATO Y GOTO Y NARITA N | 2009 | Cancer Microenviron2009，1，： | 1 |
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