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| 1 | Combination of branched-chain amino acid and angiotensin?convertingenzyme inhibitor improves liver fibrosis progression in patients with cirrhosis显示文摘 | Hitoshi Yoshiji Ryuichi Noguchi Yasuhide Ikenaka Kosuke Kaji Yosuke Aihara Akitoshi Douhara Junichi Yamao Masahisa Toyohara Akira Mitoro Masayoshi Sawai Motoyuki Yoshida Chie Morioka Masao Fujimoto Masahito Uemura Hiroshi Fukui | 2012 | Molecular Medicine Reports2012，，： | 1 |
| 2 | Combination of sorafenib and angiotensin-II receptor blocker attenuates preneoplastic lesion development in a non-diabetic rat model of steatohepatitis显示文摘 | Hitoshi Yoshiji Ryuichi Noguchi Tadashi Namisaki Kei Moriya Mitsuteru Kitade Yosuke Aihara Akitoshi Douhara Hideto Kawaratani Norihisa Nishimura Hiroshi Fukui | 2014 | Journal of Gastroenterology2014，，： | 1 |
| 3 | The effect of inflammatory eytokines in alcoholic liver disease 显示文摘 | Kawaratani H Tsujimoto T Douhara A | 2013 | Mediators Inflamm2013，2013，49： | 1 |
| 4 | The effect of in- flammatory cytokines in alcoholic liver disease显示文摘 | Kawaratani H Tsujimoto T Douhara A | 2013 | Mediators of in- flammation2013，2013，49： | 1 |
| 5 | DNA methylation of angiotensin Ⅱ receptor gene in nonalcoholic steatohepatitis-related liver fibrosis显示文摘AIM To clarify whether Agtr1 a methylation is involved in the development of nonalcoholic steatohepatitis(NASH)-related liver fibrosis in adult rats.METHODS A choline-deficient amino acid(CDAA) diet model was employed for methylation analysis of NASH-related liver fibrosis.Agtr1 a methylation levels were measured in the livers of CDAA- and control choline-sufficient amino acid(CSAA)-fed rats for 8 and 12 wk using quantitative methylation-specific PCR.Hepatic stellate cells(HSCs) were isolated by collagenase digestion of the liver,followed by centrifugation of the crude cell suspension through a density gradient.Agtr1 a methylation and its gene expression were also analyzed during the activation of HSCs.RESULTS The mean levels of Agtr1 a methylation in the livers of CDAA-fed rats(11.5% and 18.6% at 8 and 12 wk,respectively) tended to be higher(P = 0.06 and 0.09,respectively) than those in the livers of CSAA-fed rats(2.1% and 5.3% at 8 and 12 wk,respectively).Agtr1 a was not methylated at all in quiescent HSCs,but was clearly methylated in activated HSCs(13.8%,P < 0.01).Interestingly,although Agtr1 a was hypermethylated,the Agtr1 a m RNA level increased up to 2.2-fold(P < 0.05) in activated HSCs compared with that in quiescent HSCs,suggesting that Agtr1 a methylation did not silence its expression but instead had the potential to upregulate its expression.These findings indicate that Agtr1 a methylation and its upregulation of gene expression are associated with the development of NASH-related liver fibrosis.CONCLUSION This is the first study to show that DNA methylation is potential y involved in the regulation of a renin-angiotensin system-related gene expression during liver fibrosis. | Kiyoshi Asada Yosuke Aihara Hiroaki Takaya Ryuichi Noguchi Tadashi Namisaki Kei Moriya Masakazu Uejima Mitsuteru Kitade Tsuyoshi Mashitani Kosuke Takeda Hideto Kawaratani Yasushi Okura Kosuke Kaji Akitoshi Douhara Yasuhiko Sawada Norihisa Nishimura Kenichiro Seki Akira Mitoro Junichi Yamao Hitoshi Yoshiji | 2016 | World Journal of Hepatology2016，8，28： | 1 |
| 6 | Branched-chain amino acids suppress the cumulative recurrence of hepatocellularcarcinoma under conditions of insulin-resistance显示文摘 | Hitoshi Yoshiji Ryuichi Noguchi Tadashi Namisaki Kei Moriya Mitsuteru Kitade Yosuke Aihara Akitoshi Douhara Junichi Yamao Masao Fujimoto Masahisa Toyohara Akira Mitoro Masayoshi Sawai Motoyuki Yoshida Chie Morioka Masakazu Uejima Masahito Uemura Hiroshi F | 2013 | Oncology Reports2013，，2： | 1 |
| 7 | Reduction of endotoxin attenuates liver fibrosis through suppressionof hepatic stellate cell activation and remission of intestinal permeability ina rat non-alcoholic steatohepatitis model显示文摘 | Akitoshi Douhara Kei Moriya Hitoshi Yoshiji Ryuichi Noguchi Tadashi Namisaki Mitsuteru Kitade Kosuke Kaji Yosuke Aihara Norihisa Nishimura Kosuke Takeda Yasushi Okura Hideto Kawaratani Hiroshi Fukui | 2015 | Molecular Medicine Reports2015，，3： | 1 |
| 8 | Direct renin inhibitor, aliskiren, attenuates the progression of non‐alcoholic steatohepatitis in the rat model显示文摘 | Yosuke Aihara Hitoshi Yoshiji Ryuichi Noguchi Kosuke Kaji Tadashi Namisaki Yusaku Shirai Akitoshi Douhara Kei Moriya Hideto Kawaratani Hiroshi Fukui | 2013 | Hepatol Res2013，，11： | 1 |
| 9 | Cholangiocarcinoma developed in a patient with IgG4-related disease显示文摘A 77-year-old man with jaundice and a pancreatic head tumor was referred to our hospital in August2006.The initial laboratory tests,computed tomography(CT)scan,magnetic resonance imaging(MRI),and endoscopic retrograde cholangiopancreatography suggested IgG4-related cholangitis and autoimmune pancreatitis.Oral prednisolone(PSL)was then administered.This treatment reduced the size of the pancreatic parenchyma,and the lower common bile duct(CBD)returned to its normal size.Thus,the oral PSL was gradually tapered to a maintenance dose.In February 2010,a CT scan and MRI showed segmental wall thickening and stenosis of the middle CBD,the progression of which led to extrahepatic obstructive jaundice.We suspected the emergence of a cholangiocarcinoma rather than the exacerbation of the IgG4-related sclerosing cholangitis because the stricture of the CBD was short and localized.Then,a percutaneous transhepatic biliary drainage was performed.The biopsy specimens obtained via the percutaneous transhepatic tract indicated an abnormal glandular formation,suggesting the presence of a moderate,well-differencated adenocarcinoma.The gross examination,microscopic examination and immunohistochemical analysis of the pancreaticoduodenectomy specimen suggested that a cholangiocarcinoma developed from the IgG4-related sclerosing cholangitis. | Akitoshi Douhara Akira Mitoro Emi Otani Masanori Furukawa Kosuke Kaji Masakazu Uejima Masayoshi Sawai Motoyuki Yoshida Hitoshi Yoshiji Junichi Yamao Hiroshi Fukui | 2013 | World Journal of Gastrointestinal Oncology2013，5，8： | 0 |
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