|1.||Yoshiji, Hitoshi: 8 articles (03/2015 - 07/2002)|
|2.||Fukui, Hiroshi: 8 articles (03/2015 - 07/2002)|
|3.||Noguchi, Ryuichi: 7 articles (03/2015 - 07/2002)|
|4.||Tsujiuchi, Toshifumi: 7 articles (10/2011 - 02/2002)|
|5.||Namisaki, Tadashi: 6 articles (03/2015 - 07/2003)|
|6.||Sakaida, Isao: 6 articles (06/2013 - 02/2004)|
|7.||Konishi, Yoichi: 6 articles (02/2007 - 02/2002)|
|8.||Kaji, Kosuke: 5 articles (03/2015 - 11/2007)|
|9.||Kitade, Mitsuteru: 5 articles (03/2015 - 11/2007)|
|10.||Seki, Ekihiro: 5 articles (02/2014 - 10/2009)|
05/05/2015 - "In conclusion, ipragliflozin prevented hepatic TG accumulation and fibrosis in CDAA-diet rats. "
01/01/2014 - "At 1-3 months, extensive steatosis and fibrosis were observed in CDAA and CDAA+CCl4 groups. "
10/01/2013 - "NOX2(-/-) mice on the CDAA or WD had no significant change in Sirt1, Timp3, and TACE activity or the fibrosis markers assessed. "
05/01/2013 - "In contrast, fibrosis remained even after the recovery period, to an extent similar to that in continuously CDAA-fed animals. "
11/01/1998 - "These results indicate that pre-existing fibrosis with the activated stellate cells accelerates the development of preneoplastic lesions in a CDAA diet model."
01/01/2013 - "In vivo experiments showed that treatment with MIYAIRI 588 reduced CDAA-diet-induced hepatic lipid deposition and significantly improved the triglyceride content, insulin resistance, serum endotoxin levels, and hepatic inflammatory indexes. "
01/01/2014 - "CDAA-treated mice showed peripheral insulin resistance at 1 month. "
07/01/2010 - "TLR9(-/-), IL-1R(-/-), and MyD88(-/-) mice had less insulin resistance than WT mice on the CDAA diet. "
07/01/2010 - "The CDAA diet induced NASH in WT mice, characterized by steatosis, inflammation, fibrosis, and insulin resistance. "
01/01/2014 - "the CDAA model promotes the development of HCC from NAFLD-NASH in the presence of insulin resistance but in the absence of cirrhosis. "
|3.||Body Weight (Weight, Body)
10/01/2000 - "The numbers of GST-P-positive lesions demonstrated significant increment with 1200 mg/kg body weight of BHP by CDAA diet administered only after BHP and, to a significantly greater degree, by the diet administered both before and after BHP. "
10/01/2000 - "In a dose response study, rats received vechicle or DEN, at a dose of 0.001, 0.01, 0.1, 1, 10, 20, 50, 100 or 200 mg/kg body weight, 1 week after the commencement of CSAA or CDAA diet, and sacrificed 8 weeks after vehicle or DEN. "
10/01/2000 - "While CDAA diet administered only after BHP did not alter the sizes of GST-P-positive lesions, the diet administered both before and after 600 and 1200 mg/kg body weight of BHP significantly increased the sizes of the lesions. "
10/01/2000 - "Sizes became significantly larger with only 200 mg/kg body weight of DEN in the CSAA case but with 50-200 mg/kg in the CDAA case. "
10/01/2000 - "The significant increases of the numbers of GST-P-positive lesions were obtained after 50-200 mg/kg body weight of DEN under the CSAA diet administration, whereas those were detected after 10-200 mg/kg under CDAA diet administration. "
03/01/1996 - "None of the inhibitors affected the development of fatty liver caused by the CDAA diet. "
02/01/2013 - "WT mice on the CDAA diet developed profound steatohepatitis and liver fibrosis. "
11/21/2008 - "The serum and liver levels of TNF-alpha in the CDAA-fed rats increased significantly as compared with the control group, as did the immunohistochemical values and gene expressions of TNF-alpha, TLR4, and CD14 with the progression of steatohepatitis. "
10/01/1997 - "The results together with our previous findings, indicate that relatively strong COX inhibitors, acting irreversibly like aspirin or for extended periods like PIRO, can prevent the endogenous hepatocarcinogenesis associated with a CDAA diet, although not the development of a fatty liver, suggesting that an augmented COX pathway might play key roles in the causation of liver lesions in this model."
02/01/2014 - "WT mice fed a CDAA diet displayed increased activation of Smad2/3 and had marked lipid accumulation, inflammatory cell infiltration, hepatocyte death, and fibrosis; in comparison, Tgfbr2ΔHEP mice fed a CDAA diet had suppressed liver steatosis, inflammation, and fibrosis. "
|5.||Liver Cirrhosis (Hepatic Cirrhosis)
10/01/2014 - "More importantly, Nlrp3(-/-) mice showed marked protection from CDAA-induced liver fibrosis. "
04/01/2013 - "The 24-week CDAA diet induced liver cirrhosis. "
10/01/2005 - "Feeding rats a CDAA diet for 14 weeks led to the development of severe liver fibrosis and preneoplastic lesions detected as enzyme-altered lesions. "
08/01/2003 - "Our results suggest that COX-2 is involved in CDAA- and TAA-induced liver fibrosis. "
07/01/2002 - "In CDAA-induced liver fibrosis model, PE revealed a marked inhibitory effect of liver fibrosis development. "
|1.||Choline (Choline Chloride)
|2.||Prostaglandin-Endoperoxide Synthases (Cyclooxygenase)
|4.||Angiotensin Receptors (Angiotensin II Receptor)
|9.||Type 1 Angiotensin Receptor
|2.||Phototherapy (Light Therapy)
|4.||Renal Dialysis (Hemodialysis)