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RISS 인기검색어
- 검색키워드
- 저자 : ( Norifumi Kawada ) (검색결과 4 건)
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Kotani Kohei,Kawada Norifumi 거트앤리버 소화기연관학회협의회 2024 Gut and Liver Vol.18 No.1
In chronic liver disease, hepatic stellate cell activation and degeneration of liver sinusoidal endothelial cells lead to structural changes, which are secondary to fibrosis and the presence of regenerative nodules in the sinusoids, and to functional changes, which are related to vasoconstriction. The combination of such changes increases intrahepatic vascular resistance and causes portal hypertension. The subsequent increase in splanchnic and systemic hyperdynamic circulation further increases the portal blood flow, thereby exacerbating portal hypertension. In clinical practice, the hepatic venous pressure gradient is the gold-standard measure of portal hypertension; a value of ≥10 mm Hg is defined as clinically significant portal hypertension, which is severe and is associated with the risk of liver-related events. Hepatic venous pressure gradient measurement is somewhat invasive, so evidence on the utility of risk stratification by elastography and serum biomarkers is needed. The various stages of cirrhosis are associated with different outcomes. In viral hepatitis-related cirrhosis, viral suppression or elimination by nucleos(t)ide analog or direct-acting antivirals results in recompensation of liver function and portal pressure. However, careful follow-up should be continued, because some cases have residual clinically significant portal hypertension even after achieving sustained virologic response. In this study, we reviewed the current and future prospects for portal hypertension.
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Role of cytoglobin, a novel radical scavenger, in stellate cell activation and hepatic fibrosis
Le Thi Thanh Thuy,Hoang Hai,Norifumi Kawada 대한간학회 2020 Clinical and Molecular Hepatology(대한간학회지) Vol.26 No.3
Cytoglobin (Cygb), a stellate cell-specific globin, has recently drawn attention due to its association with liver fibrosis. In the livers of both humans and rodents, Cygb is expressed only in stellate cells and can be utilized as a marker to distinguish stellate cells from hepatic fibroblast-derived myofibroblasts. Loss of Cygb accelerates liver fibrosis and cancer development in mouse models of chronic liver injury including diethylnitrosamine-induced hepatocellular carcinoma, bile duct ligation-induced cholestasis, thioacetamide-induced hepatic fibrosis, and choline-deficient L-amino aciddefined diet-induced non-alcoholic steatohepatitis. This review focuses on the history of research into the role of reactive oxygen species and nitrogen species in liver fibrosis and discusses the current perception of Cygb as a novel radical scavenger with an emphasis on its role in hepatic stellate cell activation and fibrosis.
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( Chung-feng Huang ),( Yasuhiro Asahina ),( Chun-jen Liu ),( Edward Gane ),( Yoshito Itoh ),( Norifumi Kawada ),( Yoshiyuki Ueno ),( Jin Youn ),( Chen-yu Wang ),( Joe Llewellyn ),( Anu Osinusi ),( Jen 대한간학회 2018 춘·추계 학술대회 (KASL) Vol.2018 No.1
Aims: HCV genotype (GT) 2 is the second most common gen otype in several Asian countries including Taiwan and Korea. Treatment options for GT2 remain limited in these countries. The once-daily fixed-dose combination of ledipasvir/sofosbuvir (LDV/SOF) was evaluated for the treatment of GT 2, in patients with or without compensated cirrhosis, in three phase 2 and 3 studies. Methods: This was a retrospective analysis of subjects treated with LDV/SOF for 12 weeks in the GS-US-337-1655 (Taiwan), GS-US-337-1903 (Japan) and GS-US-1468 (New Zealand) stud ies. Subjects analyzed in this integrated analysis were either mono-infected with HCV GT2, or co-infected with HCV GT2 and HBV. The data was pooled and safety and efficacy were analyzed. Results: Overall 200 subjects were treated and analyzed; 88% of subjects were Asian, 46% male, 31% had prior treatment failure, 15% were cirrhotic, 25% were IL28B non-CC, 34% were 65 years or older and 22% (n=43) were co-infected with HBV. The overall SVR rate was 97% (194/200), and was 93% (27/29) among patients with cirrhosis and 97% (59/61) in pa tients who had failed previous therapy. Of the 197 patients with available testing; NS5A resistance-associated substitutions (RASs) were present in 86% (169/197) at baseline. SVR12 rate was 98% (165/169) in patients with baseline NS5A RASs com pared with 100% (28/28) in patients without NS5A RASs. No new RASs emerged in patients with virologic failure. Treatment with LDV/SOF for 12 weeks was well tolerated. Overall the most common adverse events AEs were headache and nasopharyngi tis. Few subjects experienced serious AEs, none of which were assessed as treatment related. One patient discontinued treat ment due to AE. Conclusions: Treatment with LDV/SOF for 12 weeks is highly effective and well tolerated in patients with GT2 HCV infection, including patients who are treatment experienced and/or have compensated cirrhosis, baseline NS5A RASs and with HBV/HCV coinfection.
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Anti-fibrotic treatments for chronic liver diseases: The present and the future
( Naoshi Odagiri ),( Tsutomu Matsubara ),( Misako Sato-matsubara ),( Hideki Fujii ),( Masaru Enomoto ),( Norifumi Kawada ) 대한간학회 2021 Clinical and Molecular Hepatology(대한간학회지) Vol.27 No.3
Liver fibrosis reflects tissue scarring in the liver due to the accumulation of excessive extracellular matrix in response to chronically persistent liver injury. Hepatocyte cell death can trigger capillarization of liver sinusoidal endothelial cells, stimulation of immune cells including macrophages and Kupffer cells, and activation of hepatic stellate cells (HSCs), resulting in progression of liver fibrosis. Liver cirrhosis is the terminal state of liver fibrosis and is associated with severe complications, such as liver failure, portal hypertension, and liver cancer. Nevertheless, effective therapy for cirrhosis has not yet been established, and liver transplantation is the only radical treatment for severe cases. Studies investigating HSC activation and regulation of collagen production in the liver have made breakthroughs in recent decades that have advanced the knowledge regarding liver fibrosis pathophysiology. In this review, we summarize molecular mechanisms of liver fibrosis and discuss the development of novel anti-fibrotic therapies. (Clin Mol Hepatol 2021;27:413-424)
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