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RISS 인기검색어
- 검색키워드
- 저자 : Yen-Feng Chiu (검색결과 3 건)
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Jeffrey S. Chang,Yen-Feng Chiu,Jih-Chang Yu,Li-Tzong Chen,Hui-Ju Ch’ang 대한암학회 2018 Cancer Research and Treatment Vol.50 No.2
Purpose The role of consolidation chemoradiation (CCRT) after systemic chemotherapy in locally advanced pancreatic cancer (LAPC) is still controversial. We aim to evaluate the effectiveness of CCRT in LAPC using systematic review and meta-analysis of prospective studies. Materials and Methods Prospective clinical trials of LAPC receiving chemotherapy with or without subsequent CCRT were included in the analysis. We systematically searched in PubMed, MEDLINE, Embase, and Web of Science. The primary outcome of interest was 1-year survival. Secondary endpoints were median overall survival, progression-free survival, toxicity, and resection rate. Results Forty-one studies with 49 study arms were included with a total of 1,018 patients receiving CCRT after induction chemotherapy (ICT) and 954 patients receiving chemotherapy alone. CCRT after ICT did not improve 1-year survival significantly in LAPC patients compared with chemotherapy alone (58% vs. 52%). ICT lasted for at least 3 months revealed significantly improved survival of additional CCRT to LAPC patients compared to chemotherapy alone (65% vs. 52%). A marginal survival benefit of consolidation CCRT was noted in studies using maintenance chemotherapy (59% vs. 52%), and fluorouracil-based CCRT (64% vs. 52%), as well as in studies conducted after the 2010 (64% vs. 55%). Conclusion The survival benefit of ICT+CCRT over chemotherapy alone in treating LAPC was noted when ICT lasted for at least 3 months. Fluorouracil-based CCRT, and maintenance chemotherapy were associated with improved clinical outcomes.
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Antioxidative and Hepatoprotective Effects of Magnolol on Acetaminophen-induced Liver Damage in Rats
Yung-Hsiang Chen,Feng-Yen Lin,Po-Len Liu,Yi-Tsau Huang,Jen-Hwey Chiu,Yi-Chun Chang,Kee-Ming Man,Chuang-Ye Hong,Yen-Yi Ho,Ming-Tsung Lai 대한약학회 2009 Archives of Pharmacal Research Vol.32 No.2
Acute liver failure (ALF), an often fatal condition characterized by massive hepatocyte necrosis, is frequently caused by drug poisoning, particularly with acetaminophen (N-acetyl-p-aminophenol/APAP). Hepatocyte necrosis is consecutive to glutathione (GSH) depletion and mitochondrial damage caused by reactive oxygen species (ROS) overproduction. Magnolol, one major phenolic constituent of Magnolia officinalis, have been known to exhibit potent antioxidative activity. In this study, the anti-hepatotoxic activity of magnolol on APAP-induced toxicity in the Sprague-Dawley rat liver was examined. After evaluating the changes of several biochemical parameters in serum, the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were elevated by APAP (500 mg/kg) intraperitoneal administration (8 and 24 h) and reduced by treatment with magnolol (0.5 h after APAP administration; 0.01, 0.1, and 1 μg/kg). Histological changes around the hepatic central vein, lipid peroxidation (thiobarbituric acid-reactive substance/TBARS), and GSH depletion in liver tissue induced by APAP were also recovered by magnolol treatment. The data show that oxidative stress followed by lipid peroxidation may play a very important role in the pathogenesis of APAP-induced hepatic injury; treatment with lipid-soluble antioxidant, magnolol, exerts anti-hepatotoxic activity. Our study points out the potential interest of magnolol in the treatment of toxic ALF.
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Wu, Ying,Gao, He,Li, Huaixing,Tabara, Yasuharu,Nakatochi, Masahiro,Chiu, Yen-Feng,Park, Eun Jung,Wen, Wanqing,Adair, Linda S.,Borja, Judith B.,Cai, Qiuyin,Chang, Yi-Cheng,Chen, Peng,Croteau-Chonka, Da Oxford University Press 2014 Human Molecular Genetics Vol.23 No.4
<P>Blood levels of adiponectin, an adipocyte-secreted protein correlated with metabolic and cardiovascular risks, are highly heritable. Genome-wide association (GWA) studies for adiponectin levels have identified 14 loci harboring variants associated with blood levels of adiponectin. To identify novel adiponectin-associated loci, particularly those of importance in East Asians, we conducted a meta-analysis of GWA studies for adiponectin in 7827 individuals, followed by two stages of replications in 4298 and 5954 additional individuals. We identified a novel adiponectin-associated locus on chromosome 10 near <I>WDR11-FGFR2</I> (<I>P</I> = 3.0 × 10<SUP>−14</SUP>) and provided suggestive evidence for a locus on chromosome 12 near <I>OR8S1-LALBA</I> (<I>P</I> = 1.2 × 10<SUP>−7</SUP>). Of the adiponectin-associated loci previously described, we confirmed the association at <I>CDH13</I> (<I>P</I> = 6.8 × 10<SUP>−165</SUP>), <I>ADIPOQ</I> (<I>P</I> = 1.8 × 10<SUP>−22</SUP>), <I>PEPD</I> (<I>P</I> = 3.6 × 10<SUP>−12</SUP>), <I>CMIP</I> (<I>P</I> = 2.1 × 10<SUP>−10</SUP>), <I>ZNF664</I> (<I>P</I> = 2.3 × 10<SUP>−7</SUP>) and <I>GPR109A</I> (<I>P</I> = 7.4 × 10<SUP>−6</SUP>). Conditional analysis at <I>ADIPOQ</I> revealed a second signal with suggestive evidence of association only after conditioning on the lead SNP (<I>P</I><SUB>initial</SUB> = 0.020; <I>P</I><SUB>conditional</SUB> = 7.0 × 10<SUP>−7</SUP>). We further confirmed the independence of two pairs of closely located loci (<2 Mb) on chromosome 16 at <I>CMIP</I> and <I>CDH13</I>, and on chromosome 12 at <I>GPR109A</I> and <I>ZNF664</I>. In addition, the newly identified signal near <I>WDR11-FGFR2</I> exhibited evidence of association with triglycerides (<I>P</I> = 3.3 × 10<SUP>−4</SUP>), high density lipoprotein cholesterol (HDL-C, <I>P</I> = 4.9 × 10<SUP>−4</SUP>) and body mass index (BMI)-adjusted waist–hip ratio (<I>P</I> = 9.8 × 10<SUP>−3</SUP>). These findings improve our knowledge of the genetic basis of adiponectin variation, demonstrate the shared allelic architecture for adiponectin with lipids and central obesity and motivate further studies of underlying mechanisms.</P>
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