打字猴:1.700630216e+09
1700630216
1700630217 [14] Zeisberg M, Yang C, Martino M, et al. Fibroblast derive from hepatocytes in liver fibrosis via epithelial to mesenchymal transition. J Biol Chem, 2007, 287:23337-23347.
1700630218
1700630219 [15] Gorrell MD. Liver fibrosis: The hepatocytes revisited. Hepatology, 2007, 46(5)1659-1661.
1700630220
1700630221 [16] Weng HL, Wang BE, Jia JD, et al. Effect of IFN-γ on hepatic fibrosis in chronic hepatitis B virus infection: A randomized controlled study. Chin Gastroenterol Hepatol, 2005, 3(8):819-828.
1700630222
1700630223 [17] Weng HL, Mertens PR, Gresnner AM, et al. IFN-γ abrograters profibrogenic TGFβ signaling in liver by targeting expression of inhibitory and receptor Smads. J Hepatology, 2007, 46(1):295-303.
1700630224
1700630225 [18] Weng HL, Ciuclan L, Liu Y, et al. Profibrogenic TGF-β/activin preceptor-like kinase 5 signaling via CTGF expression in hepatocytes. Hepatology, 2007, 46(4):1257-1270.
1700630226
1700630227 [19] Guha IN, Parkes J, Roderick P, et al. Noninvasive markers of fibrosis in nonalcoholic fatty liver disease: Validating the European liver fibrosis panel and exploring simpler markers. Hepatology, 2008, 47(2):455-460.
1700630228
1700630229 [20] Fontana RJ, Goodman ZD, Dienstage JL, et al. Relationship of serum fibrosis markers with liver fibrosis stage and collagen content in patients with advanced chronic hepatitis. Hepatology, 2008, 47(3):789-789.
1700630230
1700630231 [21] Lai KKY, Kolippakkam D, Beretta L. Comprehensive and quantitative proteome profiling of the mouse liver and plasma. Heptology, 2008, 47(3):1043-1051.
1700630232
1700630233 [22] Morra R, Munteanu M, Bedossa P, et al. Diagnostic value of serum protein profiliny by SELD1-TOF protein-chip compared with a biochemipal marker, fibro test for the diagnosis of advenced fibrosis in patents with chronic hepatitis C. Aliment Pharmacol Ther, 2007, 15; 26(6):847-858.
1700630234
1700630235 [23] Wasmuth HE, Trartwein C. CB1 cannabinoid receptor antagonism: A new strategy for the treatment of liver fibrosis. Hepatology, 2007, 45(2):543-545.
1700630236
1700630237 [24] Weiskirchen R, Meurer SK. Bone morphogenetic protein-7 in focus: A member of the TGFβ superfamily is implicated in the maintenance of liver health. Hepatology, 2007, 45(5):1324-1325.
1700630238
1700630239 [25] Kinoshita K, Limuro Y, Otogawa K, et al. Aenovirus-mediated expression of BMP-7 suppresses the development of liver fibrosis in rats. Gut, 2007, 56(5):706-714.
1700630240
1700630241 [26] Zou C, Ma J, Wang X, et al. Lack of fas antagonism by met in human fatty liver disease. Nat Med, 2007, 13(9):1078-1085.
1700630242
1700630243 [27] Roderfeld M, Weiskirchen R, Waq-ner S, et al. Inhibition of hepatic fibrogensis by MMP-9 mutants in mice. Fase B J, 2006, 20(3):444-454.
1700630244
1700630245 [28] Hu YB, Li DG, Lu HM, et al. Modified synthetic SiRN A targeting TIMP-2 Ihibits hepatic fibrogensis in rats. J Gene Med, 2007, 9(3):217-229.
1700630246
1700630247 [29] Wang CH, Lee TH, Lu CN, et al. Electroporative alpha-MSH gene transfer attenuate thioacetamide induced murine hepatic fibrosis by MMP and TIMP modulation. J Gene Ther, 2006, 13(13):1000-1009.
1700630248
1700630249 [30] Prockros P, Jeffers L, Afdhal N, et al. Final results of A double-blind, placebo-controlled trial of the antifibrotic efficacy of interferon-rlb in chronic hepatitis C patients with advanced fibrosis or cirrhosis. Hepatology, 2007, 45(1):569-578.
1700630250
1700630251 [31] 蔡卫民.γ干扰素抗肝纤维化研究的体会.传染病信息,2008,待发表.
1700630252
1700630253 [32] 翁红雷,蔡卫民.IFN-γ与肝纤维化治疗.中华肝脏病杂志,2008,待发表.
1700630254
1700630255 (蔡卫民)
1700630256
1700630257
1700630258
1700630259
1700630260 内科学新进展 [:1700627004]
1700630261 内科学新进展 第五节 药物性肝损害的临床类型及诊断策略
1700630262
1700630263 摘 要 药物性肝损害是指药物在治疗过程中,肝脏由于药物的毒性损害或对药物的过敏反应所致的疾病,也有称为药物性肝炎。临床上把药物性肝损害分为中毒性肝损害和变态反应性肝损害两种。导致药物性肝损害的相关因素有药物本身的因素、个体因素、原发疾病、性别和年龄、疗程与剂量等。药物性肝损害按其临床特征可分为急性和慢性两型;按其损害部位又可分为肝细胞型、肝内淤胆型、混合型、肿瘤型和胆红素代谢障碍型等。
1700630264
1700630265 Abstract Drug-induced liver injury(DILI)is defined as a hepatic disease due to the toxicity of or hepatic hypersensitive response to certain drugs. It also termed as drug-induced hepatitis. There were two types of DILI in clinic, toxic liver injury and allergic liver injury. Several conditions leading to DILI including drug, individuality, primary diseases, gender, age, course of treatment and dosage. DILI is divided into acute and chronic DILI according to the clinical characteristics. It is also divided into five subtypes according to the damage sites including hepatocyte, cholestasis, mixing, tumor, and bilirubin dysmetabolism subtypes.
[ 上一页 ]  [ :1.700630216e+09 ]  [ 下一页 ]