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| 1 | From fatty liver to fibrosis:A tale of “second hit”显示文摘Although much is known about how fat accumulates in the liver,much remains unknown about how this causes sustained hepatocellular injury.The consequences of injury are recognized as nonalcoholic steatohepatitis(NASH) and progressive fibrosis.The accumulation of fat within the hepatocytes sensitizes the liver to injury from a variety of causes and the regenerative capacity of a fatty liver is impaired.An additional stressor is sometimes referred to as a 'second hit' in a paradigm that identifies the accumulation of fat as the 'first hit'.Possible candidates for the second hit include increased oxidative stress,lipid peroxidation and release of toxic products such as malondialdehyde and 4-hydroxynonenal,decreased antioxidants,adipocytokines,transforming growth factor(TGF)-β,Fas ligand,mitochondrial dysfunction,fatty acid oxidation by CYPs(CYP 2E1,4A10 and 4A14),and peroxisomes,excess iron,small intestinal bacterial overgrowth,and the generation of gut-derived toxins such as lipopolysaccharide and ethanol.Oxidative stress is one of the most popular proposed mechanisms of hepatocellular injury.Previous studies have specifically observed increased plasma and tissue levels of oxidative stress markers and lipid peroxidation products,with reduced hepatic and plasma levels of antioxidants.There is also some indirect evidence of the benefit of antioxidants such as vitamin E,S-adenosylmethionine,betaine,phlebotomy to remove iron,and N-acetylcysteine in NASH.However,a causal relationship or a pathogenic link between NASH and oxidative stress has not been established so far.A number of sources of increased reactive oxygen species production have been established in NASH that include proinflammatory cytokines such as tumor necrosis factor(TNF)-α,iron overload,overburdened and dysfunctional mitochondria,CYPs,and peroxisomes.Briefly,the pathogenesis of NASH is multifactorial and excess intracellular fatty acids,oxidant stress,ATP depletion,and mitochondrial dysfunction are important causes of hepatocellular injury in the steatotic liver. | Metin Basaranoglu Gkcen Basaranoglu Hakan Sentürk | 2013 | World Journal of Gastroenterology2013，19，8： | 28 |
| 2 | Fructose as a key player in the development of fatty liver disease显示文摘We aimed to investigate whether increased consumption of fructose is linked to the increased prevalence of fatty liver.The prevalence of nonalcoholic steatohepatitis(NASH) is 3% and 20% in nonobese and obese subjects,respectively.Obesity is a low-grade chronic inflam-m-atory condition and obesity-related cytokines such as interleukin-6,adiponectin,leptin,and tumor necrosis factor-α may play important roles in the developm-ent of nonalcoholic fatty liver disease(NAFLD).Additionally,the prevalence of NASH associated with both cirrhosis and hepatocellular carcinom-a was reported to be high am-ong patients with type 2 diabetes with or without obesity.Our research group previously showed that consumption of fructose is associated with adverse alterations of plasma lipid profiles and metabolic changes in m-ice,the Am-erican Lifestyle-Induced Obesity Syndrom-e m-odel,which included consum-ption of a high-fructose corn syrup in amounts relevant to that consum-ed by som-e Am-ericans.The observation reinforces the concerns about the role of fructose in the obesity epidem-ic.Increased availability of fructose(e.g.,high-fructose corn syrup) increases not only abnorm-al glucose flux but also fructose m-etabolism-in the hepatocyte.Thus,the anatomic position of the liver places it in a strategic buffering position for absorbed carbohydrates and am-ino acids.Fructose was previously accepted as a beneficial dietary com-ponent because it does not stim-ulate insulin secretion.However,since insulin signaling plays an important role in central m-echanism-s of NAFLD,this property of fructose m-ay be undesirable.Fructose has a selective hepatic m-etabolism,and provokes a hepatic stress response involving activation of c-Jun N-term-inal kinases and subsequent reduced hepatic insulin signaling.As high fat diet alone produces obesity,insulin resistance,and som-e degree of fatty liver with m-inim-al inflam-m-ation and no fibrosis,the fast food diet which includes fructose and fats produces a gene expression signature of increased hepatic fibrosis,inflam-m-ation,endoplasm-ic reticulumstress and lipoapoptosis.Hepatic de novo lipogenesis(fatty acid and triglyceride synthesis) is increased in patients with NAFLD.Stable-isotope studies showed that increased de novo lipogenesis(DNL) in patients with NAFLD contributed to fat accum-ulation in the liver and the developm-ent of NAFLD.Specifically,DNL was responsible for 26% of accum-ulated hepatic triglycerides and 15%-23% of secreted very low-density lipoprotein triglycerides in patients with NAFLD com-pared to an estim-ated less than 5% DNL in healthy subjects and 10% DNL in obese people with hyperinsulinem-ia.In conclusion,understanding the underlying causes of NAFLD form-s the basis for rational preventive and treatm-ent strategies of this m-ajor form-of chronic liver disease. | Metin Basaranoglu Gokcen Basaranoglu Tevfik Sabuncu Hakan Sentürk | 2013 | World Journal of Gastroenterology2013，19，8： | 14 |
| 3 | Clindamycin-induced acute cholestatic hepatitis显示文摘我们为牙齿的感染在 clindamycin 的管理以后在一个 42 岁的女人报导尖锐 hepatotoxicity 的一个案例。在治疗的 6 d 以后,她有疲劳,恶心,呕吐,厌食,瘙痒和黄疸。她的实验室分析显示出丙氨酸 aminotransferase (中高音) , 1795 IU/L (正常范围 0-40 ) ;aspartate aminotransferase (著名计算机生产厂商) , 1337 IU/L (正常范围 5-34 ) ;硷性磷酸酯酶(高山) , 339 IU/L (正常范围 40-150 ) ;gamma-glutamyl transpeptidase (GGT ) , 148 IU/L (正常范围 9-64 IU/L ) ;全部的胆红素, 4.1 mg/dL;直接胆红素, 2.9 mg/dL 和前凝血酶时间(磅) , 13.5 s 与国际规范的比率(INR ) , 1.04。她被就医,与立即的药中止。她的肝活体检视标本显示出混合类型(肝细胞和胆汁郁积的) 肝的损害,与导致药的肝炎的诊断兼容。用 Naranjo 概率规模的一个客观诱发性评价建议 clindamycin 是尖锐肝炎的可能的原因。在易受影响的个人, clindamycin 使用可以导致尖锐混合类型肝毒性。如果在严重肝损伤被建立以前,这药被中止,完全的恢复可能是可能的。 | Cem Aygün Orhan Kocaman Yesim Gürbüz mer Sentürk Sadettin Hülagü | 2007 | World Journal of Gastroenterology2007，13，40： | 6 |
| 4 | Determining the weights of two types of artificial reefs required to resist wave action in different wa-ter depths and bottom slopes显示文摘 | DüzbastIlar F O Sentürk U | 2009 | Ocean Engineering2009，36，1213： | 1 |
| 5 | Effects of thoracic epidural anaesthesia on pulmonary venous admixture and oxygenation during one-lung ventilation显示文摘 | Ozcan PE Sentürk M Sungur Ulke Z | 2007 | J Acta Anaesthesiol Scand2007，51，8： | 1 |
| 6 | Granular cell tumor of esophagus removed with endoscopic submucosal dissection显示文摘 | Hülagü S Sentürk O Aygün C | 2007 | Turk J Gastroenterol2007，18，3： | 1 |
| 7 | Granular cell tumor of esophagus removed with endoscopic submucosal dissection显示文摘 | Hülagü S Sentürk O Aygün C | 2007 | Turk J Gastroenterol2007，18，3： | 1 |
| 8 | Prevalence and risk factors for gall bladder polvos显示文摘 | Cant u rk Z Sent u rk O Canturk NZ | 2007 | East Afr Med J2007，84，7： | 1 |
| 9 | Generalized circles in Weyl spaces and their conformal mapping显示文摘 | Ozdeger A Sentürk Z | 2002 | Publ Math Debrecen2002，60，12： | 1 |
| 10 | A Conceptual History of the E- mergence of Bounded Rationality 显示文摘 | Klaes M E-M Sent | 2005 | History of Po- litical Economy2005，37，1： | 1 |
| 11 | Psychiatric disorders and disability among leprosy patients;a review显示文摘 | Sentürk V Sagduyu A | 2004 | Turk Psikiyatri Derg2004，15，3： | 1 |
| 12 | Association between chronic obstructive pulmonary disease and systmic inflammation:a systmic review and a meta2analysis 显示文摘 | Gan WQ Man SF Sent hilsevan A | 2004 | Thorax2004，59，7： | 1 |
| 13 | The reliability of microelectromechanical systems (MEMS) in shock environments显示文摘 | Srikar V T Sent S D | 2002 | Journal of Microelectro Mechanical Systems2002，11，3： | 1 |
| 14 | A efficient control of a piezoelectric linear actuator embedded into a servovalve for aeronautic applications显示文摘 | Sente P A Labrique F M Alexandre P J | 2012 | 1EEE Transactions on Industrial Electronics2012，59，4： | 1 |
| 15 | Association betweenchronic obst ructive pulmonary disease and systmic inflammation: asystmic review and a meta2analysis显示文摘 | Gan WQ Man SF Sent hilsevan A | 2004 | Thorax2004，59，7： | 1 |
| 16 | 利用现代企业制度组织农产品生产——泰国“正大集团”考察报告显示文摘泰国“正大集团”通过向传统农村直接引进现代企业制度的方式,把分散的小农组织起来,使其同社会化的整个经济活动挂钩,成功地解决了高度分散的农产品供给与集中的农产品需求之间发生的经常性冲突问题。本文认为,对于我国经济发展的新阶段来说,制度建设和规范行为的经验非常有限,因此,借鉴“正大”的许多做法,也许要比我们直接去借鉴发达国家的一些做法意义更大,可供实验的条件也更为相似。 | Investigation Group to Zhengda sent by Institute of Development, State Council Agricultural Research Centre | 1988 | 管理世界1988，4，2： | 1 |
| 17 | FOXO signalling is required for disuse muscle atrophy and is directly regulated by HSP70显示文摘 | Sent SM Dodd SL Judge AR | 2010 | Am J Physiol Cell Physiol2010，298，1： | 1 |
| 18 | T-cell activation by recombinant receptors:CD28 costimulation is required for interleukin 2 secretion and receptor-mediated T-cell proliferation but does not affect receptor-mediated target cell lysis显示文摘 | Hombach A Sent D Schneider C | 2001 | Cancer Res2001，61，5： | 1 |
| 19 | The effect of one year's swimming exercise on oxidant stress and antioxidant capacity in aged rats显示文摘 | Gündüz F Sentürk U K Kuru O | 2004 | Physiol Res2004，，53： | 1 |
| 20 | Concrete-filled tubular steel columns under fccentric loading显示文摘 | Neogi P K Sent H K Chapman J C | 1969 | The Journal of The Institution of Structrual Engineers1969，47，5： | 1 |
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