| 1 | Cytokines as biomarkers of inflammatory response after open versus endovascular repair of abdominal aortic aneurysms: a systematic review显示文摘一个腹的大动脉的动脉瘤(AAA ) 的修理是与有煽动性的串联的随后的激活的神经质、新陈代谢的压力相关的反应有关的一个高风险的外科的过程。与开的修理相对照(或) , endovascular 大动脉的动脉瘤修理(EVAR ) 由为更少提供广泛的切口,解剖,和织物操作似乎是手术后的压力到减少。然而,这些有益的效果可以是由代谢物在用在 endovascular 的导管的血栓的 intra 钠操作期间修理的 cytokines 和 arachidonic 酸的版本的偏移量,导致全身的煽动性的反应(先生) ,它是临床上叫的培植以后的症候群。在我们比较了的这系统的评论或与 EVAR,以 post-interventional,从改变导致传播 cytokine 的煽动性的反应铺平。我们寻求了在 EVAR 以后关于培植以后的症候群总结所有最近的证据。我们寻找了为临床的研究作为煽动性的反应的部分在 cytokines 的版本上报导在以后的 Medline (PubMed ) , ClinicalTrials.gov 和 Cochrane 图书馆开 / 常规并且 AAA 的 endovascular 修理。我们鉴别 17 学习检验 cytokine 层次在以后或对 EVAR。或似乎特别地比 EVAR 与一位更大的先生被联系,由增加的 cytokine 层次证实了 IL-6 和 IL-8 而 IL-1, IL-10 和 TNF- 出现了,冲突在二之间的结果或没有差别组织。聚酯 endografts 看起来断然在 EVAR 以后与培植以后的症候群的发生被相关。未来大未来的研究被保证位于在 surgical 以后的 cytokine 相互作用下面描出的机制煽动性的反应背景。 | Diamantis I TSILIMIGRAS Fragiska SIGALA Georgios KARAOLANIS Ioannis NTANASIS-STATHOPOULOS Eleftherios SPARTALIS Michael SPARTALIS Nikolaos PATELIS Alexandros PAPALAMPROS Chandler LONG Demetrios MORIS | 2018 | Acta Pharmacologica Sinica2018，39，7： | 5 |
| 2 | Melatonin attenuates high fat diet-induced fatty liver disease in rats显示文摘AIM:To investigate melatonin's preventive action in oxidative stress in a rat model with high fat diet-induced non-alcoholic fatty liver disease(NAFLD).METHODS:NAFLD was induced by high fat diet(HFD)in adult,male,Wistar rats,weighing 180-230 g.After acclimatization for one week,they were randomly assigned to 6 experimental groups that comprised animals on regular diet plus 5 or 10 mg/kg melatonin,for 4 or 8 wk;animals on HFD,with or without 5 or 10 mg/kg melatonin,for 4 or 8 wk;and animals on HFD for 8 or 12 wk,with melatonin 10 mg/kg for the last 4 wk.Liver damage was assessed biochemically by the serum levels of alanine aminotransferase(ALT),aspartate aminotransferase(AST),and histologically.Lipid peroxidation and oxidative stress were assessed by malondialdehyde and glutathione levels in liver tissue.Lipidemic indices and portal vein pressure were also measured.RESULTS:Compared to rats not receiving melatonin,rats on 5 or 10 mg/kg of melatonin had lower mean liver weight(-5.0 g and-4.9 g)(P < 0.001)and lower liver weight to body weight ratio(-1.0%)(P < 0.001),for the two doses,respectively.All rats fed HFD without melatonin developed severe,grade Ⅲ,steatosis.Rats on HFD with concurrent use of melatonin showed significantly less steatosis,with grade Ⅲ steatosis observed in 1 of 29(3.4%)rats on 10 mg/kg melatonin and in 3 of 27(11.1%)rats on 5 mg/kg melatonin.Melatonin was ineffective in reversing established steatosis.Melatonin also had no effect on any of the common lipidemic serum markers,the levels of which did not differ significantly among the rats on HFD,irrespective of the use or not of melatonin.Liver cell necrosis was significantly less in rats on HFD receiving melatonin than in those not on melatonin,with the AST levels declining by a mean of 170 U/L(P = 0.01)and 224 U/L(P = 0.001),and the ALT levels declining by a mean of 62.9 U/L(P = 0.01)and 93.4 U/L(P < 0.001),for the 5 and 10 mg/kg melatonin dose,respectively.Melatonin mitigated liver damage due to peroxidation and oxidative stress in liver tissue as indicated by a significant decline in MDA production by 12.7(P < 0.001)and 12.2(P < 0.001)μmol/L/mg protein/mg tissue,and a significant increase in glutathione by 20.1(P = 0.004)and 29.2(P < 0.001)μmol/L/mg protein/mg tissue,for the 5 and 10 mg/kg melatonin dose,respectively.CONCLUSION:Melatonin can attenuate oxidative stress,lessen liver damage,and improve liver histology in rats with high fat diet-induced NAFLD,when given concurrently with the diet. | Gregorios Hatzis Panayiotis Ziakas Nikolaos Kavantzas Aggeliki Triantafyllou Panagiotis Sigalas Ioanna Andreadou Konstantinos Ioannidis Stamatios Chatzis Konstantinos Filis Alexandros Papalampros Fragiska Sigala | 2013 | World Journal of Hepatology2013，5，4： | 4 |
| 3 | Mechanistic insights of rapid liver regeneration after associating liver partition and portal vein ligation for stage hepatectomy显示文摘AIM To highlight the potential mechanisms of regeneration in the Associating Liver Partition and Portal vein ligation for Stage hepatectomy models(clinical and experimental) that could unlock the myth behind the extraordinary capability of the liver for regeneration,which would help in designing new therapeutic options for the regenerative drive in difficult setup,such as chronic liver diseases. Associating Liver Partition and Portal vein ligation for Stage hepatectomy has been recently advocated to induce rapid future liver remnant hypertrophy that significantly shortens the time for the second stage hepatectomy. The introduction of Associating Liver Partition and Portal vein ligation for Stage hepatectomy in the surgical armamentarium of therapeutic tools for liver surgeons represented a real breakthrough in the history of liver surgery. METHODS A comprehensive literature review of Associating Liver Partition and Portal vein ligation for Stage hepatectomy and its utility in liver regeneration is performed. RESULTS Liver regeneration after Associating Liver Partition and Portal vein ligation for Stage hepatectomy is a combination of portal flow changes and parenchymal transection that generate a systematic response inducing hepatocyte proliferation and remodeling. CONCLUSION Associating Liver Partition and Portal vein ligation for Stage hepatectomy represents a real breakthrough in the history of liver surgery because it offers rapid liver regeneration potential that facilitate resection of liver tumors that were previously though unresectable. The jury is still out though in terms of safety,efficacy and oncological outcomes. As far as Associating Liver Partition and Portal vein ligation for Stage hepatectomy-induced liver regeneration is concerned,further research on the field should focus on the role of nonparenchymal cells in liver regeneration as well as on the effect of Associating Liver Partition and Portal vein ligation for Stage hepatectomy in liver regeneration in the setup of parenchymal liver disease. | Demetrios Moris Spyridon Vernadakis Alexandros Papalampros Michail Vailas Nikolaos Dimitrokallis Athanasios Petrou Dimitrios Dimitroulis | 2016 | World Journal of Gastroenterology2016，22，33： | 2 |
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