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| 1 | Molecular mechanisms of liver ischemia reperfusion injury:Insights from transgenic knockout models显示文摘Ischemia reperfusion injury is a major obstacle in liver resection and liver transplantation surgery.Understanding the mechanisms of liver ischemia reperfusion injury(IRI) and developing strategies to counteract this injury will therefore reduce acute complications in hepatic resection and transplantation,as well as expanding the potential pool of usable donor grafts.The initial liver injury is initiated by reactive oxygen species which cause direct cellular injury and also activate a cascade of molecular mediators leading to microvascular changes,increased apoptosis and acute inflammatory changes with increased hepatocyte necrosis.Some adaptive pathways are activated during reperfusion that reduce the reperfusion injury.IRI involves a complex interplay between neutrophils,natural killer T-cells cells,CD4+ T cell subtypes,cytokines,nitric oxide synthases,haem oxygenase-1,survival kinases such as the signal transducer and activator of transcription,Phosphatidylinositol 3-kinases/Akt and nuclear factor κβ pathways.Transgenic animals,particularly genetic knockout models,have become a powerful tool at elucidating mechanisms of liver ischaemia reperfusion injury and are complementary to pharmacological studies.Targeted disruption of the protein at the genetic level is more specific and maintained than pharmacological inhibitors or stimulants of the same protein.This article reviews the evidence from knockout models of liver IRI about the cellular and molecular mechanisms underlying liver IRI. | Gourab Datta Barry J Fuller Brian R Davidson | 2013 | World Journal of Gastroenterology2013，19，11： | 50 |
| 2 | Current protective strategies in liver surgery显示文摘During liver resection surgery for cancer or liver transplantation,the liver is subject to ischaemia (reduction in blood flow) followed by reperfusion (restoration of blood flow),which results in liver injury [ischemiareperfusion (IR) or IR injury]. Modulation of IR injury can be achieved in various ways. These include hypothermia,ischaemic preconditioning (IPC) (brief cycles of ischaemia followed by reperfusion of the organ before the prolonged period of ischaemia i.e. a conditioning response),ischaemic postconditioning (conditioning after the prolonged period of ischaemia but before the reperfusion),pharmacological agents to decrease IR injury,genetic modulation of IR injury,and machine perfusion (pulsatile perfusion). Hypothermia decreases the metabolic functions and the oxygen consumption of organs. Static cold storage in University of Wisconsin solution reduces IR injury and has prolonged organ storage and improved the function of transplanted grafts. There is currently no evidence for any clinical advantage in the use of alternate solutions for static cold storage. Although experimental data from animal models suggest that IPC,ischaemic postconditioning,various pharma-cological agents,gene therapy,and machine perfusion decrease IR injury,none of these interventions can be recommended in clinical practice. This is because of the lack of randomized controlled trials assessing the safety and efficacy of ischaemic postconditioning,gene therapy,and machine perfusion. Randomized controlled trials and systematic reviews of randomized controlled trials assessing the safety and efficacy of IPC and various pharmacological agents have demonstrated biochemical or histological improvements but this has not translated to clinical benefit. Further well designed randomized controlled trials are necessary to assess the various new protective strategies in liver resection. | Kurinchi S Gurusamy Hector D Gonzalez Brian R Davidson | 2010 | World Journal of Gastroenterology2010，16，48： | 7 |
| 3 | Early acute kidney injury after liver transplantation: Predisposing factors and clinical implications显示文摘AIM To investigate the additional clinical impact of hepatic ischaemia reperfusion injury(HIRI) on patients sustaining acute kidney injury(AKI) following liver transplantation.METHODS This was a single-centre retrospective study of consecutive adult patients undergoing orthotopic liver transplantation(OLT) between January 2013 and June 2014. Early AKI was identified by measuring serum creatinine at 24 h post OLT(> 1.5 × baseline) or by the use of continuous veno-venous haemofiltration(CVVHF) during the early post-operative period. Patients with and without AKI were compared to identify risk factors associated with this complication. Peak serum aspartate aminotransferase(AST) within 24 h post-OLT was used as a surrogate marker for HIRI and severity was classified as minor(< 1000 IU/L), moderate(1000-5000 IU/L) or severe(> 5000 IU/L). The impact on time to extubation, intensive care length of stay, incidence of chronic renal failure and 90-d mortality were examined firstly for each of the two complications(AKI and HIRI) alone and then as a combined outcome. RESULTS Out of the 116 patients included in the study, 50% developed AKI, 24% required CVVHF and 70% sustainedmoderate or severe HIRI. Median peak AST levels were 1248 IU/L and 2059 IU/L in the No AKI and AKI groups respectively(P = 0.0003). Furthermore, peak serum AST was the only consistent predictor of AKI on multivariate analysis P = 0.02. AKI and HIRI were individually associated with a longer time to extubation, increased length of intensive care unit stay and reduced survival. However, the patients who sustained both AKI and moderate or severe HIRI had a longer median time to extubation(P < 0.001) and intensive care length of stay(P = 0.001) than those with either complication alone. Ninety-day survival in the group sustaining both AKI and moderate or severe HIRI was 89%, compared to 100% in the groups with either or neither complication(P = 0.049). CONCLUSION HIRI has an important role in the development of AKI post-OLT and has a negative impact on patient outcomes, especially when occurring alongside AKI. | Suehana Rahman Susan V Mallett Brian R Davidson | 2017 | World Journal of Hepatology2017，9，18： | 6 |
| 4 | 围手术期患者的安全:正确的患者、正确的手术、正确的部位——一项多因素、跨部门的干预性研究显示文摘背景为围手术期患者提供安全的环境非常重要。基于这一点,我们在围手术期实施了“患者安全第一”的政策。方法在干预性研究的第一阶段(2001—2002年),我们首先制定并实施干预性研究中组织和教育方面的内容。2003至2005年为研究的实施阶段。根据我们的零忍受原则,在手术等候区内一旦发现患者的麻醉或手术准备工作中有重大差错,该患者就被送回病房(失败),并等到差错得到纠正后再进行手术。结果共有15856例患者参加了研究。在研究实施阶段的3年中,有112例患者被送回病房(0.71%)。与2003年的数据相比,2004年和2005年发生的重大错误明显减少,且有统计学意义(2003、2004和2005年的数据分别为1.04%、0.59%和0.49%)。而且,逐步逻辑回归方法分析结果显示,手术前准备不充分所致重大错误的发生率逐年下降,具有统计学意义(比值比=1.48,95%CI:1.16~1.87)。此外,在2003、2004和2005年中,各年的失败发生平均间隔时间分别为6.6、11.2和14.7天(P〈0.03)。最后,不仅患者手术前准备工作在研究期间有显著改善(P〈0.0001);而且,使患者手术前准备工作评分为100%的可能性也有明显增加(P〈0.001)。结论教育和提高认识能减少围手术期的错误发生率。但是,即使有详细规划的制度,也无法达到无差错的环境。因此,检查和全面分析应该持续不断地进行。 | Edna Zohar Yossi Noga Ehud Davidson Margalit Kantor Brian Fredman 周全红(译) 江伟(校) | 2008 | 麻醉与镇痛2008，4，4： | 5 |
| 5 | Haemoxygenase modulates cytokine induced neutrophil chemoattractant in hepatic ischemia reperfusion injury显示文摘AIM To investigate the hepatic microcirculatory changes due to Haemoxygenase(HO),effect of HO inhibition on remote ischemic preconditioning(RIPC) and modulation of CINC.METHODS Eight groups of animals were studied- Sham,ischemia reperfusion injury(IRI) the animals were subjected to 45 min of hepatic ischemia followed by three hours of reperfusion,RIPC(remote ischemic preconditioning) + IRI group,remote ischemic preconditioning in sham(RIPC + Sham),PDTC + IR(Pyridodithiocarbamate,HO donor),Zn PP + RIPC + IRI(Zinc protoporphyrin prior to preconditioning),IR-24(45 min of ischemia followed by 24 h of reperfusion),RIPC+IR-24(preconditioning prior to. After 3 and 24 h of reperfusion the animals were killed by exsanguination and samples were taken. RESULTS Velocity of flow(160.83 ± 12.24 μm/s),sinusoidal flow(8.42 ± 1.19) and sinusoidal perfusion index(42.12 ± 7.28) in hepatic IR were lower(P < 0.05) in comparison to RIPC and PDTC(HO inducer). RIPC increased velocity of flow(328.04 ± 19.13 μm/s),sinusoidal flow(17.75 ± 2.59) and the sinusoidal perfusion index(67.28 ± 1.82)(P < 0.05). PDTC(HO induction) reproduced the effects of RIPC in hepatic IR. PDTC restored RBC velocity(300.88 ± 22.109 μm/s),sinusoidal flow(17.66 ± 3.71) and sinusoidal perfusion(82.33 ± 3.5) to near sham levels. Zn PP(HO inhibition) reduced velocity of flow of RBC in the RIPC group(170.74 ± 13.43 μm/s and sinusoidal flow in the RIPC group(9.46 ± 1.34). Zn PP in RIPC(60.29 ± 1.82) showed a fall in perfusion only at 180 min of reperfusion. Neutrophil adhesion in IR injury is seen in both postsinusoidal venules(769.05 ± 87.48) and sinusoids(97.4 ± 7.49). Neutrophil adhesion in RIPC + IR injury is reduced in both postsinusoidal venules(219.66 ± 93.79) and sinusoids(25.69 ± 9.08)(P < 0.05). PDTC reduced neutrophil adhesion in both postsinusoidal venules(89.58 ± 58.32) and sinusoids(17.98 ± 11.01)(P < 0.05) reproducing the effects of RIPC. Zn PP(HO inhibition) increased venular(589.04 ± 144.36) and sinusoidal neutrophil adhesion in preconditioned animals(121.39 ± 30.65)(P < 0.05). IR after 24 h of reperfusion increased venular and sinusoidal neutrophil adhesion in comparison to the early phase and was significantly reduced by RIPC. Hepatocellular cell death in IRI(80.83 ± 13.03),RIPC + IR(17.35 ± 2.47),and PTDC+IR(11.66 ± 1.17) Zn PP + RIPC + IR(41.33 ± 3.07) reduced hepatocellular death. Zn PP significantly increased hepatocellular death(P < 0.05 PTDC/RIPC vs Zn PP and IR). The CINC cytokine levels in sham(101.32 ± 6.42). RIPC + sham(412.18 ± 65.24) as compared to sham(P < 0.05). Hepatic IR(644.08 ± 181.24)(P < 0.05). RIPC CINC-1 levels in the early phase(401.62 ± 78.56). And PDTC(HO inducer) CINC-1 levels in hepatic IR(413.36 ± 63.06) were significantly lower. HO inhibition in preconditioned animals with Zinc protoporphyrin increased serum CINC levels(521.81 ± 74.9)(P < 0.05). The serum CINC levels were high in the late phase of hepatic IR(15306 ± 1222.04). RIPC reduced CINC levels in the late phase of IR(467.46 ± 26.06),P < 0.05.CONCLUSION RIPC protects hepatic microcirculation by induction of HO and modulation of CINC in hepatic IR. | Niteen Tapuria Sameer Junnarkar Mahmoud Abu-amara Barry Fuller Alexander M Seifalian Brian R Davidson | 2016 | World Journal of Gastroenterology2016，22，33： | 3 |
| 6 | Cholangiocarcinoma显示文摘 | Shahid A Khan Howard C Thomas Brian R Davidson Simon D Taylor-Robinson | 2005 | The Lancet . 2005 (9493)2005，，： | 3 |
| 7 | 三维三步MTT法肿瘤药敏试验与芬丹明B法的比较显示文摘目的 :比较自创的三维三步MTT法 (3D3S MTT法 )与MTT法及芬丹明B法 (SRB法 )在肿瘤药敏试验中的价值。方法 :选用Hep G2、T 2 4和SKOV3三种细胞系和丝列霉素及阿霉素两种抗癌药 ,观察暴露于两种药物 3d后再培养不同时间 ,用上述三种方法测定的药敏结果。MTT法与SRB法计算肿瘤生长抑制率 (%TGI)的公式均是 :%TGI =[1 At Ac]× 1 0 0 % ;根据自建的表达MTT代谢的数学模型 ,3D3S MTT法计算 %TGI的公式是 :%TGI =1 { [lnAmax ln(Amax At) ] [lnAmax ln(Amax Ac) ] } 1 b × 1 0 0 %。结果 :三种方法测定的药物剂量 反应曲线均呈S型。MTT法测定的 %TGI要比SRB法和 3D3S MTT法测定的结果低 ,而MTT法测定的IC50 平均为SRB法和 3D3S MTT法测定结果的 3~ 5倍。而 3D3S MTT法测定的 %TGI及IC50 与SRB法测定的结果相近似。结论 :3D3S MTT法克服了MTT法测定肿瘤药敏所存在的 3~ 5倍的低估问题 ,与SRB法相比结果可靠 。 | 王悦华 蔡亚宁 Brian R Davidson | 2002 | 军医进修学院学报2002，23，3： | 2 |
| 8 | Cholangiocarcinoma显示文摘 | Shahid A Khan Howard C Thomas Brian R Davidson Simon D Taylor-Robinson | 2005 | The Lancet2005，，9493： | 2 |
| 9 | Percutaneous biliary metal wall stenting in malignant obstructive jaundice显示文摘 | Adrian A Indar Dileep N Lobo Andrew D Gilliam Roger Gregson Ian Davidson Simon Whittaker John Doran Brian J Rowlands Ian J Beckingham | 2003 | European Journal of Gastroenterology & Hepatology2003，，： | 1 |
| 10 | Asset management modelling framework for irrigation and drainage system:Principles and case study application显示文摘 | Malano Hector M Geogre Biju A Davidson Brian | 2005 | Irrigation and Drainage Systems2005，19，2： | 1 |
| 11 | Effect of remote ischemic preconditioning on liver ischemia/reperfusion injury using a new mouse model显示文摘 | Mahmoud Abu‐Amara Shi Yu Yang Alberto Quaglia Peter Rowley Niteen Tapuria Alexander M. Seifalian Barry J. Fuller Brian R. Davidson | 2011 | Liver Transpl2011，，1： | 1 |
| 12 | Remote Ischemic Preconditioning: A Novel Protective Method From Ischemia Reperfusion Injury—A Review显示文摘 | Niteen Tapuria Yogesh Kumar Meer Mohammad Habib Mahmoud Abu Amara Alexander M. Seifalian Brian R. Davidson | 2008 | Journal of Surgical Research2008，，2： | 1 |
| 13 | Remote Ischemic Preconditioning: A Novel Protective Method From Ischemia Reperfusion Injury—A Review显示文摘 | Niteen Tapuria Yogesh Kumar Meer Mohammad Habib Mahmoud Abu Amara Alexander M. Seifalian Brian R. Davidson | 2008 | Journal of Surgical Research2008，，2： | 1 |
| 14 | Liver Transplantation and Recurrent Hepatocellular Carcinoma: Predictive Value of Nodule Size in a Retrospective and Explant Study显示文摘 | Alessandro Grasso Rosa Stigliano Filomena Morisco Hugo Martines Alberto Quaglia Amar P. Dhillon David Patch Brian R. Davidson Keith Rolles Andrew K. Burroughs | 2006 | Transplantation2006，，11： | 1 |
| 15 | Cholangiocarcinoma显示文摘 | Shahid A Khan Howard C Thomas Brian R Davidson Simon D Taylor-Robinson | 2005 | The Lancet2005，，9493： | 1 |
| 16 | Representation of DNAsequences in recormbinant DNA Libraries Prepared by restriction enzyepartial digestion显示文摘 | Brian seed Richard C Parker Normen Davidson | 1982 | Gene1982，19，： | 1 |
| 17 | Effect of ischemic preconditioning on hepatic microcirculation and function in a rat model of ischemia reperfusion injury显示文摘 | Rahul S. Koti Wenxuan Yang Michael R. Dashwood Brian R. Davidson Alexander M. Seifalian | 2002 | Liver Transplantation2002，，12： | 1 |
| 18 | Can contingent valuation be used to measure the in situ value of groundwater on the North China Plain显示文摘 | Wei Yongping Davidson Brian Chert Deli | 2007 | Water Re- sources Management2007，21，10： | 1 |
| 19 | Infection rates with and without T-tube splintage of common bile duct anastomosis in liver transplantation显示文摘 | Z. Ben-Ari Louise Neville Brian Davidson Keith Rolles Andrew K. Burroughs | 1998 | Transplant International1998，，2： | 1 |
| 20 | Cirrhosis of the human liver: an in vitro 31 P nuclear magnetic resonance study显示文摘 | Simon D. Taylor-Robinson E.Louise Thomas Janet Sargentoni Claude D. Marcus Brian R. Davidson Jimmy D. Bell | 1995 | BBA - Molecular Basis of Disease1995，，2： | 1 |
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