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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 | Hepatitis E virus in patients with acute severe liver injury显示文摘AIM: To examine the incidence of hepatitis E(HepE) in individuals with acute liver injury severe enough to warrant treatment at a transplant unit.METHODS: Hepatitis E virus(HEV) is an emerging pathogen in developed countries causing severe illness, particularly in immunocompromised patients or those with underlying chronic liver disease. HepE infection isoften under diagnosed, as clinicians can be reluctant to test patients who have not travelled to regions traditionally considered hyperendemic for HepE. There are few data regarding the significance of HEV in patients with very severe acute liver injury in developed countries. Eighty patients with acute severe liver injury attending the Scottish Liver Transplant unit were tested for HEV and anti-HEV IgG and IgM. Severe acute liver injury was defined as a sudden deterioration in liver function confirmed by abnormal liver function tests and coagulopathy or presence of hepatic encephalopathy. Eighty percent of these patients were diagnosed with paracetomol overdose. No patients had a history of chronic or decompensated chronic liver disease at time of sampling. IgG positive samples were quantified against the World Health Organization anti-HEV IgG standard. Samples were screened for HEV viral RNA by quantitative reverse transcription polymerase chain reaction.RESULTS: Four cases of hepatitis E were identified. Three of the four cases were only diagnosed on retrospective testing and were initially erroneously ascribed to drug-induced liver injury and decompensated chronic liver disease, with the cause of the decompensation uncertain. One case was caused by HEV genotype 1 in a traveller returning from Asia, the other three were autochthonous and diagnosed on retrospective testing. In two of these cases(where RNA was detected) HEV was found to be genotype 3, the most prevalent genotype in developed countries. Three patients survived, two of whom had been misdiagnosed as having drug induced liver injury. The fourth patient died from sepsis and liver failure precipitated as a result of hepatitis E infection and previously undiagnosed cirrhosis. Histopathology data to date is limited to mainly that seen for endemic HepE. All patients, with the exception of patient 1, demonstrated characteristics of HepE infection, as seen in previously described locally acquired cases.CONCLUSION: In patients with acute severe liver injury, HEV testing should be part of the initial diagnostic investigation algorithm irrespective of suspected initial diagnosis, age or travel history. | Claire Louise Crossan Kenneth J Simpson Darren G Craig Christopher Bellamy Janice Davidson Harry R Dalton Linda Scobie | 2014 | World Journal of Hepatology2014，6，6： | 4 |
| 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 | Fondaparinux预防老年急性内科患者发生静脉血栓形成的效果与安全性:随机安慰剂对照研究显示文摘目的:观察 Fondaparinux 对具有中高度静脉血栓发生危险的老年急性内科住院患者的抗凝效果与安全性。设计:双盲随机安慰剂对照研究。背景:8个国家的35个中心。参与者:849例≥60岁内科患者,住院原因分别为充血性心力衰竭、慢性肺病合并急性呼吸系统疾患、急性炎症性或感染性疾病,预期至少住院4天以上。干预:2.5 mg Fondaparinux 或安慰剂,每天1次皮下注射,持续6~14天。观察指标:主要指标为静脉血栓形成(治疗后15天内采用双侧静脉造影检查)及有症状的静脉血栓;次要指标为死亡与出血。患者随访时间为1个月。结果:Fondaparinux 治疗组425例患者和安慰剂组414例患者接受了安全性分析(10例未治疗)。644例患者(75.9%)可接受主要指标分析。静脉血栓检出率在 Fondaparinux 治疗组为5.6%(18/321),安慰剂组为10.5%(34/323),相对危险减少46.7%(95% CI 7.7%~69.3%)。安慰剂组5例患者发生有症状的静脉血栓,Fondaparinux治疗组无患者发生有症状的静脉血栓(P=0.029)。两组均有1例(0.2%)患者发生严重出血。随访结束时,安慰剂组、Fondaparinux 治疗组分别死亡25(6.0%)、14(3.3%)例患者。结论:Fondaparinux 可有效预防急性内科老年患者无症状性及有症状的静脉血栓。严重出血几率两组相似。 | Alexander T Cohen Bruce L Davidson Alexander S Gallus Michael R Lassen Martin H Prins Witold Tomkowski Alexander G G Turpie Jan F M Egberts Anthonie W A Lensing 石汉平(译) 王深明(校) | 2006 | 英国医学杂志中文版2006，9，5： | 3 |
| 8 | 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 |
| 9 | Focused-flow model of relativistic diodes显示文摘 | Goldstein S A Davidson R C Siambis J G | 1974 | PhysRev Lett1974，33，25： | 2 |
| 10 | Posterior interosseous nerve localization within the proximal forearm-a patient normalized parameter显示文摘AIM To provide a 'patient-normalized' parameter in the proximal forearm. METHODS Sixty-three cadaveric upper extremities from thirty-five cadavers were studied. A muscle splitting approach was utilized to locate the posterior interosseous nerve(PIN) at the point where it emerges from beneath the supinator. The supinator was carefully incised to expose the midpoint length of the nerve as it passes into the forearm while preserving the associated fascial connections, thereby preserving the relationship of the nerve with the muscle. We measured the transepicondylar distance(TED), PIN distance in the forearm's neutral rotation position, pronation position, supination position, and the nerve width. Two individuals performed measurements using a digital caliper with inter-observer and intraobserver blinding. The results were analyzed with the Wilcoxon-Mann-Whitney test for paired samples. RESULTS In pronation, the PIN was within two confidence intervals of 1.0 TED in 95% of cases(range 0.7-1.3 TED); in neutral, within two confidence intervals of 0.84 TED in 95% of cases(range 0.5-1.1 TED); in supination,within two confidence intervals of 0.72 TED in 95% of cases(range 0.5-0.9 TED). The mean PIN distance from the lateral epicondyle was 100% of TED in a pronated forearm, 84% in neutral, and 72% in supination. Predictive accuracy was highest in supination; in all cases the majority of specimens(90.47%-95.23%) are within 2 cm of the forearm position-specific percentage of TED. When comparing right to left sides for TEDs with the signed Wilcoxon-Mann-Whitney test for paired samples as well as a significance test(with normal distribution), the P-value was 0.0357(significance-0.05) indicating a significant difference between the two sides.CONCLUSION This 'patient normalized' parameter localizes the PIN crossing a line drawn between the lateral epicondyle and the radial styloid. Accurate PIN localization will aid in diagnosis, injections, and surgical approaches. | Srinath Kamineni Crystal R Norgren Evan M Davidson Ellora P Kamineni Andrew S Deane | 2017 | World Journal of Orthopedics2017，8，4： | 2 |
| 11 | Protection of the liver by ischemic preconditioning: a review of mechanisms and clinical applications显示文摘 | Koti R S Seifalian A M Davidson B R | 2003 | Dig Surg2003，20，5： | 2 |
| 12 | ADA与EASD对2型糖尿病高血糖处理:治疗启动与评定的新共识方案显示文摘在不到一年时间由同一批专家代表ADA和EASD先后起草和发布了两次关于'2型糖尿病高血糖处理的共识声明'同时发表在2008年1月和12月的《Diabetes Care》和《Diabetologia》上。第一次共识声明内容主要围绕TZDs药物的安全性,本刊作了摘译转载(参阅《中国糖尿病杂志》2008年第7期)。第二次修订的共识声明,关注点为降糖药的新分级,论据及观点比较清晰,故仍摘译供读者参考。 | Nathan DM Buse JB Davidson MB Ferrannini E Holman RR Sherwin R Zinman B 钱荣立(摘译) | 2009 | 中国糖尿病杂志2009，17，1： | 2 |
| 13 | Nonlinear properties of the Kapchinskij-vladimirskij equilibrium and envelope equation for an intense charged-particle beam in a periodic focusing field显示文摘 | Chen C Davidson R C | 1994 | Phy Rev E1994，49，6： | 2 |
| 14 | Cholangiocarcinoma显示文摘 | Shahid A Khan Howard C Thomas Brian R Davidson Simon D Taylor-Robinson | 2005 | The Lancet2005，，9493： | 2 |
| 15 | A model for heap bioleaching of chalcocite with heat balance: mesophiles and moderate thermophiles显示文摘 | Leahy M J Davidson M R Schwarz M P | 2007 | Hyclrometallurgy2007，85，1： | 1 |
| 16 | Ezetimibe coadministered with simvastatin In patients with primary hypercholesterolemia显示文摘 | DAVIDSON MH MCGARRY T BETTIS R | 2002 | J Am Coll Cardiol2002，40，12： | 1 |
| 17 | Diffusion and chemical activity of Zr-Sn and Zr-Ti systems 显示文摘 | ZEE R H WATTERS J F DAVIDSON R D | 1986 | Physical Review B1986，34，10： | 1 |
| 18 | The Retail Life Cycle显示文摘 | DAVIDSON W R BATES A D BASS S J | 2002 | Retailing:The Evolution and Development of Retailing2002，55，6： | 1 |
| 19 | Effect of root/leaf temperature differentials on root / shoot ratios in some pasture grasses and clover显示文摘 | Davidson R | 1969 | Annals of Bota- ny1969，33，： | 1 |
| 20 | Evaluating evidence-based medicine skills during a performance-based examination显示文摘 | Davidson ra Duerson M Romrell L Pauly R Watson rt | 2004 | Acad Med2004，79，3： | 1 |
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