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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 | 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 |
| 3 | Molecular regulation of cardiac hypertrophy显示文摘 | Barry SP Davidson SM Townsend PA | 2008 | Int J Biochem Cell Biol2008，40，10： | 1 |
| 4 | Molecular regulation of cardiac hypertrophy 显示文摘 | Sean P Barry Sean M Davidson Paul A Townsend | 2008 | Intern Biochem Cell Biol2008，40，10： | 1 |
| 5 | 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 |
| 6 | Social networks, communication styles, and learning performance in a CSCL community显示文摘 | Hichang Cho Geri Gay Barry Davidson | 2007 | Computers & Education2007，49，2： | 1 |
| 7 | Utilization of a major brown rust resistance gene in sugarcane breeding显示文摘 | Neil C. Glynn Chris Laborde R. Wayne Davidson Mike S. Irey Barry Glaz Angélique D’Hont Jack C. Comstock | 2013 | Molecular Breeding2013，，2： | 1 |
| 8 | Molecular regulation of cardiac hypertrophy显示文摘 | Barry SP Davidson SM Townsend PA | 2008 | Int J Biochem Cell Biol2008，40，： | 1 |
| 9 | Hospitality HRM: past, present and the future显示文摘 | Michael C.G. Davidson Ruth McPhail Shane Barry | 2011 | International Journal of Contemporary Hospitality Management2011，，4： | 1 |
| 10 | Determination of energy release rate and mode mix in three-dimensional layered structures using plate theory显示文摘 | Barry D. Davidson LiJie Yu Hurang Hu | 2000 | International Journal of Fracture2000，，1： | 1 |
| 11 | Genomic organization of lactic acid bacteria显示文摘 | Barrie E. Davidson Nancy Kordias Marian Dobos Alan J. Hillier | 1996 | Antonie van Leeuwenhoek (-)1996，，2： | 1 |
| 12 | Molecular regulation of cardiac hypertrophy显示文摘 | Barry SP Davidson SM Townsend PA | 2008 | Int J Biochem Cell Biol2008，40，10： | 1 |
| 13 | Molecular regulation of cardiac hypertrophy显示文摘 | Barry SP Davidson SM Townsend PA | 2008 | Int J Biochem Cell Biol2008，40，： | 1 |
| 14 | Molecular regulation of cardiac hypertrophy显示文摘 | BARRY S DAVIDSON S TOWNSEND P | 2008 | Int J Biochem Cell2008，40，10： | 1 |
| 15 | Social networks, communication styles, and learning performance in a CSCL commtmity显示文摘 | Cho Hichang Gay Geri Davidson Barry | 2007 | Computers & Education2007，49，2： | 1 |
| 16 | Molecular regulation of cardiac hypertrophy显示文摘 | Barry S P Davidson S M Townsend P A | 2008 | International Journal of Biochemistry NCell Biology2008，40，10： | 1 |
| 17 | Molecular regulation of cardiac hypertrophy显示文摘 | Barry SP Davidson SM Townsend PA | | 0，，10： | 1 |
| 18 | An expert system for the design and analysis of composite structures显示文摘 | BARRY DAVIDSON UTPAL ROY CHRIS LUDDEN | 1999 | IIE Transactions1999，，4： | 1 |
| 19 | Influence of environmental vertical wind shear on the intensity of hurricane-strength tropical cyclones in the Australian region显示文摘 | Paterson Linda A Barry Hanstrum Noel E Davidson | 2005 | Monthly Weather Review2005，133，： | 1 |
| 20 | Molecular regulation of cardiac hypertrophy显示文摘 | BARRY S P DAVIDSON S M TOWNSEND P A | 2008 | Int J Biochem Cell Biol2008，40，： | 1 |
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