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1

Serum concentrations of MCP-1 and RANTES in patients during aortic surgery: the relationship with ischemia-reperfusion

100%
Jedynak M., Siemiatkowski A., Gacko M., Mroczko B., Borkowski J.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 3
201-207
EN
Surgical trauma is associated with depression of the immune system, which results in a high complication rate following abdominal aortic aneurysm (AAA) repair. Monocyte chemotactic protein-1 (MCP-1) and regulated-on-activation normal T cell expressed and secreted (RANTES) protein are important mediators of the immune and inflammatory response. The aim of this study was to determine whether there is any relationship between MCP-1 or RANTES and operative injury and ischemia-reperfusion during AAA surgery in human. Peripheral blood samples were taken from 12 patients before surgery, after anesthesia induction, before unclamping of aorta (PreXoff), 90 min after unclamping (90minXoff), and at 24 and 48 h after surgery. The MCP-1 and RANTES serum concentrations were measured with the ELISA technique. MCP-1 concentration significantly increased after reperfusion (90minXoff) in comparison with the PreXoff level (p=0.001). Twenty-four hours after AAA repair, MCP-1 significantly decreased 269?225 pg/ml (p=0.005) and reached preoperative value. RANTES level was higher in AAA patients before surgery than in controls (p=0.025) and decreased significantly after ischemia-reperfusion to 13 ng/ml (p< 0.001) at 90minXoff. We showed increases in RANTES concentration to 26 ng/ml on the 1st and to 31 ng/ml on the 2nd day after surgery (p=0.020, p=0.012, respectively) compared with the 90minXoff level. Ischemia-reperfusion during AAA repair results in an increase in MCP-1 and decrease in RANTES concentrations in serum. The changes in chemokine concentrations may influence the development of immunosuppression after AAA repair, contributing to the postoperative course.
2
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Behavioral evaluation of ischemic damage to CA1 hippocampal neurons: Effects of preconditioning

100%
Duszczyk M., Ziembowicz A., Gadamski R., Lazarewicz J. W.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 4
311-319
EN
In Mongolian gerbils, global forebrain ischemia induces enhanced locomotor activity and the disruption of nest building immediately after the insult, followed by damage to hippocampal neurons developing 3 days later. Preconditioning by a brief episode of sublethal ischemia induces the protection of CA1 hippocampal neurons against a lethal ischemic insult. We examined how preconditioning with 2-min ischemia affects disturbances in the nest building behavior and locomotor activity induced by the injurious 3-min ischemia. Morphological examination confirmed that preconditioning significantly reduced neuronal damage in CA1 evoked by injurious ischemia. Behavioral studies demonstrated that preconditioning reduced the locomotor hyperactivity and latency in nest building after test ischemia, in comparison to sham or naive animals. The results indicate that the nest building test and measurement of locomotor activity may be used for an early in vivo prediction of the extent of ischemic brain damage and tolerance induced by ischemic preconditioning.
3
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Effect of 3-aminobenzamide on Bcl-2, Bax and AIF localization in hippocampal neurons altered by ischemia-reperfusion injury. The immunocytochemical study

100%
Strosznajder R., Gajkowska B.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 1
15-22
EN
Poly(ADP-ribose) polymerase plays an important role in cell survival and death. Our previous histological and ultrastructural studies showed that PARP inhibitor 3-aminobenzamide (3-AB) protected neurons against death after ischemia. In this study we investigated the effect of 3-AB on the localization and expression of apoptosis inducing factor (AIF) and on two proteins from Bcl-2 family: Bcl-2 and Bax in hippocampal area CA1, on the 4th day after 3 min of forebrain ischemia in gerbils. Our results indicated that after ischemia AIF is preferentially translocated from the mitochondria to the cytoplasm and to the nucleus. Intravenous administration of 3-AB (30 mg/kg b.w.) prevents AIF translocation to the nucleus. AIF was mainly seen in the structurally unchanged mitochondria and Golgi complex. Moreover, after 3-AB administration overexpression of Bcl-2 protein was observed in mitochondrial membranes, rough endoplasmatic reticulum, Golgi complex, nuclear envelopes, and also in cytoplasm and in nucleus. These data suggest that inhibition of PARP activity may have a beneficial effect on hippocampal neurons through overexpression of Bcl-2 protein and suppression of AIF translocation to the nucleus.
4
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Proteomics of experimental stroke in mice

88%
Focking M., Besselmann M., Trapp T.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 4
273-278
EN
Multi-Western blots of more than 400 proteins were performed from brain extracts of mice submitted to transient focal ischemia induced by 1 h middle cerebral artery (MCA) thread occlusion. Measurements were carried out in groups of six animals in sham-operated controls, at the end of 1 h ischemia, and after 3 and 12 h recirculation. After MCA occlusion up to 45% of proteins were up- or downregulated in the ipsilateral hemisphere by a factor of 1.5 or more, as compared to sham-operated controls. The temporal regulation of several proteins in the ischemia-affected hemisphere after 1 h MCA thread occlusion is described. In the non-ischemic hemisphere the number of regulated proteins was close to 50%, indicating a hitherto unrecognized involvement of the opposite side. The proteomic approach of brain injury analysis goes beyond previous screenings of gene expression at the transcriptional level and although our study provides further evidence for the complexity of multiinjury pathways in the evolution of ischemic brain damage it may help to identify key mediators of ischemic injury.
5
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Effect of carvedilol on neuronal survival and poly(ADP-ribose) polymerase activity in hippocampus after transient forebrain ischemia

88%
Strosznajder R., Jesko H., Dziewulska J.
Acta Neurobiologiae Experimentalis
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2005
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vol. 65
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issue 2
137-134
EN
Carvedilol a beta-adrenoreceptor antagonist with potent antioxidant properties raises high expectations in therapy of ischemia. In this study the effect of carvedilol on neuronal survival after transient forebrain ischemia in gerbils was investigated. The role of poly(ADP-ribose) polymerase (PARP-1) in this process was evaluated. Our data indicated that carvedilol administered subcutaneously in a dose of 7 or 70 mg/kg b.w. directly after 5 min of transient forebrain ischemia protects significant population of neurons in hippocampal area CA1, but has no effect after induction of prolonged 10 min ischemia. Carvedilol significantly decreased PARP activity in hippocampus that was markedly increased after both 15 min and 4 days of reperfusion following 5 min of ischemia. Moreover, carvedilol prevented NAD+ depletion after ischemic-reperfusion insult. These results indicated that carvedilol protects neurons against death and suggested that suppression of PARP activity during reperfusion could be involved in this process.
6

Ischemia-reperfusion injury of the liver

88%
Ziaja J.
Postępy Higieny i Medycyny Doświadczalnej
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2001
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vol. 55
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issue 3
433-448
EN
There is no single factor responsible for liver injury after its temporary ischemia and reperfusion. We deal with a mosaic of biochemical processes, in which a number of cells, mediators and enzymatic systems take part. The mechanism of liver injury remains far from full explanation.
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