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  • 1
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  125. Kongress der Deutschen Gesellschaft für Chirurgie; 20080422-20080425; Berlin; DOC08dgch9525 /20080416/
    Publication Date: 2008-04-14
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 2
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  129. Kongress der Deutschen Gesellschaft für Chirurgie; 20120424-20120427; Berlin; DOC12dgch566 /20120423/
    Publication Date: 2012-04-24
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 3
    Keywords: CELLS ; INHIBITOR ; CELL ; Germany ; INHIBITION ; GENERATION ; ENZYMES ; PROTEIN ; SURGERY ; INJURIES ; kidney ; GRAFT ; REDUCTION ; renal ; TRANSPLANTATION ; RAT ; treatment ; DECREASE ; Jun ; REJECTION ; OXYGEN ; RENAL-ALLOGRAFT ; reactive oxygen species ; INJURY ; INFILTRATION ; RE ; OXYGEN RADICALS ; ALLOGRAFT-REJECTION ; OXIDOREDUCTASE ; ENZYME-ACTIVITIES ; OXIDANT INJURY ; REACTIVE OXYGEN
    Abstract: Background. Increased oxygen radical production may not only contribute to posttransplant ischemia-reperfusion injury but also to acute rejection of renal allografts. Xanthine oxidoreductase (XOR) may constitute a relevant reactive oxygen species (ROS) source. The study was conducted (1) to determine ROS production as well as oxidant and antioxidant enzyme activities in renal grafts and (2) to modulate acute rejection by tungsten administration, a specific inhibitor of XOR. Methods. Syngraft (Lewis to Lewis, Fisher344 to Fisher344) and allograft (Fisher344 to Lewis) kidney transplantations were performed with or without tungsten administration. Analysis was performed at day 1, 3, or 9 posttransplantation. Results. Generation of ROS was enhanced, being 10-fold higher in renal allografts versus control kidneys at day 9 (P 〈 0.01); this was associated with histologic signs of acute rejection. Oxygen radicals were generated to a significant degree by enhanced XOR activity, which increased more than 10-fold in renal allografts at day 9 posttransplantation; XOR protein in glomeruli and tubulointerstitium was also elevated in allografts. In addition, NADPH oxidase activity increased significantly in allografts. The activity of antioxidant enzymes tended to decrease. Tungsten treatment resulted in a pronounced reduction of XOR activity and ROS production, without any effect on NADPH-oxidase activity; mononuclear cell infiltration and rejection signs were significantly ameliorated at day 9 posttransplantation by selective inhibition of XOR. Conclusions. A major part of ROS generation in acute rejection was contributed by XOR. ROS are not only associated with but also contribute to acute allograft rejection because inhibition of XOR alleviated rejection phenomena
    Type of Publication: Journal article published
    PubMed ID: 15201667
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  • 4
    Keywords: CELLS ; ENDOTHELIAL-CELLS ; EXPRESSION ; SURVIVAL ; CELL ; Germany ; IN-VIVO ; INHIBITION ; MICROSCOPY ; MODEL ; PERFUSION ; VIVO ; PROTEIN ; kidney ; MICROCIRCULATION ; REDUCTION ; TRANSPLANTATION ; RAT ; DAMAGE ; RECRUITMENT ; REJECTION ; FAILURE ; RECEPTORS ; chemokine ; ANTAGONIST ; inflammation ; endothelial cells ; ALLOGRAFT-REJECTION ; chemokines ; in vivo ; KIDNEY-TRANSPLANTATION ; ALLOGRAFT ; Allograft rejection ; ANTAGONIST VMIP-II ; Virokine ; vMIP-II
    Abstract: During rejection, leukocytes are recruited from the peripheral circulation into the graft leading to the damage of endothelial cells, capillary perfusion failure and graft loss. Chemokines play a pivotal role in the recruitment of leukocytes to the endothelium. Viral macrophage inflammatory protein-II (vMIP-II), a human herpes virus-8 DNA-encoded protein, is a broad-spectrum chemokine antagonist. The aim of the study was to prove the beneficial activity of vMIP-II treatment on acute rat kidney allograft damage. Heterotopic rat kidney transplantation was performed in the Fischer 344 to Lewis transplantation model and animals were treated with vMIP-II (2 x 15 A mu g or 100 A mu g/day) for 7 days. Rejection-induced damage was analyzed by histology, and microcirculatory changes within the graft were analyzed by in vivo microscopy. Viral macrophage inflammatory protein-II significantly improved acute glomerular damage and tubulointerstitial inflammation and lowered the extent of vascular and tubulointerstitial damage of the treated allografts. Functional microcirculation of peritubular capillaries was significantly improved in vivo, and the firm adherence of leukocytes was significantly reduced by vMIP-II treatment. The administration of the broad-spectrum antagonist vMIP-II improved acute renal allograft damage, mainly by a reduction in leukocyte recruitment with a subsequently improved renal cortical microcirculation in vivo
    Type of Publication: Journal article published
    PubMed ID: 20401660
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  • 5
    Keywords: ADHESION, ALLOGRAFTS, ALPHA(V)BETA(3), ALPHA(V)BETA(3) INTEGRIN, ALPHA-V-INTEGRINS, ANTAGONIST, ARRE
    Abstract: Integrin-mediated cell adhesion and signaling is essential to vascular development and inflammatory processes. Elevated expression of integrin alpha(v)beta(3) has been detected in ischemia-reperfusion injury and rejecting heart allografts. We thus hypothesized that the inhibition of alpha(v)-associated integrins may have potent anti-inflammatory effects in acute kidney allograft rejection. We studied the effects of a peptidomimetic antagonist of alpha(v) integrins in two rat models of renal allotransplantation, differing in degree of major histocompatibility complex mismatch. Integrin alpha(v)beta(3) was up-regulated in rejecting renal allografts. Integrin antagonist reduced the histological signs of acute rejection, the intensity of the mononuclear cell infiltration, and cell proliferation in the grafted kidneys. This could be correlated to a reduced leukocyte-endothelial interaction and an improved peritubular microcirculation observed by intravital microscopy. In vitro under laminar flow conditions, the arrest of monocytes to interleukin-1 beta-activated endothelium was decreased. Furthermore, in co-culture models the proliferation and transmigration of monocytes/macrophages, endothelium, and fibroblasts induced by renal tubular epithelia was efficiently inhibited by alpha(v) integrin antagonism. These data reveal an important role of this integrin subclass in leukocyte recruitment and development and maintenance of acute rejection; blockade of alpha(v) integrins may provide a new therapeutic strategy to attenuate acute allograft rejection
    Type of Publication: Journal article published
    PubMed ID: 17702892
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  • 6
    Keywords: 33, ACUTE REJECTION, CD40, CD40 LIGAND, CELL, CELLS, CHEMOATTRACTANT PROTEIN-1, COMBINATION, Decoy o
    Abstract: During acute rejection of cardiac transplants endothelial cell-leukocyte interaction fuelled by co-stimulatory molecules like CD40/CD154 may ultimately lead to graft loss. One key player in up-regulating the expression of such pro-inflammatory gene products is the interferon-gamma-dependent transcription factor STAT-1. Hence down-regulating interferon-gamma-stimulated pro-inflammatory gene expression in the graft endothelial cells by employing a decoy oligodeoxynucleotide (dODN) neutralising STAT-1 may protect the graft. To verify this hypothesis, heterotopic mouse heart transplantation was performed in the allogeneic B10.A(2R) to C57BL/6 and syngeneic C57BL/6 to C57BL/6 strain combination without immunosuppression. Graft vessels were pre-treated with STAT-1 dODN, mutant control ODN (10 mu M each) or vehicle (Ringer solution). Cellular rejection (vascular and interstitial component) was graded histologically and CD40, ICAM-1, VCAM-1, MCP-1, E-selectin and RANTES expression in the graft monitored by real time PCR 24 h and 9 days post-transplantation. Nine days after transplantation both rejection scores were significantly diminished by 85 and 70%, respectively, in STAT-1 dODN-treated allografts as compared to mutant control ODN-treated allografts. According to immunohistochemistry analysis, this was accompanied by a reduced infiltration of monocyte/macrophages and T cells into the graft myocardium. In addition, pro-inflammatory gene expression was strongly impaired by more than 80% in STAT-1 dODN-treated allografts 24 h post-transplantation but not in mutant control ODN or vehicle-treated allografts. This inhibitory effect on pro-inflammatory gene expression was no longer detectable 9 days post-transplantation. Single periprocedural treatment with a STAT-1 dODN thus effectively reduces cellular rejection in mouse heart allografts. This effect is associated both with an early decline in pro-inflammatory gene expression and a later drop in mononuclear cell infiltration
    Type of Publication: Journal article published
    PubMed ID: 19352584
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  • 7
    Keywords: APOPTOSIS ; CELLS ; ENDOTHELIAL-CELLS ; EXPRESSION ; proliferation ; PROTECTION ; SURVIVAL ; COMBINATION ; human ; INHIBITION ; MODEL ; MODELS ; GENE ; GENES ; TISSUE ; TIME ; NF-KAPPA-B ; ACTIVATION ; RESPONSES ; kidney ; GRAFT ; TRANSPLANTATION ; RAT ; RAT-KIDNEY ; IMMUNE-RESPONSES ; TARGET ; prevention ; UP-REGULATION ; DAMAGE ; MUSCLE ; SMOOTH-MUSCLE CELLS ; IMMUNE-RESPONSE ; REJECTION ; RENAL-ALLOGRAFT ; CHRONIC REJECTION ; ENDOTHELIAL- CELLS ; HEME OXYGENASE-1 ; TRANSPLANTS
    Abstract: Background. Chronic rejection with development of transplant arteriosclerosis is the major culprit involved in loss of kidney allografts. The allografts fate was thought to depend on the intensity of the host immune responses and the potency of immunosuppressive regimens. Recent data suggests that grafts contribute to their own survival by way of up-regulation of "cytoprotective" genes. Methods. We analyzed the expression of four cytoprotective genes. A20. Bcl-2, Bcl-x(L), and heme oxygenase (HO)-1, in three rat renal allograft models of chronic rejection: Fisher 344-Lewis (F344/Lew), Dark Agouti- Brown Norway (DA/BN), and DA-Wistar-Furth (TF). We chose these genes for their known anti-inflammatory and anti-apoptotic function in endothelial cells (EC) and the atheroprotective function of A20 in smooth muscle cells (SMC). Results. Twenty- eight and 9 weeks following transplantation, F344/Lew and DA/BN transplants had stable graft function. Histopathologic analysis showed moderate tissue damage, minimal cellular infiltrates, and preserved vascular integrity correlating with high expression of A20 in SMC. Conversely, impaired allograft function in the DA/WF combination with substantial transplant arteriosclerosis was noted in 60% of the grafts correlating with absent or decreased A20 expression in EC and SMC. In all combinations, expression of HO-1, 136-2, and Bcl-x(L) colocalized with infiltrating cells and was not informative on the graft,status. Conclusions. We demonstrate for the first time a strict correlation between A20 expression in the vessel and the absence of transplant arteriosclerosis in rat kidney- allograft models. This data is similar to data obtained in human kidney allografts and suggests that A20 may represent a novel therapeutic target for the prevention of chronic allograft rejection
    Type of Publication: Journal article published
    PubMed ID: 12544863
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  • 8
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  124. Kongress der Deutschen Gesellschaft für Chirurgie; 20070501-20070504; München; DOC07dgch7443 /20071001/
    Publication Date: 2007-10-02
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 9
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  124. Kongress der Deutschen Gesellschaft für Chirurgie; 20070501-20070504; München; DOC07dgch7543 /20071001/
    Publication Date: 2007-10-02
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 10
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Differences in kinetic properties, pH response, sensitivity to ouabain, and disc-acrylamide electrophoresis resolution, are observed when GTP and ATP are used as the substrates, for triphosphohydrolases in isolated rat brain microvessels. In brain parenchyma there are no such differences. It is concluded that substrate-specific GTPase exists in brain microvessels.
    Type of Medium: Electronic Resource
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