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33 results on '"Burggraf, Dorothe"'

1. Gender specific airway gene expression in COPD sub-phenotypes supports a role of mitochondria and of different types of leukocytes

Author

Esteve-Codina, Anna, Hofer, Thomas P., Burggraf, Dorothe, Heiss-Neumann, Marion S., Gesierich, Wolfgang, Boland, Anne, Olaso, Robert, Bihoreau, Marie-Therese, Deleuze, Jean-Francois, Moeller, Winfried, Schmid, Otmar, Soler Artigas, María, Renner, Kathrin, Hohlfeld, Jens M., Welte, Tobias, Fuehner, Thomas, Jerrentrup, Lukas, Koczulla, Andreas Rembert, Greulich, Timm, Prasse, Antje, Müller-Quernheim, Joachim, Gupta, Sumit, Brightling, Christopher, Subramanian, Deepak R., Parr, David G., Kolsum, Umme, Gupta, Vandana, Barta, Imre, Döme, Balázs, Strausz, János, Stendardo, Mariarita, Piattella, Marco, Boschetto, Piera, Korzybski, Damian, Gorecka, Dorota, Nowinski, Adam, Dabad, Marc, Fernández-Callejo, Marcos, Endesfelder, David, zu Castell, Wolfgang, Hiemstra, Pieter S., Venge, Per, Noessner, Elfriede, Griebel, Thasso, Heath, Simon, Singh, Dave, Gut, Ivo, and Ziegler-Heitbrock, Loems

Published
2021
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9. Influence of lung CT changes in chronic obstructive pulmonary disease (COPD) on the human lung microbiome

Author

Engel, Marion, primary, Endesfelder, David, additional, Schloter-Hai, Brigitte, additional, Kublik, Susanne, additional, Granitsiotis, Michael S., additional, Boschetto, Piera, additional, Stendardo, Mariarita, additional, Barta, Imre, additional, Dome, Balazs, additional, Deleuze, Jean-François, additional, Boland, Anne, additional, Müller-Quernheim, Joachim, additional, Prasse, Antje, additional, Welte, Tobias, additional, Hohlfeld, Jens, additional, Subramanian, Deepak, additional, Parr, David, additional, Gut, Ivo Glynne, additional, Greulich, Timm, additional, Koczulla, Andreas Rembert, additional, Nowinski, Adam, additional, Gorecka, Dorota, additional, Singh, Dave, additional, Gupta, Sumit, additional, Brightling, Christopher E., additional, Hoffmann, Harald, additional, Frankenberger, Marion, additional, Hofer, Thomas P., additional, Burggraf, Dorothe, additional, Heiss-Neumann, Marion, additional, Ziegler-Heitbrock, Loems, additional, Schloter, Michael, additional, and zu Castell, Wolfgang, additional

Published
2017
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10. Emphysema- and airway-dominant COPD phenotypes defined by standardised quantitative computed tomography

Author

Subramanian, Deepak R., primary, Gupta, Sumit, additional, Burggraf, Dorothe, additional, vom Silberberg, Suzan J., additional, Heimbeck, Irene, additional, Heiss-Neumann, Marion S., additional, Haeussinger, Karl, additional, Newby, Chris, additional, Hargadon, Beverley, additional, Raj, Vimal, additional, Singh, Dave, additional, Kolsum, Umme, additional, Hofer, Thomas P., additional, Al-shair, Khaled, additional, Luetzen, Niklas, additional, Prasse, Antje, additional, Müller-Quernheim, Joachim, additional, Benea, Giorgio, additional, Leprotti, Stefano, additional, Boschetto, Piera, additional, Gorecka, Dorota, additional, Nowinski, Adam, additional, Oniszh, Karina, additional, Castell, Wolfgang zu, additional, Hagen, Michael, additional, Barta, Imre, additional, Döme, Balázs, additional, Strausz, Janos, additional, Greulich, Timm, additional, Vogelmeier, Claus, additional, Koczulla, Andreas R., additional, Gut, Ivo, additional, Hohlfeld, Jens, additional, Welte, Tobias, additional, Lavae-Mokhtari, Mahyar, additional, Ziegler-Heitbrock, Loems, additional, Brightling, Christopher, additional, and Parr, David G., additional

Published
2016
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11. Einfluss exogener Plasminogenaktivatoren auf die Veränderungen der Mikrogefäße nach experimenteller fokaler zerebraler Ischämie : Schlussbericht ; Förderkennzeichen: 01 GI 9904 Projekt B3 ; Titel des Netzwerks: Kompetenznetzwerk Schlaganfall ; Titel des Projekts: B) Pathophysiologie und Akuttherapie ; Titel der Projekt Gruppe: B1-B4 Pathophysiologie und Akuttherapie: Experimentelle Untersuchungen ; Typ des Projekts: Tierexperimentelle Untersuchungen ; Laufzeit: 01.01.2000 - 31.12.2004

Author

Hamann, Gerhard and Burggraf, Dorothe

Abstract

Ill., graph. Darst.

Published
2005
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12. The EvA study: aims and strategy

Author

Ziegler-Heitbrock, Loems, primary, Frankenberger, Marion, additional, Heimbeck, Irene, additional, Burggraf, Dorothe, additional, Wjst, Matthias, additional, Häussinger, Karl, additional, Brightling, Chris, additional, Gupta, Sumit, additional, Parr, David, additional, Subramanian, Deepak, additional, Singh, Dave, additional, Kolsum, Umme, additional, Boschetto, Piera, additional, Potena, Alfredo, additional, Gorecka, Dorota, additional, Nowinski, Adam, additional, Barta, Imre, additional, Döme, Balazs, additional, Strausz, Janos, additional, Greulich, Timm, additional, Vogelmeier, Claus, additional, Bals, Robert, additional, Hohlfeld, Jens M., additional, Welte, Tobias, additional, Venge, Per, additional, Gut, Ivo, additional, Boland, Anne, additional, Olaso, Robert, additional, Hager, Jörg, additional, Hiemstra, Pieter, additional, Rabe, Klaus F., additional, Unmüßig, Martina, additional, Müller-Quernheim, Joachim, additional, and Prasse, Antje, additional

Published
2012
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31. Influence of the duration of ischemia and reperfusion on infarct volume and microvascular damage in mice.

Author

Vosko, Milan R., Burggraf, Dorothe, Liebetrau, Martin, Wunderlich, Nathalie, Jäger, Gabriele, Gröger, Moritz, Plesnila, Nikolaus, and Hamann, Gerhard F.

Subjects
CEREBRAL ischemia, REPERFUSION injury, MICROCIRCULATION disorders, IMMUNOHISTOCHEMISTRY, HEMORRHAGE, LABORATORY mice
Abstract

Objectives: Focal cerebral ischemia is responsible for alterations of vascular permeability, and the loss of microvascular integrity is a primary source of subsequent hemorrhages. We evaluated the influence of different durations of ischemia and reperfusion on infarction size and microvascular damage after focal cerebral ischemia in the mouse. Methods: C57BL/6 mice (n = 39) were subjected to focal cerebral ischemia (I) and reperfusion (R). Consecutive brain sections were analysed for infarction volumes (Nissl-staining) and for collagen type IV (immunohistochemistry and western blot). Results: Infarction size (percentage of the infarction volume versus ipsilateral hemisphere) increased with total time of ischemia and reperfusion: 19 ± 2% (I3R0), 30 ± 2% (I3R3), 36 ± 4% (I3R12), 41 ± 4% (I1R24), 45 ± 6% (I2R24) and 58 ± 2% (I3R24). The ischemic hemispheres showed a significant progressive reduction of collagen type IV positive vessels (ischemic versus non-ischemic contralateral area): 90 ± 3% (I3R0), 88 ± 1% (I3R3), 82 ± 3% (I3R12), 85 ± 3% (I1R24), 79 ± 3% (I2R24), 72 ± 2% (I3R24). Conclusions: Both prolonged ischemia and reperfusion lead to an increased infarction volume, as well as progressive microvascular damage. [ABSTRACT FROM AUTHOR]

Published
2006
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32. ACE inhibition reduces activity of the plasminogen/plasmin and MMP systems in the brain of spontaneous hypertensive stroke-prone rats

Author

Liebetrau, Martin, Burggraf, Dorothe, Wunderlich, Nathalie, Jäger, Gabriele, Linz, Wolfgang, and Hamann, Gerhard F.

Subjects
*FIBRINOLYTIC agents, *EXTRACELLULAR matrix, *BLOOD plasma, *ACE inhibitors
Abstract

Abstract: The spontaneously hypertensive stroke-prone rat (SHR-SP) is an experimental model of malignant hypertension which lead to secondary alterations of the extracellular matrix. Our aim was to determine ACE-inhibitor related changes of proteases involved in the reconstruction of the extracellular matrix in the brain. Twelve SHR-SP rats were randomized into two groups. Each group was treated with either an antihypertensive dose of ramipril or placebo for 6 months. Brain tissue plasminogen activator (t-PA) and urokinase (u-PA) were quantified by using casein-dependent plasminogen zymography, matrix metalloproteinase (MMP)-2 and MMP-9, by MMP-zymography, and tissue inhibitor of MMP (TIMP)-1 and -2, by reverse zymography. The amounts of u-PA, t-PA, and MMPs were significantly reduced in animals treated with ACE inhibitor. Plasminogen zymography showed a 39% reduction of u-PA in the basal ganglia (p <0.0001); t-PA expression was reduced by 26% in the cortex and by 33% in the basal ganglia (p <0.0001). MMP-2 expression was reduced by 15% in the cortex (p <0.05) and by 10% in the basal ganglia (p <0.05); MMP-9 expression significantly decreased by 37% in the cortex and by 25% in the basal ganglia (p <0.0001 each). No differences were observed in the amount of TIMP-1 or TIMP-2. These findings provide new insights into the biochemical mechanisms underlying extracellular matrix proliferation and its modulation by ACE inhibitors. Therapeutic alterations that influence the proteolytic systems might prove important in the prevention of extracellular matrix accumulation and secondary microvascular vessel wall changes. [Copyright &y& Elsevier]

Published
2005
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33. Matrix metalloproteinase‐9 promotes neutrophil and T cell recruitment and migration in the postischemic liver

Author

Khandoga, Andrej, Kessler, Julia S., Hanschen, Marc, Khandoga, Alexander G., Burggraf, Dorothe, Reichel, Christoph, Hamann, Gerhard F., Enders, Georg, and Krombach, Fritz

Abstract

Matrix metalloproteinases‐2 and ‐9 (MMP‐2/9) are critically involved in degradation of extracellular matrix, and their inhibition is discussed as a promising strategy against hepatic ischemia‐reperfusion (I/R) injury. Here, we analyzed the role of MMP‐2 and ‐9 for leukocyte migration and tissue injury in sham‐operated mice and in mice after I/R, treated with a MMP‐2/9 inhibitor or vehicle. Using zymography, we show that the MMP‐2/9 inhibitor abolished I/R‐induced MMP‐9 activation, whereas MMP‐2 activity was not detectable in all groups. As demonstrated by intravital microscopy, MMP‐9 inhibition attenuated postischemic rolling and adherence of total leukocytes in hepatic postsinusoidal venules, CD4+ T cell accumulation in sinusoids, and neutrophil transmigration. These effects were associated with reduction of plasma tumor necrosis factor α (TNF‐α) levels and endothelial expression of CD62P. Motility of interstitially migrating leukocytes was assessed by near‐infrared reflected light oblique transillumination microscopy in the postischemic cremaster muscle. Upon MMP‐9 blockade, leukocyte migration velocity and curve‐line and straight‐line migration distances were reduced significantly as compared with the vehicle‐treated I/R group. Postischemic sinusoidal perfusion failure, hepatocellular apoptosis, and alanine aminotransferase activity were only slightly reduced after MMP‐9 inhibition, whereas aspartate aminotransferase activity and mortality were significantly lower. In conclusion, MMP‐9 is involved in the early recruitment cascades of neutrophils and CD4+ T cells, promotes neutrophil and T cell transmigration during hepatic I/R, and is required for motility of interstitially migrating leukocytes. MMP‐9 blockade is associated with an attenuation of TNF‐α release and endothelial CD62P expression, weakly protects from early microvascular/hepatocellular I/R damage, but improves postischemic survival.

Published
2006
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