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69 results on '"Lindeman, Jan H.N."'

51. Renal Ischemia-Reperfusion Induces Release of Angiopoietin-2 From Human Grafts of Living and Deceased Donors

Author

de Vries, Dorottya K., primary, Khairoun, Meriem, additional, Lindeman, Jan H.N., additional, Bajema, Ingeborg M., additional, de Heer, Emile, additional, Roest, Mark, additional, van Zonneveld, Anton J., additional, van Kooten, Cees, additional, Rabelink, Ton J., additional, Schaapherder, Alexander F., additional, and Reinders, Marlies E.J., additional

Published
2013
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53. Correction

Author

Beenakker, Jan-Willem M., primary, Ashcroft, Brian A., additional, Lindeman, Jan H.N., additional, and Oosterkamp, Tjerk H., additional

Published
2012
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57. Expression of Vascular Endothelial Growth Factor, Stromal Cell-Derived Factor-1, and CXCR4 in Human Limb Muscle With Acute and Chronic Ischemia

Author

van Weel, Vincent, primary, Seghers, Leonard, additional, de Vries, Margreet R., additional, Kuiper, Esther J., additional, Schlingemann, Reinier O., additional, Bajema, Ingeborg M., additional, Lindeman, Jan H.N., additional, Delis-van Diemen, Pien M., additional, van Hinsbergh, Victor W.M., additional, van Bockel, J. Hajo, additional, and Quax, Paul H.A., additional

Published
2007
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58. Collagen Degradation in the Abdominal Aneurysm

Author

Abdul-Hussien, Hazem, primary, Soekhoe, Ratna G.V., additional, Weber, Ekkehard, additional, von der Thüsen, Jan H., additional, Kleemann, Robert, additional, Mulder, Adri, additional, van Bockel, J. Hajo, additional, Hanemaaijer, Roeland, additional, and Lindeman, Jan H.N., additional

Published
2007
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62. Phenotypic Modulation of Smooth Muscle Cells in Atherosclerosis Is Associated With Downregulation of LMOD1, SYNPO2, PDLIM7, PLN, and SYNM

Author

Perisic Matic, Ljubica, Rykaczewska, Urszula, Razuvaev, Anton, Sabater-Lleal, Maria, Lengquist, Mariette, Miller, Clint L., Ericsson, Ida, Röhl, Samuel, Kronqvist, Malin, Aldi, Silvia, Magné, Joelle, Paloschi, Valentina, Vesterlund, Mattias, Li, Yuhuang, Jin, Hong, Diez, Maria Gonzalez, Roy, Joy, Baldassarre, Damiano, Veglia, Fabrizio, Humphries, Steve E., de Faire, Ulf, Tremoli, Elena, Odeberg, Jacob, Vukojević, Vladana, Lehtiö, Janne, Maegdefessel, Lars, Ehrenborg, Ewa, Paulsson-Berne, Gabrielle, Hansson, Göran K., Lindeman, Jan H.N., Eriksson, Per, Quertermous, Thomas, Hamsten, Anders, and Hedin, Ulf

Abstract

Supplemental Digital Content is available in the text.

Published
2016
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67. Renal Ischemia-Reperfusion Induces Release of Angiopoietin-2 From Human Grafts of Living and Deceased Donors

Author

Vries, Dorottya K. de, Khairoun, Meriem, Lindeman, Jan H.N., Bajema, Ingeborg M., de Heer, Emile, Roest, Mark, Zonneveld, Anton J. van, van Kooten, Cees, Rabelink, Ton J., Schaapherder, Alexander F., and Reinders, Marlies E.J.

Abstract

Recent insights suggest that endothelial cell (EC) activation plays a major role in renal ischemia-reperfusion (IR) injury. Interactions between ECs and pericytes via signaling molecules, including angiopoietins, are involved in maintenance of the vascular integrity. Experimental data have shown that enhancement of Angiopoietin (Ang)-1 signaling might be beneficial in renal IR injury. However, little is known about the role of angiopoietins in human renal IR injury.

Published
2013
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68. Correction

Author

Beenakker, Jan-Willem M., Ashcroft, Brian A., Lindeman, Jan H.N., and Oosterkamp, Tjerk H.

Subjects
Biophysics, Correction
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69. No prominent role for terminal complement activation in the early myocardial reperfusion phase following cardiac surgery.

Author

Kortekaas, Kirsten A., van der Pol, Pieter, Lindeman, Jan H.N., Baan, Carla C., van Kooten, Cees, and Klautz, Robert J.M.

Subjects
*MYOCARDIAL reperfusion, *CARDIAC surgery, *HEART failure patients, *COMPLEMENT activation, *CLINICAL trials, *HEART pathophysiology, *HOMOGRAFTS, *IMMUNOLOGY
Abstract

OBJECTIVES Complement activation is considered an important mediator of myocardial ischaemia/reperfusion (I/R) injury. Although complement inhibitors are highly effective in animals, clinical trials fail to show a substantial benefit in humans. This raises questions on the role of complement activation in human myocardial I/R injury. METHODS Soluble C5b-9, i.e. terminal complement complex, and C5a were assessed in patients with non-ischaemic (n = 10) and ischaemic heart failure (n = 10), and patients without heart failure (n = 10) undergoing cardiac surgery. To study the pathophysiology of human I/R injury, a model of arteriovenous measurements over the reperfused heart was applied at consecutive time points during the early reperfusion phase. Furthermore, C3d and C5b-9 depositions in pre-reperfusion myocardial and endomyocardial tissue were evaluated and compared to pre-transplantation tissue from myocardial allografts. RESULTS Simultaneous assessment of soluble C5b-9 and C5a in systemical and myocardial venous blood samples revealed the absence of net release from the reperfused heart in all three patient groups. Biopsies of patients with non-ischaemic heart failure showed the most abundant myocardial depositions of C3d and C5b-9: 4.8 times more C3d (P = 0.008) and 4.7 times more C5b-9 (P = 0.004) than donor tissue. Also C3d was abundantly present in endomyocardial tissue of both heart failure groups compared to donors (both P = 0.02). CONCLUSIONS No evidence was obtained that terminal complement activation is involved in the acute phase following myocardial reperfusion. Since complement deposition was already present before reperfusion, human complement inhibition might be more beneficial in the preoperative phase than during reperfusion. [ABSTRACT FROM AUTHOR]

Published
2012
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