von Dr. Haitao Wang
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| [1.] Haw/Fragment 006 01 - Diskussion Zuletzt bearbeitet: 2014-10-16 17:57:41 Singulus | BauernOpfer, Fragment, Gesichtet, Haw, SMWFragment, Schaper 2009, Schutzlevel sysop |
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| Untersuchte Arbeit: Seite: 6, Zeilen: 1-9 |
Quelle: Schaper 2009 Seite(n): 7, Zeilen: r. Spalte: 33ff |
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| The pressure derived pulsatile stretch is also discussed[25, 36, 37], and the transcription factor- activator protein 1 (AP-1) is the molecular transducer. However, AP-1 is also activated by FSS[38], Pulsatile stretch can only be tested acutely and in vitro with its inherent limits. Cultured endothelium under stretch alters translation and transcription of growth factors and changes the sensitivity to cytokines[11, 39, 40]. If pulsatile stretch is a molding force, it must be demonstrated that in collateral growth pulsatile stretch is higher than the physiological levels in normal small arteries. Furthermore, in arterial occlusion the intravascular pressure downstream from the occlusion is much lower than the systemic arterial pressure[8].
8. Schaper, W., Collateral circulation: past and present. Basic Res Cardiol, 2009. 104(1): p. 5-21. 11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62. 25. Korff, T., K. Aufgebauer, and M. Hecker, Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation, 2007. 116(20): p. 2288-97. 36. Lehoux, S., et al., Differential regulation of vascular focal adhesion kinase by steady stretch and pulsatility. Circulation, 2005. 111(5): p. 643-9. 37. Popp, R., I. Fleming, and R. Busse, Pulsatile stretch in coronary arteries elicits release of endothelium-derived hyperpolarizing factor: a modulator of arterial compliance. Circ Res, 1998. 82(6): p. 696-703. 38. Miyagi, M., et al., Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells. Arterioscler Thromb Vasc Biol, 2005. 25(5): p. 970-5. 39. Busse, R. and I. Fleming, Pulsatile stretch and shear stress: physical stimuli determining the production of endothelium-derived relaxing factors. J Vasc Res, 1998. 35(2): p. 73-84. 40. Demicheva, E., M. Hecker, and T. Korff, Stretch-induced activation of the transcription factor activator protein-1 controls monocyte chemoattractant protein-1 expression during arteriogenesis. Circ Res, 2008. 103(5): p. 477-84. |
However, pressure derived pulsatile stretch is also discussed [83, 88, 110] and the transcription factor AP-1 is the molecular transducer. However, AP-1 is also activated by FSS [96]. Pulsatile stretch can only be tested acutely and in vitro with its inherent limits. Cultured endothelium under stretch alters translation and transcription of growth factors and changes the sensitivity to cytokines[14, 32, 110]. If pulsatile stretch is a molding force it must be demonstrated that in collateral growth pulsatile stretch is higher than the physiological levels in normal small arteries. Furthermore, in arterial occlusion the intravascular pressure downstream from the occlusion (and hence in the receiving end of the collateral arcade) is much lower than the systemic arterial pressure [...]
14. Busse R, Fleming I (1998) Pulsatile stretch and shear stress: physical stimuli determining the production of endothelium-derived relaxing factors. J Vasc Res 35:73–84 32. Demicheva E, Hecker M, Korff T (2008) Stretch-induced activation of the transcription factor activator protein-1 controls monocyte chemoattractant protein-1 expression during arteriogenesis. Circ Res (in press) 83. Korff T, Aufgebauer K, Hecker M (2007) Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation 116:2288–2297 88. Lehoux S, Esposito B, Merval R, Tedgui A (2005) Differential regulation of vascular focal adhesion kinase by steady stretch and pulsatility. Circulation 111:643–649 96. Miyagi M, Miwa Y, Takahashi-Yanaga F, Morimoto S, Sasaguri T (2005) Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells. Arterioscler Thromb Vasc Biol 25:970–975 110. Popp R, Fleming I, Busse R (1998) Pulsatile stretch in coronary arteries elicits release of endothelium-derived hyperpolarizing factor: a modulator of arterial compliance. Circ Res 82:696–703 |
Die Quelle ist am Ende genannt, der Umfang der Übernahme (die auf der Vorseite beginnt), ist aber so nicht gekennzeichnet, auch weil es zahlreiche andere Literaturverweise gibt. |
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| [2.] Haw/Fragment 006 10 - Diskussion Zuletzt bearbeitet: 2014-10-17 17:21:58 Singulus | Buschmann and Schaper 1999, Fragment, Gesichtet, Haw, SMWFragment, Schutzlevel sysop, Verschleierung |
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| Untersuchte Arbeit: Seite: 6, Zeilen: 10-14 |
Quelle: Buschmann and Schaper 1999 Seite(n): 122, Zeilen: l. Spalte: letzte Zeilen |
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| In the case of a sudden arterial occlusion or a slowly progressing stenosis, a steep pressure gradient develops along the shortest path within the interconnecting network that increases the blood flow velocity and FSS in these vessels. The effect of this sustained increase in shear is the upregulation of distinct processes in the collateral arteries. | In the case of a sudden arterial occlusion or a slowly progressing stenosis, a steep pressure gradient along the shortest path within the interconnecting network develops that increases the blood flow velocity and hence fluid shear stress in these vessels, which now assume the new function as “collaterals” [normal femoral artery blood flow 4.8 x 10-3 dyn/cm2; blood flow via anastomoses (occlusion) 889 x 10-3 dyn/cm2]. The effect of this sustained increase in shear is the upregulation of distinct processes in the collateral arteries. |
Ein Verweis auf die Quelle fehlt. |
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| [3.] Haw/Fragment 006 15 - Diskussion Zuletzt bearbeitet: 2014-10-12 16:31:50 Schumann | BauernOpfer, Fragment, Gesichtet, Haw, SMWFragment, Schaper and Scholz 2003, Schutzlevel sysop |
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| Untersuchte Arbeit: Seite: 6, Zeilen: 15-21 |
Quelle: Schaper and Scholz 2003 Seite(n): 1145, Zeilen: l. Spalte: 10 ff. |
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| FSS is proportional to the blood flow velocity and inversely related to the cube of the radius[41]. It is sensed by the endothelium, which, in response, changes the expression of growth factors, secretes nitric oxide (NO)[42, 43], prostacyclin, and probably other transmitters, and leads, with prolonged exposure, to positive arterial remodeling. However, even small increases in the radius of collateral arteries lead to a precipitous fall of the FSS because of the cubic relationship, and the FSS-related growth ends prematurely[20].
20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51. 41. Schmidt, V.J., et al., Gap junctions synchronize vascular tone within the microcirculation. Pharmacol Rep, 2008. 60(1): p. 68-74. 42. Busse, R. and I. Fleming, Regulation and functional consequences of endothelial nitric oxide formation. Ann Med, 1995. 27(3): p. 331-40. 43. Fleming, I., et al., Isometric contraction induces the Ca2+-independent activation of the endothelial nitric oxide synthase. Proc Natl Acad Sci U S A, 1999. 96(3): p. 1123-8. |
FSS is proportional to the blood flow velocity and inversely related to the cube of the radius.21 It is sensed by the endothelium, which, in response, changes the expression of growth factors, secretes NO,22,23 prostacyclin, and probably other transmitters, and leads, with prolonged exposure, to positive arterial remodeling. However, even small increases in the radius of collateral arteries lead to a precipitous fall of the FSS because of the cubic relationship, and the FSS-related growth ends prematurely.
21. Schmidt RF, Thews G. Physiologie des Menschen. Berlin: Springer; 1997. 22. Busse R, Fleming I. Regulation and functional consequences of endothelial nitric oxide formation. Ann Med. 1995;27:331–340. 23. Fleming I, Bauersachs J, Schäfer A, Scholz D, Aldershvile J, Busse R. Isometric contraction induces the Ca2+ independent activation of the endothelial nitric oxide synthase. Proc Natl Acad Sci U S A. 1999;96: 1123–1128. |
Die Quelle ist in Fn. 20 angegeben. Der Umfang der Übernahme, die drei Literaturverweise miteinschließt, wird aber ebensowenig deutlich wie der Umstand, dass es sich um eine beinahe wörtliche Übernahme handelt. |
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| [4.] Haw/Fragment 006 21 - Diskussion Zuletzt bearbeitet: 2014-10-12 16:33:19 Schumann | Fragment, Gesichtet, Haw, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Van Oostrom et al 2008 |
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| Untersuchte Arbeit: Seite: 6, Zeilen: 21-30 |
Quelle: Van Oostrom et al 2008 Seite(n): 1380, 1381, Zeilen: 1380: r. Spalte: 15 ff.; 1381: l. Spalte: 1 ff. |
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| Furthermore, FSS is almost impossible to measure in small collaterals. Pipp and colleagues[44] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic force in collateral growth.
Collaterals increase their diameter up to 20 times during arteriogenesis, which is possible through mitosis of vascular cells[45]. Given that the collateral vessels grow in length as well as in width, the expanding vessel arranges itself in loops and turns to accommodate the extra length. This gives the vessels a typical corkscrew pattern and causes energy loss[10]. 10. Heil, M., et al., Arteriogenesis versus angiogenesis: similarities and differences. J Cell Mol Med, 2006. 10(1): p. 45-55. 44. Pipp, F., et al., Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hindlimb. Arterioscler Thromb Vasc Biol, 2004. 24(9): p. 1664-8. 45. Wolf, C., et al., Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J Mol Cell Cardiol, 1998. 30(11): p. 2291-305. |
Furthermore, FSS is almost impossible to measure in small collaterals.
[Seite 1381] Pipp and colleagues [14] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further, significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic power in collateral growth. Collaterals increase their diameter up to 20 times during arteriogenesis, which is possible through mitosis of vascular cells [15]. Given that the collateral vessels grow in length as well as in width, the expanding vessel arranges itself in loops and turns to accommodate the extra length. This gives the vessels a typical corkscrew pattern [16] and causes energy loss. 14. Pipp, F., Boehm, S., Cai, W. J., Adili, F., Ziegler, B., Karanovic, G., Ritter, R., Balzer, J., Scheler, C., Schaper, W., Schmitz-Rixen, T. (2004) Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler. Thromb. Vasc. Biol. 24, 1664–1668. 15. Wolf, C., Cai, W. J., Vosschulte, R., Koltai, S., Mousavipour, D., Scholz, D., Afsah-Hedjri, A., Schaper, W., Schaper, J. (1998) Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J. Mol. Cell. Cardiol. 30, 2291–2305. 16. Heil, M., Eitenmuller, I., Schmitz-Rixen, T., Schaper, W. (2006) Arteriogenesis versus angiogenesis: similarities and differences. J. Cell. Mol. Med. 10, 45–55. |
Ein Verweis auf die Quelle fehlt. |
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Letzte Bearbeitung dieser Seite: durch Benutzer:Singulus, Zeitstempel: 20141016180003