von Dr. Haitao Wang
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| [1.] Haw/Fragment 015 02 - Diskussion Zuletzt bearbeitet: 2014-10-17 17:14:55 [[Benutzer:|]] | BauernOpfer, Fragment, Gesichtet, Haw, SMWFragment, Schaper and Scholz 2003, Schutzlevel sysop |
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| Untersuchte Arbeit: Seite: 15, Zeilen: 2-8 |
Quelle: Schaper and Scholz 2003 Seite(n): 1150, Zeilen: 6ff |
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| After peripheral artery occlusion in rabbits and mice, arteriogenesis proceeds much faster than angiogenesis because of a structural dilatation of pre-existing collateral vessels followed by mitosis of all vascular cell types, which restores resting blood flow within 3 days. Recovery of dilatory reserve (maximal flow) takes longer[20]. The slower angiogenesis is unable to significantly restore flow even if angiogenesis reduces the minimal terminal resistance of the entire chain of resistors by new capillaries in parallel. Future therapeutic efforts should be directed at stimulating arteriogenesis.
20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51. |
After peripheral artery occlusion in rabbits and mice, arteriogenesis proceeds much faster than angiogenesis because of a structural dilatation of preexisting collateral vessels followed by mitosis of all vascular cell types, which restores resting blood flow within 3 days. Recovery of dilatory reserve (maximal flow) takes longer. The slower angiogenesis is unable to significantly restore flow even if angiogenesis reduces the minimal terminal resistance of the entire chain of resistors by new capillaries in parallel. Future therapeutic aims should be directed at stimulating arteriogenesis. |
Die Quelle ist angegeben. Dem Leser wird aber durch die Platzierung des Quellenverweises nicht klar, dass der gesamte Abschnitt aus der Quelle stammt. |
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| [2.] Haw/Fragment 015 16 - Diskussion Zuletzt bearbeitet: 2014-10-12 16:46:07 [[Benutzer:|]] | Ebong et al 2006, Fragment, Gesichtet, Haw, KomplettPlagiat, SMWFragment, Schutzlevel sysop |
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| Untersuchte Arbeit: Seite: 15, Zeilen: 16-18 |
Quelle: Ebong et al 2006 Seite(n): H2015, Zeilen: l. Spalte: 34 ff. |
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| Intercellular communication is a key regulator of vascular function[69, 70]. In the vessel wall, cell-to-cell communication occurs by extracellular diffusion and convection of humoral factors or by intercytoplasmic exchange of ions, metabolites, [and small signaling molecules (<1 kDa) via gap junctions.]
69. Haefliger, J.A., P. Nicod, and P. Meda, Contribution of connexins to the function of the vascular wall. Cardiovasc Res, 2004. 62(2): p. 345-56. 70. Ross, R., Cell biology of atherosclerosis. Annu Rev Physiol, 1995. 57: p. 791-804. |
INTERCELLULAR COMMUNICATION is a key regulator of vascular function (23, 40). In the vessel wall, cell-to-cell communication occurs by extracellular diffusion and convection of humoral factors or by intercytoplasmic exchange of ions, metabolites, and small signaling molecules (<1 kDa) via gap junctions.
23. Haefliger JA, Nicod P, and Meda P. Contribution of connexins to the function of the vascular wall. Cardiovasc Res 62: 345–356, 2004. 40. Ross R. Cell biology of atherosclerosis. Annu Rev Physiol 57: 791–804, 1995. |
Ein Verweis auf die Quelle fehlt. Fortsetzung auf der nächsten Seite. |
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Letzte Bearbeitung dieser Seite: durch Benutzer:Singulus, Zeitstempel: 20141017171638
