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Arteriogenesis in Gja5 (Connexin-40) deficient mice

von Dr. Haitao Wang

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[1.] Haw/Fragment 007 01 - Diskussion
Zuletzt bearbeitet: 2014-10-12 16:36:35 Schumann
Fragment, Gesichtet, Haw, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Van Oostrom et al 2008

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 7, Zeilen: 1-6
Quelle: Van Oostrom et al 2008
Seite(n): 1381, Zeilen: l. Spalte: 12 ff.
[This, together with the premature arrest of arteriogenic growth,] as a result of the drop in FSS in the growing collateral, is a reason that collateral arteries cannot completely compensate the conductance of the artery they have replaced. Initially, during arteriogenesis, several collateral vessels are recruited and proliferate. However, as it is hemodynamically more efficient for fewer, larger arteries to conduct the blood than a greater number of smaller arteries, the smaller vessels regress later on, and those with the higher shear forces continue growing[46].

46. Hoefer, I.E., J.J. Piek, and G. Pasterkamp, Pharmaceutical interventions to influence arteriogenesis: new concepts to treat ischemic heart disease. Curr Med Chem, 2006. 13(9): p. 979-87.

This, together with the premature arrest of arteriogenic growth, as a result of the drop in FSS in the growing collateral, is a reason that collateral arteries cannot completely compensate the conductance of the artery they have replaced. Initially, during arteriogenesis, several collateral vessels are recruited and proliferate. However, as it is hemodynamically more efficient for fewer, larger arteries to conduct the blood than a greater number of smaller arteries, the smaller vessels regress later on, and those with the higher shear forces continue growing [17].

17. Hoefer, I. E., Piek, J. J., Pasterkamp, G. (2006) Pharmaceutical interventions to influence arteriogenesis: new concepts to treat ischemic heart disease. Curr. Med. Chem. 13, 979–987.

Anmerkungen

Kein Verweis auf die Quelle.

Die Übernahme beginnt auf der Vorseite.

Sichter
(Hindemith), SleepyHollow02

[2.] Haw/Fragment 007 07 - Diskussion
Zuletzt bearbeitet: 2014-10-20 22:09:34 WiseWoman
Buschmann and Schaper 1999, Fragment, Gesichtet, Haw, SMWFragment, Schutzlevel sysop, Verschleierung

Typus
Verschleierung
Bearbeiter
Hindemith
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Untersuchte Arbeit:
Seite: 7, Zeilen: 7-9, 12-26
Quelle: Buschmann and Schaper 1999
Seite(n): 122, Zeilen: r. Spalte: 10ff
FSS as a molding force was recognized over 100 years ago; the embryologist Thoma described the relationship between the diameter of an artery and its blood flow velocity[47]. [...] Any sustained deviation from that relationship initiates processes of either growth or atrophy. A sustained increase of fluid shear stress leads to activation of the endothelium.

1.3.3. Activation of the endothelium

It is currently not well enough known how the stimulus of increased shear stress is transmitted from the endothelial cell membrane to the nucleus, where it initiates the transcriptional activity of a number of genes, partially via a protein that binds to the shear stress responsive element that is present in the promotor of several genes (nitric oxide synthase (NOS), platelet-derived growth factor (PDGF), monocyte chemoattractant protein-1 (MCP-1))[49]. The first step in the activation of the endothelium is the opening of chloride channels that are also responsible for the volume control of endothelial cells. Characteristically stress-activated endothelium appears swollen in scanning electron microscopic images[50], adhesion molecules are upregulated[51], and the conditions are perfect for the adhesion and invasion of circulating cells.


47. Yancopoulos, G.D., M. Klagsbrun, and J. Folkman, Vasculogenesis, angiogenesis, and growth factors: ephrins enter the fray at the border. Cell, 1998. 93(5): p. 661-4.

49. Shyy, Y.J., et al., Fluid shear stress induces a biphasic response of human monocyte chemotactic protein 1 gene expression in vascular endothelium. Proc Natl Acad Sci U S A, 1994. 91(11): p. 4678-82.

50. Ziegelstein, R.C., et al., Cytosolic alkalinization of vascular endothelial cells produced by an abrupt reduction in fluid shear stress. Circ Res, 1998. 82(7): p. 803-9.

51. Chappell, D.C., et al., Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium. Circ Res, 1998. 82(5): p. 532-9.

Shear stress as a molding force was recognized over 100 years ago; the embryologist Thoma described the relationship between the diameter of an artery and its blood flow velocity (14). Any sustained deviation from that relationship initiates processes of either growth or atrophy. A sustained increase of fluid shear stress leads to activation of the endothelium.

Activation of the endothelium

It is presently not well enough known how the stimulus of increased shear stress is transmitted from the endothelial cell membrane to the nucleus, where it initiates the transcriptional activity of a number of genes (12), partially via a protein that binds to the shear stress responsive element that is present in the promotor of several genes (NOS, PDGF, MCP-1). The first step in the activation of the endothelium is the opening of chloride channels that are also responsible for the volume control of endothelial cells. Characteristically stress-activated endothelium appears swollen in scanning electron microscopic images (15). Adhesion molecules are upregulated (4), and the conditions are perfect for the adhesion and invasion of circulating cells.


4. Chappell, D. C., S. E. Varner, R. M. Nerem, R. M. Medford, and R. W. Alexander. Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium. Circ. Res. 82: 532–539, 1998.

12. Shyy, Y.-J., H.-J. Hsieh, S. Usami, and S. Chien. Fluid shear stress induces a biphasic response of human monocyte chemotactic protein 1 expression in vascular endothelium. Proc. Natl. Acad. Sci. USA 91: 4678–4682, 1994.

14. Yancopoulos, G. D., M. Klagsbrun, and J. Folkman: Vasculogenesis, angiogenesis, and growth factors: ephrins enter the fray at the border. Cell 93: 661–664, 1998.

15. Ziegelstein, R. C., P. S. Blank, L. Cheng, and M. C. Capogrossi. Cytosolic alkalinization of vascular endothelial cells produced by an abrupt reduction in fluid shear stress. Circ. Res. 82: 803–809, 1998.

Anmerkungen

Ein Verweis auf die Quelle fehlt.

Sichter
(Hindemith) P.Schwartz

[3.] Haw/Fragment 007 09 - Diskussion
Zuletzt bearbeitet: 2014-10-12 16:37:19 Schumann
Fragment, Gesichtet, Haw, KomplettPlagiat, SMWFragment, Schaper and Scholz 2003, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 7, Zeilen: 9-12
Quelle: Schaper and Scholz 2003
Seite(n): 1145, Zeilen: l. Spalte: 22 ff.
Murray[48] proposed that the vascular system is optimally configured to minimize the amount of mechanical and metabolic work to provide adequate blood flow, and he predicted that FSS is constant throughout the vasculature and that blood flow through each vessel is proportional to that vessel’s diameter cube.

48. Murray, C.D., The Physiological Principle of Minimum Work Applied to the Angle of Branching of Arteries. J Gen Physiol, 1926. 9(6): p. 835-841.

Murray25 proposed that the vascular sytem [sic] is optimally configured to minimize the amount of mechanical and metabolic work to provide adequate blood flow, and he predicted that FSS is constant throughout the vasculature and that blood flow through each vessel is proportional to that vessel’s diameter cube.

25. Murray CD. The physiological principle of minimum work applied to the angle of branching arteries. J Gen Physiol. 1926;9:835–841.

Anmerkungen

Ein Verweis auf die Quelle fehlt.

Sichter
(Hindemith), SleepyHollow02

[4.] Haw/Fragment 007 27 - Diskussion
Zuletzt bearbeitet: 2014-10-12 16:38:10 Schumann
Fragment, Gesichtet, Haw, KomplettPlagiat, SMWFragment, Schaper and Scholz 2003, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 7, Zeilen: 27-30
Quelle: Schaper and Scholz 2003
Seite(n): 1145, 1146, Zeilen: 1145: r. Spalte: letzte Zeilen; 1146; l. Spalte: 1 ff.
Chronically increased shear stress activates endothelium in a morphologically visible way. It loses volume control and swells, because chloride channels change their open probability[52]. Inhibitors of the chloride channel also inhibit arteriogenesis. The location and nature of the mechanotransducer of shear stress are controversially [discussed[53], and protein kinases and stretch sensitive K-channels were studied[54].]

52. Nilius, B., et al., Volume-activated Cl- channels. Gen Pharmacol, 1996. 27(7): p. 1131-40.

53. Ali, M.H. and P.T. Schumacker, Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med, 2002. 30(5 Suppl): p. S198-206.

54. Nilius, B. and G. Droogmans, Ion channels and their functional role in vascular endothelium. Physiol Rev, 2001. 81(4): p. 1415-59.

Chronically increased shear stress activates endothelium in a morphologically visible way. It loses volume control and swells,

[Seite 1146]

because chloride channels change their open probability.33 Inhibitors of the chloride channel also inhibit arteriogenesis.34 The location and nature of the mechanotransducer of shear stress are controversially discussed,35 and protein kinases and stretch sensitive K+ channels were studied.36


33. Nilius B, Eggermont J, Voets T, Droogmans G. Volume-activated Cl-channels. Gen Pharmacol. 1996;27:1131–1140.

34. Ziegelhoeffer T, Scholz D, Helish A, Wagner S, Schaper W. Swelling cell-doing well? Volume-regulated chloride channels and arteriogenesis. J Mol Cell Cardiol. 2002;34:A71. Abstract

35. Ali MH, Schumacker PT. Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med. 2002;30:S198–S206.

36. Nilius B, Droogmans G. Ion channels and their functional role in vascular endothelium. Physiol Rev. 2001;81:1415–1459.

Anmerkungen

Ein Verweis auf die Quelle fehlt.

Sichter
(Hindemith), SleepyHollow02


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