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Autor     I. Buschmann, W. Schaper
Titel    Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth
Zeitschrift    News in physiological sciences
Ausgabe    14
Datum    June 1999
Seiten    121-125
URL    http://physiologyonline.physiology.org/content/nips/14/3/121.full.pdf

Literaturverz.   

ja
Fußnoten    ja
Fragmente    8


Fragmente der Quelle:
[1.] Haw/Fragment 003 16 - Diskussion
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The presence of these native collaterals, which may not be utilized to provide perfusion under normal conditions, varies widely among species and also within individuals. However, these vessels have the ability to dramatically increase the lumen by growth so as to provide enhanced perfusion to the jeopardized ischemic regions. In case of chronic or acute occlusion of a major artery, collateral arteries can relieve the ensuing harmful effects in many regions of the body (hindlimb, heart, brain and kidney). It is important to recognize that this process is not a passive dilatation but one of active proliferation and remodeling. Under normal flow conditions and depending on the pressure gradient between the interconnecting arterial networks there is only minimal net forward flow, but small amounts of flow may oscillate within the network. The presence of these native collaterals, which may not be utilized to provide perfusion under normal conditions, varies widely among species and also within individuals. However, these vessels have the ability to dramatically increase the lumen by growth so as to provide enhanced perfusion to the jeopardized ischemic regions. In case of chronic or acute occlusion of a major artery, collateral arteries can ameliorate the ensuing detrimental effects in many regions of the body (hindlimb, heart, brain, kidney). It is important to recognize that this process is not a passive dilatation but one of active proliferation and remodeling. Under normal flow conditions and depending on the pressure gradient between the interconnecting arterial networks there is only minimal net forward flow, but small amounts of flow may oscillate within the network.
Anmerkungen

Ein Verweis auf die Quelle fehlt hier. Sie ist weiter oben genannt, aber ohne irgendeinen Hinweis, dass sich dieser Verweis auch auf die hier dokumentierte Passage beziehen soll.

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(Hindemith) Klgn

[2.] Haw/Fragment 006 10 - Diskussion
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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.
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Ein Verweis auf die Quelle fehlt.

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(Hindemith) Klgn

[3.] Haw/Fragment 007 07 - Diskussion
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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

[4.] Haw/Fragment 009 20 - Diskussion
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Upregulation of survival factors for monocytes (granulocyte macrophage colony-stimulating factor (GM-CSF)) provides the environment for a stable function of monocytes (Fig.1.3. C). These in turn produce fairly large amounts of growth factors, including VEGF, colony stimulating factor, transforming growth factor-β, in particular, FGF-2[20]. The adhesion and invasion of monocytes and platelets (also potent producers of growth factors) is soon followed by the first wave of mitosis of the endothelial and smooth muscle cells. The cell invasion is most prominent in the intima, the initial entrance, but even more pronounced later in the adventitia, where they create an inflammatory environment that is later accompanied by T cells. One of the effects of the perivascular inflammation is that it creates the space (by forcing neighboring tissue cells into apoptosis) for the greatly expanding collateral vessel, which can increase its [diameter up to 20 times[21].]

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

Upregulation of survival factors for monocytes (granulocyte macrophage colony-stimulating factor) provides the environment for a stable function of monocytes (Fig. 1C). These in turn produce fairly large amounts of growth factors, in particular, fibroblast growth factor-2. The adhesion and invasion of monocytes and platelets (also potent producers of growth factors) is soon followed by the first wave of mitosis of the endothelial and smooth muscle cells. [...]

[S. 123]

[...] The cell invasion is most prominent in the intima, the initial entrance, but even more pronounced later in the adventitia, where they create an inflammatory environment that is later accompanied by T cells. One of the effects of the perivascular inflammation is that it creates the space (by forcing neighboring tissue cells into apoptosis) for the greatly expanding collateral vessel, which can increase its diameter up to 20 times.

Anmerkungen

Die Quelle ist am Ende des Absatzes genannt, aber es ist nicht klar, dass der gesamte Absatz aus ihr stammt.

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(Hindemith), WiseWoman

[5.] Haw/Fragment 012 08 - Diskussion
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1.3.6. Therapeutic arteriogenesis

In previous studies, Ito, W.D., et al., showed that chronic intra-arterial infusion of MCP-1 greatly increased the development of arterial collateral blood vessels (arteriogenesis) after FAO[7, 60]. These collaterals were more numerous on angiograms, and their ability to conduct blood had increased by six fold. (Fig. 1.3., A and B) The histological appearance of these typical corkscrew vessels was that of muscular arteries[20].

Therapeutic arteriogenesis

In previous studies we showed that chronic intra-arterial infusion of MCP-1 greatly increased the development of arterial collateral blood vessels (arteriogenesis) after femoral artery occlusion (6, 7). These collaterals were more numerous on angiograms, and their ability to conduct blood had increased by sixfold (Fig. 1, A and B). The histological appearance of these typical corkscrew vessels was that of muscular arteries.

Anmerkungen

Ein Verweis auf die Quelle fehlt hier. Man findet ihn auf der nächsten Seite.


"FAO" statt "femoral arterial occlusion"; "six fold" statt "sixfold". Übernahme der referenzierten Bilder aus Quelle:HAW/Buschmann and Schaper 1999 mit komplett plagierter Bildunterschrift.

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(Hindemith) P.Schwartz

[6.] Haw/Fragment 013 01 - Diskussion
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[In another study, Arras, M., et al.[14] injected a single dose of] lipopolysaccharide intravenously into New Zealand white rabbits 3 days after ligation of the femoral artery. This potent stimulator of TNF-a also markedly enhanced the number of monocyte-derived macrophages accumulated around growing collateral arteries. Peripheral and collateral conductance was markedly increased. Nevertheless, on a molar basis MCP-1 is the most potent arteriogenic peptide[21]. VEGF is a peptide with angiogenic properties. It is produced by cells in close vicinity of endothelial cells, its chemoattractive action on monocytes is dose dependent; and its expression is highly regulated by hypoxia and hence by a physiological feedback mechanism to tissue hypoxia[67].

14. Arras, M., et al., Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J Clin Invest, 1998. 101(1): p. 40-50.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

67. Carmeliet, P. and D. Collen, Vascular development and disorders: molecular analysis and pathogenic insights. Kidney Int, 1998. 53(6): p. 1519-49.

In another study, we injected a single dose of lipopolysaccharide intravenously into New Zealand White rabbits 3 days after ligation of the femoral artery (1). This potent stimulator of tumor necrosis factor- a also markedly enhanced the number of monocyte-derived macrophages accumulated around growing collateral arteries. Peripheral and collateral conductances were markedly increased. Nevertheless, on a molar basis MCP-1 is the most potent arteriogenic peptide. Vascular endothelial growth factor (VEGF) is a peptide with angiogenic properties. It is produced by cells in close vicinity of endothelial cells, suggesting paracrine regulation of capillary formation; it is secreted and exerts a direct effect via interaction with endothelial receptors Flk-1 and Flt-1; its chemoattractive action on monocytes is dose dependent; and its expression is highly regulated by hypoxia and thereby a physiological feedback mechanism to tissue hypoxia (3).

1. Arras, M., W. D. Ito, D. Scholz, B. Winkler, J. Schaper, and W. Schaper. Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J. Clin. Invest. 101: 40–50, 1997.

3. Carmeliet, P., and D. Collen. Vascular development and disorders—molecular analysis and pathogenic insights. Kidney Int. 53: 1519–1549, 1998.

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Die Quelle ist in der Mitte genannt, der Umfang der Übernahme wird durch diesen Verweis aber nicht klar. Auch zwei Literaturverweise sind übernommen.

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(Hindemith), WiseWoman

[7.] Haw/Fragment 013 20 - Diskussion
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Angiogenesis is a process by which new capillary blood vessels sprout from a pre-existing blood vessel[68]. It is an important component of various normal and pathological conditions such as wound healing, fracture repair, folliculogenesis, ovulation, and pregnancy. These periods of angiogenesis are tightly regulated. However, if not properly controlled, angiogenesis can also represent a significant pathogenic component of tumor growth and metastasis, rheumatic arthritis, and retinopathies[21]. Angiogenesis is a complex phenomenon consisting of several distinct processes, which include endothelial migration and proliferation, extracellular proteolysis, endothelial differentiation (capillary tube formation), and vascular wall remodeling. It is important to recognize that these newly formed capillary tubes lack vascular smooth muscle cells.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

68. Risau, W., Mechanisms of angiogenesis. Nature, 1997. 386(6626): p. 671-4.

Angiogenesis is a process by which new capillary blood vessels sprout from a preexisting blood vessel

[Seite 122]

(10). It is an important component of various normal and pathological conditions such as wound healing, fracture repair, folliculogenesis, ovulation, and pregnancy. These periods of angiogenesis are tightly regulated. However, if not properly controlled, angiogenesis can also represent a significant pathogenic component of tumor growth and metastasis, rheumatic arthritis, and retinopathies. Angiogenesis is a complex phenomenon consisting of several distinct processes, which include endothelial migration and proliferation, extracellular proteolysis, endothelial differentiation (capillary tube formation), and vascular wall remodeling. It is important to recognize that these newly formed capillary tubes lack vascular smooth muscle cells.


10. Risau, W. Mechanisms of angiogenesis. Nature 386: 671–674, 1997.

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Auf die Quelle wird in der Mitte der Passage verwiesen, der Umfang der Übernahme bleibt so im Unklaren.

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[8.] Haw/Fragment 014 01 - Diskussion
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Arteriogenesis differs from angiogenesis in several aspects, (Table 1.1., Fig.1.5.) the most important being the dependence of angiogenesis on hypoxia and the dependence of arteriogenesis on inflammation[20]. However, angiogenesis and arteriogenesis share several mechanisms of action, e.g., their dependence on growth factors. Whereas angiogenesis can be largely explained by the actions of VEGF, arteriogenesis is probably a multifactorial process in which several growth factors are orchestrated. The role of VEGF in arteriogenesis is not clear, but a chemoattractive role for monocytes and hence an indirect contribution is imaginable[21].

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

Arteriogenesis differs from angiogenesis in several aspects, the most important being the

[S. 125]

dependence of angiogenesis on hypoxia and the dependence of arteriogenesis on inflammation.

However, angiogenesis and arteriogenesis share several mechanisms of action (Fig. 2), e.g., their dependence on growth factors. Whereas angiogenesis can be largely explained by the actions of VEGF, arteriogenesis is probably a multifactorial process in which several growth factors are orchestrated. The role of VEGF in arteriogenesis is not clear, but a chemoattractive role for monocytes and hence an indirect contribution is imaginable.

Anmerkungen

Die Quelle ist angegeben, doch durch die Literaturverweise wird nicht klar, dass die gesamte Passage übernommen ist.

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(Hindemith), WiseWoman

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