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2 ungesichtete Fragmente: "verdächtig" oder "Keine Wertung"

[1.] Arc/Fragment 027 04 - Diskussion
Bearbeitet: 25. February 2014, 21:40 (Guckar)
Erstellt: 24. February 2014, 15:19 Hindemith
Arc, Fragment, Haghighat et al 2007, KeineWertung, SMWFragment, Schutzlevel, ZuSichten

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KeineWertung
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Hindemith
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Untersuchte Arbeit:
Seite: 27, Zeilen: 4-19
Quelle: Haghighat et al 2007
Seite(n): 2051, 2052, 2053, Zeilen: 2051: r.col: 23ff; 2052: r.col: 8ff; 2053: l.col: 17ff
Haghighat et al.71 were the first group to investigate the effect of short-term administration of G-CSF or GM-CSF on atherosclerotic plaque progression in a murine model of atherosclerosis. The study revealed that when combined with high-fat diet, both G-CSF and GM-CSF accelerated the formation of atherosclerotic lesions in Apo E-/- mice, rather than ameliorating the extent of lesions. Surprisingly, these effects could not be explained with any consistent changes in hemodynamics, local inflammation, lipid profiles or systemic inflammation that could provide a plausible explanation for the striking effects of G-CSF and GM-CSF treatment on atherosclerotic lesions. A potential reason for the deleterious effects of the cytokines was the induction of neovascularization in the arterial wall, which was markedly increased with GM-CSF or G-CSF treatments in comparison with controls. Previously, the association that coronary vasa vasorum neovascularization precedes the development of endothelial dysfunction and atherosclerotic development had already been made72, 73. Although the study by Haghighat et al.71 clearly demonstrate an association between G-CSF and GM-CSF-enhanced atherosclerosis and neovascularization in the arterial wall, causality has not yet been proven.

71. Haghighat A WD, Whalin MK, Cowan DP, Taylor WR. . Granulocyte colonystimulating factor and granulocyte macrophage colony-stimulating factor exacerbate atherosclerosis in apolipoprotein E-deficient mice. Circulation. 2007;115:2049-2054.

72. Herrmann J, Lerman LO, Rodriguez-Porcel M, Holmes DR, Jr., Richardson DM, Ritman EL, Lerman A. Coronary vasa vasorum neovascularization precedes epicardial endothelial dysfunction in experimental hypercholesterolemia. Cardiovasc Res. 2001;51:762-766.

73. Kwon HM, Sangiorgi G, Ritman EL, McKenna C, Holmes DR, Jr., Schwartz RS, Lerman A. Enhanced coronary vasa vasorum neovascularization in experimental hypercholesterolemia. J Clin Invest. 1998;101:1551-1556.

In summary, we found no consistent changes in hemodynamics, local inflammation, lipid profiles, or systemic inflammation that could provide a plausible explanation for the striking effects of G-CSF and GM-CSF treatment on atherosclerotic lesion area.

[...]

Another potentially deleterious effect of G-CSF and GM-CSF is the induction of neovascularization in the arterial wall. As shown in Figure 3, neovascularization within the atherosclerotic lesions and adventitia was markedly increased in the animals treated with GM-CSF (15.3±6.4 vessels per cross section) and G-CSF (18.0±2.5 vessels per cross section) compared with controls (2.0±1.2 vessels per cross section; P<0.05 versus control).

[...] The present study is the first to investigate the effect of short-term administration of G-CSF or GM-CSF on atherosclerotic plaque progression in a murine model of atherosclerosis.

[page 2052]

Our study found that when combined with a high-fat diet, both G-CSF and GM-CSF accelerated the formation of atherosclerotic lesions in ApoE-/- mice as opposed to ameliorating the extent of lesion involvement.

[page 2053]

Subsequent animal studies have shown that coronary vasa vasorum neovascularization precedes the development of endothelial dysfunction and atherosclerotic lesion formation.31,32 Although the present study clearly demonstrates an association between G-CSF– and GM-CSF-enhanced atherosclerosis and vascularity, causality has not been shown.33


31. Herrmann J, Lerman LO, Rodriguez-Porcel M, Holmes DR Jr, Richardson DM, Ritman EL, Lerman A. Coronary vasa vasorum neovascularization precedes epicardial endothelial dysfunction in experimental hypercholesterolemia. Cardiovasc Res. 2001;51:762–766.

32. Kwon HM, Sangiorgi G, Ritman EL, McKenna C, Holmes DR Jr, Schwartz RS, Lerman A. Enhanced coronary vasa vasorum neovascularization in experimental hypercholesterolemia. J Clin Invest. 1998;101: 1551–1556.

33. Moulton KS. Angiogenesis in atherosclerosis: gathering evidence beyond speculation. Curr Opin Lipidol. 2006;17:548 –555.

Anmerkungen

The source is given and it is clear to the reader that in this paragraph the findings of Haghighat et al. (2007) are being described. However, it is not clear to the reader that the interpretations and conclusions have been taken verbatim from the source and that two additional references to the literature are also taken from it.

Sichter
(Hindemith)

[2.] Arc/Fragment 016 22 - Diskussion
Bearbeitet: 26. February 2014, 23:10 (Guckar)
Erstellt: 25. February 2014, 12:00 Hindemith
Arc, Basu et al 2002, Fragment, KeineWertung, SMWFragment, Schutzlevel, ZuSichten

Typus
KeineWertung
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Untersuchte Arbeit:
Seite: 16, Zeilen: 22-25
Quelle: Basu et al 2002
Seite(n): 854, Zeilen: l.col: 12ff
In an “emergency” or “stress” situation, such as infection with pathogenic organisms, a component of a typical host response includes increased production of neutrophils for tissue restoration by eliminating invading organisms and removing damaged cells1, 28.

1. Basu S, Dunn A, Ward A. G-CSF: function and modes of action (Review). Int J Mol Med. 2002;10:3-10.

28. Basu S, Hodgson G, Zhang H-H, Katz M, Quilici C, Dunn AR. "Emergency" granulopoiesis in G-CSF-deficient mice in response to Candida albicans infection. Blood. 2000;95:3725-3733.

In an emergency situation, such as infection with pathogenic organisms, a component of a typical host response includes increased production of neutrophils for tissue restoration by eliminating invading organisms and removing damaged cells.
Anmerkungen

The source is not given.

Basu et al. (2000) have a similar, but different phrase: "During an emergency, such as infection with pathogenic organisms, the response of the host involves a series of inflammatory events, with macrophages and neutrophils playing an important role in the cellular phase, followed by an acquired immunity specific to the pathogen."

Basu et al (2002b) has not been checked yet.

Sichter
(Hindemith)

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