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Typus
KeinPlagiat
Bearbeiter
Graf Isolan
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 8, Zeilen: 1ff (complete)
Quelle: Malik et al 2010
Seite(n): 1802, Zeilen: left col. 14-19, 38-47
[This process is regulated at multiple levels but it may also] depend in part on the local production of chemoattractant cytokines (IFN-γ, TNF-α etc) or chemokines that function to modulate the activity of cell-surface adhesion receptors as well as to direct migration of targeted cells into the tissue site (Baggiolini 1998;Gerard and Rollins 2001). CXCL1, CXCL2 and CXCL5 (their receptor is CXCR2) are CXC chemokines that promote chemotaxis of inflammatory cells to sites of inflammation. Induction of CXCL2 and CXCL5 was observed in myocardial cells in an ischemia-reperfusion rat model and also after lipopolysaccharide (LPS) treatment (Chandrasekar et al. 2001). CXCL2 has been shown able to attract neutrophils to the site of inflammation (Tessier et al. 1997). Local expression of CXCL1 and of CXCL2 is important for neutrophil-dependent hepatic injury induced by ischemia and reperfusion in mice (Lentsch et al. 1998).

Chandrasekar B, Smith JB, Freeman GL (2001) Ischemia-reperfusion of rat myocardium activates nuclear factor-KappaB and induces neutrophil infiltration via lipopolysaccharide-induced CXC chemokine. Circulation 103:2296-2302

Lentsch AB, Yoshidome H, Cheadle WG, Miller FN, Edwards MJ (1998) Chemokine involvement in hepatic ischemia/reperfusion injury in mice: roles for macrophage inflammatory protein-2 and Kupffer cells. Hepatology 27:507-512

Tessier PA, Naccache PH, Clark-Lewis I, Gladue RP, Neote KS, McColl SR (1997) Chemokine networks in vivo: involvement of C-X-C and C-C chemokines in neutrophil extravasation in vivo in response to TNF-alpha. J Immunol 159:3595-3602

This process is regulated at multiple levels, but it may also depend in part on the local production of chemoattractant cytokines (interferon-γ [IFN-γ], tumor necrosis factor-α, etc) or chemokines that function to modulate the activity of cell-surface adhesion receptors as well as to direct migration of targeted cells into the tissue site.10,12

[...]

CXCL1, CXCL2, and CXCL5 (their receptor is CXCR2) are CXC chemokines that promote chemotaxis of inflammatory cells to sites of inflammation. Induction of CXCL2 and CXCL5 was observed in myocardial cells in an ischemia-reperfusion rat model and also after lipopolysaccharide treatment.11 CXCL2 has been shown able to attract neutrophils to the site of inflammation.20 Local expression of CXCL1 and of CXCL2 is important for neutrophil-dependent hepatic injury induced by ischemia and reperfusion in mice.21


10. Baggiolini M: Chemokines and leukocyte traffic. Nature 1998, 392:565–568

11. Chandrasekar B, Smith JB, Freeman GL: Ischemia-reperfusion of rat myocardium activates nuclear factor-KappaB and induces neutrophil infiltration via lipopolysaccharide-induced CXC chemokine. Circulation 2001, 103:2296–2302

12. Gerard C, Rollins BJ: Chemokines and disease. Nat Immunol 2001, 2:108–115

20. Tessier PA, Naccache PH, Clark-Lewis I, Gladue RP, Neote KS, McColl SR: Chemokine networks in vivo: involvement of C-X-C and C-C chemokines in neutrophil extravasation in vivo in response to TNF-alpha. J Immunol 1997, 159:3595–3602

21. Lentsch AB, Yoshidome H, Cheadle WG, Miller FN, Edwards MJ: Chemokine involvement in hepatic ischemia/reperfusion injury in mice: roles for macrophage inflammatory protein-2 and Kupffer cells. Hepatology 1998, 27:507–512

Anmerkungen

According to Iam, pg. 95, the article Malik et al 2010 - note the ten co-authors - already existed, when the thesis was finished in 2009, and had already been "Submitted in Am. J. of path.". The paper was accepted for publication December 15, 2009.

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