Fandom

VroniPlag Wiki

Quelle:Iam/Malik et al 2010

< Quelle:Iam

31.380Seiten in
diesem Wiki
Seite hinzufügen
Diskussion0

Störung durch Adblocker erkannt!


Wikia ist eine gebührenfreie Seite, die sich durch Werbung finanziert. Benutzer, die Adblocker einsetzen, haben eine modifizierte Ansicht der Seite.

Wikia ist nicht verfügbar, wenn du weitere Modifikationen in dem Adblocker-Programm gemacht hast. Wenn du sie entfernst, dann wird die Seite ohne Probleme geladen.

Angaben zur Quelle [Bearbeiten]

Autor     Ihtzaz Ahmed Malik, Federico Moriconi, Nadeem Sheikh, Naila Naz, Sajjad Khan, Jozsef Dudas, Tümen Mansuroglu, Clemens Friedrich Hess, Margret Rave-Fränk, Hans Christiansen, and Giuliano Ramadori
Titel    Single-Dose Gamma-Irradiation Induces Up-Regulation of Chemokine Gene Expression and Recruitment of Granulocytes into the Portal Area but

Not into Other Regions of Rat Hepatic Tissue

Zeitschrift    The American Journal of Pathology
Datum    April 2010
Nummer    176 (4)
Seiten    1801-1815
Anmerkung    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.
DOI    0.2353/ajpath.2010.090505
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2843471/

Literaturverz.   

yes
Fußnoten    no
Fragmente    3


Fragmente der Quelle:
[1.] Iam/Fragment 003 22 - Diskussion
Zuletzt bearbeitet: 2014-03-13 10:15:34 Singulus
Fragment, Iam, KeineWertung, Malik et al 2010, SMWFragment, Schutzlevel, ZuSichten

Typus
KeineWertung
Bearbeiter
Singulus
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 3, Zeilen: 22-26
Quelle: Malik et al 2010
Seite(n): 1801, Zeilen: r. col. 7-13
Radiation therapy has played a minor role in the treatment of patients with liver cancer or liver metastases because the liver has been considered sensitive to radiation. Indeed, radiation-induced liver diseases (RILD) is a serious clinical complication (Shim et al. 2007), due chiefly to radiation-induced inflammation. Radiation induced liver damage seems to be worst if diseased liver is irradiated (Cheng et al. 2002).

Shim SJ, Seong J, Lee IJ, Han KH, Chon CY, Ahn SH (2007) Radiation-induced hepatic toxicity after radiotherapy combined with chemotherapy for hepatocellular carcinoma. Hepatol Res 37:906-913

Cheng JC, Wu JK, Huang CM, Huang DY, Cheng SH, Lin YM, Jian JJ, Yang PS, Chuang VP, Huang AT (2002) Radiation-induced liver disease after radiotherapy for hepatocellular carcinoma: clinical manifestation and dosimetric description. Radiother Oncol 63:41-45

Radiation therapy has played a minor role in the treatment of patients with liver cancer or liver metastases because the liver has been considered sensitive to radiation. Indeed, radiation-induced liver diseases is a serious clinical complication 1, due chiefly to radiation-induced inflammation. Radiation induced liver damage seems to be worst if diseased liver is irradiated 2.

1. Shim SJ, Seong J, Lee IJ, Han KH, Chon CY, Ahn SH: Radiation-induced hepatic toxicity after radiotherapy combined with chemotherapy for hepatocellular carcinoma. Hepatol Res 2007, 37:906-913

2. Cheng JC, Wu JK, Huang CM, Huang DY, Cheng SH, Lin YM, Jian JJ, Yang PS, Chuang VP, Huang AT: Radiation-induced liver disease after radiotherapy for hepatocellular carcinoma: clinical manifestation and dosimetric description. Radiother Oncol 2002, 63:41-45

Anmerkungen
Sichter
(Singulus)

[2.] Iam/Fragment 007 10 - Diskussion
Zuletzt bearbeitet: 2014-03-11 18:33:30 Graf Isolan
Fragment, Iam, KeinPlagiat, Malik et al 2010, SMWFragment, Schutzlevel, ZuSichten

Typus
KeinPlagiat
Bearbeiter
Graf Isolan
Gesichtet
No.png
Untersuchte Arbeit:
Seite: 7, Zeilen: 10-31
Quelle: Malik et al 2010
Seite(n): 1801-1802, Zeilen: 1801: right col. 14ff - 1802:left col. 1ff
Chemokines are thought to be responsible for recruiting inflammatory cells. They are actively involved in inflammation, tissue repair and development of fibrosis (Marra 2002). The chemokine family is divided into four main groups based on their structure and chemotactic activity for specific leukocyte populations: C, CC, CXC and CX3C. The subset of CXC chemokines containing a glycine-leucine-arginine (ELR) motif, which immediately precedes the CXC residues, selectively targets neutrophils. While there are seven ELR+ CXC chemokines in the human genome, only four have been identified in the murine genome: keratinocyte-derived chemokine (KC)/CXCL1, macrophage-inflammatory protein-2 (MIP-2)/CXCL2, LPS-induced chemokine (LIX)/CXCL5 and CXCL15/lungkine (Bozic et al. 1995;Rossi et al. 1999;Wolpe et al. 1989).

The CXC (or α) chemokines, such as Interleukin-8 (IL-8)/CXCL8, CXCL9/MIG, CXCL10/IP10, CXCL11/ITAC and CXCL12/SDF1 have the potential to activate and attract neutrophils and T lymphocytes (Harris et al. 1996) while the C-C (or β) chemokines, such as MCP1/CCL2, MIP-1α/CCL3, MIP-1β/CCL4, MIP-3α/CCL20 and MIP-3β/CCL19, are predominantly chemoattractants for multiple leukocyte subtypes, including monocytes, eosinophils, basophils, T lymphocytes, dendritic cells, natural killer (NK) cells and, to a lesser extent, neutrophils (Ajuebor et al. 1998). Neutrophil recruitment is regulated by a complex array of signals (Frangogiannis et al. 2002) including activated complement and the CXC family chemokines interleukin-8 (IL-8/CXCL8 or CINC-1), macrophage inflammatory protein-2 (MIP-2/CXCL2), cytokine-induced neutrophil chemoattractant (KC/CXCL1/Gro-α), and lipopolysaccharide-induced CXC-chemokine (LIX/CXCL5) (Baggiolini 1998;Chandrasekar et al. 2001).


Ajuebor MN, Flower RJ, Hannon R, Christie M, Bowers K, Verity A, Perretti M (1998) Endogenous monocyte chemoattractant protein-1 recruits monocytes in the zymosan peritonitis model. J Leukoc Biol 63:108-116

Baggiolini M (1998) Chemokines and leukocyte traffic. Nature 392:565-568

Bozic CR, Kolakowski LF, Jr., Gerard NP, Garcia-Rodriguez C, von Uexkull-Guldenband C, Conklyn MJ, Breslow R, Showell HJ, Gerard C (1995) Expression and biologic characterization of the murine chemokine KC. J Immunol 154:6048-6057

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

Frangogiannis NG, Smith CW, Entman ML (2002) The inflammatory response in myocardial infarction. Cardiovasc Res 53:31-47

Harris JG, Flower RJ, Watanabe K, Tsurufuji S, Wolitzky BA, Perretti M (1996) Relative contribution of the selectins in the neutrophil recruitment caused by the chemokine cytokine-induced neutrophil chemoattractant (CINC). Biochem Biophys Res Commun 221:692-696

Marra F (2002) Chemokines in liver inflammation and fibrosis. Front Biosci 7:d1899-d1914

Rossi DL, Hurst SD, Xu Y, Wang W, Menon S, Coffman RL, Zlotnik A (1999) Lungkine, a novel CXC chemokine, specifically expressed by lung bronchoepithelial cells. J Immunol 162:5490-5497

Wolpe SD, Sherry B, Juers D, Davatelis G, Yurt RW, Cerami A (1989) Identification and characterization of macrophage inflammatory protein 2. Proc Natl Acad Sci U S A 86:612-616

[Page 1801]

Chemokines are thought to be responsible for recruiting inflammatory cells. They are actively involved in inflammation, tissue repair, and development of fibrosis.3 The chemokine family is divided into four main groups based on their structure and chemotactic activity for specific leukocyte populations: C, CC, CXC, and CX3C. The subset of CXC chemokines containing a glycine-leucine-arginine (ELR) motif, which immediately precedes the CXC residues, selectively targets neutrophils. Although there are seven ELR+ CXC chemokines in the human genome, only four have been identified in the murine genome: keratinocyte-derived chemokine (KC)/CXCL1, macrophage-inflammatory protein-2 (MIP-2)/CXCL2, lipopolysaccharide-induced chemokine (LIX)/CXCL5, and CXCL15/lungkine.4–6

The CXC (or α) chemokines, such as interleukin-8 (IL-8)/CXCL8, CXCL9/MIG, CXCL10/IP-10, CXCL11/ITAC,

[Page 1802]

and CXCL12/SDF1, have the potential to activate and attract neutrophils and T lymphocytes,7 whereas the CC (or β) chemokines, such as monocyte chemoattractant protein-1 (MCP-1)/CCL2, MIP-1α/CCL3, MIP-1β/CCL4, MIP-3α/CCL20, and MIP-3β/CCL19, are predominantly chemoattractants for multiple leukocyte subtypes, including monocytes, eosinophils, basophils, T lymphocytes, dendritic cells, natural killer cells, and, to a lesser extent, neutrophils.8 Neutrophil recruitment is regulated by a complex array of signals,9 including activated complement and the CXC family chemokines IL-8/CXCL8 or CINC-1, MIP-2/CXCL2, cytokine-induced neutrophil chemoattractant (KC/CXCL1/Gro-α), and LIX/CXCL5.10,11


3. Marra F: Chemokines in liver inflammation and fibrosis. Front Biosci 2002, 7:d1899–d1914

4. Bozic CR, Kolakowski LF Jr, Gerard NP, Garcia-Rodriguez C, von Uexkull-Guldenband C, Conklyn MJ, Breslow R, Showell HJ, Gerard C: Expression and biologic characterization of the murine chemokine KC. J Immunol 1995, 154:6048–6057

5. Rossi DL, Hurst SD, Xu Y, Wang W, Menon S, Coffman RL, Zlotnik A: Lungkine, a novel CXC chemokine, specifically expressed by lung bronchoepithelial cells. J Immunol 1999, 162:5490–5497

6. Wolpe SD, Sherry B, Juers D, Davatelis G, Yurt RW, Cerami A: Identification and characterization of macrophage inflammatory protein 2. Proc Natl Acad Sci USA 1989, 86:612–616

7. Harris JG, Flower RJ, Watanabe K, Tsurufuji S, Wolitzky BA, Perretti M: Relative contribution of the selectins in the neutrophil recruitment caused by the chemokine cytokine-induced neutrophil chemoattractant (CINC). Biochem Biophys Res Commun 1996, 221:692–696

8. Ajuebor MN, Flower RJ, Hannon R, Christie M, Bowers K, Verity A, Perretti M: Endogenous monocyte chemoattractant protein-1 recruits monocytes in the zymosan peritonitis model. J Leukoc Biol 1998, 63:108–116

9. Frangogiannis NG, Smith CW, Entman ML: The inflammatory response in myocardial infarction. Cardiovasc Res 2002, 53:31–47

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

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.

Sichter
(Graf Isolan)

[3.] Iam/Fragment 008 01 - Diskussion
Zuletzt bearbeitet: 2014-03-11 18:34:44 Graf Isolan
Fragment, Iam, KeinPlagiat, Malik et al 2010, SMWFragment, Schutzlevel, ZuSichten

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.

Sichter
(Graf Isolan)

Auch bei Fandom

Zufälliges Wiki