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[1.] Iam/Fragment 081 01 - Diskussion
Zuletzt bearbeitet: 2014-03-12 16:58:50 Hindemith
Fragment, Gesichtet, Iam, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Wouters et al 2007

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 81, Zeilen: 1-16
Quelle: Wouters et al 2007
Seite(n): 693, 698, Zeilen: 693:left col. 6-21 - right col. 1-4; 698: right col. 36-41
[It has been reported that this accumulation results from three processes:] (a) retinoblastoma protein (pRb)- mediated cell cycle arrest in mid-G1; (b) activation of an oxygen-sensitive restriction point in late G1, close to the G1/S border; and (c) inhibition of DNA replication. It was furthermore demonstrated that cells in G2, mitosis, or early G1 by the onset of hypoxia progress to the pRb mediated checkpoint in mid-G1 during continuation of hypoxic exposure. In contrast, pRb-incompetent cells or cells that have already passed this mid-G1 checkpoint continue cell cycle progression until they are blocked in the oxygen-sensitive restriction point close to the G1/S boundary. Moreover, cells in the S phase, when rendered hypoxic, are immediately arrested and are inactivated after only a few hours of oxygen deprivation. In general, cells residing in the S phase at the time of hypoxic conditions are much more sensitive to the lethal effects of hypoxia than cells in any other stage of the cell cycle. Consequently, following prolonged severe hypoxia, most clonogenic cells are arrested in one of the two restriction points in G1 (Amellem and Pettersen 1991; Amellem et al. 1998; Koritzinsky et al. 2001). The reason why low oxygen tension is associated with radioresistance relies on the fact that cell killing by ionizing radiation is caused by damage to the DNA. Either direct ionization or reaction of the radiation with hydroxyl radicals produced by radiolysis of nearby water molecules results in the origin of DNA radicals.

Amellem O, Pettersen EO (1991) The role of protein accumulation on the kinetics of entry into S phase following extreme hypoxia. Anticancer Res 11:1083-1087

Amellem O, Sandvik JA, Stokke T, Pettersen EO (1998) The retinoblastoma protein-associated cell cycle arrest in S-phase under moderate hypoxia is disrupted in cells expressing HPV18 E7 oncoprotein. Br J Cancer 77:862-872

Koritzinsky M, Wouters BG, Amellem O, Pettersen EO (2001) Cell cycle progression and radiation survival following prolonged hypoxia and re-oxygenation. Int J Radiat Biol 77:319-328

[Page 693]

It has been reported that this accumulation results from three processes: (a) retinoblastoma protein (pRb)- mediated cell cycle arrest in mid-G1; (b) activation of an oxygen- sensitive restriction point in late G1, close to the G1/S border; and (c) inhibition of DNA replication.

It was furthermore demonstrated that cells in G2, mitosis, or early G1 by the onset of hypoxia progress to the pRb-mediated checkpoint in mid-G1 during continuation of hypoxic exposure. In contrast, pRb-incompetent cells or cells that have already passed this mid-G1 checkpoint continue cell cycle progression until they are blocked in the oxygen-sensitive restriction point close to the G1/S boundary. Moreover, cells in the S phase, when rendered hypoxic, are immediately arrested and are inactivated after only a few hours of oxygen deprivation. In general, cells residing in the S phase at the time of hypoxic conditions are much more sensitive to the lethal effects of hypoxia than cells in any other stage of the cell cycle. Consequently, following prolonged severe hypoxia, most clonogenic cells are arrested in one of the two restriction points in G1 [31, 43, 44].

[Page 698]

The reason why low oxygen tension is associated with radioresistance relies on the fact that cell killing by ionizing radiation is caused by damage to the DNA. Either direct ionization or reaction of the radiation with hydroxyl radicals produced by radiolysis of nearby water molecules results in the origin of DNA radicals.


31 Koritzinsky M, Wouters BG, Amellem O et al. Cell cycle progression and radiation survival following prolonged hypoxia and re-oxygenation. Int J Radiat Biol 2001;77:319 –328.

43 Amellem O, Pettersen E. Cell inactivation and cell cycle inhibition as induced by extreme hypoxia: The possible role of cell cycle arrest as a protection against hypoxia-induced lethal damage. Cell Prolif 1991;24:127–141.

44 Amellem O, Sandvik JA, Stokke T et al. The retinoblastoma protein-associated cell cycle arrest in S-phase under moderate hypoxia is disrupted in cells expressing HPV18 E7 oncoprotein. Br J Cancer 1998;77:862–872.

Anmerkungen

From the final chapter of Iam's thesis ("Discussion"): Nothing has been marked as a citation, though the texts are identical but for one of the references given. The source is not even mentioned.

Sichter
(Graf Isolan) Schumann

[2.] Iam/Fragment 081 18 - Diskussion
Zuletzt bearbeitet: 2014-03-19 21:39:19 Hindemith
BauernOpfer, Fragment, Gesichtet, Iam, Moriconi et al 2008, SMWFragment, Schutzlevel sysop

Typus
BauernOpfer
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 81, Zeilen: (17-18), 18-22
Quelle: Moriconi et al 2008
Seite(n): 167, Zeilen: right col. 31ff
This mechanism could be true in our case as leucopoenia has also been observed in current model (Moriconi et al. 2008). Another possible explanation could be considered: radiation-induced chemokines and cytokines expression may influence leukocyte production in the bone marrow. It may modify the expression of adhesion molecule genes in blood leukocytes in a way that is different from that necessary for adhesion and transmigration of inflammatory cells. This question is now under investigation.

Moriconi F, Christiansen H, Raddatz D, Dudas J, Hermann RM, Rave-Frank M, Sheikh N, Saile B, Hess CF, Ramadori G (2008) Effect of radiation on gene expression of rat liver chemokines: in vivo and in vitro studies. Radiat Res 169:162-169

Radiation-induced cytokine expression may influence leukocyte production in the bone marrow. Another reason for the lack of leukocyte infiltration may be that radiation modifies the expression of adhesion molecule genes in both liver cells and blood leukocytes in a way that is different from that necessary for adhesion and transmigration of inflammatory cells. This question is now under investigation.
Anmerkungen

Though the source is named right before the parallel text starts nothing has been marked as a citation. The text does not suggest that the reference to the source should also refer to the text coming after the reference.

Sichter
(Graf Isolan), Hindemith


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