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45 gesichtete, geschützte Fragmente: Plagiat

[1.] Iam/Fragment 003 03 - Diskussion
Bearbeitet: 12. March 2014, 19:26 Graf Isolan
Erstellt: 2. March 2014, 09:16 (Hindemith)
Fragment, Gesichtet, Hawkins and Dawson 2006, Iam, KomplettPlagiat, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 3, Zeilen: 3-12
Quelle: Hawkins and Dawson 2006
Seite(n): 1653, 1654, Zeilen: 1653: 33-43 - 1654, l.col: 1-3
Hepatocellular carcinoma (HCC) is the sixth most common cancer in the world (626,000 diagnoses per year) and is the third most common cause of cancer-related death (598,000 deaths per year). Although HCC predominantly is a problem in developing countries, its incidence is expected to rise over the next decade in North America largely because of the increasing incidence of hepatitis C2 and the 1% to 4% risk per year of HCC developing in patients with cirrhosis (Helton et al. 2003). Unfortunately, the overall 5-year survival rate for all patients with HCC has remained steady at 3% to 5% (Parkin 2001). HCC is particularly challenging to treat because of to the common locally advanced or multifocal presentation of disease that develops in a background of cirrhosis because the survival of patients with HCC is related strongly to underlying liver function (Chevret et al. 1999).

Chevret S, Trinchet JC, Mathieu D, Rached AA, Beaugrand M, Chastang C (1999) A new prognostic classification for predicting survival in patients with hepatocellular carcinoma. Groupe d'Etude et de Traitement du Carcinome Hepatocellulaire. J Hepatol 31:133-141

Helton WS, Di BA, Chari R, Schwartz M, Bruix J (2003) Treatment strategies for hepatocellular carcinoma in cirrhosis. J Gastrointest Surg 7:401-411

Parkin DM (2001) Global cancer statistics in the year 2000. Lancet Oncol 2:533-543

[page 1653]

Hepatocellular carcinoma (HCC) is the sixth most common cancer in the world (626,000 diagnoses per year) and is the third most common cause of cancer-related death (598,000 deaths per year).1 Although HCC predominantly is a problem in developing countries, its incidence is expected to rise over the next decade in North America largely because of the increasing incidence of hepatitis C2 and the 1% to 4% risk per year of HCC developing in patients with cirrhosis.3 Unfortunately, the overall 5-year survival rate for all patients with HCC has remained steady at 3% to 5%.1

HCC is particularly challenging to treat because of to the common locally advanced or multifocal presentation of disease that de-

[page 1654]

velops in a background of cirrhosis. Because the survival of patients with HCC is related strongly to underlying liver function,4 [...]


1. Parkin DM, Bray F, Ferlay J, Pisani P. Global cancer statistics, 2002. CA Cancer J Clin. 2005;55:74-108.

2. El-Serag HB, Mason AC. Rising incidence of hepatocellular carcinoma in the United States. N Engl J Med. 1999;340:745- 750.

3. Helton WS, Di Bisceglie A, Chari R, Schwartz M, Bruix J. Treatment strategies for hepatocellular carcinoma in cirrhosis. J Gastrointest Surg. 2003;7:401-411.

4. Chevret S, Trinchet JC, Mathieu D, Rached AA, Beaugrand M, Chastang C. A new prognostic classification for predicting survival in patients with hepatocellular carcinoma. Groupe d’Etude et de Traitement du Carcinome Hepatocellulaire. J Hepatol. 1999;31:133-141.

Anmerkungen

The first lines of the thesis are taken verbatim from a source that is mentioned nowhere in the thesis. Also references to the literature have been taken (except one, where apparently the superscript "2" has been overlooked, such that the thesis talks now about "hepatitis C2")

Sichter
(Hindemith) Schumann

[2.] Iam/Fragment 003 13 - Diskussion
Bearbeitet: 12. March 2014, 19:44 Graf Isolan
Erstellt: 2. March 2014, 15:26 (Graf Isolan)
Fragment, Gesichtet, Iam, Robbins and Zhao 2007, SMWFragment, Schutzlevel sysop, Verschleierung

Typus
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Graf Isolan
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Untersuchte Arbeit:
Seite: 3, Zeilen: 13-22
Quelle: Robbins and Zhao 2007
Seite(n): 135, Zeilen: 8-18
Consequently, for most patients, cancer can be considered a chronic disease. The total radiation dose that can be administered safely to cancer patients is limited by the risk of complications arising in those normal tissues unavoidably included within the treatment volume. Of particular concern are the late effects that arise several months to years post irradiation. While improvements in radiation oncology such as intensity-modulated radiation therapy (IMRT) have led to a reduction in the dose of normal tissue irradiated, late effects remain a significant risk (Robbins and Zhao 2004). The National Cancer Institute has identified long-term survival from cancer as one of the new areas of public health emphasis, particularly studying adverse long-term or late effects of cancer and its treatment (National Cancer Institute’s Plans and Priorities for Cancer Research: http://plan.cancer.gov/public/survivor.htm).

Robbins ME, Zhao W (2004) Chronic oxidative stress and radiation-induced late normal tissue injury: a review. Int J Radiat Biol 80:251-259

Consequently, for most patients, cancer can be considered a chronic disease. The total radiation dose that can be administered safely to cancer patients is limited by the risk of complications arising in those normal tissues unavoidably included within the treatment volume. Of particular concern are the late effects that can arise several months to years postirradiation. While improvements in radiation oncology such as intensity-modulated radiation therapy (IMRT) have led to a reduction in the volume of normal tissue irradiated, late effects remain a significant risk. The National Cancer Institute has identified long-term survival from cancer as one of the new areas of public health emphasis, particularly studying adverse long-term or late effects of cancer and its treatment (National Cancer Institute’s Plans and Priorities for Cancer Research).
Anmerkungen

The names of the original authors are given in passing (though to a different article). Nothing has been marked as a citation although the wording is nearly identical.

Sichter
(Graf Isolan) Schumann

[3.] Iam/Fragment 003 27 - Diskussion
Bearbeitet: 13. March 2014, 12:21 Graf Isolan
Erstellt: 13. March 2014, 10:31 (Singulus)
Fragment, Gesichtet, Iam, KomplettPlagiat, Quesaraku et al. 2009, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Singulus
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 3, Zeilen: 27-32
Quelle: Quesaraku et al. 2009
Seite(n): 910, Zeilen: r. col. 4ff.
The efficacy of this therapy is limited, among other things, by the fact that it cannot be delivered without hitting normal, healthy tissue surrounding the tumour, with radiation-induced acute and chronic side effects. Radiation is known to induce DNA damage and chromosomal instability of cells both from tumorous and normal tissue (Sakata et al. 2007). However, beyond this, there are further [mechanisms involved in the actions occurring after the exposure of cells and tissue to ionizing radiation, such as radiation-induced apoptosis (Hasegawa et al. 2002).]

Sakata K, Someya M, Matsumoto Y, Hareyama M (2007) Ability to repair DNA double-strand breaks related to cancer susceptibility and radiosensitivity. Radiat Med 25:433-438

[Hasegawa M, Imai R, Nojima K, Sakurai H, Suzuki Y, Kawashima M, Matsuura M, Nakamura Y, Nakano T (2002) [Radiation-induced apoptosis in vivo: therapeutic significance of apoptosis in radiation therapy]. Nippon Igaku Hoshasen Gakkai Zasshi 62:535-539]

The efficacy of this therapy is limited, among other things, by the fact that it cannot be delivered without hitting normal, healthy tissue surrounding the tumour, with radiation-induced acute and chronic side effects. Radiation is known to induce DNA damage and chromosomal instability of cells both from tumorous and normal tissue (24). However, beyond this, there are further mechanisms involved in the actions occurring after the exposure of cells and tissue to ionizing radiation, such as radiation-induced apoptosis (25) and radiation-induced changes in gene expression (26–28).

24. Sakata K, Someya M,Matsumoto Y, Hareyama M. Ability to repair DNA double-strand breaks related to cancer susceptibility and radiosensitivity. Radiat Med 2007; 25: 433–8.

25. Hasegawa M, Imai R, Nojima K, et al. Radiation-induced apoptosis in vivo: therapeutic significance of apoptosis in radiation therapy. Nippon Igaku Hoshasen Gakkai Zasshi 2002; 62: 535–9.

26. Christiansen H, Batusic D, Saile B, et al. Identification of genes responsive to gamma radiation in rat hepatocytes and rat liver by cDNA array gene expression analysis. Radiat Res 2006; 165: 318–25.

27. Christiansen H, Sheikh N, Saile B, et al. X-irradiation in rat liver: consequent upregulation of hepcidin and downregulation of hemojuvelin and ferroportin-1 gene expression. Radiology 2007; 242: 189–97.

28. Moriconi F, Christiansen H, Raddatz D, et al. Effect of radiation on gene expression of rat liver chemokines: in vivo and in vitro studies. Radiat Res 2008; 169: 162–9.

Anmerkungen

Nothing has been marked as a citation.

Sichter
(Singulus), Graf Isolan

[4.] Iam/Fragment 004 01 - Diskussion
Bearbeitet: 13. March 2014, 12:23 Graf Isolan
Erstellt: 13. March 2014, 10:40 (Singulus)
Fragment, Gesichtet, Iam, KomplettPlagiat, Quesaraku et al. 2009, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Singulus
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 4, Zeilen: 1-2
Quelle: Quesaraku et al. 2009
Seite(n): 910, Zeilen: r. col. 10-15
[However, beyond this, there are further] mechanisms involved in the actions occurring after the exposure of cells and tissue to ionizing radiation, such as radiation-induced apoptosis (Hasegawa et al. 2002).

Hasegawa M, Imai R, Nojima K, Sakurai H, Suzuki Y, Kawashima M, Matsuura M, Nakamura Y, Nakano T (2002) [Radiation-induced apoptosis in vivo: therapeutic significance of apoptosis in radiation therapy]. Nippon Igaku Hoshasen Gakkai Zasshi 62:535-539

However, beyond this, there are further mechanisms involved in the actions occurring after the exposure of cells and tissue to ionizing radiation, such as radiation-induced apoptosis (25) and radiation-induced changes in gene expression (26–28).

25. Hasegawa M, Imai R, Nojima K, et al. Radiation-induced apoptosis in vivo: therapeutic significance of apoptosis in radiation therapy. Nippon Igaku Hoshasen Gakkai Zasshi 2002; 62: 535–9.

26. Christiansen H, Batusic D, Saile B, et al. Identification of genes responsive to gamma radiation in rat hepatocytes and rat liver by cDNA array gene expression analysis. Radiat Res 2006; 165: 318–25.

27. Christiansen H, Sheikh N, Saile B, et al. X-irradiation in rat liver: consequent upregulation of hepcidin and downregulation of hemojuvelin and ferroportin-1 gene expression. Radiology 2007; 242: 189–97.

28. Moriconi F, Christiansen H, Raddatz D, et al. Effect of radiation on gene expression of rat liver chemokines: in vivo and in vitro studies. Radiat Res 2008; 169: 162–9.

Anmerkungen

Nothing has been marked as a citation.

Sichter
(Singulus), Graf Isolan

[5.] Iam/Fragment 004 03 - Diskussion
Bearbeitet: 13. March 2014, 22:00 Singulus
Erstellt: 13. March 2014, 12:37 (Graf Isolan)
Fragment, Gesichtet, Iam, KomplettPlagiat, Moriconi et al 2008, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Graf Isolan
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 4, Zeilen: 3-10
Quelle: Moriconi et al 2008
Seite(n): 162, Zeilen: left col. 29-35 - right col. 1-2.12-15
The interest of gastroenterologists, radiation oncologists and pathologists in radiation-induced liver disease has been generated by clinical observations of the deterioration of liver function occurring after abdominal irradiation with at least 30 Gy in patients with chronic liver diseases or even in patients with a healthy liver. This toxicity limits the use of radioimmunotherapy for malignant lymphomas, radio-chemotherapy for biliopancreatic carcinomas, and radiotherapy for liver malignancies (Greco et al. 2004;Wang et al. 1995). The molecular pathogenesis of hepatocellular damage after irradiation and the development of radiation-induced liver disease is still unknown.

Greco C, Catalano G, Di GA, Orecchia R (2004) Radiotherapy of liver malignancies. From whole liver irradiation to stereotactic hypofractionated radiotherapy. Tumori 90:73-79

Wang S, Quadri SM, Tang XZ, Stephens LC, Lollo CP, Bartholomew RM, Vriesendorp HM (1995) Liver toxicity induced by combined external-beam irradiation and radioimmunoglobulin therapy. Radiat Res 141:294-302

Introduction

The interest of gastroenterologists, radiation oncologists and pathologists in radiation-induced liver disease has been generated by clinical observations of the deterioration of liver function occurring after abdominal irradiation with at least 30 Gy in patients with chronic liver diseases or even in patients with a healthy liver. This toxicity limits the use of radioimmunotherapy for malignant lymphomas, radio-chemotherapy for biliopancreatic carcinomas, and radiotherapy for liver malignancies (1-3).

[...] The molecular pathogenesis of hepatocellular damage after irradiation and the development of radiation-induced liver disease is still unknown.


1. S. Wang, S. M. Quadri, X. Z. Tang, L. C. Stephens, C. T. Lollo, R. M. Bartholomew and H. M. Vriesendorp, Liver toxicity induced by combined external-beam irradiation and radioimmunoglobulin therapy. Radiat. Res. 141, 294–302 (1995).

2. C. Sempoux, Y. Horsmans, A. Geubel, J. Fraikin, B. E. Van Beers, J. F. Gigot, J. Lerut and J. Rahier, Severe radiation-induced liver disease following localized radiation therapy for biliopancreatic carcinoma: activation of hepatic stellate cells as an early event. Hepatology 26, 128–134 (1997).

3. C. Greco, G. Catalano, A. Di Grazia and R. Orecchia, Radiotherapy of liver malignancies. From whole liver irradiation to stereotactic hypofractionated radiotherapy. Tumori 90, 73–79 (2004).

Anmerkungen

No part of this has been marked as a citation.

Sichter
(Graf Isolan) Schumann

[6.] Iam/Fragment 004 12 - Diskussion
Bearbeitet: 6. April 2014, 12:13 Guckar
Erstellt: 2. March 2014, 13:44 (Hindemith)
Butterfield et al 2006, Fragment, Gesichtet, Iam, KomplettPlagiat, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
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Untersuchte Arbeit:
Seite: 4, Zeilen: 12-17
Quelle: Butterfield et al 2006
Seite(n): 457, Zeilen: l.col: 19-23, 32-36
Inflammation is often used to describe a series of signs and symptoms after soft tissue or bone injury. Appropriately, this term was originally used to describe the 4 classic signs of the affected tissue’s response to trauma: redness, swelling, heat and pain (Rocha e Silva 1978). The inflammatory process can be initiated through a variety of mechanisms, which include the introduction of pathogens as well as challenges to the system through chemical, thermal and mechanical stresses. Regardless of the inciting factors, the events accompanying [inflammation are somewhat consistent.]

Rocha e Silva (1978) A brief survey of the history of inflammation. Agents Actions 8:45-49

In sports medicine, the term inflammation is often used to describe a series of signs and symptoms after soft tissue or bony injury. Appropriately, this term was originally used to describe the 4 classic signs of the affected tissue’s response to trauma: redness, swelling, heat, and pain.1 [...]

The inflammatory process can be initiated through a variety of mechanisms, which include the introduction of pathogens as well as challenges to the system through chemical, thermal, and mechanical stresses. Regardless of the inciting factors, the events accompanying inflammation are somewhat consistent.


1. Rocha e Silva M. A brief survey of the history of inflammation, 1978. Agents Actions. 1994;43:86–90.

Anmerkungen

The source is not mentioned here.

Sichter
(Hindemith) Schumann

[7.] Iam/Fragment 005 08 - Diskussion
Bearbeitet: 6. April 2014, 12:12 Guckar
Erstellt: 2. March 2014, 14:29 (Hindemith)
BauernOpfer, Butterfield et al 2006, Fragment, Gesichtet, Iam, SMWFragment, Schutzlevel sysop

Typus
BauernOpfer
Bearbeiter
Hindemith
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Untersuchte Arbeit:
Seite: 5, Zeilen: 8-19
Quelle: Butterfield et al 2006
Seite(n): 457, 458, 459, Zeilen: 457: r.col: 33-37; 458: l.col:15-19; 459: l.col: 12-15,22-27,33-34, r.col: 7-10
The cellular processes of inflammation are regulated by a series of specific cell signals that stimulate a variety of cell types, resulting in a cascade of events including white blood cell (WBC) recruitment and activation. Neutrophils are the first subpopulation of WBCs to enter traumatized or stressed tissues (Cannon and St Pierre 1998). The traditional thinking has been that these cytokines were released only by injured or stressed tissue, resulting in the localization of neutrophils to these injured tissues. The role of neutrophils in liver injury remains controversial. Although neutrophils contribute to liver damage by generating reactive oxygen species (ROS) (Jaeschke and Hasegawa 2006).

Currently, researchers are focused on the mechanisms for neutrophil recruitment and the function of these neutrophils in otherwise healthy, uninjured tissue. Among the most important questions regarding neutrophils and inflammation is whether the localization of neutrophils after passing the endothelium facilitates healing or tissue destruction. An early [intervention may prove the most beneficial strategy to minimizing tissue injury and facilitating tissue repair and recovery of function after soft bone injury (Butterfield et al. 2006).]


Butterfield TA, Best TM, Merrick MA (2006) The dual roles of neutrophils and macrophages in inflammation: a critical balance between tissue damage and repair. J Athl Train 41:457-465

Cannon JG, St Pierre BA (1998) Cytokines in exertion-induced skeletal muscle injury. Mol Cell Biochem 179:159-167

Jaeschke H, Hasegawa T (2006) Role of neutrophils in acute inflammatory liver injury. Liver Int 26:912-919

[page 457]

The cellular processes of inflammation are regulated by a series of specific cell signals that stimulate a variety of cell types, resulting in a cascade of events including white blood cell (WBC) recruitment and activation.

[page 458]

Although the implications for clinical therapeutics are not fully realized at this time, early intervention may prove the most beneficial strategy to minimizing tissue injury and facilitating tissue repair and recovery of function.

[page 459]

The traditional thinking has been that these cytokines were released only by injured or damaged myocytes, resulting in the localization of neutrophils to these injured tissues. [...] Currently, researchers are focused on the mechanisms for neutrophil recruitment and the function of these neutrophils in otherwise healthy, uninjured muscle. Among the most important questions regarding neutrophils and inflammation is whether the localization of neutrophils in the ECM facilitates healing or tissue destruction. [...]

[...]

Neutrophils are the first subpopulation of WBCs to enter traumatized or stressed tissues.17 [...] Currently, the role of neutrophils in muscle injury remains controversial. Although neutrophils contribute to preexisting muscle damage,47 evidence is mounting that they may provide the principal insult to the muscle membrane.39


17. Cannon JG, St Pierre BA. Cytokines in exertion-induced skeletal muscle injury. Mol Cell Biochem. 1998;179:159–167.

39. Pizza FX, Koh TJ, McGregor SJ, Brooks SV. Muscle inflammatory cells after passive stretches, isometric contractions, and lengthening contractions. J Appl Physiol. 2002;92:1873–1878.

47. Frenette J, St-Pierre M, Cote CH, Mylona E, Pizza FX. Muscle impairment occurs rapidly and precedes inflammatory cell accumulation after mechanical loading. Am J Physiol Regul Integr Comp Physiol. 2002;282: R351–R357.

Anmerkungen

The source is given at the very end, but without indication that most of the preceding two paragraphs has been taken verbatim from it.

Note that the source is largely about muscle injury, whereas the thesis discusses liver damage in rats. The copied text is adapted accordingly.

Sichter
(Hindemith) Schumann

[8.] Iam/Fragment 006 01 - Diskussion
Bearbeitet: 6. April 2014, 12:13 Guckar
Erstellt: 2. March 2014, 15:22 (Hindemith)
BauernOpfer, Butterfield et al 2006, Fragment, Gesichtet, Iam, SMWFragment, Schutzlevel sysop

Typus
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Hindemith
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Untersuchte Arbeit:
Seite: 6, Zeilen: 1-3
Quelle: Butterfield et al 2006
Seite(n): 458, Zeilen: l.col: 15-19
[An early] intervention may prove the most beneficial strategy to minimizing tissue injury and facilitating tissue repair and recovery of function after soft bone injury (Butterfield et al. 2006). Although the implications for clinical therapeutics are not fully realized at this time, early intervention may prove the most beneficial strategy to minimizing tissue injury and facilitating tissue repair and recovery of function.
Anmerkungen

The copied text starts already on the previous page: Iam/Fragment 005 08

Although the source is given, it is not clear to the reader how much text has been taken and that the text has been copied verbatim.

Sichter
(Hindemith) Schumann

[9.] Iam/Fragment 006 20 - Diskussion
Bearbeitet: 12. March 2014, 19:44 Graf Isolan
Erstellt: 2. March 2014, 14:59 (Graf Isolan)
Fragment, Gesichtet, Iam, SMWFragment, Schutzlevel sysop, Sheikh 2006, Verschleierung

Typus
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Graf Isolan
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Untersuchte Arbeit:
Seite: 6, Zeilen: 20-28
Quelle: Sheikh 2006
Seite(n): 4, Zeilen: 8-16
Interleukin (IL)-6 itself from the group of IL-6-type cytokines and IL-1β together with tumor necrosis factor (TNF)-α from the IL-1-type cytokine group are considered to be the major mediators of the acute-inflamamtion. At the inflammatory sites, IL-6 is produced by macrophages, endothelial cells and fibroblasts (Ramadori and Christ 1999). The release of mature IL-1β by macrophages seems to take place only during or after cell death (Perregaux and Gabel 1998). TNF-α is synthesized mainly by mononuclear phagocytes recruited at the sites of damage and by tissue macrophages. While IL-6, IL-1β, and TNF-α are the inducers of acute phase protein gene expression, other cytokines were shown to modulate this expression (Ramadori and Christ 1999).

Perregaux DG, Gabel CA (1998) Post-translational processing of murine IL-1: evidence that ATP-induced release of IL-1 alpha and IL-1 beta occurs via a similar mechanism. J Immunol 160:2469-2477

Ramadori G, Christ B (1999) Cytokines and the hepatic acute-phase response. Semin Liver Dis 19:141-155

Interleukin- (IL) 6 from the group of IL-6-type cytokines and IL-1β together with tumor necrosis factor (TNF)-α from the group of IL-1-type cytokine are considered to be the major mediators of the APR. At the inflammatory sites, IL-6 is produced by macrophages, endothelial cells, and fibroblasts (Ramadori and Christ, 1999). The release of mature IL-1β by macrophages seems to take place only during or after cell death (Perregaux and Gabel, 1998). TNF-α is synthesized mainly by mononuclear phagocytes recruited at the sites of damage and by tissue macrophages (Ramadori and Christ, 1999). While IL-6, IL-1β, and TNF-α are the inducers of acute-phase protein gene expression, other cytokines (Table 1) were shown to modulate this expression (Moshage, 1997).

Moshage H. Cytokines and the hepatic acute phase response. J Pathol 181: 257-266, 1997.

Perregaux DG and Gabel CA. Post-translational processing of murine IL-1: evidence that ATP-induced release of IL-1{alpha} and IL-1{beta} occurs via a similar mechanism. J Immunol 160: 2469-2477, 1998.

Ramadori G and Christ B. Cytokines and the hepatic acute-phase response. Semin Liver Dis 19: 141-155, 1999.

Anmerkungen

Nearly identical - nevertheless nothing has been marked as a citation.

Sichter
(Graf Isolan) Schumann

[10.] Iam/Fragment 007 12 - Diskussion
Bearbeitet: 12. March 2014, 20:04 Graf Isolan
Erstellt: 3. March 2014, 11:45 (Hindemith)
Fragment, Gesichtet, Iam, Lin et al 2006, SMWFragment, Schutzlevel sysop, Verschleierung

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Hindemith, Graf Isolan
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Untersuchte Arbeit:
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Quelle: Lin et al 2006
Seite(n): 1, Zeilen: right col. 5-15
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).

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

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

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, immediately preceding the CXC residues, selectively target neutrophils. Although there are seven ELR+ CXC chemokines in the human genome, only four have been identified in the murine genome: CXCL1/keratinocyte-derived chemokine (KC)1, CXCL2/MIP-21, CXCL5/LPS-induced chemokine (LIX)1, and CXCL15/lungkine [8–12].

8. Smith, J. B., Herschman, H. R. (1997) Identification of inflammatory mediators by screening for glucocorticoid-attenuated response genes. Methods Enzymol. 287, 250–265.

9. Wolpe, S. D., Sherry, B., Juers, D., Davatelis, G., Yurt, R. W., Cerami, A. (1989) Identification and characterization of macrophage inflammatory protein 2. Proc. Natl. Acad. Sci. USA 86, 612–616.

10. Wuyts, A., Haelens, A., Proost, P., Lenaerts, J. P., Conings, R., Opdenakker, G., Van Damme, J. (1996) Identification of mouse granulocyte chemotactic protein-2 from fibroblasts and epithelial cells. Functional comparison with natural KC and macrophage inflammatory protein-2. J. Immunol. 157, 1736–1743.

11. Rossi, D. L., Hurst, S. D., Xu, Y., Wang, W., Menon, S., Coffman, R. L., Zlotnik, A. (1999) Lungkine, a novel CXC chemokine, specifically expressed by lung bronchoepithelial cells. J. Immunol. 162, 5490–5497.

12. Bozic, C. R., Kolakowski Jr., L. F., Gerard, N. P., Garcia-Rodriguez, C., von Uexkull-Guldenband, C., Conklyn, M. J., Breslow, R., Showell, H. J., Gerard, C. (1995) Expression and biologic characterization of the murine chemokine KC. J. Immunol. 154, 6048–6057.

Anmerkungen

The source is not mentioned.

Sichter
(Hindemith), (Graf Isolan) Schumann

[11.] Iam/Fragment 007 20 - Diskussion
Bearbeitet: 19. March 2014, 21:11 Hindemith
Erstellt: 13. March 2014, 23:33 (Graf Isolan)
Fragment, Gesichtet, Iam, Moriconi et al 2008, SMWFragment, Schutzlevel sysop, Verschleierung

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Untersuchte Arbeit:
Seite: 7, Zeilen: 20-26
Quelle: Moriconi et al 2008
Seite(n): 162-163, Zeilen: 162: right col. 39-42 - 163: left col. 1-5
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).

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

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

[Page 162]

The C-X-C (or α) chemokines, such as CINC1, IP10, MIG, ITAC and SDF1, have the potential to activate and attract neutrophils and T lymphocytes (18), while the C-C (or β) chemokines, such as

[Page 163]

MCP1, MIP1α, MIP1β, MIP3α and MIP3β, 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 (19).


18. J. G. Harris, R. J. Flower, K. Watanabe, S. Tsurufuji, B. A. Wolitzky and M. Perretti, 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 (1996).

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

Anmerkungen

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Note: Ajuebor et al. (1998) does not contain the parallel text.

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[12.] Iam/Fragment 010 08 - Diskussion
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The liver is a highly radiosensitive organ because of the danger of development of radiation-induced liver disease. It could be that cell-cell interactions between different cell systems occurring in the liver probably play a decisive role in the development of radiation-induced liver disease (Christiansen et al. 2007).

The molecular pathogenesis of hepatocellular damage after irradiation is obscure.


Christiansen H, Sheikh N, Saile B, Reuter F, Rave-Frank M, Hermann RM, Dudas J, Hille A, Hess CF, Ramadori G (2007) x-Irradiation in rat liver: consequent upregulation of hepcidin and downregulation of hemojuvelin and ferroportin-1 gene expression. Radiology 242:189-197

The liver is a highly radiosensitive organ because of the danger of development of radiation-induced liver disease. Because isolated primary hepatocytes in vitro are known to be radioresistant (14–20), cell-cell interactions between different cell systems occurring in the liver probably play a decisive role in the development of radiation-induced liver disease. [...]

The molecular pathogenesis of hepatocellular damage after irradiation is obscure.

Anmerkungen

The source is given, but it is not clear that the text is taken mostly verbatim and that also the sentence after the reference to the source is taken from it.

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[13.] Iam/Fragment 010 12 - Diskussion
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For research purposes, a reproducible injury model of tissue inflammation and repair is required; one of such model is radiation induced liver injury (Christiansen et al. 2006). Specifically, it serves as an accepted paradigm to aid in the understanding of the body’s generalized inflammatory process after irradiation and, therefore, of a significant number of liver injuries.

Christiansen H, Batusic D, Saile B, Hermann RM, Dudas J, Rave-Frank M, Hess CF, Schmidberger H, Ramadori G (2006) Identification of genes responsive to gamma radiation in rat hepatocytes and rat liver by cDNA array gene expression analysis. Radiat Res 165:318-325

For research purposes, a reproducible injury model of tissue inflammation and repair is required; one such model involves eccentric overload to skeletal muscle.2–4 [...] Specifically, it serves as an accepted paradigm to aid in the understanding of the body’s generalized inflammatory process and, therefore, of a significant number of athletic injuries.

2. Best TM, Fiebig R, Corr DT, Brickson S, Ji L. Free radical activity, antioxidant enzyme, and glutathione changes with muscle stretch injury in rabbits. J Appl Physiol. 1999;87:74–82.

3. Brickson S, Hollander J, Corr DT, Ji LL, Best TM. Oxidant production and immune response after stretch injury in skeletal muscle. Med Sci Sports Exerc. 2001;33:2010–2015.

4. Tsivitse SK, Mylona E, Peterson JM, Gunning WT, Pizza FX. Mechanical loading and injury induce human myotubes to release neutrophil chemoattractants. Am J Physiol Cell Physiol. 2005;288:C721–C729.

Anmerkungen

The source is not given, its text has been adapted from muscle to liver injuries.

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[14.] Iam/Fragment 011 01 - Diskussion
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Previous studies has reported that the chemokines and cytokines are important for hepatocellular damage, repair, and fibrosis development in other toxic liver injuries (Jaeschke et al. 1996;Ramadori and Armbrust 2001;Ramadori et al. 2008). Similarly, cell types of different organs interact by way of cytokines in the development of normal tissue reactions after radiation therapy (Herskind et al. 1998).

Herskind C, Bamberg M, Rodemann HP (1998) The role of cytokines in the development of normal-tissue reactions after radiotherapy. Strahlenther Onkol 174 Suppl 3:12-15

Jaeschke H, Smith CW, Clemens MG, Ganey PE, Roth RA (1996) Mechanisms of inflammatory liver injury: adhesion molecules and cytotoxicity of neutrophils. Toxicol Appl Pharmacol 139:213-226

Ramadori G, Armbrust T (2001) Cytokines in the liver. Eur J Gastroenterol Hepatol 13:777- 784

Ramadori G, Moriconi F, Malik I, Dudas J (2008) Physiology and pathophysiology of liver inflammation, damage and repair. J Physiol Pharmacol 59 Suppl 1:107-117

Cytokines are important for hepatocellular damage, repair, and fibrosis development in other toxic liver injuries (26–28). Similarly, cell types of different organs interact by way of cytokines in the development of normal tissue reactions after radiation therapy (29).

26. Jaeschke H, Smith CW, Clemens MG, Ganey PE, Roth RA. Mechanisms of inflammatory liver injury: adhesion molecules and cytotoxicity of neutrophils. Toxicol Appl Pharmacol 1996;139:213–216.

27. Neubauer K, Saile B, Ramadori G. Liver fibrosis and altered matrix synthesis. Can J Gastroenterol 2001;15:187–193.

28. Ramadori G, Armbrust T. Cytokines in the liver. Eur J Gastroenterol Hepatol 2001;13: 777–784.

29. Herskind C, Bamberg M, Rodemann HP. The role of cytokines in the development of normal-tissue reactions after radiotherapy. Strahlenther Onkol 1998;174:12–15.

Anmerkungen

The source is not mentioned.

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[15.] Iam/Fragment 011 05 - Diskussion
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The response of hepatocytes to radiation is heterogeneous and is dependent on oxygen concentration. However, in general, hepatocytes are considered more radioresistant than other cells (Alati et al. 1989b;Alati et al. 1989a). In contrast, the liver is a radiosensitive organ. The threshold dose for injury after whole-liver irradiation has been reported to be between 20 and 30 Gy (Anscher et al. 1990). In animal studies, liver irradiation above a threshold dose is not followed by a recovery phase and a complete return to normal. Instead, progressive liver fibrosis and cirrhosis may occur (Geraci et al. 1993).

Alati T, Eckl P, Jirtle RL (1989a) An in vitro micronucleus assay for determining the radiosensitivity of hepatocytes. Radiat Res 119:562-568

Alati T, Van CM, Jirtle RL (1989b) Radiosensitivity of parenchymal hepatocytes as a function of oxygen concentration. Radiat Res 118:488-501

Anscher MS, Crocker IR, Jirtle RL (1990) Transforming growth factor-beta 1 expression in irradiated liver. Radiat Res 122:77-85

Geraci JP, Mariano MS (1993) Radiation hepatology of the rat: parenchymal and nonparenchymal cell injury. Radiat Res 136:205-213

Geraci JP, Mariano MS, Jackson KL (1993) Radiation hepatology of the rat: time-dependent recovery. Radiat Res 136:214-221

The response of hepatocytes to radiation is heterogeneous and is dependent on oxygen concentration (4). However, in general, hepatocytes are considered more radioresistant than other cells (5–10). In contrast, the liver is a radiosensitive organ. The threshold dose for injury after whole-liver irradiation has been reported to be between 20 and 30 Gy (11). In animal studies, liver irradiation above a threshold dose is not followed by a recovery phase and a complete return to normal. Instead, progressive liver fibrosis and cirrhosis may occur (12).

4. T. Alati, M. Van Cleeff and R. L. Jirtle, Radiosensitivity of parenchymal hepatocytes as a function of oxygen concentration. Radiat. Res. 118, 488–501 (1989).

5. T. Alati, P. Eckl and R. L. Jirtle, An in vitro micronucleus assay for determining the radiosensitivity of hepatocytes. Radiat. Res. 119, 562–568 (1989).

6. T. Alati, M. Van Cleeff, S. C. Strom and R. L. Jirtle, Radiation sensitivity of adult human parenchymal hepatocytes. Radiat. Res. 115, 152–160 (1988).

7. R. L. Jirtle, G. Michalopoulos, J. R. McLain and J. Crowley, Transplantation system for determining the clonogenic survival of parenchymal hepatocytes exposed to ionizing radiation. Cancer Res. 41, 3512–3518 (1981).

8. R. L. Jirtle, J. R. McLain, S. C. Strom and G. Michalopoulos, Repair of radiation damage in noncycling parenchymal hepatocytes. Br. J. Radiol. 55, 847–851 (1982).

9. R. L. Jirtle, G. Michalopoulos, S. C. Strom, P. M. DeLuca and M. N. Gould, The survival of parenchymal hepatocytes irradiated with low and high LET radiation. Br. J. Cancer 6, 197–201 (1984).

10. R. L. Jirtle, P. M. DeLuca, W. M. Hinshaw and M. N. Gould, Survival of parenchymal hepatocytes irradiated with 14.3 MeV neutrons. Int. J. Radiat. Oncol. Biol. Phys. 10, 895–899 (1984).

11. R. L. Jirtle, M. S. Anscher and T. Alati, Radiation sensitivity of the liver. Adv. Radiat. Biol. 14, 269–311 (1990).

12. J. P. Geraci, M. S. Mariano and K. L. Jackson, Radiation hepatology of the rat: Time-dependent recovery. Radiat. Res. 136, 214–221 (1993).

Anmerkungen

Nothing is marked as a citation.

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[16.] Iam/Fragment 011 12 - Diskussion
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Investigators have shown that hepatocytes are not substantially damaged by radiation. Still, radiation can weaken the defense mechanisms of hepatocytes, and this weakening can lead to the susceptibility to apoptosis mediated by tumor necrosis factor alpha (TNF-α) in-vitro in some hepatocytes (Christiansen et al. 2004). Furthermore, results of a recent study indicate that whole-liver irradiation in the rat leads to development of steatosis within the first 48 hours after irradiation (Christiansen et al. 2006).

Christiansen H, Batusic D, Saile B, Hermann RM, Dudas J, Rave-Frank M, Hess CF, Schmidberger H, Ramadori G (2006) Identification of genes responsive to gamma radiation in rat hepatocytes and rat liver by cDNA array gene expression analysis. Radiat Res 165:318-325

Christiansen H, Saile B, Neubauer-Saile K, Tippelt S, Rave-Frank M, Hermann RM, Dudas J, Hess CF, Schmidberger H, Ramadori G (2004) Irradiation leads to susceptibility of hepatocytes to TNF-alpha mediated apoptosis. Radiother Oncol 72:291-296

Investigators have shown that hepatocytes are not substantially damaged by radiation. Still, radiation can weaken the defense mechanisms of hepatocytes, and this weakening can lead to the susceptibility to apoptosis mediated by tumor necrosis factor α (TNF-α) in vitro in some hepatocytes (30). Furthermore, results of a recent study indicate that whole-liver irradiation in the rat leads to development of steatosis within the first 48 hours after irradiation (31).

30. Christiansen H, Saile B, Neubauer-Saile K, et al. Irradiation leads to susceptibility of hepatocytes to TNF-alpha mediated apoptosis. Radiother Oncol 2004;72:291–296.

31. Christiansen H, Batusic D, Saile B, et al. Identification of genes responsive to gamma radiation in rat hepatocytes and rat liver by cDNA array gene expression analysis. Radiat Res 2006;165:318–325.

Anmerkungen

The source is not mentioned.

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[17.] Iam/Fragment 011 17 - Diskussion
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The acute clinical period of radiation-induced liver disease after irradiation tends to be relatively silent; the subacute phase is characterized by the development of anicteric ascites, elevation of liver enzymes, rapid weight gain, and liver enlargement 2 weeks to 4 months after treatment (Lawrence et al. 1995).

Lawrence TS, Robertson JM, Anscher MS, Jirtle RL, Ensminger WD, Fajardo LF (1995) Hepatic toxicity resulting from cancer treatment. Int J Radiat Oncol Biol Phys 31:1237-1248

The acute clinical period of radiation-induced liver disease after irradiation tends to be relatively silent; the subacute phase is characterized by the development of anicteric ascites, elevation of liver enzymes, rapid weight gain, and liver enlargement 2 weeks to 4 months after treatment (12).

12. T. S. Lawrence, J. M. Robertson, M. S. Anscher, R. L. Jirtle, W. D. Ensminger and L. F. Fajardo, Hepatic toxicity resulting from cancer treatment. Int. J. Radiat. Oncol. Biol. Phys. 31, 1237–1248 (1995).

Anmerkungen

Identical, not marked as a citation, no source given.

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[18.] Iam/Fragment 011 22 - Diskussion
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Once it became obvious that the liver is injured after irradiation, the individual liver cell types would be introduced in culture to investigate a hierarchy of the events triggering after irradiation in the liver. Besides the ability to respond to the cytokine action, liver parenchyma and non-parenchaymal cells express a great variety of receptors for chemokines, cytokines, growth factors, and prostaglandins and represent therefore the major target for a multiple set of mediators involved in defense reaction after liver irradiation (Christiansen et al. 2007).

Christiansen H, Sheikh N, Saile B, Reuter F, Rave-Frank M, Hermann RM, Dudas J, Hille A, Hess CF, Ramadori G (2007) x-Irradiation in rat liver: consequent upregulation of hepcidin and downregulation of hemojuvelin and ferroportin-1 gene expression. Radiology 242:189-197

Once it became obvious that the liver is a primary target organ for the APR, the individual liver cell types were introduced in culture to investigate a hierarchy of the events triggering the full APR in the liver. Besides the ability to respond to the cytokine action, different cell types within the liver are also able to express IL-1β, TNF-α, IL-6, and other modulator cytokines of the hepatic APR (Ramadori and Christ, 1999). [...] Hepatocytes express a great variety of receptors for cytokines, growth factors, and prostaglandins and therefore, represent the major target for a multiple set of mediators involved in both systemic and local host defense reactions.

Ramadori G and Christ B. Cytokines and the hepatic acute-phase response. Semin Liver Dis 19: 141-155, 1999.

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Adapted to fit Iam's subject, but still in large parts identical. Nothing has been marked as a citation.

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[19.] Iam/Fragment 011 30 - Diskussion
Bearbeitet: 6. April 2014, 12:13 Guckar
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Resection and liver transplantation are the treatments for HCC with the most mature outcome data (Cheng et al. 2004a;Iwatsuki et al. 1991) but above 15% of patients with HCC are candidates for resection or transplantation, many other therapies have been investigated.

Cheng JC, Wu JK, Lee PC, Liu HS, Jian JJ, Lin YM, Sung JL, Jan GJ (2004a) Biologic susceptibility of hepatocellular carcinoma patients treated with radiotherapy to radiation-induced liver disease. Int J Radiat Oncol Biol Phys 60:1502-1509

Iwatsuki S, Starzl TE, Sheahan DG, Yokoyama I, Demetris AJ, Todo S, Tzakis AG, Van Thiel DH, Carr B, Selby R, . (1991) Hepatic resection versus transplantation for hepatocellular carcinoma. Ann Surg 214:221-228

Resection and liver transplantation are the treatments for HCC with the most mature outcome data.12–15 [...]

Because <15% of patients with HCC are candidates for resection or transplantation, many other therapies have been investigated.


12. Iwatsuki S, Starzl TE, Sheahan DG, et al. Hepatic resection versus transplantation for hepatocellular carcinoma. Ann Surg. 1991;214:221-228; discussion, 228-229.

13. Carr BI, Selby R, Madariaga J, Iwatsuki S, Starzl TE. Prolonged survival after liver transplantation and cancer chemotherapy for advanced-stage hepatocellular carcinoma. Transplant Proc. 1993;25(1 Pt 2):1128-1129.

14. Stone MJ, Klintmalm GB, Polter D, et al. Neoadjuvant chemotherapy and liver transplantation for hepatocellular carcinoma: a pilot study in 20 patients. Gastroenterology. 1993; 104:196-202.

15. Cherqui D. Role of adjuvant treatment in liver transplantation for advanced hepatocellular carcinoma [review]. J Hepatobiliary Pancreat Surg. 1998;5:35-40.

36. Cheng JC, Wu JK, Lee PC, et al. Biologic susceptibility of hepatocellular carcinoma patients treated with radiotherapy to radiation-induced liver disease. Int J Radiat Oncol Biol Phys. 2004;60:1502-1509.

Anmerkungen

To be continued on the next page: Iam/Fragment 012 01

Note that the meaning of the copied text is badly reproduced: "<15%" --> "above 15%", causality "because" is lost.

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[20.] Iam/Fragment 012 01 - Diskussion
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Systemic chemotherapy has had limited impact in HCC (Leung et al. 2002;Mathurin et al. 1998). Historically, radiation therapy (RT) has played a minor role in the management of patients with unresectable liver cancer, primarily because of the low tolerance of the whole liver to RT and challenges associated with delivering highly conformal, high-dose RT to liver tumors while sparing dose to the uninvolved liver. There is a below 5% risk of radiation-induced liver injury after uniform whole-liver RT of 28 to 35 Gy delivered over 3 weeks, (Emami et al. 1991;Leung et al. 2002) doses that are far less than those required to eradicate tumor. The most common liver toxicity observed in North America is radiation-induced liver disease (RILD), which is a clinical syndrome of anicteric hepatomegaly, ascites and elevated liver enzymes (particularly serum alkaline phosphatase) that occurs from 2 weeks to 3 months after external beam RT (Leung et al. 2002). Treatment for RILD consists of supportive measures and in the minority of patients, it can result in liver failure. Reactivation of viral hepatitis and precipitation of underlying liver disease also can occur after RT for HCC (Cheng et al. 2004b).

Cheng JC, Wu JK, Lee PC, Liu HS, Jian JJ, Lin YM, Sung JL, Jan GJ (2004b) Biologic susceptibility of hepatocellular carcinoma patients treated with radiotherapy to radiation-induced liver disease. Int J Radiat Oncol Biol Phys 60:1502-1509

Emami B, Lyman J, Brown A, Coia L, Goitein M, Munzenrider JE, Shank B, Solin LJ, Wesson M (1991) Tolerance of normal tissue to therapeutic irradiation. Int J Radiat Oncol Biol Phys 21:109-122

Leung TW, Tang AM, Zee B, Yu SC, Lai PB, Lau WY, Johnson PJ (2002) Factors predicting response and survival in 149 patients with unresectable hepatocellular carcinoma treated by combination cisplatin, interferon-alpha, doxorubicin and 5-fluorouracil chemotherapy. Cancer 94:421-427

Mathurin P, Rixe O, Carbonell N, Bernard B, Cluzel P, Bellin MF, Khayat D, Opolon P, Poynard T (1998) Review article: Overview of medical treatments in unresectable hepatocellular carcinoma--an impossible meta-analysis? Aliment Pharmacol Ther 12:111-126

Systemic chemotherapy has had limited impact in

HCC.31–33 [...]

Historically, radiation therapy (RT) has played a minor role in the management of patients with unresectable liver cancer, primarily because of the low tolerance of the whole liver to RT and challenges associated with delivering highly conformal, high-dose RT to liver tumors while sparing dose to the uninvolved liver. There is a >5% risk of radiation-induced liver injury after uniform whole-liver RT of 28 gray (Gy) to 35 Gy delivered over 3 weeks,34,35 doses that are far less than those required to eradicate tumor. The most common liver toxicity observed in North America is radiation-induced liver disease (RILD), which is a clinical syndrome of anicteric hepatomegaly, ascites, and elevated liver enzymes (particularly serum alkaline phosphatase) that occurs from 2 weeks to 3 months after external beam RT.35 Treatment for RILD consists of supportive measures, and, in the minority of patients, it can result in liver failure. Reactivation of viral hepatitis and precipitation of underlying liver disease also can occur after RT for HCC.36


31. Mathurin P, Rixe O, Carbonell N, et al. Review article: overview of medical treatments in unresectable hepatocellular carcinoma—an impossible metaanalysis? Aliment Pharmacol Ther. 1998;12:111-126.

32. Burroughs A, Hochhauser D, Meyer T. Systemic treatment and liver transplantation for hepatocellular carcinoma: two ends of the therapeutic spectrum. Lancet Oncol. 2004;5:409-418.

33. Leung TW, Tang AM, Zee B, et al. Factors predicting response and survival in 149 patients with unresectable hepatocellular carcinoma treated by combination cisplatin, interferon-alpha, doxorubicin and 5-fluorouracil chemotherapy. Cancer. 2002;94:421-427.

34. Emami B, Lyman J, Brown A, et al. Tolerance of normal tissue to therapeutic irradiation. Int J Radiat Oncol Biol Phys. 1991;21:109-122.

35. Lawrence TS, Robertson JM, Anscher MS, Jirtle RL, Ensminger WD, Fajardo LF. Hepatic toxicity resulting from cancer treatment. Int J Radiat Oncol Biol Phys. 1995;31:1237-1248.

36. Cheng JC, Wu JK, Lee PC, et al. Biologic susceptibility of hepatocellular carcinoma patients treated with radiotherapy to radiation-induced liver disease. Int J Radiat Oncol Biol Phys. 2004;60:1502-1509.

Anmerkungen

The copied text starts on the previous page: Iam/Fragment 011 30

Note that the copied material is not always correctly reproduced: ">5% risk" --> "below 5% risk".

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[21.] Iam/Fragment 012 16 - Diskussion
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[Induction of chemokines in tumors after irradiation has already been reported (Matsumura et al. 2008).] Evidence is accumulating that ionizing radiation (IR) therapy, a treatment modality routinely used to kill cancer cells, can modulate the expression of several [receptors and cytokines by cancer cells and tumor stroma, resulting in modifications of the tumor microenvironment that can be exploited to enhance the effects of immunotherapy (Demaria and Formenti 2007).]

Demaria S, Formenti SC (2007) Sensors of ionizing radiation effects on the immunological microenvironment of cancer. Int J Radiat Biol 83:819-825

Evidence is accumulating that ionizing radiation (IR) therapy, a treatment modality routinely employed to kill cancer cells, can modulate the expression of several receptors and cytokines by cancer cells and tumor stroma, resulting in modifications of the tumor microenvironment that can be exploited to enhance the effects of IT (reviewed in references 20 and 21).

20. Demaria S, Bhardwaj N, McBride WH, Formenti SC. Combining radiotherapy and immunotherapy: a revived partnership. Int J Radiat Oncol Biol Phys 2005;63:655–666. [PubMed: 16199306]

21. Demaria S, Formenti SC. Sensors of ionizing radiation effects on the immunological microenvironment of cancer. Int J Radiat Biol 2007;83:1–7. [PubMed: 17357435]

Anmerkungen

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12a diss Iam.png

Figure 6: The combined use of radiation, immunotherapy and angiogenesis inhibitors-by normalizing blood flow and lowering intratumoral pressure, angiogenesis inhibitors enable T cells to gain efficient access to the tumor, while increasing the necessary components for effective T-cell function at the tumor site. Furthermore, by reducing hypoxia, antiangiogenic agents allow for optimization of radiotherapy, thereby providing the immune system with a rich supply of tumor antigens while modulating tumor-cell phenotype for enhanced T-cell killing (adapted by Kamrava et al. 2009)


Kamrava M, Bernstein MB, Camphausen K, Hodge JW (2009) Combining radiation, immunotherapy, and antiangiogenesis agents in the management of cancer: the Three Musketeers or just another quixotic combination? Mol Biosyst 5:1262-1270

12a source Iam.png

Fig. 4 The combined use of radiation, immunotherapy, and angiogenesis inhibitors-by normalizing blood flow and lowering intratumoral pressure, angiogenesis inhibitors enable T cells to gain efficient access to the tumor, while increasing the necessary components for effective T-cell function at the tumor site. Furthermore, by reducing hypoxia, antiangiogenic agents allow for optimization of radiotherapy, thereby providing the immune system with a rich supply of tumor antigens while modulating tumor-cell phenotype for enhanced T-cell killing.

Anmerkungen

The source is given, but it is not clear to the reader that the image as well as the extensive caption have both been taken from it.

"adapted by Kamrava et al. 2009" should probably be "adopted from Kamrava et al. 2009"

Sichter
(Hindemith) Schumann

[23.] Iam/Fragment 013 01 - Diskussion
Bearbeitet: 12. March 2014, 16:28 Klgn
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BauernOpfer, Fragment, Gesichtet, Iam, Matsumura et al 2008, SMWFragment, Schutzlevel sysop

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[Evidence is accumulating that ionizing radiation (IR) therapy, a treatment modality routinely used to kill cancer cells, can modulate the expression of several] receptors and cytokines by cancer cells and tumor stroma, resulting in modifications of the tumor microenvironment that can be exploited to enhance the effects of immunotherapy (Demaria and Formenti 2007). The molecular mechanism(s) responsible for up-regulation of chemokines following IR of cancer cells are presently undefined. A possible candidate is the PI3K/Akt signaling pathway, which is activated by IR in tumor and endothelial cells (Zingg et al. 2004). This pathway promotes survival of tumor cells and has been recently linked to the induction of CXCL16 in a mouse model of mammary tumorigenesis (Ju et al. 2007).

Demaria S, Formenti SC (2007) Sensors of ionizing radiation effects on the immunological microenvironment of cancer. Int J Radiat Biol 83:819-825

Ju X, Katiyar S, Wang C, Liu M, Jiao X, Li S, Zhou J, Turner J, Lisanti MP, Russell RG, Mueller SC, Ojeifo J, Chen WS, Hay N, Pestell RG (2007) Akt1 governs breast cancer progression in vivo. Proc Natl Acad Sci U S A 104:7438-7443

Zingg D, Riesterer O, Fabbro D, Glanzmann C, Bodis S, Pruschy M (2004) Differential activation of the phosphatidylinositol 3'-kinase/Akt survival pathway by ionizing radiation in tumor and primary endothelial cells. Cancer Res 64:5398-5406

[Page 3099]

Evidence is accumulating that ionizing radiation (IR) therapy, a treatment modality routinely employed to kill cancer cells, can modulate the expression of several receptors and cytokines by cancer cells and tumor stroma, resulting in modifications of the tumor microenvironment that can be exploited to enhance the effects of IT (reviewed in references 20 and 21).

[Page 3106]

The molecular mechanism(s) responsible for up-regulation of CXCL16 following IR of breast cancer cells are presently undefined. A possible candidate is the PI3K/Akt signaling pathway, which is activated by IR in tumor and endothelial cells (49). This pathway promotes survival of tumor cells, and has been recently linked to induction of CXCL16 in a mouse model of mammary tumorigenesis (50).


20. Demaria S, Bhardwaj N, McBride WH, Formenti SC. Combining radiotherapy and immunotherapy: a revived partnership. Int J Radiat Oncol Biol Phys 2005;63:655–666. [PubMed: 16199306]

21. Demaria S, Formenti SC. Sensors of ionizing radiation effects on the immunological microenvironment of cancer. Int J Radiat Biol 2007;83:1–7. [PubMed: 17357435]

49. Zingg D, Riesterer O, Fabbro D, Glanzmann C, Bodis S, Pruschy M. Differential activation of the phosphatidylinositol 3′-kinase/Akt survival pathway by ionizing radiation in tumor and primary endothelial cells. Cancer Res 2004;64:5398–5406. [PubMed: 15289348]

50. Ju X, Katiyar S, Wang C, Liu M, Jiao X, Li S, Zhou J, Turner J, Lisanti MP, Russell RG, Mueller SC, Ojeifo J, Chen WS, Hay N, Pestell RG. Akt1 governs breast cancer progression in vivo. Proc Natl Acad Sci U S A 2007;104:7438–7443. [PubMed: 17460049]

Anmerkungen

The source is mentioned right before the passage starts on the previous page. Nothing has been marked as a citation though the wording (and the list of references) are identical.

The reader should take note: The reference to "breast cancer" from the original source has been deleted since Iam does research with regard to liver cancer.

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[24.] Iam/Fragment 015 01 - Diskussion
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2. MATERIALS

2.1 Animals

Male Wistar rats (about 200 g body weight) were purchased from Harlan-Winkelmann (Borchen, Germany) and kept under standard conditions with 12-hours light/dark cycles and access to fresh water and food pellets ad libitum at room temperature of 19-23°C. The rats consumed 12-15 g food (rat diet "ssniff", Spezialitäten GmbH, Soest, Germany) and 12-25 ml water per day and had a 30-40 g gain of weight per week. Animals were used for the experiments not earlier than 6 days after arrival. The preparation of hepatocytes was performed during the first 3 hours of the light phase.

2. MATERIALS

2.1 Animals

Male Wistar rats (about 200 g body weight) were purchased from Harlan-Winkelmann (Borchen, Germany) and kept under standard conditions with 12-hours light/dark cycles, access to fresh water and food pellets ad libitum at room temperature of 19-23°C. The rats consumed 12-15 g food (rat diet "ssniff", Spezialitäten GmbH, Soest, Germany) and 12-25 ml water per day and had a 30-40 g gain of weight per week. Animals were used for the experiments not earlier than 6 days after arrival. The preparation of hepatocytes was performed during the first 3 h of the light phase.

Anmerkungen

Identical; not marked as a citation.

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[25.] Iam/Fragment 024 04 - Diskussion
Bearbeitet: 12. March 2014, 20:03 Graf Isolan
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Christiansen et al 2007, Fragment, Gesichtet, Iam, SMWFragment, Schutzlevel sysop, Verschleierung

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The in-vivo experiments were performed as described previously: (Christiansen et al. 2006). Before irradiation planning computed tomography (CT) was performed with a scanner (Somatom Balance; Siemens Medical Solutions, Erlangen, Germany) in each rat to delineate the livers of the animals. The rats were anaesthetized intraperitoneally (IP) with 90 mg ketamine per kilogram of body weight (Intervet, Unterschleissheim, Germany) and 7.5 mg/kg of 2% xylazine (Serumwerk Bernburg, Bernburg/Saale, Germany). The margins of the liver were marked on the skin of the animals and a dose distribution was calculated. The livers were irradiated selectively with 6–MeV photons (dose rate, 2.4 Gy/min) by using an accelerator (Clinac 600 C; Varian, Palo Alto, Calif). A dose of 25 Gy in a single treatment was delivered by using an anteroposterior and posteroanterior treatment technique. Normal sham-irradiated animals, which were transported and anesthetized simultaneously with the irradiated animals, served as specific controls. Animals were observed at specified times up to 48 hours after irradiation and seemed to behave normally without signs of discomfort. Livers and serum samples were taken from five animals each at 1, 3, 6, 12, 24, and 48 hours after irradiation and frozen.

Christiansen H, Batusic D, Saile B, Hermann RM, Dudas J, Rave-Frank M, Hess CF, Schmidberger H, Ramadori G (2006) Identification of genes responsive to gamma radiation in rat hepatocytes and rat liver by cDNA array gene expression analysis. Radiat Res 165:318-325

[page 190]

In vivo experiments were performed by several authors (H.C., F.R., M.R., R.M.H., A.H.) in consensus, as described previously by Christiansen et al (31): Planning computed tomography (CT) was performed with a scanner (Somatom Balance; Siemens Medical Solutions, Erlangen, Germany) in each rat to delineate the livers of the animals. The rats were intraperitoneally anesthetized with 90 mg per kilogram of body weight of ketamine (Intervet, Unterschleissheim, Germany) and 7.5 mg/kg of 2% xylazine (Serumwerk Bernburg, Bernburg/Saale, Germany). The margins of the liver were marked

[page 191]

on the skin of each animal, and a dose distribution was calculated.

The livers were irradiated selectively with 6–MeV photons (dose rate, 2.4 Gy/min) by using an accelerator (Clinac 600 C; Varian, Palo Alto, Calif). A dose of 25 Gy in a single treatment was delivered by using an anteroposterior and posteroanterior treatment technique. Normal sham-irradiated animals, which were transported and anesthetized simultaneously with the irradiated animals, served as specific controls. Animals were observed at specified times up to 48 hours after irradiation and seemed to behave normally without signs of discomfort. Livers and serum samples were taken from five animals each at 1, 3, 6, 12, 24, and 48 hours after irradiation and frozen.


31. Christiansen H, Batusic D, Saile B, et al. Identification of genes responsive to gamma radiation in rat hepatocytes and rat liver by cDNA array gene expression analysis. Radiat Res 2006;165:318–325.

Anmerkungen

Christiansen et al. (2006) does not have the passage in this formulation.

It is not surprising that the same research group follows a similar or the same protocol for different experiments. However, text re-use should be clearly marked and the correct source given.

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[26.] Iam/Fragment 025 01 - Diskussion
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3.1.2 Isolation of rat hepatocytes and irradiation

Hepatocytes were isolated from male Wistar rats by circulating perfusion with collagenase essentially as described previously (Seglen 1972).

3.1.2.a. Liver perfusion

After laparotomy, the vena portae was canulated, vena cava inferior was ligated above the diaphragm to prevent flow of the perfusion media into a whole body circulation. Finally, the vena cava inferior was cut beneath the liver and canulated. The liver was perfused in non-recirculative mode through the portal vein with 150-200 ml CO2-enriched preperfusion medium at a flow rate of 30 ml/min until the liver was free from blood. To break down components of extracellular matrix, the liver was perfused in recirculative mode with collagenase perfusion medium until it started to feel soft (about 7-11 min).


Seglen PO (1972) Preparation of rat liver cells. I. Effect of Ca 2+ on enzymatic dispersion of isolated, perfused liver. Exp Cell Res 74:450-454

3.1.1 Isolation of rat hepatocytes

Hepatocytes were isolated from male Wistar rats by circulating perfusion with collagenase essentially as described previously (Seglen, 1973; Katz et al., 1979).

3.1.1.I Liver perfusion

After laparotomy, the vena portae was canulated, vena cava inferior was ligated above the diaphragm to prevent flow of the perfusion media into a whole body circulation. Finally, the vena cava inferior was cut beneath the liver and canulated. The liver was perfused in non-recirculative mode through the portal vein with 150-200 ml CO2-enriched preperfusion medium at a flow rate of 30 ml/min until the liver was free from blood. To break down components of extracellular matrix, the liver was perfused in recirculative mode with collagenase perfusion medium until it started to feel soft (about 7-11 min).

Anmerkungen

Though identical nothing has been marked as a citation.

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[27.] Iam/Fragment 026 01 - Diskussion
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3.1.2.b. Preparation of the hepatocyte suspension

After perfusion, the liver was excised and transferred into a sterile glass beaker filled with culture medium M 199 with additives. Glisson’s capsule, i. e. collagen tissue around the liver, was carefully removed and discarded. To obtain a cell suspension, the tissue was disrupted mechanically using sterile forceps. Connective tissue and remainder of the liver capsule as well as big cell aggregates were removed by filtration of the primary cell suspension through a nylon mesh (pore-size 79 μm). Non-parenchymal cells and cell debris were removed by numerous selective sedimentations (20 g, 2 min, 4°C) in wash medium. After the last centrifugation, hepatocytes were suspended in medium M 199 with additives. 50 ml of M 199 was added per 1 g of wet weight of the sedimented cells; the cell suspension typically had a density of about 106/2.5 ml.

3.1.2.c. Media and solutions for hepatocyte preparation and culture

All media and solutions for cell culture were prepared in double distilled water, further purified by sterile filtration and stored at 4°C. All solutions were prepared not more than one day before the isolation.

Krebs-Ringer stock solution

    Final concentration
NaCl   120 mM
KCl   4.8 mM
MgSO4×7H2O   1.2 mM
KH2PO4   1.2 mM
NaHCO3   24.4 mM

The solution was equilibrated with carbogen and pH was adjusted to 7.35 [sic]

Pre-perfusion medium (prepared in 1X Krebs-Ringer solution)

    Final concentration
EGTA   0.25 mM

Collagenase perfusion medium (prepared in 1X Krebs-Ringer solution)

    Final concentration
HEPES   15 mM
CaCl2×2H2O   4 mM
[Collagenase 50 mg

The medium was prepared directly prior to isolation, equilibrated with carbogen for 30 min and finally sterile filtered.]

[Page 25]

3.1.1.II Preparation of the hepatocyte suspension

After perfusion, the liver was excised and transferred into a sterile glass beaker filled with culture medium M 199 with additives. Glisson’s capsule, i.e. collagen tissue around the liver, was carefully removed and discarded. To obtain a cell suspension, the tissue was disrupted mechanically using sterile forceps. Connective tissue and remainder of the liver capsule as well as big cell aggregates were removed by filtration of the primary cell suspension through a nylon mesh (pore-size 79 μm). Non-parenchymal cells and cell debris were removed by numerous selective sedimentations (20 g, 2 min, and 4°C) in wash medium. After the last centrifugation, hepatocytes were suspended in medium M 199 with additives. 50 ml of M 199 was added per 1 g of wet weight of the sedimented cells; the cell suspension typically had a density of about 106/2.5 ml.

[Page 26]

3.1.1.III Media and solutions for hepatocyte preparation and culture

All media and solutions for cell culture were prepared in double distilled water, further purified by sterile filtration and stored at 4°C. All solutions were prepared not more than one day before the isolation.

Krebs-Ringer stock solution
  For 1l Final concentration
NaCl 7 g 120 mM
KCl 0.36 g 4.8 mM
MgSO4×7H2O 0.296 g 1.2 mM
KH2PO4 0.163 g 1.2 mM
NaHCO3 2.016 g 24.4 mM
dd H2O to 1 l  
The solution was equilibrated with carbogen and pH was adjusted to 7.35 [sic]
Pre-perfusion medium
  For 1 l Final concentration
EGTA 95.1 mg 0.25 mM
Krebs-Ringer stock solution to 1 l  
Collagenase perfusion medium
  For 100 ml Final concentration
HEPES 360 mg 15 mM
CaCl2×2H2O 58.8 mg 4 mM
Collagenase 50 mg
Krebs-Ringer stock solution to 100 ml  
The medium was prepared directly prior to isolation, equilibrated with carbogen for 30 min and finally sterile filtered.
Anmerkungen

Though identical nothing has been marked as a citation.

Typical C&P-mistake: The author has overlooked that the "6" in "106/2.5 ml" is an exponent and not just another digit.

Sichter
(Graf Isolan) Schumann

[28.] Iam/Fragment 027 01 - Diskussion
Bearbeitet: 12. March 2014, 20:16 Graf Isolan
Erstellt: 7. March 2014, 09:35 (Singulus)
Fragment, Gesichtet, Iam, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Sheikh 2006

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Collagenase 50 mg
The medium was prepared directly prior to isolation, equilibrated with carbogen for 30 min and finally sterile filtered.


Wash medium

    Final concentration
HEPES/NaOH pH 7.4   20 mM
NaCl   120 mM
KCl   4.8 mM
MgSO4×7H2O   1.2 mM
KH2PO4   1.2 mM
Bovine serum albumin   0.4%

Medium M 199 with additives

M199 with Earle’s salts without NaHCO3   Final concentration
Glucose×H2O   5.5 mM
HEPES   15 mM
NaHCO3   18 mM
Bovine serum albumin   0.4%
The medium was equilibrated with carbogen until pH reached a value of 7.35. Finally, the medium was sterile filtered.
[page 26]

Collagenase 50 mg

[...]

The medium was prepared directly prior to isolation, equilibrated with carbogen for 30 min and finally sterile filtered.

[page 27]

Wash medium
  For 1l Final concentration
HEPES/NaOH pH 7.4 4.77 g 20 mM
NaCL 7.00 g 120 mM
KCl 0.36 g 4.8 mM
MgSO4×7H2O 0.30 g 1.2 mM
KH2PO4 0.16 g 1.2 mM
Bovine serum albumin 4.00 g 0.4%
dd H2O to 1 l  
Medium M 199 with additives
  For 1l Final concentration
M199 with Earle’s salts without NaHCO3 1 l
Glucose × H2O 1.1 g 5.5 mM
HEPES 3.6 g 15 mM
NaHCO3 1.5 g 18 mM
Bovine serum albumin 4.0 g 0.4%
The medium was equilibrated with carbogen until pH reached a value of 7.35. Finally, the medium was sterile filtered.
Anmerkungen

Continuation of Fragment 026 01.

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[29.] Iam/Fragment 031 11 - Diskussion
Bearbeitet: 12. March 2014, 20:03 Graf Isolan
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Irradiation was performed 24 hours after the hepatocytes were plated, and the culture medium was replaced immediately before irradiation: On the first day after isolation, hepatocytes were irradiated with 8 Gy (6–megaelectron volt photons) at a dose rate of 2.4 Gy/min by using the accelerator mentioned before. Irradiation was performed 24 hours after the hepatocytes were plated, and the culture medium was replaced immediately before irradiation: On the first day after isolation, hepatocytes were irradiated with 8 Gy (6–megaelectron volt photons) at a dose rate of 2.4 Gy/min by using the accelerator mentioned before.
Anmerkungen

The source is not given.

Sichter
(Hindemith) Schumann

[30.] Iam/Fragment 036 01 - Diskussion
Bearbeitet: 12. March 2014, 20:03 Graf Isolan
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3.2.2.b. Thermal cycler amplification program

The amplification was performed at 50 °C for 2 min, 95°C for 2 min., 95°C for 15 seconds to 60°C for 30 seconds for 45 cycles (Figure 8) in an ABI prism 7000 sequence detection system. All samples were assayed in duplicate. Expression of different genes was analyzed using Platinum SYBR Green qPCR mix UDG. The PCR amplification program was followed by dissociation curve protocol for controlling the specificity of the PCR products. Specific temperature of dissociation of the PCR product was calculated by the Primer Express software. Curves of amplification were analyzed to measure the Ct value in the linear range of the amplification. The results were normalized to the house keeping gene and fold change expression was calculated using Ct values by Prism Graph Pad 4 software.

36a diss Iam.png

Figure 8: Thermal cycler amplification program for the quantitative real-time PCR amplification of the mRNA using Platinum® SYBR® Green qPCR SuperMix UDG, specific forward, reverse primer and template cDNA in ABI Prism® 7000 Sequence Detection System by Applied Biosystems. Stage 1; 2 minutes incubation at 50°C, Stage 2; 2 minutes incubation at 95°C for hot start, Stage 3; 15 sec at 95°c and 30sec at 60°C for 45 repeats, Stage 4; 15 sec 95°C, 15sec 60°C and 15 sec 95°C to get dissociation curve.

[Page 30]

3.2.1.II Thermal cycler amplification program

The amplification was performed at 50 °C for 2 min., 95°C for 2 min., 95°C for 15 sec to 60°C for 30 sec for 45 cycles (Figure 2) in an ABI prism 7000 sequence detection system. All samples were assayed in duplicate. Expression of different genes was analysed using Platinum SYBR Green qPCR mix UDG. The PCR amplification program was followed by dissociation curve protocol for controlling the specificity of the PCR products. Specific temperature of dissociation of the PCR product was calculated by the Primer Express software. Curves of amplification were analysed to measure the Ct value in the linear range of the amplification. The results were normalized to the

[Page 31]

housekeeping gene and fold change expression was calculated using Ct values by Prism Graph Pad 4 software.

36a source Iam.png

Figure 3: Thermal cycler amplification program for the quantitative real-time PCR amplification of the mRNA using Platinum® SYBR® Green qPCR SuperMix UDG, specific forward, reverse primer pairs and template cDNA in ABI Prism® 7000 Sequence Detection System by Applied Biosystems. Stage 1; 2 min. incubation at 50°C, Stage 2; 2 min. incubation at 95°C for hot start, Stage 3; 15 sec at 95°C and 30 sec at 60°C for 45 repeats. Stage 4; 15 sec at 95°C; 15 sec at 60°C and 15 sec at 95°C to get dissociation curve.

Anmerkungen

But for some "corrections" identical up to the breaks between words ("50 °C" vs. "95°C" in both texts), though nothing has been marked as a citation. Iam's "figure 8" is also identical to Sheiks "figure 3"

Sichter
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[31.] Iam/Fragment 037 01 - Diskussion
Bearbeitet: 12. March 2014, 20:03 Graf Isolan
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3.2.2.c. Primer designing

Primers for different genes were designed using the program “Primer Express” (ABI System) and the gene bank data (http://www.ncbi.nlm.nih.gov). All the primer sets used for real-time PCR are listed in the Table 1.

3.2.3 Isolation of total RNA

3.2.3.a. RNA isolation procedure using silica columns

The isolation of total RNA from cultured rat liver hepatocytes, Kupffer cells, myofibroblasts and laser-microdissected samples of the liver was conducted using the NucleoSpin® RNAII kit (Macherey-Nagel) in accordance to the protocol for cultured animal cells.

3.2.3.b. Isolation of RNA by density-gradient ultracentrifugation

Total RNA was isolated from the liver by means of guanidine isothiocyanate extraction, cesium chloride density-gradient ultracentrifugation and ethanol precipitation according to method of Chirgwin (Chirgwin et al. 1979). This method is a versatile and efficient way to extract intact RNA from most tissues and cultured cells, even if the endogenous level of RNase is high.

Cell lysis: The cells were rapidly lysed in guanidine isothiocyanate-containing buffer, which ensures inactivation of RNases. The lysates were layered onto a CsCl gradient and spun in an ultracentrifuge. Proteins remain in the aqueous guanidine portion, DNA bands in the CsCl, and RNA settle down at the bottom of the tubes as a pallet [sic]. The RNA was recovered by dissolving the pellet. The recovery of RNA was usually excellent if the capacity of the gradient did not exceed.

Homogenization of the tissue sample: About 100 mg of frozen tissue was homogenized with Ultra-Turrax TP 18/10 homogenizer 3 times for 10 sec each in 3 ml of ice-cold GITC buffer with freshly added Antifoam A (Sigma). The homogenates were centrifuged for 10 min at 3,500 rpm in a Rotixa /RP centrifuge (Hettich) at 4°C to pellet connective tissue and large cell debris.

CsCl gradient and ultra centrifugation: To prepare the gradient 2 ml of CsCl buffer was poured into 5-ml polyallomer ultracentrifuge tubes (6 per preparation). The cleared guanidine lysed samples were carefully layered on top of the CsCl buffer.


Chirgwin JM, Przybyla AE, MacDonald RJ, Rutter WJ (1979) Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease. Biochemistry 18:5294-5299

[Page 32]

3.2.1.IV Primers designing

Primers for different genes were designed using the program “Primer Express” (ABI System) and the gene bank data (http://www.ncbi.nlm.nih.gov). All the primer sets used for real-time PCR are listed in the Table 1.

3.2.2 Isolation of total RNA

3.2.2.I RNA isolation procedure using silica columns

The isolation of total RNA from cultured rat hepatocytes was conducted using the NucleoSpin® RNAII kit (Macherey-Nagel) in accordance to the protocol for cultured animal cells.

[Page 34]

3.2.2.IV Isolation of RNA by density-gradient ultracentrifugation

Total RNA was isolated from the liver, the skeletal muscle and extrahepatic organs by means of guanidine isothiocyanate extraction, cesium chloride density-gradient ultracentrifugation and ethanol precipitation according to method of Chirgwin (Chirgwin et al, 1979). This method is a versatile and efficient way to extract intact RNA from most tissues and cultured cells, even if the endogenous level of RNase is high.

Cell lysis

The cells were rapidly lysed in guanidine isothiocyanate-containing buffer, which ensures inactivation of RNases. The lysates were layered onto a CsCl gradient and spun in an ultracentrifuge. Proteins remain in the aqueous guanidine portion, DNA bands in the CsCl, and RNA settle down at the bottom of the tubes as a pellet. The RNA was recovered by dissolving the pellet. The recovery of RNA was usually excellent if the capacity of the gradient does not exceed.

Homogenization of the tissue sample

About 100 mg of frozen tissue was homogenized with ultra-turrax TP 18/10 homogenizer 3 times for 10 sec each in 3 ml of ice-cold GITC buffer with freshly added antifoam A (Sigma). The homogenates were centrifuged for 10 min at 3,500 rpm in a Rotixa/RP centrifuge (Hettich) at 4°C to pellet connective tissue and large cell debris.

[Page 35]

CsCl gradient and ultra centrifugation

To prepare the gradient 2 ml of CsCl buffer was poured into 5-ml polyallomer ultracentrifuge tubes (6 per preparation). The cleared guanidine lysed samples were carefully layered on top of the CsCl buffer.


Chirgwin JM, Przybyla AE, MacDonald RJ and Rutter WJ. Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease. Biochemistry 18: 5294- 5299, 1979.

Anmerkungen

Slightly adapted, but otherwise nearly identical, though not marked as a citation.

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[The samples were centrifuged] overnight (21 h) at 35,000 rpm in a Kontron TST55 rotor at 20°C. The supernatants were carefully removed by aspiration and the transparent gelatin-like RNA pellets were gently washed (preserving undisturbed) with 200 μl of 70% ethanol at room temperature. The pellets were reconstituted in 200 μl of RNase-free water by pipetting and transferred into sterile 1.5 ml eppendorf tubes and the procedure was immediately continued to RNA precipitation.

RNA precipitation: The RNA was precipitated with 450 μl of 100% ethanol in the presence of sodium acetate, pH 5.4 (20 μl of 2 M solution per pellet) overnight at –20°C. The RNA precipitates were centrifuged for 30 min at 12,000 rpm in an Eppendorf bench-top centrifuge at 4°C to get RNA pellet.

Washing of the RNA pellet: Supernatants were discarded and pellet was washed with 200 μl of ice-cold 70% ethanol to remove all traces of sodium acetate. The RNA precipitates were centrifuged as described above, the supernatants were discarded and the pellet was dried for 30 min. at room temperature.

Reconstitution of RNA: The pellets were reconstituted in 100 μl of RNase-free water. To determine the concentration and purity of the RNA obtained, the aliquot of RNA sample was diluted 1:100 in RNase-free H2O and the concentration was measured at 260 nm and 280 nm by spectrophotometer (GeneQuant II, Pharmacia Biotech).

Solutions used for Ultracentrifugation

Guanidine isothiocyanate (GITC) buffer

    Final concentration
Guanidine isothiocyanate   4 M
0.25 M sodium citrate   25 mM
N-lauroylsarcosyl   0.5%

The solution was sterile filtered and stored in the dark at 4°C. β-Mercaptoethanol was added just prior to use at a ration of 1 to 100 μl of GITC buffer.

Cesium chloride (CsCl) buffer

    Final concentration
Cesium chloride   5.7 M
0.25 M sodium citrate   25 mM
0.5 M EDTA   100 mM

pH was adjusted with 0.25 M citric acid to 7.5; the solution was dissolved in RNase-free [H2O, sterile filtered and stored at room temperature.]

[Page 35]

The samples were centrifuged overnight (21 h) at 35,000 rpm in a Kontron TST55 rotor at 20°C. The supernatants were carefully removed by aspiration and the transparent gelatin-like RNA pellets were gently washed (preserving undisturbed) with 200 μl of 70% ethanol at room temperature. The pellets were reconstituted in 200 μl of RNase-free water by pipetting and transferred into sterile 1.5 ml eppendorf tubes and the procedure was immediately continued to RNA precipitation.

RNA precipitation

The RNA was precipitated with 450 μl of 100% ethanol in the presence of sodium acetate, pH 5.4 (20 μl of 2 M solution per pellet) overnight at –20°C. The RNA precipitates were centrifuged for 30 min at 12,000 rpm in an Eppendorf bench-top centrifuge at 4°C to get RNA pellet.

Washing of the RNA pellet

Supernatants were discarded and pellets were washed with 200 μl of ice-cold 70% ethanol to remove all traces of sodium acetate. The RNA precipitates were centrifuged as described above, the supernatants were discarded and the pellets were dried for 30 minutes at room temperature.

Reconstitution of RNA

The pellets were reconstituted in 100 μl of RNase-free water. To determine the concentration and purity of the RNA obtained, the aliquot of RNA sample was diluted 1:100 in RNase-free H2O and the concentration was measured at 260 nm and 280 nm by spectrophotometer (GeneQuant II, Pharmacia Biotech).

[Page 36]

Solutions used for Ultracentrifugation

Guanidine isothiocyanate (GITC) buffer
  For 200 ml Final concentration
Guanidine isothiocyanate 94.53 g 4 M
0.25 M sodium citrate 20 ml 25 mM
N-lauroylsarcosyl 1 g 0.5%
RNase-free H2O to 200 ml  

The solution was sterile filtered and stored in the dark at 4°C. β-Mercaptoethanol was added just prior to use at a ration of 1 to 100 μl of GITC buffer.

Cesium chloride (CsCl) buffer
  For 200 ml Final concentration
Cesium chloride 192 g 5.7 M
0.25 M sodium citrate 20 ml 25 mM
0.5 M EDTA 40 ml 100 mM
RNase-free H2O to 200 ml  

pH was adjusted with 0.25 M citric acid to 7.5; the solution was sterile filtered and stored at room temperature.

Anmerkungen

Nearly identical, nevertheless not marked as a citation.

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[33.] Iam/Fragment 039 01 - Diskussion
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[pH was adjusted with 0.25 M citric acid to 7.5; the solution was dissolved in RNase-free] H2O, sterile filtered and stored at room temperature.

3.2.4 Northern blot analysis

Northern blot analysis is a method to quantify RNA expression. The RNA is separated in a denaturing formaldehyde/agarose gel, transferred by capillary transfer to a nylon membrane and fixed by UV cross linking. The RNA of interest is identified by hybridization with a specific radiolabeled cDNA probe. All solutions used for the northern blot were autoclaved, the electrophoresis and blot chambers, gel plates and combs were kept in freshly prepared 0.1% DEPC solution for 10-20 min before use to inactivate RNases.

3.2.4.a. Preparation of RNA samples

Each RNA probe (5-10 μg of total RNA) in a volume not more than 5 μl was mixed with 7.5 μl of sample buffer. In case of dilute sample where the volume of the probe exceeded 5 μl, the sample was concentrated in a vacuum centrifuge until the volume was reduced to 5 μl. RNA probes mixed with sample buffer were denatured by heating at 65°C for 10 min. Afterwards, the samples were briefly cooled on ice and centrifuged for 1 min at 10,000 rpm in an Eppendorf bench-top centrifuge. Each sample was mixed with 3 μl of loading buffer and centrifuged for 1 min at 10,000 rpm in an Eppendorf bench-top centrifuge.

3.2.4.b. Electrophoresis

The electrophoresis was performed at constant voltage of 80 V for 1-1.5 h. After electrophoresis, the quality of RNA was estimated under UV transilluminator built-in Eagle Eye™ system (Stratagene); the gel was photographed and the procedure was immediately continued to blotting.

3.2.4.c. Transfer of RNA to nylon membrane

After the separation of RNA in the gel, it was transferred to a nylon membrane by capillary transfer method. A plastic tray was filled with 500 ml of 20X SSC and a piece of Whatman 3MM filter was soaked in 20X SSC and swaddled over the glass plate placed over the tray with both ends hanging into buffer to act as wick. The transfer was carried out overnight. After the transfer, RNA was fixed on the membrane by UV cross linking for 2 min from both sides using Stratalinker™ 180 (Stratagene) set at “autocross link” mode.

Pre-hybridization: Afterwards, the membrane was placed into a hybridization tube and any bubbles between the membrane and internal wall of the tube were carefully removed.

[Page 36]

pH was adjusted with 0.25 M citric acid to 7.5; the solution was sterile filtered and stored at room temperature.

3.2.3 Northern blot analysis

Northern blot analysis is a method to quantify RNA expression. The RNA is separated in a denaturing formaldehyde/agarose gel, transferred by capillary transfer to a nylon membrane and fixed by UV cross linking. The RNA of interest is identified by hybridization with a specific radiolabeled cDNA probe. All solutions used for the northern blot were autoclaved, the electrophoresis and blot chambers, gel plates and combs were kept in freshly prepared 0.1% DEPC solution for 10-20 min before use to inactivate RNases.

3.2.3.I Preparation of RNA samples

Each RNA probe (5-10 μg of total RNA) in a volume not more than 5 μl was mixed with 7.5 μl of sample buffer. In case of dilute sample where the volume of the

[Page 37]

probe exceeded 5 μl, the sample was concentrated in a vacuum centrifuge until the volume was reduced to 5 μl. RNA probes mixed with sample buffer were denatured by heating at 65°C for 10 min. Afterwards, the samples were briefly cooled on ice and centrifuged for 1 min at 10,000 rpm in an Eppendorf bench-top centrifuge. Each sample was mixed with 3 μl of loading buffer and centrifuged for 1 min at 10,000 rpm in an Eppendorf bench-top centrifuge.

[...]

3.2.3.III Electrophoresis

The electrophoresis was performed at constant voltage of 80 V for 1-1.5 h. After electrophoresis, the quality of RNA was estimated under UV transilluminator built-in Eagle Eye™ system (Stratagene); the gel was photographed, and the procedure was immediately continued to blotting.

3.2.3.IV Transfer of RNA to nylon membrane

After the separation of RNA in the gel, it was transferred to a nylon membrane by capillary transfer method. The system for transfer was assembled as depicted in Figure 4. A plastic tray was filled with 500 ml of 20×SSC. A piece of Whatman 3MM filter was soaked in 20×SSC and swaddled over the glass plate placed over the tray with both ends hanging into buffer to act as wick. [Any bubbles between the filter and glass plate were smoothed out. The gel was carefully placed upside down over the filter. The bubbles between the gel and wick were carefully removed. The nylon membrane wetted in 2×SSC was placed on top of the gel and smoothed. Two other pieces of Whatman 3MM filters soaked in 2×SSC were sequentially flat laid on top of nylon filter and smoothed. A stack]

[Page 38]

[of paper towels was placed on top, covered with another glass plate and pressed with 1 kg blotting weight.] The transfer was carried out overnight. After the transfer, RNA was fixed on the membrane by UV cross linking for 2 min from both sides using Stratalinker™ 180 (Stratagene) set at “autocross link” mode.

[...]

Pre-hybridization

Afterwards, the membrane was placed into a hybridization tube, and any bubbles between the membrane and internal wall of the tube were carefully removed.

Anmerkungen

Identical, without a hint that Iam is not the author of this text.

In "3.2.4.c." Iam has left out some of the original text, thus in fact the description of the procedure is incomplete.

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(Graf Isolan) Schumann

[34.] Iam/Fragment 044 09 - Diskussion
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Aliquots of prepared tissue homogenates and cell lysates were denatured in sample buffer containing 2% SDS, 10% glycerol, 50 μg/ml bromphenol blue, 2% β- mercaptoethanol and 50 mM Tris-HCl, pH 6.8 by boiling at 95°C for 10 min and 15 μg of total protein was subjected to SDS-polyacrylamide gel electrophoresis (SDS-PAGE).

3.3.2.b SDS-polyacrylamide gel

For all applications described, a 12.5% separating Tris/glycine SDS polyacrylamide ready made gel (SDS-PAGE) was used from invitrogen as instructed. The western blot was performed according to the method of Laemmli (Laemmli 1970).

3.3.2.c SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and electrophoretic transfer

The samples were loaded onto the bottom of the wells. Electrophoresis was run at constant 20 mA per gel. The Rainbow™ colored protein markers (Amersham Pharmacia Biotech) were used as molecular weight standards. Electrophoretic transfer was carried out essentially as described by Towbin (Towbin et al. 1979). Prior to stopping the gel running, fiber pads, filter paper and nitrocellulose transfer membrane (0.45 μM pore size) were soaked in transfer buffer. After electrophoresis, the gel was removed out of the plates and immersed in transfer buffer. For electrophoretic transfer of proteins from the gel to a membrane, a Mini-Trans-Blot® Cell (Bio-Rad), compatible with described system for electrophoresis, was utilized. The transblot sandwich was assembled according to the manufacturer’s instructions from Bio-Rad in the following order starting from the anode side: sponge, 2 sheets of filter paper, nitrocellulose membrane, gel, 2 sheets of filter paper, sponge. The assembled transblot sandwich was inserted into the transblot cell filled with transfer buffer. Ice-cooling unit was set behind the cathode side of transblot cell. The transfer ran for 2 h at 350 mA with one change of the ice-cooling unit after the first hour.


Laemmli UK (1970) Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227:680-685

Towbin H, Staehelin T, Gordon J (1979) Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: procedure and some applications. Proc Natl Acad Sci U S A 76:4350-4354

[Page 48]

Aliquots of the prepared lysates were denatured in sample buffer containing 2% β-mercaptoethanol by boiling at 95°C for 5 minutes and 20-60 μg of total protein was subjected to SDS-polyacrylamide gel electrophoresis (SDS-PAGE).

[Page 63]

Casting of SDS-polyacrylamide gel

For all applications described, a Tris/glycine SDS polyacrylamide gel (SDS-PAAG) system was used according to the method of Laemmli (Laemmli, 1970). [...]

SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and electrophoretic transfer

The samples were loaded onto the bottom of the wells. Electrophoresis was run at a constant current of 25 mA per gel. Electrophoretic transfer was carried out essentially as described by Towbin (Towbin et al., 1979). Prior to stopping the gel running, fiber pads, filter paper and nitrocellulose transfer membrane (0.45 μM pore size) were soaked in transfer buffer. After electrophoresis, the gel was removed out of the plates and immersed in transfer buffer. For electrophoretic transfer of proteins from the gel to a membrane, a Mini-Trans-Blot® Cell (BioRad), compatible with the described system for electrophoresis, was utilized. The transblot sandwich was assembled according to the manufacturer’s instructions from BioRad in the following order starting from the anode side: sponge, 2 sheets of filter paper, nitrocellulose membrane, gel, 2 sheets of filter paper, sponge. The assembled transblot sandwich was inserted into the transblot cell

[Page 64]

filled with transfer buffer. An ice-cooling unit was set behind the cathode side of transblot cell. For most of the proteins, the transfer ran for 2 hours at 500 mA with one change of the ice-cooling unit after the first hour.


40. Laemmli U.K. Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature. 227: 680-685, 1970.

90. Towbin H., Staehelin T., and Gordon J. Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: procedure and some applications. Proc.Natl.Acad.Sci.U.S.A. 76: 4350-4354, 1979.

Anmerkungen

Nothing has been marked as a citation. No source given.

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[35.] Iam/Fragment 045 01 - Diskussion
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3.3.2.d Immunovisualization

After transfer, the membrane was incubated on the rocking platform with blocking solution overnight at 4°C. Next, the membrane was incubated with primary antibody diluted in antibody dilution buffer for 2 h at room temperature. After washing (six times, five min on each occasion), the membrane was incubated with HRP-conjugated secondary antibody diluted in antibody dilution buffer for 1 h at room temperature. Afterwards, the membrane was washed as before. For the chemiluminescent detection SuperSignal® West Pico Chemiluminescent Substrate (Pierce) was used. Substrate working solution was prepared by mixing of equal volumes of two substrate components. The membrane was incubated with substrate working solution for 5 min at room temperature, laid between two sheets of transparent plastic protector and exposed to X-ray film, which was developed afterward according to the manufacturer’s instructions.

Immunovisualization

After transfer, the membrane was incubated on a rocking platform with blocking solution overnight at 4°C (or alternatively, for 60 minutes at room temperature). Next, the membrane was incubated with primary antibody diluted in antibody dilution buffer for 1 hour at room temperature. After washing (six times five minutes each), the membrane was incubated with HRP-conjugated secondary antibody diluted in antibody dilution buffer for 1 hour at room temperature. Afterwards the membrane was washed as before. For the chemiluminescent detection, SuperSignal® West Pico Chemiluminescent Substrate (Pierce) was used. Substrate working solution was prepared by mixing of equal volumes of two substrate components. The membrane was incubated with substrate working solution for 5 minutes at room temperature, laid between sheets of transparent plastic protector and exposed to X-ray film, which was developed afterwards according to manufacturer’s instructions.

Anmerkungen

Nearly identical but for "corrections" (and a minimal adaption). Nevertheless no part has been marked as a citation.

Sichter
(Graf Isolan) Schumann

[36.] Iam/Fragment 046 01 - Diskussion
Bearbeitet: 12. March 2014, 20:16 Graf Isolan
Erstellt: 3. March 2014, 17:34 (Hindemith)
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3.3.3 Enzyme-Linked Immunosorbent Assay (ELISA)

To measure MIP-2/CXCL2 concentration in rat serum, the Quantikine® M rat CXCL2 immunoassay kit (R&D Systems, Wiesbaden, Germany), based on solid phase ELISA, was used.

3.3.3.a. Reagent preparation

Since all samples should be pipette within 15 min, reagents needed for the assay were prepared prior to assay procedure. All reagents were provided with Quantikine® immunoassay kit.

3.3.3.b. Rat CXCL2 control

The control provided with kit, was reconstituted with 1 ml double distilled water.

3.3.3.c. Rat CXCL2 conjugate concentrate

For 96 wells

Conjugate concentrate 0.5 ml

Conjugate diluent 11 ml

3.3.3.d. Washing buffer

For 96 wells

Washing buffer concentrate 25 ml

ddH2O to 625 ml

3.3.3.e. Substrate solution

Equal volumes of color reagents A and B, provided by kit, were mixed together, and solution was used with 15 min.

3.3.3.f. Standard and sample preparation

The standards were reconstituted with 2 ml of calibrator diluent. This stock solution (2000 pg/ml) was used to prepare a serial dilution ranging from 31.2 pg/ml to 2000 pg/ml. Calibrator diluent served as zero standard. Prior to assay, serum samples were diluted 2 fold into calibration diluent.

3.3.1 Enzyme-Linked Immunosorbent Assay (ELISA)

To measure IL-6, IL-1β, TNF-α and IFN-γ concentration in rat serum, the Quantikine® rat IL-6, IL-1β, TNF-α and IFN γ immunoassay kit (R&D Systems, Wiesbaden, Germany), based on solid phase ELISA, was used.

[page 50]

3.3.1.II Reagent preparation

Since all samples should be pipette within 15 min, reagents needed for the assay were prepared prior to assay procedure. All reagents were provided with Quantikine® immunoassay kit.

3.3.1.III Rat IL-6, IL-1β, TNF-α and IFN-γ control

The control provided with kit, was reconstituted with 1 ml double distilled water.

3.3.1.IV Rat IL-6 IL-1β, TNF-α and IFN-γ conjugate concentrate

For 96 wells

Conjugate concentrate 0.5 ml

Conjugate diluent 11 ml

3.3.1.V Washing buffer

For 96 wells

Washing buffer concentrate 25 ml

dd H2O to 625 ml

3.3.1.VI Substrate solution

Equal volumes of color reagents A and B, provided by kit, were mixed together, and solution was used with 15 min.

3.3.1.VII Standard and sample preparation

[page 51]

The standards were reconstituted with 2 ml of calibrator diluent. This stock solution (2000 pg/ml) was used to prepare a serial dilution ranging from 31.2 pg/ml to 2000 pg/ml. Calibrator diluent served as zero standard. Prior to assay, serum samples were diluted 2 fold into calibration diluent.

Anmerkungen

The source is not given.

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3.3.3.g. Assay procedure

The whole procedure was performed at room temperature. All samples, standards and controls were brought to the RT and assayed in duplicates. To synchronize the reaction in each well, all reagents were pipette using a multi-channel pipette. 50 μl of assay diluent was added to each well. Standards, control and samples were added in a quantity of 50 μl per well. The components were mixed by gentle tapping the plate frame for 1 min. After that, the plate was covered with the adhesive strip provided and incubated for 2 h at room temperature. After the incubation period each well was aspirated and washed with 400 μl of wash buffer using a manifold dispenser, and procedure was repeated four times for a total of five washes. After washing, 100 μl of rat CXCL2 conjugate was added to each well. The plate was covered with a new adhesive strip and incubated for another 2 h at room temperature. The aspiration and washing procedure was performed as described above. Subsequently, 100 μl of substrate solution was added to each well to start enzymatic reaction and plate was incubated in the dark for 30 min at room temperature. To stop the enzymatic reaction, 100 μl of stop solution was added to each well, followed by determination of optical density of each well using a microplate reader (Dynatech Laboratories) set to dual wavelength mode (test filter –450 nm, reference filter –570 nm). The calculation of results was performed with a program (Dynatech MRX software, version 1.33) created in accordance to the manual instructions (Quantikine® immunoassay kit).

3.4 Methods in clinical chemistry

3.4.1 Transaminases

Transminases (ALT and AST) are the most important representatives of a group of enzymes, the aminotransferases or transaminases, which catalyze the conversion of α-keto acids into amino acids by transfer of amino groups. As a liver specific enzyme AST is significantly elevated in hepatobiliary disease, increased ALT levels, however can occur in connection with damages of heart or skeletal muscle as well as of liver parenchyma. Serum level of transaminases (AP, ALT and AST) were determined by routine clinical laboratory test using diasys kit (diagnostic systems international Holzheim Germany)

[Page 51]

3.3.1.VIII Assay procedure

The whole procedure was performed at room temperature. All samples, standards and controls were brought to the RT and assayed in duplicates. To synchronize the reaction in each well, all reagents were pipette using a multi-channel pipette. 50 μl of assay diluent was added to each well. Standards, control and samples were added in a quantity of 50 μl per well. The components were mixed by gentle tapping the plate frame for 1 min. After that, the plate was covered with the adhesive strip provided and incubated for 2 h at room temperature. After the incubation period each well was aspirated and washed with 400 μl of wash buffer using a manifold dispenser, and procedure was repeated four times for a total of five washes. After washing, 100 μl of rat IL-6, IL-1β, TNF-α or IFN γ conjugate was added to each well. The plate was covered with a new adhesive strip and incubated for another 2 hours at room temperature. The aspiration and washing procedure was performed as described above. Subsequently, 100 μl of substrate solution was added to each well to start enzymatic reaction and plate was incubated in the dark for 30 min at room temperature. To stop the enzymatic reaction, 100 μl of stop solution was added to each well, followed by determination of optical density of each well using a microplate reader (Dynatech Laboratories) set to dual wavelength mode (test filter 450 nm, reference filter 570 nm). The calculation of results was performed with a program (Dynatech MRX software, version 1.33) created in accordance to the manual instructions (Quantikine® immunoassay kit).

[Page 54]

3.4 Methods in clinical chemistry

[Page 56]

3.4.2 Transaminases

Transminases (ALT and AST) are the most important representatives of a group of enzymes, the aminotransferases or transaminases, which catalyze the conversion of α- keto acids into amino acids by transfer of amino groups. As a liver specific enzymes ALT is significantly elevated in hepatobiliary disease, increased AST levels however, can occur in connection with damages of heart or skeletal muscle as well as of liver parenchyma. [...] Serum level of transaminases were determined by routine clinical laboratory test using diasys kit (diagnostic systems international Holzheim Germany)

Anmerkungen

But for minutiae (that adapt the existing text to Iam's research subject) identical, nevertheless not marked as a citation.

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[38.] Iam/Fragment 048 01 - Diskussion
Bearbeitet: 12. March 2014, 20:16 Graf Isolan
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3.4.2 Statistical Analysis

The data were analyzed using Prism Graph pad 4 software (San Diego, USA). All experimental errors are shown as S.E.M. Statistical significance was calculated by Student’s t test and one way ANOVA and Dunnett post hoc test. Significance was accepted at P < 0.05.

3.4.3 Safety Measures

All operations with genetically modified organisms and plasmid DNA were performed in accordance to the ‘‘Gentechnikgesetz’’ of 1990 and to the rules prescribed by the ‘‘Gentechnik-Sicherheitsverordnung’’ of 1990. Ethidium bromide, formaldehyde, DEPC and other chemicals deleterious for the environment, when used in the course of the work, were carefully managed and disposed properly in accordance with institutional guidelines. All the operations with radioactive chemicals were performed in a radioactivity class II laboratory and the radioactive waste was disposed off according to the institutional instructions.

3.5 Statistical analysis

The data were analysed using Prism Graph pad 4 software (San Diego, USA). All experimental errors are shown as SEM. Statistical significance was calculated by Student’s t test and one way ANOVA with Dunnett post hoc test. Significance was accepted at P < 0.05.

3.6 Safety measures

All operations with genetically modified organisms and plasmid DNA were performed in accordance to the ‘‘Gentechnikgesetz’’ of 1990 and to the rules prescribed by the ‘‘Gentechnik-Sicherheitsverordnung’’ of 1990. Ethidium bromide, formaldehyde, DEPC and other chemicals deleterious for the environment, when used in the course of the work, were carefully managed and disposed properly in accordance with institutional guidelines. All the operations with radioactive chemicals were performed in a radioactivity class II laboratory and the radioactive waste was disposed off according to the institutional instructions.

Anmerkungen

Identical, nevertheless not marked as a citation.

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(Graf Isolan) Schumann

[39.] Iam/Fragment 074 02 - Diskussion
Bearbeitet: 12. March 2014, 19:43 Graf Isolan
Erstellt: 2. March 2014, 16:30 (Hindemith)
Fragment, Gesichtet, Iam, Kamrava et al 2009, KomplettPlagiat, SMWFragment, Schutzlevel sysop

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With the advent of new cancer therapies in the last few years, the goals of reducing disease burden and improving quality of life are frequently achieved. Yet despite the advances seen with numerous monotherapies, a multimodality approach that targets different aspects of tumor biology may yield the greatest clinical benefit for patients with late-stage disease. Many such strategies have been employed with varying degrees of success. The addition of immunotherapy to standard-of-care radiation therapy has shown evidence of efficacy in some preclinical models and in the clinical setting. However, exploiting these two modalities safely and effectively remains an ongoing challenge. It is feasible that the addition of another therapeutic modality could further enhance the antitumor effects of these treatments. With the advent of new cancer therapies in the last few years, the goals of reducing disease burden and improving quality of life are frequently achieved. Yet despite the advances seen with numerous monotherapies, a multimodality approach that targets different aspects of tumor biology may yield the greatest clinical benefit for patients with late stage disease. Many such strategies have been employed with varying degrees of success. The addition of immunotherapy to standard-of-care radiation therapy has shown evidence of efficacy in some preclinical models and in the clinical setting. However, exploiting these two modalities safely and effectively remains an ongoing challenge. It is feasible that the addition of another therapeutic modality could further enhance the antitumor effects of these treatments.
Anmerkungen

The source is not mentioned.

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[40.] Iam/Fragment 074 20 - Diskussion
Bearbeitet: 12. March 2014, 19:42 Graf Isolan
Erstellt: 2. March 2014, 20:56 (Graf Isolan)
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Gene array analysis of RNA from irradiated tissues is an effective tool for identifying genes of potential interest in the development of tissue injury (Kruse et al. 2004).

Kruse JJ, te Poele JA, Russell NS, Boersma LJ, Stewart FA (2004) Microarray analysis to identify molecular mechanisms of radiation-induced microvascular damage in normal tissues. Int J Radiat Oncol Biol Phys 58:420-426

Gene array analysis of RNA from irradiated tissues is an effective tool for identifying genes of potential interest in the development of normal tissue injury (15).

15. J. J. Kruse, J. A. Te Poele, N. S. Russell, L. J. Boersma and F. A. Stewart, Microarray analysis to identify molecular mechanisms of radiation-induced microvascular damage in normal tissues. Int. J. Radiat. Oncol. Biol. Phys. 58, 420–426 (2004).

Anmerkungen

From the final chapter of Iam's thesis ("Discussion"): Nearly identical with identical reference; not marked as a citation; no source given.

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(Graf Isolan) Schumann

[41.] Iam/Fragment 077 21 - Diskussion
Bearbeitet: 12. March 2014, 19:32 Graf Isolan
Erstellt: 2. March 2014, 13:04 (Hindemith)
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Ionizing radiation initiates an oxidative event within a mitochondrion that results in the localized release of Ca2+. Adjacent mitochondria take up the Ca2+ and, as a consequence, undergo the mitochondrial permeability transition and release Ca2+ to further propagate the signal to adjacent mitochondria. Elevated mitochondrial Ca2+ levels and/or direct current (DC) depolarization can enhance mitochondrial ROS generation (Vercesi et al. 1997). This explanation could support our data as mitochondrial damage was also observed in our model. In dividing cells, a substantial fraction of the cellular mitochondria are recruited to and concentrated near the nucleus as part of the mitochondrial replication component of cell division (Davis and Clayton 1996).

Davis AF, Clayton DA (1996) In situ localization of mitochondrial DNA replication in intact mammalian cells. J Cell Biol 135:883-893

Vercesi AE, Kowaltowski AJ, Grijalba MT, Meinicke AR, Castilho RF (1997) The role of reactive oxygen species in mitochondrial permeability transition. Biosci Rep 17:43-52

In this model, ionizing radiation initiates an oxidative event within a mitochondrion that results in the localized release of Ca2+. Adjacent mitochondria take up the Ca2+ and, as a consequence, undergo the mitochondrial permeability transition (exemplified by ΔΨ depolarization) and release Ca2+ to further propagate the signal to adjacent mitochondria. Elevated mitochondrial Ca2+ levels and/or ΔΨ depolarization can enhance mitochondrial ROS/RNS generation (34), although this may not be the only source of elevated ROS/RNS, as discussed below.

[...] In dividing cells, a substantial fraction of the cellular mitochondria are recruited to and concentrated near the nucleus as part of the mitochondrial replication component of cell division (38).


34. Vercesi, A. E., Kowaltowski, A. J., Grijalba, M. T., Meinicke, A. R., and Castilho, R. F. The role of reactive oxygen species in mitochondrial permeability transition. Biosci. Rep., 17: 43–52, 1997.

38. Davis, A., and Clayton, D. In situ localization of mitochondrial DNA replication in intact mammalian cells. J. Cell Biol., 135: 883–893, 1996.

Anmerkungen

The source is mentioned a bit further up, but with no indication whatsoever that further down a passage is taken from it verbatim and including references to the literature.

Note: copying ΔΨ and pasting it leads naturally to "DC".

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(Hindemith) Schumann

[42.] Iam/Fragment 078 01 - Diskussion
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[One function of NF-κB is promotion of cell survival through induction of] target genes, whose products inhibit components of the apoptotic machinery in normal and cancerous cells. NF-κB can also prevent programmed necrosis by inducing genes encoding antioxidant proteins. Regardless of mechanism, many cancer cells of either epithelial or hematopoietic origin use NF-κB to achieve resistance to anticancer drugs, radiation, and death cytokines (Luo et al. 2005a).

Two NF-κB activation pathways exist. The first, the classical pathway (Fig. 25), is normally triggered in response to microbial and viral infections or exposure to proinflammatory cytokines that activate the tripartite IKK complex, leading to phosphorylation- induced IκB degradation. This pathway, which mostly targets p50: RelA and p50:c-Rel dimers, depends mainly on IKKβ activity (Li et al. 1999). The second pathway, the alternative pathway, leads to selective activation of p52:RelB dimers by inducing processing of the NF-κB2/p100 precursor protein, which mostly occurs as a heterodimer with RelB in the cytoplasm. This pathway is triggered by certain members of the TNF cytokine family, through selective activation of IKKα homodimers by the upstream kinase NIK (Senftleben et al. 2001). Both pathways regulate cell survival and death (Senftleben and Karin 2002).


Li ZW, Chu W, Hu Y, Delhase M, Deerinck T, Ellisman M, Johnson R, Karin M (1999) The IKKbeta subunit of IkappaB kinase (IKK) is essential for nuclear factor kappaB activation and prevention of apoptosis. J Exp Med 189:1839-1845

Luo JL, Kamata H, Karin M (2005a) IKK/NF-kappaB signaling: balancing life and death--a new approach to cancer therapy. J Clin Invest 115:2625-2632

Senftleben U, Cao Y, Xiao G, Greten FR, Krahn G, Bonizzi G, Chen Y, Hu Y, Fong A, Sun SC, Karin M (2001) Activation by IKKalpha of a second, evolutionary conserved, NF-kappa B signaling pathway. Science 293:1495-1499

Senftleben U, Karin M (2002) The IKK/NF-kappa B pathway. Crit Care Med 30:S18-S26

One function of NF-κB is promotion of cell survival through induction of target genes, whose products inhibit components of the apoptotic machinery in normal and cancerous cells. NF-κB can also prevent programmed necrosis by inducing genes encoding antioxidant proteins. Regardless of mechanism, many cancer cells, of either epithelial or hematopoietic origin, use NF-κB to achieve resistance to anticancer drugs, radiation, and death cytokines. [...]

[...]

Two NF-κB activation pathways exist (Figure 1). The first, the classical pathway, is normally triggered in response to microbial and viral infections or exposure to proinflammatory cytokines that activate the tripartite IKK complex, leading to phosphorylation-induced IκB degradation. This pathway, which mostly targets p50:RelA and p50:c-Rel dimers, depends mainly on IKKβ activity (4). The other pathway, the alternative pathway, leads to selective activation of p52:RelB dimers by inducing processing of the NF-κB2/p100 precursor protein, which mostly occurs as a heterodimer with RelB in the cytoplasm. This pathway is triggered by certain members of the TNF cytokine family, through selective activation of IKKα homodimers by the upstream kinase NIK (5). Both pathways regulate cell survival and death (6); [...]


4. Li, Z.W., et al. 1999. The IKKbeta subunit of IkappaB kinase (IKK) is essential for nuclear factor kappaB activation and prevention of apoptosis. J. Exp. Med. 189:1839–1845.

5. Senftleben, U., et al. 2001. Activation by IKKalpha of a second, evolutionary conserved, NF-kappa B signaling pathway. Science. 293:1495–1499.

6. Senftleben, U., and Karin, M. 2002. The IKK/NF-kappa B pathway. Crit. Care Med. 30(1 Suppl.):S18–S26.

Anmerkungen

The source is given, but only for the first part and without indication that text has been copied verbatim.

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(Hindemith) Schumann

[43.] Iam/Fragment 080 08 - Diskussion
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80a diss Iam.png

Figure 26: Overview of the influence of hypoxia on the cell in culture (adopted by (Wouters et al. 2007)

Abbreviations: ASK-1, apoptosis signal-regulating kinase 1; ERK, extracellular signal–regulated kinase; HIF-1, hypoxia inducible factor 1; IAP-2, inhibitor of apoptosis protein 2; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; PI3K, phosphatidylinositol 3-kinase; ROS, reactive oxygen species

Hypoxia mediates a striking effect on cell cycle progression (Amellem and Pettersen 1991;Amellem et al. 1998) revealed that mammalian cells in general tend to accumulate in the G1 phase of the cell cycle during prolonged hypoxia. 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.]


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

Wouters A, Pauwels B, Lardon F, Vermorken JB (2007) Review: implications of in vitro research on the effect of radiotherapy and chemotherapy under hypoxic conditions. Oncologist 12:690-712

80a source Iam.png

Figure 1. Overview of the influence of hypoxia on the cell in culture.

Abbreviations: ASK-1, apoptosis signal-regulating kinase 1; ERK, extracellular signal–regulated kinase; HIF-1, hypoxia inducible factor 1; IAP-2, inhibitor of apoptosis protein 2; JNK, c-Jun N-terminal kinase; MAPK, mitogen-activated protein kinase; PI3K, phosphatidylinositol 3-kinase; ROS, reactive oxygen species.

As mentioned above, exposure to hypoxia mediates a striking effect on cell cycle progression. Amellem et al. [43, 44] revealed that mammalian cells in general tend to accumulate in the G1 phase of the cell cycle during prolonged hypoxia. 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.


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 and the list of the references are identical. The source is mentioned in the legend to the accompanying figure 26.

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[44.] Iam/Fragment 081 01 - Diskussion
Bearbeitet: 12. March 2014, 16:58 Hindemith
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[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.

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[45.] Iam/Fragment 081 18 - Diskussion
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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.

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