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Diese Zusammenstellung basiert auf Befunden einer laufenden Plagiatsanalyse (Stand: 2014-10-23) – es handelt sich insofern nicht um einen abschließenden Bericht. Zur weiteren Meinungsbildung wird daher empfohlen, den jeweiligen Stand der Analyse auf der Seite http://de.vroniplag.wikia.com/wiki/Haw zum Vergleich heranzuziehen.

Eine kritische Auseinandersetzung mit der Dissertation von Dr. Haitao Wang: Arteriogenesis in Gja5 (Connexin-40) deficient mice

Dissertation zur Erlangung des akademischen Grades Doctor medicinae (Dr. med.) der Medizinischen Fakultät Charité - Universitätsmedizin Berlin, Datum der Promotion: 9. September 2011. 1. Gutachter: PD Dr. Ivo Buschmann, 2. Gutachter: Prof. Dr. Joachim Jankowski, 3. Gutachter: PD Dr. med. Prof. Dr. Karl-Ludwig Schulte. Veröffentlicht: Berlin, 2011.
→ Nachweis: Deutsche Nationalbibliothek
→ Nachweis: UB FU Berlin

Der Barcode drückt den Anteil der Seiten aus, die Fremdtextübernahmen enthalten, nicht den Fremdtextanteil am Fließtext. Je nach Menge des übernommenen Textes werden drei Farben verwendet:

  • schwarz: bis zu 50 % Fremdtextanteil auf der Seite
  • dunkelrot: zwischen 50 % und 75 % Fremdtextanteil auf der Seite
  • hellrot: über 75 % Fremdtextanteil auf der Seite

Weiße Seiten wurden entweder noch nicht untersucht oder es wurde nichts gefunden. Blaue Seiten umfassen Titelblatt, Inhaltsverzeichnis, Literaturverzeichnis, Vakatseiten und evtl. Anhänge, die in die Berechnung nicht einbezogen werden.

Der Barcode stellt den momentanen Bearbeitungsstand dar. Er gibt nicht das endgültige Ergebnis der Untersuchung wieder, da Untersuchungen im VroniPlag Wiki stets für jeden zur Bearbeitung offen bleiben, und somit kein Endergebnis existiert.

33 Seiten mit Plagiatstext

Seiten mit weniger als 50% Plagiatstext

13 Seiten: 017 019 023 044 045 046 047 050 055 025 032 049 012

Seiten mit 50%-75% Plagiatstext

2 Seiten: 010 014

Seiten mit mehr als 75% Plagiatstext

18 Seiten: 001 002 006 007 008 009 015 016 056 013 003 020 022 005 004 011 018 021

Kapitelübersicht

  • Die Dissertation enthält zahlreiche wörtliche und sinngemäße Textübernahmen, die nicht als solche kenntlich gemacht sind. Als betroffen festgestellt wurden bisher (Stand: 24. Oktober 2014) folgende Kapitel, die sich zum Teil als vollständig übernommen erwiesen haben – siehe Klammervermerke:
  • CHAPTER ONE: INTRODUCTION
  • 1. Arteriogenesis
  • 1.1. Three different ways of neovascularization (S. 1): Seite 1 – [vollständig (wörtlich)]
  • 1.2. The definition of arteriogenesis (S. 1-3): Seiten 1, 2 – [vollständig (exkl. Abb. 1.1)]
  • 1.3. The process of arteriogenesis [Anf.] (S. 3): Seite 3 – [vollständig]
  • 1.3.1. Arteriole (S. 3-4): Seiten 3, 4
  • 1.3.2. Fluid shear stress (FSS) as initial triggering (S. 4-7): Seiten 4, 5, 6, 7
  • 1.3.3. Activation of the endothelium (S. 7-8): Seiten 7, 8 – [vollständig]
  • 1.3.4. Circulating cells invade arterioles with activated endothelium (S. 8-10): Seiten 8, 9
  • 1.3.5. Remodeling (S. 10-12): Seiten 10, 11
  • 1.3.6. Therapeutic arteriogenesis (S. 12-13): Seiten 12, 13 – [vollständig]
  • 2. Angiogenesis
  • 2.1. The definition of angiogenesis (S. 13): Seite 13
  • 2.2. The process of angiogenesis (S. 13): Seite 13 – [vollständig]
  • 2.3. The differences between arteriogenesis and angiogenesis (S. 14): Seite 14
  • 2.4. Conclusion (S. 14-15): Seite 15
  • 3. Gap junctions (S. 15-19): Seiten 15, 16, 17, 18, 19
  • 5. Laser Doppler Flow (LDF) Imaging
  • 5.1. The definition of Laser Doppler Flow (LDF) Imaging (S. 20): Seite 20 – [vollständig (wörtlich)]
  • 5.2. Operating principles (S. 20-22): Seiten 20, 21, 22 – [vollständig (Text, exkl. Abb. 1.8.a und 1.8.b)]
  • 5.3. The definition of perfusion units (S. 22): Seite 22 – [vollständig (wörtlich)]
  • 6. Prospects and challenges (S. 23-24): Seite 23
  • 7. Objectives (S. 25): Seite 25
  • CHAPTER TWO: MATERIALS AND METHODS
  • 2. Methods
  • 2.2. Assessment of blood flow with Laser Doppler Flow (LDF) Imaging (S. 32): Seite 32
  • CHAPTER FOUR: DISCUSSION [Anf.] (S. 44): Seite 44
  • 1. Gja5 plays a functional role in arteriogenesis (S. 45): Seite 45
  • 2. Smaller and fewer collateral arteries in Gja5-/- mice (S. 45-46): Seite 46
  • 4. Reduced Gja5 in endothelial cells may play a functional role in arteriogenesis (S. 47-48): Seite 47
  • CHAPTER FIVE: SUMMARY
  • Background (Seite 49): Seite 49
  • Methods (S. 50): Seite 50
  • CHAPTER SIX: STUDY LIMITATIONS AND PERSPECTIVES (S. 55-56): Seiten 55, 56.

Herausragende Quellen

  • Limbourg et al. (2009): Eine Quelle aus der umfangreich übernommen wurde, die aber nirgends in der untersuchten Arbeit erwähnt ist.
  • Buschmann & Schaper (1999): Eine Publikation des Doktorvaters, die zwar in der untersuchten Arbeit erwähnt wird, aus der aber trotzdem einige Passagen ungekennzeichnet bzw. nicht ausreichend gekennzeichnet übernommen wurden.
  • Wikipedia Connexin (2010): Es gibt auch ungekennzeichnete Übernahmen aus der Wikipedia.

Herausragende Fundstellen

  • Fragment 004 01: Ein Beispiel für eine Übernahme, bei der die Quelle zwar angegeben ist, der Umfang der Übernahme aber für den Leser keineswegs klar wird.
  • Fragment 020 03: Eine fast ganzseitige Übernahme aus einer Instrumentenbeschreibung des Herstellers.
  • Fragment 016 01: Eine ungekennzeichnete Übernahme, bei der auch zehn Literaturverweise kopiert wurden.

Andere Beobachtungen

  • Es gibt auch umfangreiche Textparallelen zwischen der untersuchten Dissertation und der Publikation Buschmann et al. (2010) (auf den Seiten 22, 23, 33, 45, 49, 50). Diese Textparallelen wurden nicht als Plagiate dokumentiert, da H. W. elfter Autor dieser Publikation ist und Selbstplagiate im Vroniplag Wiki grundsätzlich nicht als Plagiate dokumentiert werden. Trotzdem hätten natürlich die Übernahmen gekennzeichnet und hätte Buschmann et al. (2010) im Literaturverzeichnis angegeben werden müssen.
  • Der Satz "Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest." stammt aus Limbourg et al. (2009). Er wurde in der hier untersuchten Arbeit dreimal verwendet, jeweils ohne Quellenverweis:
  • Die zur Zeit der Einreichung der untersuchten Arbeit gültige Promotionsordnung der Medizinischen Fakultät der Charité - Universitätsmedizin Berlin vom 8. Dezember 2004 (PDF) zur Promotion zum Doctor medicinae (Dr. med.) und zum Doctor medicinae dentariae (Dr. med. dent.) enthält u.a. folgende Ausführungen und Bestimmungen:
  • § 4 Anmeldung von Promotionsvorhaben
    "(1) [...] Bei der Anmeldung sind vorzulegen: [...]
    f) eine schriftliche Erklärung, dass die an der Medizinischen Fakultät der Charité – Universitätsmedizin Berlin geltende Richtlinie der guten wissenschaftlichen Praxis zur Kenntnis genommen wurde."
  • § 5 Schriftliche Promotionsleistung
    "(2) Die Dissertation muss eine in selbständiger wissenschaftlicher Arbeit verfasste Abhandlung und eine in sich geschlossene Darstellung der Forschungsarbeiten und ihrer Ergebnisse sein, die einen Fortschritt der wissenschaftlichen Erkenntnis zum Gegenstand hat. [...]"
  • § 13 Entzug des Doktorgrades
    "Nach Aushändigung der Promotionsurkunde gelten die für den Entzug des Doktorgrades gültigen gesetzlichen Bestimmungen."
  • Auf Seite 71 der Dissertation findet man folgende "Erklärung":
    "Ich, [H. W.], erkläre, dass ich die vorgelegte Dissertation mit dem Thema: [Arteriogenesis in Gja5 (Connexin-40) deficient mice] selbst verfasst und keine anderen als die angegebenen Quellen und Hilfsmittel benutzt, ohne die (unzulässige) Hilfe Dritter verfasst und auch in Teilen keine Kopien anderer Arbeiten dargestellt habe."

Statistik

  • Es sind bislang 58 gesichtete Fragmente dokumentiert, die als Plagiat eingestuft wurden. Bei 36 von diesen handelt es sich um Übernahmen ohne Verweis auf die Quelle („Verschleierungen“ oder „Komplettplagiate“). Bei 22 Fragmenten ist die Quelle zwar angegeben, die Übernahme jedoch nicht ausreichend gekennzeichnet („Bauernopfer“).
  • Die untersuchte Arbeit hat 56 Seiten im Hauptteil. Auf 33 dieser Seiten wurden bislang Plagiate dokumentiert, was einem Anteil von 58.9 % entspricht.
    Die 56 Seiten lassen sich bezüglich des Textanteils, der als Plagiat eingestuft ist, wie folgt einordnen:
Plagiatsanteil Anzahl Seiten
keine Plagiate dokumentiert 23
0 % - 50 % Plagiatsanteil 13
50 % - 75 % Plagiatsanteil 2
75 % - 100 % Plagiatsanteil 18
Ausgehend von dieser Aufstellung lässt sich abschätzen, wieviel Text der untersuchten Arbeit gegenwärtig als plagiiert dokumentiert ist: Es sind, konservativ geschätzt, rund 30 % des Textes im Hauptteil der Arbeit.


Illustration

Folgende Grafik illustriert das Ausmaß und die Verteilung der dokumentierten Fundstellen. Die Farben bezeichnen den diagnostizierten Plagiatstyp:
(grau=Komplettplagiat, rot=Verschleierung, gelb=Bauernopfer)

Haw2 col

Die Nichtlesbarkeit des Textes ist aus urheberrechtlichen Gründen beabsichtigt.

Zum Vergrößern auf die Grafik klicken.


Anmerkung: Die Grafik repräsentiert den Analysestand vom 24. Oktober 2014.

Definition von Plagiatkategorien

Die hier verwendeten Plagiatkategorien basieren auf den Ausarbeitungen von Wohnsdorf / Weber-Wulff: Strategien der Plagiatsbekämpfung, 2006. Eine vollständige Beschreibung der Kategorien findet sich im VroniPlag-Wiki. Die Plagiatkategorien sind im Einzelnen:

Übersetzungsplagiat

Ein Übersetzungsplagiat entsteht durch wörtliche Übersetzung aus einem fremdsprachlichen Text. Natürlich lässt hier die Qualität der Übersetzung einen mehr oder weniger großen Interpretationsspielraum. Fremdsprachen lassen sich zudem höchst selten mit mathematischer Präzision übersetzen, so dass jede Übersetzung eine eigene Interpretation darstellt. Zur Abgrenzung zwischen Paraphrase und Kopie bei Übersetzungen gibt es ein Diskussionsforum.

Komplettplagiat

Text, der wörtlich aus einer Quelle ohne Quellenangabe übernommen wurde.

Verschleierung

Text, der erkennbar aus fremder Quelle stammt, jedoch umformuliert und weder als Paraphrase noch als Zitat gekennzeichnet wurde.

Bauernopfer

Text, dessen Quelle ausgewiesen ist, der jedoch ohne Kenntlichmachung einer wörtlichen oder sinngemäßen Übernahme kopiert wurde.

Quellen nach Fragmentart

Die folgende Tabelle schlüsselt alle gesichteten Fragmente zeilenweise nach Quellen und spaltenweise nach Plagiatskategorien auf.

Tabelle: Haw: Quellen / Fragmente (dynamische Auszählung)
Quelle
Jahr ÜP
KP
VS
BO
KW
KeinP

ZuSichten
Unfertig
Buschmann and Schaper 1999 0 0 4 4 0 0 8 0 0
Dbouk et al 2009 0 0 0 1 0 0 1 0 0
Ebong et al 2006 0 4 1 0 0 0 5 0 0
Figueroa and Duling 2009 0 2 0 0 0 0 2 0 0
Heil and Schaper 2004 0 0 0 5 0 0 5 0 0
Limbourg et al 2009 0 7 1 0 0 0 8 0 0
Moor instruments 2006 0 2 0 1 0 0 3 0 0
Schaper 2009 0 0 0 2 0 0 2 0 0
Schaper and Scholz 2003 0 2 1 6 0 0 9 0 0
Van Oostrom et al 2008 0 6 1 1 0 0 8 0 0
Wikipedia Connexin 2010 0 3 0 0 0 0 3 0 0
Willems 2009 0 0 2 0 0 0 2 0 0
Zagorchev et al 2010 0 0 0 2 0 0 2 0 0
- 0 26 10 22 0 0 58 0 0

Fragmentübersicht

58 gesichtete, geschützte Fragmente

FragmentSeiteArbeitZeileArbeitQuelleSeiteQuelleZeileQuelleTypus
Haw/Fragment 001 0414-16Van Oostrom et al 20081379l. Spalte: 30 ff.KomplettPlagiat
Haw/Fragment 001 17117-23Limbourg et al 20091737l. Spalte: 6ffKomplettPlagiat
Haw/Fragment 001 25125-28Van Oostrom et al 20081380l. Spalte: 9 ff.KomplettPlagiat
Haw/Fragment 002 0121-6Limbourg et al 20091737l. Spalte: 19ffKomplettPlagiat
Haw/Fragment 002 0727-16Van Oostrom et al 20081380Figure 1, l.Sp. 13 ff.BauernOpfer
Haw/Fragment 003 0434-10Heil and Schaper 2004449AbstractBauernOpfer
Haw/Fragment 003 16316-26Buschmann and Schaper 1999122l. Spalte: 36ffVerschleierung
Haw/Fragment 003 27327-30Heil and Schaper 2004450l. Spalte: 6ffBauernOpfer
Haw/Fragment 004 0141-17Heil and Schaper 2004450l. Spalte: 11ffBauernOpfer
Haw/Fragment 004 25425-28Heil and Schaper 2004450r. Spalte: 20ffBauernOpfer
Haw/Fragment 005 0151-5Heil and Schaper 2004450r. Spalte: 26ffBauernOpfer
Haw/Fragment 005 0656-12Schaper 20097r. Spalte: 15ffBauernOpfer
Haw/Fragment 006 0161-9Schaper 20097r. Spalte: 33ffBauernOpfer
Haw/Fragment 006 10610-14Buschmann and Schaper 1999122l. Spalte: letzte ZeilenVerschleierung
Haw/Fragment 006 15615-21Schaper and Scholz 20031145l. Spalte: 10 ff.BauernOpfer
Haw/Fragment 006 21621-30Van Oostrom et al 20081380, 13811380: r. Spalte: 15 ff.; 1381: l. Spalte: 1 ff.KomplettPlagiat
Haw/Fragment 007 0171-6Van Oostrom et al 20081381l. Spalte: 12 ff.KomplettPlagiat
Haw/Fragment 007 0777-9, 12-26Buschmann and Schaper 1999122r. Spalte: 10ffVerschleierung
Haw/Fragment 007 0979-12Schaper and Scholz 20031145l. Spalte: 22 ff.KomplettPlagiat
Haw/Fragment 007 27727-30Schaper and Scholz 20031145, 11461145: r. Spalte: letzte Zeilen; 1146; l. Spalte: 1 ff.KomplettPlagiat
Haw/Fragment 008 0181-19Schaper and Scholz 20031146l. Spalte: 2 ff.BauernOpfer
Haw/Fragment 008 24824-29Schaper and Scholz 20031146r. Spalte: 9 ff.Verschleierung
Haw/Fragment 009 0191-19Schaper and Scholz 20031146r. Spalte:17 ff.BauernOpfer
Haw/Fragment 009 20920-30Buschmann and Schaper 1999122, 123122: r. Spalte: 45ff: 123: l. Spalte: 6ffBauernOpfer
Haw/Fragment 010 07107-13Schaper and Scholz 20031148r. Spalte: 36 ff.BauernOpfer
Haw/Fragment 011 01111-24Schaper and Scholz 20031148, 11491148: r. Spalte: 44ff; 1149: l. Spalte: 1ffBauernOpfer
Haw/Fragment 012 08128-14Buschmann and Schaper 1999124l. Spalte: 34ffVerschleierung
Haw/Fragment 013 01131-9Buschmann and Schaper 1999124l. Spalte: 43ffBauernOpfer
Haw/Fragment 013 151315-18Limbourg et al 20091737l. Spalte: 15ffKomplettPlagiat
Haw/Fragment 013 201320-29Buschmann and Schaper 1999121, 122121: r. Spalte: letzte Zeilen; 122: l. Spalte: 1ffBauernOpfer
Haw/Fragment 014 01141-8Buschmann and Schaper 1999124, 125124: r. Spalte: letzte Zeilen; 125: l. Spalte: 1ffBauernOpfer
Haw/Fragment 015 02152-8Schaper and Scholz 200311506ffBauernOpfer
Haw/Fragment 015 161516-18Ebong et al 2006H2015l. Spalte: 34 ff.KomplettPlagiat
Haw/Fragment 016 01161-7, 10-13Ebong et al 2006H2015l. Spalte: 39 ff.KomplettPlagiat
Haw/Fragment 016 08168-10Wikipedia Connexin 20101 (Internetquelle)-KomplettPlagiat
Haw/Fragment 016 191619-26Wikipedia Connexin 20101 (Internetquelle)-KomplettPlagiat
Haw/Fragment 017 101710-16Ebong et al 2006H2015r. Spalte: 6 ff.KomplettPlagiat
Haw/Fragment 018 01181-15Dbouk et al 20093Figure 1BauernOpfer
Haw/Fragment 019 01191-6Ebong et al 2006H2015r. Spalte: 16 ff.KomplettPlagiat
Haw/Fragment 019 06196-8, 13-15Wikipedia Connexin 20101 (Internetquelle)-KomplettPlagiat
Haw/Fragment 020 03203-26Moor instruments 20061, 21: 4ff; 2: 1ffKomplettPlagiat
Haw/Fragment 021 01211ff (komplett)Moor instruments 200625ffBauernOpfer
Haw/Fragment 022 01221ff (komplett)Moor instruments 20062, 32: letzte Zeilen; 3: 1ffKomplettPlagiat
Haw/Fragment 023 02232-4Limbourg et al 20091737l. Spalte: 2ffKomplettPlagiat
Haw/Fragment 023 192319-26, 27-28Ebong et al 2006H2015r. Spalte: 6 ff.Verschleierung
Haw/Fragment 025 02252-3Limbourg et al 20091737l. Spalte: 3ffKomplettPlagiat
Haw/Fragment 032 03323-10Limbourg et al 20091738, 17391738: r. Spalte: 12ff; 1739: l. Spalte: 1ffKomplettPlagiat
Haw/Fragment 044 02442-5Willems 200931 ff.Verschleierung
Haw/Fragment 044 05445-9, 11-16Figueroa and Duling 2009249, 260249: r. Spalte: 11 ff.; 260: l. Spalte: 25 ff.KomplettPlagiat
Haw/Fragment 045 03453-7Limbourg et al 20091737abstractVerschleierung
Haw/Fragment 045 284528-29Zagorchev et al 20101l. Spalte: 17 ff.BauernOpfer
Haw/Fragment 046 01461-6Zagorchev et al 20101l. Spalte: 17 ff.BauernOpfer
Haw/Fragment 047 154715-23Van Oostrom et al 20081380, 13811380: r. Spalte: 16 ff.; 1381: 1 ff.KomplettPlagiat
Haw/Fragment 049 03493-5Limbourg et al 20091737l. Spalte: 2ffKomplettPlagiat
Haw/Fragment 050 03503-6Figueroa and Duling 2009260l. Spalte: 25 ff.KomplettPlagiat
Haw/Fragment 055 02552-5Willems 200931 ff.Verschleierung
Haw/Fragment 055 275527-29Van Oostrom et al 20081379l. Spalte: 30 ff.Verschleierung
Haw/Fragment 056 01561 ff. (komplett)Van Oostrom et al 20081387l. Spalte: 22 ff.KomplettPlagiat

Textfragmente

Anmerkung zur Farbhinterlegung

Die Farbhinterlegung dient ausschließlich der leichteren Orientierung des Lesers im Text. Das Vorliegen einer wörtlichen, abgewandelten oder sinngemäßen Übernahme erschließt sich durch den Text.

Hinweis zur Zeilenzählung

Bei der Angabe einer Fundstelle wird alles, was Text enthält (außer Kopfzeile mit Seitenzahl), als Zeile gezählt, auch Überschriften. In der Regel werden aber Abbildungen, Tabellen, etc. inklusive deren Titel nicht mitgezählt. Die Zeilen der Fußnoten werden allerdings beginnend mit 101 durchnummeriert, z. B. 101 für die erste Fußnote der Seite.

58 gesichtete, geschützte Fragmente

[1.] Haw/Fragment 001 04

KomplettPlagiat
Untersuchte Arbeit:
Seite: 1, Zeilen: 4-16
Quelle: Van Oostrom et al 2008
Seite(n): 1379, Zeilen: l. Spalte: 30 ff.
Cardiovascular disorders are currently the leading cause of death globally. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients who do not benefit from these treatment options. For a long time, it has been known that patients suffering from coronary heart disease can recruit collateral vessels and thereby improve symptoms of myocardial ischemia[1]. Also, it is well established that an increased demand for oxygen, as occurs during exercise and placental development, can induce formation of new capillaries[2]. Thus, it seems that the body already possesses an “in-house” rescue system to increase blood flow in ischemic circumstances. Stimulation of this system, termed neovascularization, could be a promising new direction in treating cardiovascular diseases[3]. Neovascularization in humans can be brought about by three distinct mechanisms: vasculogenesis, angiogenesis, or arteriogenesis (depicted in Fig. 1.1.)[3].

1. Helfant, R.H., P.S. Vokonas, and R. Gorlin, Functional importance of the human coronary collateral circulation. N Engl J Med, 1971. 284(23): p. 1277-81.

2. Prior, B.M., H.T. Yang, and R.L. Terjung, What makes vessels grow with exercise training? J Appl Physiol, 2004. 97(3): p. 1119-28.

3. Carmeliet, P., Mechanisms of angiogenesis and arteriogenesis. Nat Med, 2000. 6(4): p. 389-95.

In fact, cardiovascular disorders are currently the leading cause of death globally [1]. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients who do not benefit from these treatment options.

For a long time, it has been known that patients suffering from coronary heart disease can recruit collateral vessels and thereby improve symptoms of myocardial ischemia [2]. Also, it is well established that an increased demand in oxygen, as occurs during exercise and placental development, can induce formation of new capillaries [3]. Thus, it seems that the body already possesses an “in-house” rescue system to increase blood flow in ischemic circumstances. Stimulation of this system, termed neovascularization, could be a promising new direction in treating cardiovascular diseases. Neovascularization in humans can be fulfilled by three distinct mechanisms: vasculogenesis, angiogenesis, or arteriogenesis (depicted in Fig. 1) [4].


1. World Health Organization (February 2007) Factsheet 317.

2. Helfant, R. H., Vokonas, P. S., Gorlin, R. (1971) Functional importance of the human coronary collateral circulation. N. Engl. J. Med. 284, 1277–1281.

3. Prior, B. M., Yang, H. T., Terjung, R. L. (2004) What makes vessels grow with exercise training? J. Appl. Physiol. 97, 1119–1128.

4. Carmeliet, P. (2000) Mechanisms of angiogenesis and arteriogenesis. Nat. Med. 6, 389–395.

Anmerkungen

Ein Verweis auf die Quelle fehlt.


[2.] Haw/Fragment 001 17

KomplettPlagiat
Untersuchte Arbeit:
Seite: 1, Zeilen: 17-23
Quelle: Limbourg et al 2009
Seite(n): 1737, Zeilen: l. Spalte: 6ff
During embryonic development, blood vessels form de novo from angiogenic blood islands in a process termed vasculogenesis. This primary plexus extends by capillary sprouting and eventually remodels into a highly organized network of capillaries, arteries and veins[4]. The postnatal vascular system is critical for maintaining homeostasis and adapts readily to environmental cues and physiological or pathological conditions[5]. This adaptation comprises two different and characteristic responses, angiogenesis and arteriogenesis.

4. Adams, R.H. and K. Alitalo, Molecular regulation of angiogenesis and lymphangiogenesis. Nat Rev Mol Cell Biol, 2007. 8(6): p. 464-78.

5. Carmeliet, P., Angiogenesis in health and disease. Nat Med, 2003. 9(6): p. 653-60.

During the embryonic development, blood vessels form de novo from angiogenic blood islands in a process termed vasculogenesis. This primary plexus extends by capillary sprouting and eventually remodels into a highly organized network of capillaries, arteries and veins2. The postnatal vascular system is critical for maintaining homeostasis and adapts readily to environmental cues and physiological or pathological conditions3. This adaptation comprises two different and characteristic responses, angiogenesis and arteriogenesis.

2. Adams, R.H. & Alitalo, K. Molecular regulation of angiogenesis and lymphangiogenesis. Nat. Rev. Mol. Cell. Biol. 8, 464–478 (2007).

3. Carmeliet, P. Angiogenesis in health and disease. Nat. Med. 9, 653–660 (2003).

Anmerkungen

Ein Verweis auf die Quelle fehlt.


[3.] Haw/Fragment 001 25

KomplettPlagiat
Untersuchte Arbeit:
Seite: 1, Zeilen: 25-28
Quelle: Van Oostrom et al 2008
Seite(n): 1380, Zeilen: l. Spalte: 9 ff.
The term “arteriogenesis”—the development of large collateral arteries from pre-existing arteriolar anastomoses—was proposed in 1997 by W. Schaper, R. Chapuli-Munoz, and W. Risau[7] to discriminate between arteriogenesis and true angiogenesis.

7. Ito, W.D., et al., Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am J Physiol, 1997. 273(3 Pt 2): p. H1255-65.

The term “arteriogenesis”—the development of large collateral arteries from pre-existing arteriolar anastomoses—was proposed in 1997 by W. Schaper, R. Chapuli-Munoz, and W. Risau [10] to discriminate between arteriogenesis and true angiogenesis.

10. Ito, W. D., Arras, M., Scholz, D., Winkler, B., Htun, P., Schaper, W. (1997) Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am. J. Physiol. 273, H1255–H1265.

Anmerkungen

Kein Verweis auf die Quelle


[4.] Haw/Fragment 002 01

KomplettPlagiat
Untersuchte Arbeit:
Seite: 2, Zeilen: 1-6
Quelle: Limbourg et al 2009
Seite(n): 1737, Zeilen: l. Spalte: 19ff
[Arteriogenesis is defined as the enlargement of pre-existing collateral arteries and their remodelling into conductance vessels[8]. This process is driven by an] increased blood flow in collateral arteries leading to an increase in wall tension and fluid shear stress[9-11]. Specific arterial signaling pathways, angiogenic growth factors, as well as resident cells in the vessel wall and circulating cells participate in this complex biological process of luminal expansion and wall growth[12-17]. It is important to note that arteriogenesis is the key mechanism to enhance perfusion and is, thus, critical for the rescue of ischemic organs[18, 19].

8. Schaper, W., Collateral circulation: past and present. Basic Res Cardiol, 2009. 104(1): p. 5-21.

9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

10. Heil, M., et al., Arteriogenesis versus angiogenesis: similarities and differences. J Cell Mol Med, 2006. 10(1): p. 45-55.

11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62.

12. Limbourg, A., et al., Notch ligand Delta-like 1 is essential for postnatal arteriogenesis. Circ Res, 2007. 100(3): p. 363-71.

13. Schaper, W., Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia, 1967. 23(7): p. 595-6.

14. Arras, M., et al., Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J Clin Invest, 1998. 101(1): p. 40-50.

15. Jacobi, J., et al., Adenoviral gene transfer with soluble vascular endothelial growth factor receptors impairs angiogenesis and perfusion in a murine model of hindlimb ischemia. Circulation, 2004. 110(16): p. 2424-9.

16. Kondoh, K., et al., Conduction performance of collateral vessels induced by vascular endothelial growth factor or basic fibroblast growth factor. Cardiovasc Res, 2004. 61(1): p. 132-42.

17. Ziegelhoeffer, T., et al., Bone marrow-derived cells do not incorporate into the adult growing vasculature. Circ Res, 2004. 94(2): p. 230-8.

18. Scholz, D., et al., Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol, 2002. 34(7): p. 775-87.

19. Simons, M., Angiogenesis: where do we stand now? Circulation, 2005. 111(12): p. 1556-66.

Arteriogenesis, on the other hand, is defined as the enlargement of pre-existing collateral arteries and their remodelling to conductance vessels5. This process is driven by an increased blood flow in collateral arteries leading to an increase in wall tension and fluid shear stress6–8. Specific arterial signaling pathways, angiogenic growth factors, as well as resident cells in the vessel wall and circulating cells participate in this complex biological process of luminal expansion and wall growth9–14. It is important to note that arteriogenesis is the key mechanism to enhance perfusion and is, thus, critical for the rescue of ischemic organs15,16.

5. Schaper, W. Collateral circulation: past and present. Basic Res. Cardiol. 104, 5–21 (2009).

6. Heil, M. & Schaper, W. Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ. Res. 95, 449–458 (2004).

7. Heil, M., Eitenmuller, I., Schmitz-Rixen, T. & Schaper, W. Arteriogenesis versus angiogenesis: similarities and differences. J. Cell. Mol. Med. 10, 45–55 (2006).

8. Eitenmuller, I. et al. The range of adaptation by collateral vessels after femoral artery occlusion. Circ. Res. 99, 656–662 (2006).

9. Limbourg, A. et al. Notch ligand Delta-like 1 is essential for postnatal arteriogenesis. Circ. Res. 100, 363–371 (2007).

10. Schaper, W., Jageneau, A. & Xhonneux, R. The development of collateral circulation in the pig and dog heart. Cardiologia 51, 321–335 (1967).

11. Arras, M. et al. Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J. Clin. Invest. 101, 40–50 (1998).

12. Jacobi, J. et al. Adenoviral gene transfer with soluble vascular endothelial growth factor receptors impairs angiogenesis and perfusion in a murine model of hindlimb ischemia. Circulation 110, 2424–2429 (2004).

13. Kondoh, K. et al. Conduction performance of collateral vessels induced by vascular endothelial growth factor or basic fibroblast growth factor. Cardiovasc. Res. 61, 132–142 (2004).

14. Ziegelhoeffer, T. et al. Bone marrow-derived cells do not incorporate into the adult growing vasculature. Circ. Res. 94, 230–238 (2004).

15. Scholz, D. et al. Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J. Mol. Cell. Cardiol. 34, 775–787 (2002).

16. Simons, M. Angiogenesis: where do we stand now? Circulation 111, 1556–1566 (2005).

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Fig. 1.1.

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[6] (Van Oostrom, M.C., et al., J Leukoc Biol, 2008;84(6): 1379-91)

Fig.1.1. Neovascularization can occur via vasculogenesis (A), angiogenesis (B), or arteriogenesis (C). (A) In vasculogenesis, circulating endothelial progenitor cells (EPC; purple) contribute to new blood vessel growth (capillaries). (B) During angiogenesis, endothelial cells are activated by ischemia and develop a lumen, thereby forming a new, small capillary vessel[3]. (C) In arteriogenesis, circulating leukocytes (green) are attracted to the activated endothelium. They assist in enlarging collateral anastomoses. Activated endothelial cells (blue), activated vascular smooth muscle cells (yellow)[3].

Normally, there is only a minimal net flow in these pre-existing connections. However, a sudden arterial occlusion or a slow progressing stenosis in the main artery can cause an increased pressure gradient in these small vessels to respond by actively proliferating and remodeling, which results in an increased lumen size and enhanced [perfusion to the ischemic tissue[20]. Hence, it seems that arteriogenesis is initiated differently and progresses differently from angiogenesis.]


3. Carmeliet, P., Mechanisms of angiogenesis and arteriogenesis. Nat Med, 2000. 6(4): p. 389-95.

6. van Oostrom, M.C., et al., Insights into mechanisms behind arteriogenesis: what does the future hold? J Leukoc Biol, 2008. 84(6): p. 1379-91.

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

Haw 02a source

Fig. 1. Neovascularization can occur via vasculogenesis (A), angiogenesis (B), or arteriogenesis (C). (A) In vasculogenesis, circulating endothelial progenitor cells (EPC; purple) contribute to new blood vessel growth (capillaries) by secreting the necessary growth factors and chemokines for endothelial cells to migrate (upper) or by incorporating into the newly formed vessels (lower). (B) During angiogenesis, endothelial cells are activated by ischemia and grow in the direction of angiogenic signals. The endothelial cells fuse and develop a lumen, thereby forming a new, small capillary vessel. (C) In arteriogenesis, circulating leukocytes (green) are attracted to the activated endothelium. They assist in enlarging collateral anastomoses. Activated endothelial cells (blue), activated vascular smooth muscle cells (yellow), quiescent endothelial cells (gray), quiescent smooth muscle cells (brown).

[...]

Normally, as a result of the high resistance of arteriolar anastomoses and the lack of a pressure gradient, there is only a minimal net flow in these pre-existing connections. However, a sudden arterial occlusion or a slow progressing stenosis in the main artery can cause an increased pressure gradient in the anastomoses, leading to increased blood flow inside. These small vessels respond by actively proliferating and remodeling, which results in an increased lumen size and enhanced perfusion to the ischemic tissue [11]. Hence, it seems that arteriogenesis is initiated differently and progresses differently to angiogenesis.


11. Schaper, W., Scholz, D. (2003) Factors regulating arteriogenesis. Arterioscler. Thromb. Vasc. Biol. 23, 1143–1151.

Anmerkungen

Die Quelle ist für die Abbildung angegeben, nicht jedoch für die Bildunterschrift und den darauffolgenden Text. Auf die Bildunterschrift könnte man die Quellenangabe bei großzügiger Handhabung erstrecken, auf den Text schwerlich.


[6.] Haw/Fragment 003 04

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Growth of collateral blood vessels (arteriogenesis) is potentially able to preserve structure and function of limbs and organs after occlusion of a major artery. The success of the remodeling process depends on the following conditions: (1) existence of an arteriolar network that connects the preocclusive with the postocclusive microcirculation; (2) activation of the arteriolar endothelium by elevated fluid shear stress; (3) invasion (but not incorporation) of bone marrow–derived cells; and (4) proliferation of endothelial and smooth muscle cells[9].

9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

Growth of collateral blood vessels (arteriogenesis) is potentially able to preserve structure and function of limbs and organs after occlusion of a major artery. The success of the remodeling process depends on the following conditions: (1) existence of an arteriolar network that connects the preocclusive with the postocclusive microcirculation; (2) activation of the arteriolar endothelium by elevated fluid shear stress; (3) invasion (but not incorporation) of bone marrow–derived cells; and (4) proliferation of endothelial and smooth muscle cells.
Anmerkungen

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[7.] Haw/Fragment 003 16

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The presence of these native collaterals, which may not be utilized to provide perfusion under normal conditions, varies widely among species and also within individuals. However, these vessels have the ability to dramatically increase the lumen by growth so as to provide enhanced perfusion to the jeopardized ischemic regions. In case of chronic or acute occlusion of a major artery, collateral arteries can relieve the ensuing harmful effects in many regions of the body (hindlimb, heart, brain and kidney). It is important to recognize that this process is not a passive dilatation but one of active proliferation and remodeling. Under normal flow conditions and depending on the pressure gradient between the interconnecting arterial networks there is only minimal net forward flow, but small amounts of flow may oscillate within the network. The presence of these native collaterals, which may not be utilized to provide perfusion under normal conditions, varies widely among species and also within individuals. However, these vessels have the ability to dramatically increase the lumen by growth so as to provide enhanced perfusion to the jeopardized ischemic regions. In case of chronic or acute occlusion of a major artery, collateral arteries can ameliorate the ensuing detrimental effects in many regions of the body (hindlimb, heart, brain, kidney). It is important to recognize that this process is not a passive dilatation but one of active proliferation and remodeling. Under normal flow conditions and depending on the pressure gradient between the interconnecting arterial networks there is only minimal net forward flow, but small amounts of flow may oscillate within the network.
Anmerkungen

Ein Verweis auf die Quelle fehlt hier. Sie ist weiter oben genannt, aber ohne irgendeinen Hinweis, dass sich dieser Verweis auch auf die hier dokumentierte Passage beziehen soll.


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Mature collateral vessels differ only in minor histological aspects from normal arteries of the conductance type: they are muscular and contain more collagen and exhibit transiently, during the growth process, a significant intima consisting of smooth muscle cells in the synthetic and proliferative phenotype. Mature collateral vessels differ only in minor histological aspects from normal arteries of the conductance type: they are muscular and contain more collagen and exhibited transiently during the growth process a significant intima consisting of smooth muscle cells in the synthetic and proliferative phenotype.
Anmerkungen

Ein Verweis auf die Quelle findet man weiter unten auf der nächsten Seite. Dieser Verweis macht keineswegs deutlich, dass die hier dokumentierte Passage wörtlich aus der Quelle stammt.


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[However, they differ markedly in their] anatomical appearance: they are sometimes excessively tortuous[13, 25]. In the re-entry region, they join up with the distal part of the occluded artery at nonphysiological angles, which adds to the resistance to flow. Collateral arteries can develop relatively quickly provided a pre-existent network of arterioles had existed before occlusion of the artery but they can also quickly regress when the occluded artery is opened up again[22]. This may also be the case when the subtended tissue had atrophied or is not used to full potential like in the peripheral circulation supplying the muscles of the leg. Most often, an occluded artery is not replaced by one single large collateral vessel but rather by several smaller ones. But this arrangement is inefficient because according to the Poiseuille’s Law the energy losses created by the resistance of the contributing vessels are additive[9]. During the course of collateral artery development many of the smaller contributing vessels regress, whereas the larger ones increase in diameter and make the system more efficient. However, no ideal adaptation is reached. At optimal conditions (no tissue loss after arterial occlusion), collateral vessels recover only approximately 40% of the maximal conductance (flow at a given blood pressure at maximal vasodilatation). This was shown for the canine heart and for the peripheral circulation in pigs, rabbits, and mice[7, 26].

7. Ito, W.D., et al., Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am J Physiol, 1997. 273(3 Pt 2): p. H1255-65.

9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

13. Schaper, W., Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia, 1967. 23(7): p. 595-6.

22. Fulton, W.F., The Time Factor in the Enlargement of Anastomoses in Coronary Artery Disease. Scott Med J, 1964. 9: p. 18-23.

25. Korff, T., K. Aufgebauer, and M. Hecker, Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation, 2007. 116(20): p. 2288-97.

26. Kumada, T., et al., Comparison of postpacing and exercise-induced myocardial dysfunction during collateral development in conscious dogs. Circulation, 1982. 65(6): p. 1178-85.

However, they differ markedly in their anatomical appearance: they are sometimes excessively tortuous.1 In the reentry region, they join up with the distal part of the occluded artery at nonphysiological angles, which adds to the resistance toward flow. Collateral arteries can develop relatively quickly provided a preexistent network of arterioles had existed before occlusion of the artery but they can also quickly regress when the occluded artery is opened up again.2 This may also be the case when the subtended tissue had atrophied or is not used to full potential like in the peripheral circulation supplying the muscles of the leg. Most often, an occluded artery is not replaced by one single large collateral vessel but rather by several smaller ones. But this arrangement is inefficient because according to the Poiseuille’s Law the energy losses created by the resistance of the contributing vessels are additive. During the course of collateral artery development many of the smaller contributing vessels regress, whereas the larger ones increase in diameter and make the system more efficient. However, no ideal adaptation is reached. At optimal conditions (no tissue loss after arterial occlusion), collateral vessels recover only approximately 40% of the maximal conductance (flow at a given blood pressure at maximal vasodilatation). This was shown for the canine heart and for the peripheral circulation in pigs, rabbits, and mice.3–5

1. Schaper W. The Collateral Circulation of the Heart. Amsterdam London: Elsevier North Holland Publishing Company; 1971.

2. Fulton WFM. The time factor in the enlargement of anastomoses in coronary artery disease. Scot Med J. 1964;9:18–23.

3. Kumada T, Gallagher KP, Battler A, White F, Kemper WS, Ross Jr J. Comparison of postpacing and exercise-induced myocardial dysfunction during collateral development in conscious dogs. Circulation. 1982;65:1178–1185.

4. Ito WD, Arras M, Scholz D, Winkler B, Htun P, Schaper W. Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am J Physiol. 1997;273:H1255–H1265.

5. Elsaesser H, Sauer A, Friedrich C, Helisch A, Luttun A, Carmeliet P, Scholz D, Schaper W. Bone marrow transplants abolish inhibition of arteriogenesis in placenta growth factor k.o. mice. J Mol Cell Cardiol. 2000;32:A29. Abstract

Anmerkungen

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The collateral vessel wall is now exposed to various pronounced mechanical forces: increased blood flow directly augments FSS, i.e., the viscous drag that flowing blood exerts on the endothelial lining. Assuming Newtonian fluid dynamics, FSS can be estimated using the following equation: Hence, the collateral vessel wall is now exposed to various pronounced mechanical forces: increased blood flow directly augments fluid shear stress (FSS), ie, the viscous drag that flowing blood exerts on the endothelial lining. Assuming Newtonian fluid dynamics, FSS can be estimated using the following equation:
Anmerkungen

Fortsetzung auf der nächsten Seite, dort findet sich dann auch ein Quellenverweis.


[11.] Haw/Fragment 005 01

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The equation that already includes blood viscosity (η) and the internal radius of a vessel (R), demonstrates that increased blood flow (Q) will directly result in increased FSS (τ)[9]. Furthermore, the wall of the collateral arteriole is influenced by pressure-related forces like longitudinal-, circumferential-, and radial wall stresses.


9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

Haw 05a source

The equation that already includes blood viscosity (η) and the internal radius of a vessel (R), demonstrates that increased blood flow (Q) will directly result in increased FSS (τ).8 Furthermore, the wall of the collateral arteriole is influenced by pressure-related forces like longitudinal-, circumferential-, and radial wall stresses.


8. Cox R. Physiology and hemodynamics of the macrocirculation. In: Stehbens W, eds. Hemodynamics and the Blood Vessel Wall. Springfield, Ill: Charles C. Thomas; 1979:75–156.

Anmerkungen

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[12.] Haw/Fragment 005 06

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It is generally assumed that a physical stimulus starts the remodeling process whereby increased pressure leads to increased wall thickness and increased flow to increased arterial diameter. Pressure-dependent forces are by far the highest in magnitude and they affect both the endothelium as well as the muscular media. It is therefore logical to assume that these are important factors for remodeling[13, 25]. However, in collateral growth with its pressure gradient driven increase in flow, the much weaker FSS, which the viscous drag of flowing blood exerts on the endothelial [lining, is the determining force[11, 29-35].]

11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62.

13. Schaper, W., Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia, 1967. 23(7): p. 595-6.

25. Korff, T., K. Aufgebauer, and M. Hecker, Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation, 2007. 116(20): p. 2288-97.

29. Ben Driss, A., et al., Arterial expansive remodeling induced by high flow rates. Am J Physiol, 1997. 272(2 Pt 2): p. H851-8.

30. Buus, C.L., et al., Smooth muscle cell changes during flow-related remodeling of rat mesenteric resistance arteries. Circ Res, 2001. 89(2): p. 180-6.

31. Girard, P.R. and R.M. Nerem, Shear stress modulates endothelial cell morphology and F-actin organization through the regulation of focal adhesion-associated proteins. J Cell Physiol, 1995. 163(1): p. 179-93.

32. Langille, B.L., Remodeling of developing and mature arteries: endothelium, smooth muscle, and matrix. J Cardiovasc Pharmacol, 1993. 21 Suppl 1: p. S11-7.

33. Resnick, N., et al., Fluid shear stress and the vascular endothelium: for better and for worse. Prog Biophys Mol Biol, 2003. 81(3): p. 177-99.

34. Tronc, F., et al., Role of NO in flow-induced remodeling of the rabbit common carotid artery. Arterioscler Thromb Vasc Biol, 1996. 16(10): p. 1256-62.

35. Tzima, E., et al., A mechanosensory complex that mediates the endothelial cell response to fluid shear stress. Nature, 2005. 437(7057): p. 426-31.

It is generally assumed that a physical stimulus starts the remodeling process whereby increased pressure leads to increased wall thickness and increased flow to increased arterial diameter. Pressure-dependent forces are by far the highest in magnitude and they affect both the endothelium as well as the muscular media. It is therefore logical to assume that these are important factors for remodeling [83, 121, 122]. [...] However, in collateral growth with its pressure gradient driven increase in flow the much weaker FSS, which the viscous drag of flowing blood exerts on the endothelial lining, is the determining force [8, 17, 35, 49, 85, 114, 142, 145, 149].

8. Ben Driss A, Benessiano J, Poitevin P, Levy BI, Michel JB (1997) Arterial expansive remodeling induced by high flow rates. Am J Physiol 272:H851–H858

17. Buus CL, Pourageaud F, Fazzi GE, Janssen G, Mulvany MJ, De Mey JG (2001) Smooth muscle cell changes during flow-related remodeling of rat mesenteric resistance arteries. Circ Res 89:180–186

35. Eitenmuller I, Volger O, Kluge A, Troidl K, Barancik M, Cai WJ, Heil M, Pipp F, Fischer S, Horrevoets AJ, Schmitz-Rixen T, Schaper W (2006) The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res 99:656–662

49. Girard PR, Nerem RM (1995) Shear stress modulates endothelial cell morphology and F-actin organization through the regulation of focal adhesion- associated proteins. J Cell Physiol 163:179–193

83. Korff T, Aufgebauer K, Hecker M (2007) Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation 116:2288–2297

85. Langille BL (1993) Remodeling of developing and mature arteries: endothelium, smooth muscle, and matrix. J Cardiovasc Pharmacol 21(Suppl 1):S11–S17

114. Resnick N, Yahav H, Shay-Salit A, Shushy M, Schubert S, Zilberman LC, Wofovitz E (2003) Fluid shear stress and the vascular endothelium: for better and for worse. Prog Biophys Mol Biol 81:177–199

121. Schaper W (1967) Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia 23:595– 596

122. Schaper W (1971) The collateral circulation of the heart. Elsevier North Holland Publishing Company, Amsterdam

142. Thoma R (1893) Untersuchungen über die Histogenese und Histomechanik des Gefäßsystems. F.Enke, Stuttgart

145. Tronc F, Wassef M, Esposito B, Henrion D, Glagov S, Tedgui A (1996) Role of NO in flow-induced remodeling of the rabbit common carotid artery. Arterioscler Thromb Vasc Biol 16:1256–1262

149. Tzima E, Irani-Tehrani M, Kiosses WB, Dejana E, Schultz DA, Engelhardt B, Cao G, DeLisser H, Schwartz MA (2005) A mechanosensory complex that mediates the endothelial cell response to fluid shear stress. Nature 437:426–431

Anmerkungen

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The pressure derived pulsatile stretch is also discussed[25, 36, 37], and the transcription factor- activator protein 1 (AP-1) is the molecular transducer. However, AP-1 is also activated by FSS[38], Pulsatile stretch can only be tested acutely and in vitro with its inherent limits. Cultured endothelium under stretch alters translation and transcription of growth factors and changes the sensitivity to cytokines[11, 39, 40]. If pulsatile stretch is a molding force, it must be demonstrated that in collateral growth pulsatile stretch is higher than the physiological levels in normal small arteries. Furthermore, in arterial occlusion the intravascular pressure downstream from the occlusion is much lower than the systemic arterial pressure[8].

8. Schaper, W., Collateral circulation: past and present. Basic Res Cardiol, 2009. 104(1): p. 5-21.

11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62.

25. Korff, T., K. Aufgebauer, and M. Hecker, Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation, 2007. 116(20): p. 2288-97.

36. Lehoux, S., et al., Differential regulation of vascular focal adhesion kinase by steady stretch and pulsatility. Circulation, 2005. 111(5): p. 643-9.

37. Popp, R., I. Fleming, and R. Busse, Pulsatile stretch in coronary arteries elicits release of endothelium-derived hyperpolarizing factor: a modulator of arterial compliance. Circ Res, 1998. 82(6): p. 696-703.

38. Miyagi, M., et al., Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells. Arterioscler Thromb Vasc Biol, 2005. 25(5): p. 970-5.

39. Busse, R. and I. Fleming, Pulsatile stretch and shear stress: physical stimuli determining the production of endothelium-derived relaxing factors. J Vasc Res, 1998. 35(2): p. 73-84.

40. Demicheva, E., M. Hecker, and T. Korff, Stretch-induced activation of the transcription factor activator protein-1 controls monocyte chemoattractant protein-1 expression during arteriogenesis. Circ Res, 2008. 103(5): p. 477-84.

However, pressure derived pulsatile stretch is also discussed [83, 88, 110] and the transcription factor AP-1 is the molecular transducer. However, AP-1 is also activated by FSS [96]. Pulsatile stretch can only be tested acutely and in vitro with its inherent limits. Cultured endothelium under stretch alters translation and transcription of growth factors and changes the sensitivity to cytokines[14, 32, 110]. If pulsatile stretch is a molding force it must be demonstrated that in collateral growth pulsatile stretch is higher than the physiological levels in normal small arteries. Furthermore, in arterial occlusion the intravascular pressure downstream from the occlusion (and hence in the receiving end of the collateral arcade) is much lower than the systemic arterial pressure [...]

14. Busse R, Fleming I (1998) Pulsatile stretch and shear stress: physical stimuli determining the production of endothelium-derived relaxing factors. J Vasc Res 35:73–84

32. Demicheva E, Hecker M, Korff T (2008) Stretch-induced activation of the transcription factor activator protein-1 controls monocyte chemoattractant protein-1 expression during arteriogenesis. Circ Res (in press)

83. Korff T, Aufgebauer K, Hecker M (2007) Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation 116:2288–2297

88. Lehoux S, Esposito B, Merval R, Tedgui A (2005) Differential regulation of vascular focal adhesion kinase by steady stretch and pulsatility. Circulation 111:643–649

96. Miyagi M, Miwa Y, Takahashi-Yanaga F, Morimoto S, Sasaguri T (2005) Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells. Arterioscler Thromb Vasc Biol 25:970–975

110. Popp R, Fleming I, Busse R (1998) Pulsatile stretch in coronary arteries elicits release of endothelium-derived hyperpolarizing factor: a modulator of arterial compliance. Circ Res 82:696–703

Anmerkungen

Die Quelle ist am Ende genannt, der Umfang der Übernahme (die auf der Vorseite beginnt), ist aber so nicht gekennzeichnet, auch weil es zahlreiche andere Literaturverweise gibt.


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In the case of a sudden arterial occlusion or a slowly progressing stenosis, a steep pressure gradient develops along the shortest path within the interconnecting network that increases the blood flow velocity and FSS in these vessels. The effect of this sustained increase in shear is the upregulation of distinct processes in the collateral arteries. In the case of a sudden arterial occlusion or a slowly progressing stenosis, a steep pressure gradient along the shortest path within the interconnecting network develops that increases the blood flow velocity and hence fluid shear stress in these vessels, which now assume the new function as “collaterals” [normal femoral artery blood flow 4.8 x 10-3 dyn/cm2; blood flow via anastomoses (occlusion) 889 x 10-3 dyn/cm2]. The effect of this sustained increase in shear is the upregulation of distinct processes in the collateral arteries.
Anmerkungen

Ein Verweis auf die Quelle fehlt.


[15.] Haw/Fragment 006 15

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FSS is proportional to the blood flow velocity and inversely related to the cube of the radius[41]. It is sensed by the endothelium, which, in response, changes the expression of growth factors, secretes nitric oxide (NO)[42, 43], prostacyclin, and probably other transmitters, and leads, with prolonged exposure, to positive arterial remodeling. However, even small increases in the radius of collateral arteries lead to a precipitous fall of the FSS because of the cubic relationship, and the FSS-related growth ends prematurely[20].

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

41. Schmidt, V.J., et al., Gap junctions synchronize vascular tone within the microcirculation. Pharmacol Rep, 2008. 60(1): p. 68-74.

42. Busse, R. and I. Fleming, Regulation and functional consequences of endothelial nitric oxide formation. Ann Med, 1995. 27(3): p. 331-40.

43. Fleming, I., et al., Isometric contraction induces the Ca2+-independent activation of the endothelial nitric oxide synthase. Proc Natl Acad Sci U S A, 1999. 96(3): p. 1123-8.

FSS is proportional to the blood flow velocity and inversely related to the cube of the radius.21 It is sensed by the endothelium, which, in response, changes the expression of growth factors, secretes NO,22,23 prostacyclin, and probably other transmitters, and leads, with prolonged exposure, to positive arterial remodeling. However, even small increases in the radius of collateral arteries lead to a precipitous fall of the FSS because of the cubic relationship, and the FSS-related growth ends prematurely.

21. Schmidt RF, Thews G. Physiologie des Menschen. Berlin: Springer; 1997.

22. Busse R, Fleming I. Regulation and functional consequences of endothelial nitric oxide formation. Ann Med. 1995;27:331–340.

23. Fleming I, Bauersachs J, Schäfer A, Scholz D, Aldershvile J, Busse R. Isometric contraction induces the Ca2+ independent activation of the endothelial nitric oxide synthase. Proc Natl Acad Sci U S A. 1999;96: 1123–1128.

Anmerkungen

Die Quelle ist in Fn. 20 angegeben. Der Umfang der Übernahme, die drei Literaturverweise miteinschließt, wird aber ebensowenig deutlich wie der Umstand, dass es sich um eine beinahe wörtliche Übernahme handelt.


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Furthermore, FSS is almost impossible to measure in small collaterals. Pipp and colleagues[44] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic force in collateral growth.

Collaterals increase their diameter up to 20 times during arteriogenesis, which is possible through mitosis of vascular cells[45]. Given that the collateral vessels grow in length as well as in width, the expanding vessel arranges itself in loops and turns to accommodate the extra length. This gives the vessels a typical corkscrew pattern and causes energy loss[10].


10. Heil, M., et al., Arteriogenesis versus angiogenesis: similarities and differences. J Cell Mol Med, 2006. 10(1): p. 45-55.

44. Pipp, F., et al., Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hindlimb. Arterioscler Thromb Vasc Biol, 2004. 24(9): p. 1664-8.

45. Wolf, C., et al., Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J Mol Cell Cardiol, 1998. 30(11): p. 2291-305.

Furthermore, FSS is almost impossible to measure in small collaterals.

[Seite 1381]

Pipp and colleagues [14] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further, significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic power in collateral growth.

Collaterals increase their diameter up to 20 times during arteriogenesis, which is possible through mitosis of vascular cells [15]. Given that the collateral vessels grow in length as well as in width, the expanding vessel arranges itself in loops and turns to accommodate the extra length. This gives the vessels a typical corkscrew pattern [16] and causes energy loss.


14. Pipp, F., Boehm, S., Cai, W. J., Adili, F., Ziegler, B., Karanovic, G., Ritter, R., Balzer, J., Scheler, C., Schaper, W., Schmitz-Rixen, T. (2004) Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler. Thromb. Vasc. Biol. 24, 1664–1668.

15. Wolf, C., Cai, W. J., Vosschulte, R., Koltai, S., Mousavipour, D., Scholz, D., Afsah-Hedjri, A., Schaper, W., Schaper, J. (1998) Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J. Mol. Cell. Cardiol. 30, 2291–2305.

16. Heil, M., Eitenmuller, I., Schmitz-Rixen, T., Schaper, W. (2006) Arteriogenesis versus angiogenesis: similarities and differences. J. Cell. Mol. Med. 10, 45–55.

Anmerkungen

Ein Verweis auf die Quelle fehlt.


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[This, together with the premature arrest of arteriogenic growth,] as a result of the drop in FSS in the growing collateral, is a reason that collateral arteries cannot completely compensate the conductance of the artery they have replaced. Initially, during arteriogenesis, several collateral vessels are recruited and proliferate. However, as it is hemodynamically more efficient for fewer, larger arteries to conduct the blood than a greater number of smaller arteries, the smaller vessels regress later on, and those with the higher shear forces continue growing[46].

46. Hoefer, I.E., J.J. Piek, and G. Pasterkamp, Pharmaceutical interventions to influence arteriogenesis: new concepts to treat ischemic heart disease. Curr Med Chem, 2006. 13(9): p. 979-87.

This, together with the premature arrest of arteriogenic growth, as a result of the drop in FSS in the growing collateral, is a reason that collateral arteries cannot completely compensate the conductance of the artery they have replaced. Initially, during arteriogenesis, several collateral vessels are recruited and proliferate. However, as it is hemodynamically more efficient for fewer, larger arteries to conduct the blood than a greater number of smaller arteries, the smaller vessels regress later on, and those with the higher shear forces continue growing [17].

17. Hoefer, I. E., Piek, J. J., Pasterkamp, G. (2006) Pharmaceutical interventions to influence arteriogenesis: new concepts to treat ischemic heart disease. Curr. Med. Chem. 13, 979–987.

Anmerkungen

Kein Verweis auf die Quelle.

Die Übernahme beginnt auf der Vorseite.


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FSS as a molding force was recognized over 100 years ago; the embryologist Thoma described the relationship between the diameter of an artery and its blood flow velocity[47]. [...] Any sustained deviation from that relationship initiates processes of either growth or atrophy. A sustained increase of fluid shear stress leads to activation of the endothelium.

1.3.3. Activation of the endothelium

It is currently not well enough known how the stimulus of increased shear stress is transmitted from the endothelial cell membrane to the nucleus, where it initiates the transcriptional activity of a number of genes, partially via a protein that binds to the shear stress responsive element that is present in the promotor of several genes (nitric oxide synthase (NOS), platelet-derived growth factor (PDGF), monocyte chemoattractant protein-1 (MCP-1))[49]. The first step in the activation of the endothelium is the opening of chloride channels that are also responsible for the volume control of endothelial cells. Characteristically stress-activated endothelium appears swollen in scanning electron microscopic images[50], adhesion molecules are upregulated[51], and the conditions are perfect for the adhesion and invasion of circulating cells.


47. Yancopoulos, G.D., M. Klagsbrun, and J. Folkman, Vasculogenesis, angiogenesis, and growth factors: ephrins enter the fray at the border. Cell, 1998. 93(5): p. 661-4.

49. Shyy, Y.J., et al., Fluid shear stress induces a biphasic response of human monocyte chemotactic protein 1 gene expression in vascular endothelium. Proc Natl Acad Sci U S A, 1994. 91(11): p. 4678-82.

50. Ziegelstein, R.C., et al., Cytosolic alkalinization of vascular endothelial cells produced by an abrupt reduction in fluid shear stress. Circ Res, 1998. 82(7): p. 803-9.

51. Chappell, D.C., et al., Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium. Circ Res, 1998. 82(5): p. 532-9.

Shear stress as a molding force was recognized over 100 years ago; the embryologist Thoma described the relationship between the diameter of an artery and its blood flow velocity (14). Any sustained deviation from that relationship initiates processes of either growth or atrophy. A sustained increase of fluid shear stress leads to activation of the endothelium.

Activation of the endothelium

It is presently not well enough known how the stimulus of increased shear stress is transmitted from the endothelial cell membrane to the nucleus, where it initiates the transcriptional activity of a number of genes (12), partially via a protein that binds to the shear stress responsive element that is present in the promotor of several genes (NOS, PDGF, MCP-1). The first step in the activation of the endothelium is the opening of chloride channels that are also responsible for the volume control of endothelial cells. Characteristically stress-activated endothelium appears swollen in scanning electron microscopic images (15). Adhesion molecules are upregulated (4), and the conditions are perfect for the adhesion and invasion of circulating cells.


4. Chappell, D. C., S. E. Varner, R. M. Nerem, R. M. Medford, and R. W. Alexander. Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium. Circ. Res. 82: 532–539, 1998.

12. Shyy, Y.-J., H.-J. Hsieh, S. Usami, and S. Chien. Fluid shear stress induces a biphasic response of human monocyte chemotactic protein 1 expression in vascular endothelium. Proc. Natl. Acad. Sci. USA 91: 4678–4682, 1994.

14. Yancopoulos, G. D., M. Klagsbrun, and J. Folkman: Vasculogenesis, angiogenesis, and growth factors: ephrins enter the fray at the border. Cell 93: 661–664, 1998.

15. Ziegelstein, R. C., P. S. Blank, L. Cheng, and M. C. Capogrossi. Cytosolic alkalinization of vascular endothelial cells produced by an abrupt reduction in fluid shear stress. Circ. Res. 82: 803–809, 1998.

Anmerkungen

Ein Verweis auf die Quelle fehlt.


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Murray[48] proposed that the vascular system is optimally configured to minimize the amount of mechanical and metabolic work to provide adequate blood flow, and he predicted that FSS is constant throughout the vasculature and that blood flow through each vessel is proportional to that vessel’s diameter cube.

48. Murray, C.D., The Physiological Principle of Minimum Work Applied to the Angle of Branching of Arteries. J Gen Physiol, 1926. 9(6): p. 835-841.

Murray25 proposed that the vascular sytem [sic] is optimally configured to minimize the amount of mechanical and metabolic work to provide adequate blood flow, and he predicted that FSS is constant throughout the vasculature and that blood flow through each vessel is proportional to that vessel’s diameter cube.

25. Murray CD. The physiological principle of minimum work applied to the angle of branching arteries. J Gen Physiol. 1926;9:835–841.

Anmerkungen

Ein Verweis auf die Quelle fehlt.


[20.] Haw/Fragment 007 27

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Chronically increased shear stress activates endothelium in a morphologically visible way. It loses volume control and swells, because chloride channels change their open probability[52]. Inhibitors of the chloride channel also inhibit arteriogenesis. The location and nature of the mechanotransducer of shear stress are controversially [discussed[53], and protein kinases and stretch sensitive K-channels were studied[54].]

52. Nilius, B., et al., Volume-activated Cl- channels. Gen Pharmacol, 1996. 27(7): p. 1131-40.

53. Ali, M.H. and P.T. Schumacker, Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med, 2002. 30(5 Suppl): p. S198-206.

54. Nilius, B. and G. Droogmans, Ion channels and their functional role in vascular endothelium. Physiol Rev, 2001. 81(4): p. 1415-59.

Chronically increased shear stress activates endothelium in a morphologically visible way. It loses volume control and swells,

[Seite 1146]

because chloride channels change their open probability.33 Inhibitors of the chloride channel also inhibit arteriogenesis.34 The location and nature of the mechanotransducer of shear stress are controversially discussed,35 and protein kinases and stretch sensitive K+ channels were studied.36


33. Nilius B, Eggermont J, Voets T, Droogmans G. Volume-activated Cl-channels. Gen Pharmacol. 1996;27:1131–1140.

34. Ziegelhoeffer T, Scholz D, Helish A, Wagner S, Schaper W. Swelling cell-doing well? Volume-regulated chloride channels and arteriogenesis. J Mol Cell Cardiol. 2002;34:A71. Abstract

35. Ali MH, Schumacker PT. Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med. 2002;30:S198–S206.

36. Nilius B, Droogmans G. Ion channels and their functional role in vascular endothelium. Physiol Rev. 2001;81:1415–1459.

Anmerkungen

Ein Verweis auf die Quelle fehlt.


[21.] Haw/Fragment 008 01

BauernOpfer
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[The location and nature of the mechanotransducer of shear stress are controversially] discussed[53], and protein kinases and stretch sensitive K-channels were studied[54]. We found that high shear stress in vitro causes a transient phosphorylation of focal adhesions, which could also act as mechanoreceptors[55]. By whatever way the mechanical force is transmitted from the deformed cell (membrane) to its nucleus, it will activate transcription factors, like early growth response 1 (egr-1) (upregulated during the early phases of arteriogenesis), that switch on gene expression, notably of chemokines like MCP-1 but also adhesion molecules like intracellular adhesion molecule-1 (ICAM-1), that are necessary for the docking of monocytes[56]. Shear stress is also known to release NO, but it is not known whether chronically increased shear stress will lead to chronically increased amounts of released NO. A lasting steep increase in shear stress leads only to a transient increase of egr-1, and this may also happen with the NO response[57]. The increased permeability of immature collaterals may have been caused by NO. However, expression studies on the RNA level have not shown any changes related to the early stages of collateral growth[20]. Immunofluorescence studies have shown the presence of PDGF antigen in neointima formation in canine collaterals, which supports findings by the Geary,R.L., et al[58]. showing that PDGF is increased under low-flow conditions that favor intima proliferation. The necessity of a cell-to cell transmitter (i.e., from endothelium to smooth muscle) is not very high, because the adhering monocyte assumes that function.

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

53. Ali, M.H. and P.T. Schumacker, Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med, 2002. 30(5 Suppl): p. S198-206.

54. Nilius, B. and G. Droogmans, Ion channels and their functional role in vascular endothelium. Physiol Rev, 2001. 81(4): p. 1415-59.

55. Scholz, D., et al., Ultrastructure and molecular histology of rabbit hind-limb collateral artery growth (arteriogenesis). Virchows Arch, 2000. 436(3): p. 257-70.

56. Gimbrone, M.A., Jr., et al., Hemodynamics, endothelial gene expression, and atherogenesis. Ann N Y Acad Sci, 1997. 811: p. 1-10; discussion 10-1.

57. Khachigian, L.M., et al., Egr-1 is activated in endothelial cells exposed to fluid shear stress and interacts with a novel shear-stress-response element in the PDGF A-chain promoter. Arterioscler Thromb Vasc Biol, 1997. 17(10): p. 2280-6.

58. Geary, R.L., et al., Time course of flow-induced smooth muscle cell proliferation and intimal thickening in endothelialized baboon vascular grafts. Circ Res, 1994. 74(1): p. 14-23.

The location and nature of the mechanotransducer of shear stress are controversially discussed,35 and protein kinases and stretch sensitive K+ channels were studied.36 We found that high shear stress in vitro causes a transient phosphorylation of focal adhesions,11 which could also act as mechanoreceptors. By whatever way the mechanical force is transmitted from the deformed cell (membrane) to its nucleus, it will activate transcription factors, like egr-1 (upregulated during the early phases of arteriogenesis), that switch on gene expression, notably of chemokines like MCP-1 but also adhesion molecules like intracellular adhesion molecule-1 (ICAM-1), that are necessary for the docking of monocytes. Other transcription factors that are so far not structurally identified may bind to the GAGACC motif present in the promoter region of several growth factors initiating their expression.37 Shear stress is also known to release NO, but it is not known whether chronically increased shear stress will lead to chronically increased amounts of released NO. A lasting step increase in shear stress leads only to a transient increase of egr-1,38 and this may also happen with the NO response. The increased permeability of immature collaterals may have been caused by NO. [...] However, expression studies on the RNA level have, in our hands, not shown any changes related to the early stages of collateral growth. Immunofluorescence studies have shown the presence of PDGF antigen in neointima formation in canine collaterals,39 which supports findings by the Geary et al40 showing that PDGF is increased under low-flow conditions that favor intima proliferation. The necessity of a cell-to-cell transmitter (ie, from endothelium to smooth muscle) is not very high, because the adhering monocyte assumes that function.

11. Scholz D, Ito W, Fleming I, Deindl E, Sauer A, Babiak A, Bühler A, Wiesnet M, Busse R, Schaper J, Schaper W. Ultrastructure and molecular histology of rabbit hindlimb collateral artery growth. Virchows Arch. 2000;436:257–270.

35. Ali MH, Schumacker PT. Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med. 2002;30:S198–S206.

36. Nilius B, Droogmans G. Ion channels and their functional role in vascular endothelium. Physiol Rev. 2001;81:1415–1459.

37. Gimbrone MA Jr, Resnick N, Nagel T, Khachigian LM, Collins T, Topper JN. Hemodynamics, endothelial gene expression, and atherogenesis. Ann N Y Acad Sci. 1997;801:1–10.

38. Khachigian LM, Anderson KR, Halnon NJ, Gimbrone MJ, Resnick N, Collins T. Egr-1 is activated in endothelial cells exposed to fluid shear stress and interacts with a novel shear-stress-response element in the PDGF A-chain promoter. Arterioscler Thromb Vasc Biol. 1997;17: 2280–2286.

39. Vosschulte R. Kollateralwachstum. Einflüsse von Wachstumsfaktoren und Matrixmetalloproteinasen auf die Zellproliferation und Zellmigration. In: Max-Planck-Institut für Physiologische und Klinische Forschung. Abteilung Experimentelle Kardiologie. Giessen: Justus-Liebig-Universität Giessen; 1999:88.

40. Geary RL, Kohler TR, Vergel S, Kirkman TR, Clowes AW. Time course of flow-induced smooth muscle cell proliferation and intimal thickening in endothelialized baboon vascular grafts. Circ Res. 1994;74:14–23.

Anmerkungen

Die Quelle wird in der Mitte der Übernahme erwähnt, ohne irgendeinen Hinweis, dass der gesamte Abschnitt aus ihr stammt.


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The endothelial lining of growing canine coronary collaterals is studded with monocytes that had attached, during phase 1 of arteriogenesis, to the now much rougher surface of the swollen endothelial cells that, activated by shear stress, upregulate the MCP-1 and adhesion molecules to which the macrophage 1 antigen (Mac-1) receptor of monocytes binds[55]. Infusion of soluble ICAM-1 binds to circulating monocytes and prevents their adhesion to transforming arterioles.

55. Scholz, D., et al., Ultrastructure and molecular histology of rabbit hind-limb collateral artery growth (arteriogenesis). Virchows Arch, 2000. 436(3): p. 257-70.

The endothelial lining of growing canine coronary collaterals is studded with monocytes that had attached, during phase 1 of arteriogenesis, to the now much rougher surface of the swollen endothelial cells that, activated by shear stress, upregulate the monocyte chemoattractant MCP-1 and adhesion molecules11 to which the Mac-1 receptor of monocytes binds. Infusion of soluble ICAM-1 binds to circulating monocytes and prevents their adhesion to transforming arterioles.

11. Scholz D, Ito W, Fleming I, Deindl E, Sauer A, Babiak A, Bühler A, Wiesnet M, Busse R, Schaper J, Schaper W. Ultrastructure and molecular histology of rabbit hindlimb collateral artery growth. Virchows Arch. 2000;436:257–270.

Anmerkungen

Ein Verweis auf die Quelle fehlt.


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[The same results can be obtained with] intravenous infusion of anti–ICAM-1 antibodies that also prevent monocyte attachment. Targeted disruption of the MCP-1 receptor (CC chemokines receptor-2) (CCR-2) in mice prevented almost all collateral growth after femoral artery occlusion[59], but infusion of MCP-1 into the proximal stump of the occluded femoral artery led to increased monocyte influx and elicited a strong arteriogenic effect[60]. We also discovered that the weak arteriogenic effects of chronically infused vascular endothelial growth factor-A (VEGF-A) is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes[61]. A similar effect was discovered with placenta growth factor (PlGF). The arteriogenesis-inhibiting effect of targeted disruption of PlGF in mice [62] could be lifted by bone marrow transplantation, i.e., an effect of monocytes[62, 63]. Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation[64]. Intravenous infusion of liposome-packaged phosphonates (alendronate) destroyed all monocytes/macrophages for a period of ≈1 week. During this time, VEGF and PlGF infusions remained completely inactive, showing again the importance of monocytes in arteriogenesis[64]. Suppression of monocyte counts by treatment with 5-fluorouracil (5-FU) significantly delayed arteriogenesis, but the rebound effect after chemical bone marrow suppression had the opposite effect[20, 59].

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

59. Heil, M., et al., Blood monocyte concentration is critical for enhancement of collateral artery growth. Am J Physiol Heart Circ Physiol, 2002. 283(6): p. H2411-9.

60. Ito, W.D., et al., Monocyte chemotactic protein-1 increases collateral and peripheral conductance after femoral artery occlusion. Circ Res, 1997. 80(6): p. 829-37.

61. Breier, G., et al., Transforming growth factor-beta and Ras regulate the VEGF/VEGF-receptor system during tumor angiogenesis. Int J Cancer, 2002. 97(2): p. 142-8.

62. Carmeliet, P., et al., Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions. Nat Med, 2001. 7(5): p. 575-83.

63. Scholz, D., et al., Bone marrow transplantation abolishes inhibition of arteriogenesis in placenta growth factor (PlGF) -/- mice. J Mol Cell Cardiol, 2003. 35(2): p. 177-84.

64. Pipp, F., et al., VEGFR-1-selective VEGF homologue PlGF is arteriogenic: evidence for a monocyte-mediated mechanism. Circ Res, 2003. 92(4): p. 378-85.

The same results can be obtained with intravenous infusion of anti–ICAM-1 antibodies that also prevent monocyte attachment. Targeted disruption of the MPC-1 receptor (CCR-2) in mice prevents almost all collateral growth after femoral artery occlusion,43 but infusion of MCP-1 into the proximal stump of the occluded femoral artery led to increased monocyte influx and elicited a strong arteriogenic effect.44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.45 A similar effect was discovered with placenta growth factor (PlGF). The arteriogenesis-inhibiting effect of targeted disruption of PlGF in mice46 could be lifted by bone marrow transplantation, ie, an effect of monocytes.46,47 Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.48 Intravenous infusion of liposome-packaged phosphonates (alendronate) destroyed all monocytes/macrophages for a period of ≈1 week. During this time, VEGF and PlGF infusions remained completely inactive, showing again the importance of monocytes in arteriogenesis.48

Suppression of monocyte counts by treatment with 5-fluorouracil significantly delayed arteriogenesis, but the rebound effect after chemical bone marrow suppression had the opposite effect.49


43. Heil M, Ziegelhoeffer T, Helisch A, Wagner S, Martin S, Kuziel WA, Schaper W. Arteriogenesis (collateral artery growth) after femoral artery occlusion is reduced in mice lacking CC-chemokine-receptor-2. Circulation. 2002;106 (Suppl II):1390. Abstract.

44. Ito W, Arras M, Winkler B, Scholz D, Schaper J, Schaper W. Monocyte chemotactic protein-1 increases collateral and peripheral conductance after femoral artery occlusion. Circ Res. 1997;80:829–837.

45. Breier G, Blum S, Peli J, Groot M, Wild C, Risau W, Reichmann E. Transforming growth factor-b1 and Ras regulate the VEGF/VEGF receptor system during tumor angiogenesis. Int J Cancer. 2002;97: 142–148.

46. Carmeliet P, Moons L, Luttun A, Vincenti V, Compernolle V, De Mol M, Wu Y, Bono F, Devy L, Beck H, Scholz D, Acker T, DiPalma T, Dewerchin M, Noel A, Stalmans I, Barra A, Blacher S, Vandendriessche T, Ponten A, Eriksson U, Plate K, Foidart J-M, Schaper W, Charnock-Jones DS, Hicklin DJ, Herbert J-M, Collen D, Persico G. Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions. Nature Med. 2001;7:575–583.

47. Scholz D, Elsaesser H, Sauer A, Friedrich C, Luttun A, Carmeliet P, Schaper W. Bone marrow transplantation abolishes inhibition of arteriogenesis in placenta growth factor (PlGF) -/- mice. J Mol Cell Cardiol. 2003;35:177–184.

48. Pipp F, Heil M, Issbrücker K, Ziegelhöffer T, Martin S, van den Heuvel J, Weich H, Fernandez B, Clauss M, Schaper W. VEGFR-1-selective VEGF homologue PlGF is arteriogenic: evidence for a monocytemediated mechanism. Circ Res. 2003;92:378–385.

49. Heil M, Ziegelhoeffer T, Pipp F, Kostin S, Martin S, Clauss M, Schaper W. Blood monocytes concentration is critical for enhancement of collateral artery growth. Am J Physiol Heart Circ Physiol. 2002;283: H2411–H2419.

Anmerkungen

Die Quelle wird am Ende zusammen mit einem anderen Literaturverweis genannt. Der Umfang der Übernahme wird aber so nicht deutlich.


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Upregulation of survival factors for monocytes (granulocyte macrophage colony-stimulating factor (GM-CSF)) provides the environment for a stable function of monocytes (Fig.1.3. C). These in turn produce fairly large amounts of growth factors, including VEGF, colony stimulating factor, transforming growth factor-β, in particular, FGF-2[20]. The adhesion and invasion of monocytes and platelets (also potent producers of growth factors) is soon followed by the first wave of mitosis of the endothelial and smooth muscle cells. The cell invasion is most prominent in the intima, the initial entrance, but even more pronounced later in the adventitia, where they create an inflammatory environment that is later accompanied by T cells. One of the effects of the perivascular inflammation is that it creates the space (by forcing neighboring tissue cells into apoptosis) for the greatly expanding collateral vessel, which can increase its [diameter up to 20 times[21].]

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

Upregulation of survival factors for monocytes (granulocyte macrophage colony-stimulating factor) provides the environment for a stable function of monocytes (Fig. 1C). These in turn produce fairly large amounts of growth factors, in particular, fibroblast growth factor-2. The adhesion and invasion of monocytes and platelets (also potent producers of growth factors) is soon followed by the first wave of mitosis of the endothelial and smooth muscle cells. [...]

[S. 123]

[...] The cell invasion is most prominent in the intima, the initial entrance, but even more pronounced later in the adventitia, where they create an inflammatory environment that is later accompanied by T cells. One of the effects of the perivascular inflammation is that it creates the space (by forcing neighboring tissue cells into apoptosis) for the greatly expanding collateral vessel, which can increase its diameter up to 20 times.

Anmerkungen

Die Quelle ist am Ende des Absatzes genannt, aber es ist nicht klar, dass der gesamte Absatz aus ihr stammt.


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1.3.5. Remodeling

After the acute phase of arteriogenesis that is dominated by the inflammatory events, remodelling begins (phase 2 of arteriogenesis), i.e., the much slower consolidation of the arterial structure after the final diameter was almost reached. A new elastic lamina is synthesized by the SMCs, and the rebuilding of the media and the formation of an intima begins with the downregulation of the tissue inhibitor of matrixmetalloproteinases (TIMP and MMP)[65].


65. Cai, W., et al., Altered balance between extracellular proteolysis and antiproteolysis is associated with adaptive coronary arteriogenesis. J Mol Cell Cardiol, 2000. 32(6): p. 997-1011

Remodelling

After the acute phase of arteriogenesis that is dominated by the inflammatory events, remodelling begins (phase 2 of arteriogenesis), ie, the much slower consolidation of the arterial structure after the final diameter was almost reached. A new elastic lamina is synthesized by the SMCs, and the rebuilding of the media and the formation of an intima begins with the downregulation of the tissue inhibitor of matrixmetalloproteinases (TIMP and MMP).80,81


80. Cai WJ, Vosschulte R, Koltai S, Kostin S, Schaper W, Schaper J. Extracellular proteolysis is involved in coronary collateral vessel development in dog. J Mol Cell Cardiol. 1997;29:A128.

81. Cai WJ, Vosschulte R, Afsah-Hedrij A, Koltai S, Koscic E, Scholz D, Kostin S, Schaper W, Schaper J. Altered balance between extracellular proteolysis and antiproteolysis is associated with adaptive coronary arteriogenesis. J Mol Cell Cardiol. 2000;32:997–1011.

Anmerkungen

Ein Verweis auf die Quelle fehlt.

Fortsetzung auf der nächsten Seite. Dort findet sich dann auch ein Quellenverweis.


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[This is followed by an upregulation of] the expression and activity of the MMPs that digest the matrix and provide the space for new cells and enable SMCs to migrate toward the intima. Many SMCs of the old media undergo apoptosis and are replaced by new ones. Those that proliferate change their phenotype and lose most of their contractile material, which is replaced by endoplasmic reticulum (ER) and free ribosomes, an indication of their synthetic activity[18, 55]. The loss of the contractile phenotype is ascribed to the combined activities of protein kinase G, activin, and regulators of G protein signaling-5 (RGS-5). In addition to actin and myosin, desmin and calponin are downregulated and fibronectin is upregulated[66]. In general, protein synthesis in SMCs switches to an embryonic pattern. Because the thickening of the vessel wall occurs under markedly increased tangential wall stress, the intercellular connections and the communication between cells change. The remodelling process of large collaterals is finally characterized by the significant increase in length (tortuosity) and by the formation of a substantial intima (Fig. 1.3.)[21]. At very late stages, the intima disappears in mature collaterals, probably because the longitudinal muscle had assumed first a helical and later a circumferential orientation. In very small animals, like mice, neither intima formation nor pruning is observed, most probably because the increase in new tissue mass is so small that remodelling processes are not required[20]. However, already in the rabbit a sizeable intima is seen in hindlimb collaterals sometime after FAO. It is tempting to speculate that collateral arteries develop from the inside out using the intima as a platform; this is the incubator where the growth factors are produced, where the MMPs and other proteases are activated, and where the SMCs migrate to and then proliferate, thereby weakening the media from which they leave, producing the bulge of later tortuosity[20].

18. Scholz, D., et al., Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol, 2002. 34(7): p. 775-87.

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

55. Scholz, D., et al., Ultrastructure and molecular histology of rabbit hind-limb collateral artery growth (arteriogenesis). Virchows Arch, 2000. 436(3): p. 257-70.

66. Cai, W.J., et al., Remodeling of the adventitia during coronary arteriogenesis. Am J Physiol Heart Circ Physiol, 2003. 284(1): p. H31-40.

This is followed by an upregulation of the expression and activity of the MMPs that digest the matrix and provide the space for new cells and enable SMCs to migrate toward the intima. Many SMCs of the old media die an apoptotic death and are replaced by new ones. Those that proliferate change their phenotype and lose most of their contractile material, which is replaced by endoplasmic reticulum and free ribosomes, an indication of their synthetic activity.11,12 The loss of the contractile phenotype is ascribed to the combined activities of protein kinase G, activin, and RGS-5. In addition to actin and myosin, desmin and calponin are downregulated and fibronectin is upregulated.82 In general, protein synthesis in SMCs switches to an embryonic pattern.

[Seite 1149]

Because the thickening of the vessel wall occurs under markedly increased tangential wall stress, the intercellular connections and the communication between cells change. [...] The remodelling process of large collaterals is finally characterized by the significant increase in length (tortuosity) and by the formation of a substantial intima (Figure 3). At very late stages, the intima disappears in mature collaterals, probably because the longitudinal muscle had assumed first a helical and later a circumferential orientation. In very small animals, like mice, neither intima formation nor pruning is observed, most probably because the increase in new tissue mass is so small that remodelling processes are not required. However, already in the rabbit a sizeable intima is seen in hindlimb collaterals sometime after femoral artery occlusion.

It is tempting to speculate that collateral arteries develop from the inside out using the intima as a platform; this is the incubator where the growth factors are produced, where the MMPs and other proteases are activated, and where the SMCs migrate to and then proliferate, thereby weakening the media from which they leave, producing the bulge of later tortuosity.


11. Scholz D, Ito W, Fleming I, Deindl E, Sauer A, Babiak A, Bühler A, Wiesnet M, Busse R, Schaper J, Schaper W. Ultrastructure and molecular histology of rabbit hindlimb collateral artery growth. Virchows Arch. 2000;436:257–270.

12. Scholz D, Ziegelhoeffer T, Helisch A, Wagner S, Friedrich C, Podzuweit T, Schaper W. Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol. 2002;34: 775–787.

82. Cai W-J, Koltai S, Kocsis E, Scholz D, Kostin S, Luo X, Schaper W, Schaper J. Remodeling of the adventitia during coronary arteriogenesis. Am J Physiol. 2003;284:H31–H40.

Anmerkungen

Auf die Quelle wird zweimal verwiesen, es wird aber nicht klar, dass die gesamte Passage inkl. einiger Literaturverweise aus der Quelle stammt.


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Verschleierung
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1.3.6. Therapeutic arteriogenesis

In previous studies, Ito, W.D., et al., showed that chronic intra-arterial infusion of MCP-1 greatly increased the development of arterial collateral blood vessels (arteriogenesis) after FAO[7, 60]. These collaterals were more numerous on angiograms, and their ability to conduct blood had increased by six fold. (Fig. 1.3., A and B) The histological appearance of these typical corkscrew vessels was that of muscular arteries[20].

Therapeutic arteriogenesis

In previous studies we showed that chronic intra-arterial infusion of MCP-1 greatly increased the development of arterial collateral blood vessels (arteriogenesis) after femoral artery occlusion (6, 7). These collaterals were more numerous on angiograms, and their ability to conduct blood had increased by sixfold (Fig. 1, A and B). The histological appearance of these typical corkscrew vessels was that of muscular arteries.

Anmerkungen

Ein Verweis auf die Quelle fehlt hier. Man findet ihn auf der nächsten Seite.


"FAO" statt "femoral arterial occlusion"; "six fold" statt "sixfold". Übernahme der referenzierten Bilder aus Quelle:HAW/Buschmann and Schaper 1999 mit komplett plagierter Bildunterschrift.


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[In another study, Arras, M., et al.[14] injected a single dose of] lipopolysaccharide intravenously into New Zealand white rabbits 3 days after ligation of the femoral artery. This potent stimulator of TNF-a also markedly enhanced the number of monocyte-derived macrophages accumulated around growing collateral arteries. Peripheral and collateral conductance was markedly increased. Nevertheless, on a molar basis MCP-1 is the most potent arteriogenic peptide[21]. VEGF is a peptide with angiogenic properties. It is produced by cells in close vicinity of endothelial cells, its chemoattractive action on monocytes is dose dependent; and its expression is highly regulated by hypoxia and hence by a physiological feedback mechanism to tissue hypoxia[67].

14. Arras, M., et al., Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J Clin Invest, 1998. 101(1): p. 40-50.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

67. Carmeliet, P. and D. Collen, Vascular development and disorders: molecular analysis and pathogenic insights. Kidney Int, 1998. 53(6): p. 1519-49.

In another study, we injected a single dose of lipopolysaccharide intravenously into New Zealand White rabbits 3 days after ligation of the femoral artery (1). This potent stimulator of tumor necrosis factor- a also markedly enhanced the number of monocyte-derived macrophages accumulated around growing collateral arteries. Peripheral and collateral conductances were markedly increased. Nevertheless, on a molar basis MCP-1 is the most potent arteriogenic peptide. Vascular endothelial growth factor (VEGF) is a peptide with angiogenic properties. It is produced by cells in close vicinity of endothelial cells, suggesting paracrine regulation of capillary formation; it is secreted and exerts a direct effect via interaction with endothelial receptors Flk-1 and Flt-1; its chemoattractive action on monocytes is dose dependent; and its expression is highly regulated by hypoxia and thereby a physiological feedback mechanism to tissue hypoxia (3).

1. Arras, M., W. D. Ito, D. Scholz, B. Winkler, J. Schaper, and W. Schaper. Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J. Clin. Invest. 101: 40–50, 1997.

3. Carmeliet, P., and D. Collen. Vascular development and disorders—molecular analysis and pathogenic insights. Kidney Int. 53: 1519–1549, 1998.

Anmerkungen

Die Quelle ist in der Mitte genannt, der Umfang der Übernahme wird durch diesen Verweis aber nicht klar. Auch zwei Literaturverweise sind übernommen.


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Angiogenesis, i.e., the sprouting of capillaries from the pre-existing vasculature, is mainly initiated by hypoxia in ischemic tissue[3]. These newly formed capillaries consist of endothelial tubes lacking proper wall structures. Angiogenesis alone has a limited capacity to increase perfusion of the surrounding ischemic tissue.

3. Carmeliet, P., Mechanisms of angiogenesis and arteriogenesis. Nat Med, 2000. 6(4): p. 389-95.

Angiogenesis, i.e., the sprouting of capillaries from the pre-existing vasculature, is mainly initiated by hypoxia in ischemic tissue4. These newly formed capillaries consist of endothelial tubes lacking proper wall structures. Angiogenesis alone has a limited capacity to increase perfusion of the surrounding ischemic tissue.

4. Carmeliet, P. Mechanisms of angiogenesis and arteriogenesis. Nat. Med. 6, 389–395 (2000).

Anmerkungen

Ein Verweis auf die Quelle fehlt.


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Angiogenesis is a process by which new capillary blood vessels sprout from a pre-existing blood vessel[68]. It is an important component of various normal and pathological conditions such as wound healing, fracture repair, folliculogenesis, ovulation, and pregnancy. These periods of angiogenesis are tightly regulated. However, if not properly controlled, angiogenesis can also represent a significant pathogenic component of tumor growth and metastasis, rheumatic arthritis, and retinopathies[21]. Angiogenesis is a complex phenomenon consisting of several distinct processes, which include endothelial migration and proliferation, extracellular proteolysis, endothelial differentiation (capillary tube formation), and vascular wall remodeling. It is important to recognize that these newly formed capillary tubes lack vascular smooth muscle cells.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

68. Risau, W., Mechanisms of angiogenesis. Nature, 1997. 386(6626): p. 671-4.

Angiogenesis is a process by which new capillary blood vessels sprout from a preexisting blood vessel

[Seite 122]

(10). It is an important component of various normal and pathological conditions such as wound healing, fracture repair, folliculogenesis, ovulation, and pregnancy. These periods of angiogenesis are tightly regulated. However, if not properly controlled, angiogenesis can also represent a significant pathogenic component of tumor growth and metastasis, rheumatic arthritis, and retinopathies. Angiogenesis is a complex phenomenon consisting of several distinct processes, which include endothelial migration and proliferation, extracellular proteolysis, endothelial differentiation (capillary tube formation), and vascular wall remodeling. It is important to recognize that these newly formed capillary tubes lack vascular smooth muscle cells.


10. Risau, W. Mechanisms of angiogenesis. Nature 386: 671–674, 1997.

Anmerkungen

Auf die Quelle wird in der Mitte der Passage verwiesen, der Umfang der Übernahme bleibt so im Unklaren.


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Arteriogenesis differs from angiogenesis in several aspects, (Table 1.1., Fig.1.5.) the most important being the dependence of angiogenesis on hypoxia and the dependence of arteriogenesis on inflammation[20]. However, angiogenesis and arteriogenesis share several mechanisms of action, e.g., their dependence on growth factors. Whereas angiogenesis can be largely explained by the actions of VEGF, arteriogenesis is probably a multifactorial process in which several growth factors are orchestrated. The role of VEGF in arteriogenesis is not clear, but a chemoattractive role for monocytes and hence an indirect contribution is imaginable[21].

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

Arteriogenesis differs from angiogenesis in several aspects, the most important being the

[S. 125]

dependence of angiogenesis on hypoxia and the dependence of arteriogenesis on inflammation.

However, angiogenesis and arteriogenesis share several mechanisms of action (Fig. 2), e.g., their dependence on growth factors. Whereas angiogenesis can be largely explained by the actions of VEGF, arteriogenesis is probably a multifactorial process in which several growth factors are orchestrated. The role of VEGF in arteriogenesis is not clear, but a chemoattractive role for monocytes and hence an indirect contribution is imaginable.

Anmerkungen

Die Quelle ist angegeben, doch durch die Literaturverweise wird nicht klar, dass die gesamte Passage übernommen ist.


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After peripheral artery occlusion in rabbits and mice, arteriogenesis proceeds much faster than angiogenesis because of a structural dilatation of pre-existing collateral vessels followed by mitosis of all vascular cell types, which restores resting blood flow within 3 days. Recovery of dilatory reserve (maximal flow) takes longer[20]. The slower angiogenesis is unable to significantly restore flow even if angiogenesis reduces the minimal terminal resistance of the entire chain of resistors by new capillaries in parallel. Future therapeutic efforts should be directed at stimulating arteriogenesis.

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

After peripheral artery occlusion in rabbits and mice, arteriogenesis proceeds much faster than angiogenesis because of a structural dilatation of preexisting collateral vessels followed by mitosis of all vascular cell types, which restores resting blood flow within 3 days. Recovery of dilatory reserve (maximal flow) takes longer. The slower angiogenesis is unable to significantly restore flow even if angiogenesis reduces the minimal terminal resistance of the entire chain of resistors by new capillaries in parallel. Future therapeutic aims should be directed at stimulating arteriogenesis.
Anmerkungen

Die Quelle ist angegeben. Dem Leser wird aber durch die Platzierung des Quellenverweises nicht klar, dass der gesamte Abschnitt aus der Quelle stammt.


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KomplettPlagiat
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Intercellular communication is a key regulator of vascular function[69, 70]. In the vessel wall, cell-to-cell communication occurs by extracellular diffusion and convection of humoral factors or by intercytoplasmic exchange of ions, metabolites, [and small signaling molecules (<1 kDa) via gap junctions.]

69. Haefliger, J.A., P. Nicod, and P. Meda, Contribution of connexins to the function of the vascular wall. Cardiovasc Res, 2004. 62(2): p. 345-56.

70. Ross, R., Cell biology of atherosclerosis. Annu Rev Physiol, 1995. 57: p. 791-804.

INTERCELLULAR COMMUNICATION is a key regulator of vascular function (23, 40). In the vessel wall, cell-to-cell communication occurs by extracellular diffusion and convection of humoral factors or by intercytoplasmic exchange of ions, metabolites, and small signaling molecules (<1 kDa) via gap junctions.

23. Haefliger JA, Nicod P, and Meda P. Contribution of connexins to the function of the vascular wall. Cardiovasc Res 62: 345–356, 2004.

40. Ross R. Cell biology of atherosclerosis. Annu Rev Physiol 57: 791–804, 1995.

Anmerkungen

Ein Verweis auf die Quelle fehlt.

Fortsetzung auf der nächsten Seite.


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Endothelial gap junctions are channels that permit and strictly regulate communication throughout the endothelial monolayer and between endothelial cells and adjacent smooth muscle and circulating blood cells. Endothelial cell migration and growth, particularly following injury and during angiogenesis, depend on communication through gap junctions[71-75]. In addition, gap junctions coordinate vascular tone and vasomotion [76-78] and participate in the regulation of immunoinflammatory responses[79, 80].

[...] Gap junctions are formed by a pair of hemichannels called connexons, each contributed by one of two neighboring cells. Connexons are composed of six connexin monomer subunits arranged around a central pore(Fig.1.6.)[82].


71. Kwak, B.R., et al., Inhibition of endothelial wound repair by dominant negative connexin inhibitors. Mol Biol Cell, 2001. 12(4): p. 831-45.

72. Larson, D.M., et al., Differential regulation of connexin43 and connexin37 in endothelial cells by cell density, growth, and TGF-beta1. Am J Physiol, 1997. 272(2 Pt 1): p. C405-15.

73. Pepper, M.S., et al., Junctional communication is induced in migrating capillary endothelial cells. J Cell Biol, 1989. 109(6 Pt 1): p. 3027-38.

74. Xie, H.Q. and V.W. Hu, Modulation of gap junctions in senescent endothelial cells. Exp Cell Res, 1994. 214(1): p. 172-6.

75. Yeh, H.I., et al., Age-related alteration of gap junction distribution and connexin expression in rat aortic endothelium. J Histochem Cytochem, 2000. 48(10): p. 1377-89.

76. Chaytor, A.T., W.H. Evans, and T.M. Griffith, Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries. J Physiol, 1998. 508 ( Pt 2): p. 561-73.

77. Christ, G.J., et al., Gap junctions in vascular tissues. Evaluating the role of intercellular communication in the modulation of vasomotor tone. Circ Res, 1996. 79(4): p. 631-46.

78. de Wit, C., et al., Impaired conduction of vasodilation along arterioles in connexin40-deficient mice. Circ Res, 2000. 86(6): p. 649-55.

79. Oviedo-Orta, E., R.J. Errington, and W.H. Evans, Gap junction intercellular communication during lymphocyte transendothelial migration. Cell Biol Int, 2002. 26(3): p. 253-63.

80. Wong, C.W., T. Christen, and B.R. Kwak, Connexins in leukocytes: shuttling messages? Cardiovasc Res, 2004. 62(2): p. 357-67.

82. Sohl, G. and K. Willecke, Gap junctions and the connexin protein family. Cardiovasc Res, 2004. 62(2): p. 228-32.

Endothelial gap junctions are channels that permit and strictly regulate communication throughout the endothelial monolayer and between endothelial cells and adjacent smooth muscle and circulating blood cells. Endothelial cell migration and growth, particularly following injury and during angiogenesis, depend on communication through gap junctions (31, 33, 38, 51, 52). In addition, gap junctions coordinate vascular tone and vasomotion (11, 13, 17) and participate in the regulation of immunoinflammatory responses (36, 50).

Gap junctions are formed by a pair of hemichannels called connexons, each contributed by one of two neighboring cells. Connexons are composed of six connexin monomer subunits arranged around a central pore.


11. Chaytor AT, Evans WH, and Griffith TM. Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries. J Physiol 508: 561–573, 1998.

13. Christ GJ, Spray DC, el-Sabban M, Moore LK, and Brink PR. Gap junctions in vascular tissues. Evaluating the role of intercellular communication in the modulation of vasomotor tone. Circ Res 79: 631–646, 1996.

17. De Wit C, Roos F, Bolz SS, Kirchhoff S, Krüger O, Willecke K, and Pohl U. Impaired conduction of vasodilation along arterioles in connexin40-deficient mice. Circ Res 86: 649–655, 2000.

31. Kwak BR, Pepper MS, Gros DB, and Meda P. Inhibition of endothelial wound repair by dominant negative connexin inhibitors. Mol Biol Cell 12: 831–845, 2001.

33. Larson DM, Wrobleski MJ, Sagar GD, Westphale EM, and Beyer EC. Differential regulation of connexin43 and connexin37 in endothelial cells by cell density, growth, and TGF-beta1. Am J Physiol Cell Physiol 272: C405–C415, 1997.

36. Oviedo-Orta E, Errington RJ, and Evans WH. Gap junction intercellular communication during lymphocyte transendothelial migration. Cell Biol Int 26: 253–263, 2002.

38. Pepper MS, Spray DC, Chanson M, Montesano R, Orci L, and Meda P. Junctional communication is induced in migrating capillary endothelial cells. J Cell Biol 109: 3027–3038, 1989.

50. Wong CW, Christen T, and Kwak BR. Connexins in leukocytes: shuttling messages? Cardiovasc Res 62: 357–367, 2004.

51. Xie HQ and Hu VW. Modulation of gap junctions in senescent endothelial cells. Exp Cell Res 214: 172–176, 1994.

52. Yeh HI, Chang HM, Lu WW, Lee YN, Ko YS, Severs NJ, and Tsai CH. Age-related alteration of gap junction distribution and connexin expression in rat aortic endothelium. J Histochem Cytochem 48: 1377–1389, 2000.

Anmerkungen

Ein Verweis auf die Quelle fehlt.


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KomplettPlagiat
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Connexins, or gap junction proteins, are a family of structurally-related transmembrane proteins that assemble to form vertebrate gap junctions (an entirely different family of proteins, the innexins, form gap junctions in invertebrates)[81].

81. Lodish, H.F., R.K. Rodriguez, and D.J. Klionsky, Points of view: lectures: can't learn with them, can't learn without them. Cell Biol Educ, 2004. 3(4): p. 202-11.

Connexins, or gap junction proteins, are a family of structurally-related transmembrane proteins that assemble to form vertebrate gap junctions (an entirely different family of proteins, the innexins, form gap junctions in invertebrates).[1]

1. Lodish, Harvey F.; Arnold Berk, Paul Matsudaira, Chris A. Kaiser, Monty Krieger, Mathew P. Scott, S. Lawrence Zipursky, James Darnell (2004). Molecular Cell Biology (5th ed.). New York: W.H. Freeman and Company. pp. 230–1. ISBN 0-7167-4366-3.

Anmerkungen

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Die angegebene Quelle enthält den Text nicht.


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KomplettPlagiat
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Connexins are four-pass transmembrane proteins with both C and N cytoplasmic termini, a cytoplasmic loop (CL) and two extra-cellular loops, (EL-1) and (EL-2). Connexins are assembled in groups of six to form hemichannels, or connexons, and two hemichannels then combine to form a gap junction. They usually weigh between 26 and 60 kDa, and have an average length of 380 amino acids. The various connexins have been observed to combine into both homomeric and heteromeric gap junctions, each of which may exhibit different functional properties including pore conductance, size selectivity, charge selectivity, voltage gating, and chemical gating. Connexins are four-pass transmembrane proteins with both C and N cytoplasmic termini, a cytoplasmic loop (CL) and two extra-cellular loops, (EL-1) and (EL-2). Connexins are assembled in groups of six to form hemichannels, or connexons, and two hemichannels then combine to form a gap junction. [...] They usually weigh between 26 and 60 kDa, and have an average length of 380 amino acids. The various connexins have been observed to combine into both homomeric and heteromeric gap junctions, each of which may exhibit different functional properties including pore conductance, size selectivity, charge selectivity, voltage gating, and chemical gating.
Anmerkungen

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Connexins 37, 40, and 43 (Cx37, Cx40, Cx43, respectively) are the major gap junction proteins expressed in vascular endothelial cells[85-89]. These proteins are very dynamic, exhibiting rapid turnover times and variable expression patterns. Because of the unique gating and permselective characteristics of Cx37, Cx40, and Cx43, different combinations of these connexin isoforms contribute to homo- or heteromeric connexons and homo- or heterotypic gap junctions leading to a variety of channel types with different functional properties[83, 90-96].

83. Kumar, N.M. and N.B. Gilula, The gap junction communication channel. Cell, 1996. 84(3): p. 381-8.

85. Bruzzone, R., et al., Connexin40, a component of gap junctions in vascular endothelium, is restricted in its ability to interact with other connexins. Mol Biol Cell, 1993. 4(1): p. 7-20.

86. Larson, D.M., C.C. Haudenschild, and E.C. Beyer, Gap junction messenger RNA expression by vascular wall cells. Circ Res, 1990. 66(4): p. 1074-80.

87. Little, T.L., E.C. Beyer, and B.R. Duling, Connexin 43 and connexin 40 gap junctional proteins are present in arteriolar smooth muscle and endothelium in vivo. Am J Physiol, 1995. 268(2 Pt 2): p. H729-39.

88. Reed, K.E., et al., Molecular cloning and functional expression of human connexin37, an endothelial cell gap junction protein. J Clin Invest, 1993. 91(3): p. 997-1004.

89. Van Rijen, H., et al., Gap junctions in human umbilical cord endothelial cells contain multiple connexins. Am J Physiol, 1997. 272(1 Pt 1): p. C117-30.

90. Beblo, D.A. and R.D. Veenstra, Monovalent cation permeation through the connexin40 gap junction channel. Cs, Rb, K, Na, Li, TEA, TMA, TBA, and effects of anions Br, Cl, F, acetate, aspartate, glutamate, and NO3. J Gen Physiol, 1997. 109(4): p. 509-22.

91. Bruzzone, R., T.W. White, and D.A. Goodenough, The cellular Internet: on-line with connexins. Bioessays, 1996. 18(9): p. 709-18.

92. Bruzzone, R., T.W. White, and D.L. Paul, Connections with connexins: the molecular basis of direct intercellular signaling. Eur J Biochem, 1996. 238(1): p. 1-27.

93. Elfgang, C., et al., Specific permeability and selective formation of gap junction channels in connexin-transfected HeLa cells. J Cell Biol, 1995. 129(3): p. 805-17.

94. Veenstra, R.D., Size and selectivity of gap junction channels formed from different connexins. J Bioenerg Biomembr, 1996. 28(4): p. 327-37.

95. Wang, H.Z. and R.D. Veenstra, Monovalent ion selectivity sequences of the rat connexin43 gap junction channel. J Gen Physiol, 1997. 109(4): p. 491-507.

96. White, T.W. and R. Bruzzone, Multiple connexin proteins in single intercellular channels: connexin compatibility and functional consequences. J Bioenerg Biomembr, 1996. 28(4): p. 339-50.

Connexin 37, 40, and 43 (Cx37, Cx40, Cx43, respectively) are the major gap junction proteins expressed in vascular endothelial cells (7, 32, 34, 39, 45). These proteins are very dynamic, exhibiting rapid turnover times and variable expression patterns. Because of the unique gating and permselective characteristics of Cx37, Cx40, and Cx43, different combinations of these connexin isoforms contribute to homo- or heteromeric connexons and homo- or heterotypic gap junctions leading to a variety of channel types with different functional properties (1, 8, 9, 19, 28, 47–49).

1. Beblo DA and Veenstra RD. Monovalent cation permeation through the connexin40 gap junction channel: Cs, Rb, K, Na, Li, TEA, TMA, TBA, and effects of anions Br, Cl, F, acetate, aspartate, glutamate, and NO3. J Gen Physiol 109: 509–522, 1997.

7. Bruzzone R, Haefliger JA, Gimlich RL, and Paul DL. Connexin40, a component of gap junctions in vascular endothelium, is restricted in its ability to interact with other connexins. Mol Biol Cell 4: 7–20, 1993.

8. Bruzzone R, White TW, and Goodenough DA. The cellular internet: on-line with connexins. Bioessays 18: 709–718, 1996.

9. Bruzzone R, White TW, and Paul DL. Connections with connexins: the molecular basis of direct intercellular signaling. Eur J Biochem 238: 1–27, 1996.

19. Elfgang C, Eckert R, Lichtenberg-Frate´ H, Butterweck A, Traub O, Klein TA, Hüsler DF, and Willecke K. Specific permeability and selective formation of gap junction channels in connexin-transfected HeLa cells. J Cell Biol 129: 805–817, 1995.

28. Kumar NM and Gilula NB. The gap junction communication channel. Cell 84: 381–388, 1996.

29. Kwak BR and Jongsma HJ. Selective inhibition of gap junction channel activity by synthetic peptides. J Physiol 516: 679–685, 1999.

32. Larson DM, Haudenschild CC, and Beyer EC. Gap junction messenger RNA expression by vascular wall cells. Circ Res 66: 1074–1080, 1990.

34. Little TL, Beyer EC, and Duling BR. Connexin 43 and connexin 40 gap junctional proteins are present in arteriolar smooth muscle and endothelium in vivo. Am J Physiol Heart Circ Physiol 268: H729–H739, 1995.

39. Reed KE, Westphale EM, Larson DM, Wang HZ, Veenstra RD, and Beyer EC. Molecular cloning and functional expression of human connexin37, an endothelial cell gap junction protein. J Clin Invest 91: 997–1004, 1993.

45. Van Rijen H, van Kempen MJ, Analbers LJ, Rook MB, van Ginneken AC, Gros D, and Jongsma HJ. Gap junctions in human umbilical cord endothelial cells contain multiple connexins. Am J Physiol Cell Physiol 272: C117–C130, 1997.

47. Veenstra RD. Size and selectivity of gap junction channels formed from different connexins. J Bioenerg Biomembr 28:b 327–337, 1996.

48. Wang HZ and Veenstra RD. Monovalent ion selectivity sequences of the rat connexin43 gap junction channel. J Gen Physiol 109: 491–507, 1997.

49. White TW and Bruzzone R. Multiple connexin proteins in single intercellular channels: connexin compatibility and functional consequences. J Bioenerg Biomembr 28: 339–350, 1996.

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Haw 18a diss

[84](Dbouk HA, et al., Cell Commun Signal, 2009; 7: 4)

Fig. 1.7. Life cycle and protein associations of connexins. Connexins are synthesized on ER-bound ribosomes and inserted into the ER cotranslationally. This is followed by oligomerization between the ER and trans-Golgi network (depending on the connexin type) into connexons, which are then delivered to the membrane via the actin or microtubule networks. Connexons may also be delivered to the plasma membrane by direct transfer from the rough ER. Upon insertion into the membrane, connexons may remain as hemichannels or they dock with compatible connexons on adjacent cells to form gap junctions[84]. Newly delivered connexons are added to the periphery of pre-formed gap junctions, while the central "older" gap junction fragments are degraded by internalization of a double-membrane structure called an annular junction into one of the two cells, where subsequent lysosomal or proteasomal degradation occurs, or in some cases the connexons are recycled to the membrane (indicated by dashed arrow). During their life cycle, connexins associate with different proteins, including (1) cytoskeletal components as microtubules, actin, and actin-binding proteins α-spectrin and drebrin, (2) junctional molecules including adherens junction components such as cadherins, α-catenin, and β-catenin, as well as tight junction components such as ZO-1 and ZO-2, (3) enzymes such as kinases and phosphatases which regulate the assembly, function, and degradation, and (4) other proteins such as caveolin[84].


84. Dbouk, H.A., et al., Connexins: a myriad of functions extending beyond assembly of gap junction channels. Cell Commun Signal, 2009. 7: p. 4.

Haw 18a source

Figure I

Life cycle and protein associations of connexins. Connexins are synthesized on ER-bound ribosomes and inserted into the ER cotranslationally. This is followed by oligomerization between the ER and trans-Golgi network (depending on the connexin type) into connexons, which are then delivered to the membrane via the actin or microtubule networks. Connexons may also be delivered to the plasma membrane by direct transfer from the rough ER. Upon insertion into the membrane, connexons may remain as hemichannels or they dock with compatible connexons on adjacent cells to form gap junctions. Newly delivered connexons are added to the periphery of pre-formed gap junctions, while the central "older" gap junction fragment are degraded by internalization of a double-membrane structure called an annular junction into one of the two cells, where subsequent lysosomal or proteasomal degradation occurs, or in some cases the connexons are recycled to the membrane (indicated by dashed arrow). During their life cycle, connexins associate with different proteins, including (1) cytoskeletal components as microtubules, actin, and actin-binding proteins α-spectrin and drebrin, (2) junctional molecules including adherens junction components such as cadherins, α-catenin, and β-catenin, as well as tight junction components such as ZO-1 and ZO-2, (3) enzymes such as kinases and phosphatases which regulate the assembly, function, and degradation, and (4) other proteins such as caveolin.

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Man beachte auch, dass sich das Bild samt Bildunterschrift auch in der Quelle Wikipedia Connexin (2010) finden läßt. Aus dieser Quelle wurde auf der folgenden Seite Text ungekennzeichnet übernommen.


[39.] Haw/Fragment 019 01

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[Although the extent of combinations of different connexins within connexons and] channels remains unclear, immunohistochemical and immunocytochemical studies demonstrate differential expression and localization patterns of all three vascular connexins in the endothelium, depending on species[97], vascular bed[98-100], and local hemodynamics[101]. In vivo studies implicate Cx40 as the constitutive vascular gap junction protein across species and vascular bed, playing an important role in coupling between cells in the vascular wall[97].

97. van Kempen, M.J. and H.J. Jongsma, Distribution of connexin37, connexin40 and connexin43 in the aorta and coronary artery of several mammals. Histochem Cell Biol, 1999. 112(6): p. 479-86.

98. Hill, C.E., et al., Heterogeneity in the distribution of vascular gap junctions and connexins: implications for function. Clin Exp Pharmacol Physiol, 2002. 29(7): p. 620-5.

99. Pepper, M.S., et al., Coupling and connexin 43 expression in microvascular and large vessel endothelial cells. Am J Physiol, 1992. 262(5 Pt 1): p. C1246-57.

100. Yeh, H.I., et al., Individual gap junction plaques contain multiple connexins in arterial endothelium. Circ Res, 1998. 83(12): p. 1248-63.

101. Gabriels, J.E. and D.L. Paul, Connexin43 is highly localized to sites of disturbed flow in rat aortic endothelium but connexin37 and connexin40 are more uniformly distributed. Circ Res, 1998. 83(6): p. 636-43.

Although the extent of combinations of different connexins within connexons and channels remains unclear, immunohistochemical and immunocytochemical studies demonstrate differential expression and localization patterns of all three vascular connexins in endothelium, depending on species (44), vascular bed (25, 37, 53), and local hemodynamics (21). In vivo studies implicate Cx40 as the constitutive vascular gap junction protein across species and vascular bed, playing an important role in coupling between cells in the vascular wall (44).

21. Gabriels JE and Paul DL. Connexin43 is highly localized to sites of disturbed flow in rat aortic endothelium but connexin37 and connexin40 are more uniformly distributed. Circ Res 83: 636–643, 1998.

25. Hill CE, Rummery N, Hickey H, and Sandow SL. Heterogeneity in the distribution of vascular gap junctions and connexins: implications for function. Clin Exp Pharmacol Physiol 29: 620–625, 2002.

37. Pepper MS, Montesano R, el Aoumari A, Gros D, Orci L, and Meda P. Coupling and connexin 43 expression in microvascular and large vessel endothelial cells. Am J Physiol Cell Physiol 262: C1246–C1257, 1992.

44. Van Kempen MJ and Jongsma HJ. Distribution of connexin37, connexin40 and connexin43 in the aorta and coronary artery of several mammals. Histochem Cell Biol 112: 479–486, 1999.

53. Yeh HI, Rothery S, Dupont E, Coppen SR, and Severs NJ. Individual gap junction plaques contain multiple connexins in arterial endothelium. Circ Res 83: 1248–1263, 1998.

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Gap junctions are essential for many physiological processes, such as the coordinated depolarization of cardiac muscle, and proper embryonic development. [...] For this reason, mutations in connexin-encoding genes can lead to functional and developmental abnormalities. Gap junctions are essential for many physiological processes, such as the coordinated depolarization of cardiac muscle, and proper embryonic development. For this reason, mutations in connexin-encoding genes can lead to functional and developmental abnormalities.
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[41.] Haw/Fragment 020 03

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Laser Doppler is a standard technique for the non-invasive blood flow monitoring and measurement of blood flow in the microcirculatory system. The strength of the technique is in looking at changes in flow - either over time or differences in flow over an area of skin or other exposed tissue.

5.2. Operating principles

The laser Doppler technique measures blood flow in the very small blood vessels of the microvasculature, such as the low-speed flows associated with nutritional blood flow in capillaries close to the skin surface and flow in the underlying arterioles and venules involved in regulation of skin temperature. The tissue thickness sampled is typically 1mm, the capillary diameters 10 microns and the velocity spectrum measurement typically 0.01 to 10mm/s.

The technique depends on the Doppler principle whereby low power light from a monochromatic stable laser, e.g. a helium neon gas laser or a single mode laser diode, incident on tissue is scattered by moving red blood cells and as a consequence is frequency broadened. The frequency broadened light, together with laser light scattered from static tissue, is photo-detected and the resulting photocurrent processed to provide a blood flow measurement. Please note, where laser light is scattered for tissue with a low red blood cell concentration, the average Doppler frequency shift is proportional to the average speed of red blood cells.

Laser light can be directed to the tissue surface either via an optic fibre (Fig.1.8.a) or as a light beam (Fig.1.8.b). For ‘fibre optic’ monitors (LDF instruments) the optic fibre terminates in an optic probe which can be attached to the tissue surface. One or more light collecting fibres also terminate in the probe head and these fibres transmit a proportion of the scattered light to a photo-detector and the electronic signal processing [system.]

Laser Doppler is a standard technique for the non-invasive blood flow monitoring and measurement of blood flow in the microcirculation. The strength of the technique is in looking at changes in flow - either over time or differences in flow over an area of skin or other exposed tissue.

[...]

Operating Principles

The laser Doppler technique measures blood flow in the very small blood vessels of the microvasculature, such as the low-speed flows associated with nutritional blood flow in capillaries close to the skin surface and flow in the underlying arterioles and venules involved in regulation of skin temperature. The tissue thickness sampled is typically 1mm, the capillary diameters 10 microns and the velocity spectrum measurement typically 0.01 to 10mm/s. The technique depends on the Doppler principle whereby low power light from a monochromatic stable laser (a), e.g. a Helium Neon gas laser or a single mode laser diode, incident on tissue is scattered by moving red blood cells and as a consequence is frequency broadened (b). The frequency broadened light, together with laser light scattered from static tissue, is photodetected and the resulting photocurrent processed to provide a blood flow measurement. Please note, where laser light is scattered for tissue with a low red blood cell concentration the average Doppler frequency shift is proportional to the average speed of red blood cells.

[Seite 2]

Laser light can be directed to the tissue surface either via an optic fibre (c) or as a light beam (d). For ‘fibre optic’ monitors (LDF instruments) the optic fibre terminates in an optic probe which can be attached to the tissue surface. One or more light collecting fibres also terminate in the probe head and these fibres transmit a proportion of the scattered light to a photodetector and the signal processing electronics.

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[42.] Haw/Fragment 021 01

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Normal fibre separations in the probe head are a few tenths of 1mm, consequently blood flow is measured in a tissue volume of typically 1mm3 or smaller.

(Fig.1.8.a)

Haw 21a diss

(Basic Theory and Operating Principles of LDF & LDI, Moor instruments Ltd User manual, 2003)

In a Laser Doppler blood flow Imager (LDI) the low intensity laser beam is scanned across a tissue surface in a raster fashion using a moving mirror. There is no direct contact with the tissue being assessed. The basic elements of the moorLDI are shown schematically in the following figure.

(Fig.1.8.b)

Haw 21b diss

(Basic Theory and Operating Principles of LDF & LDI, Moor instruments Ltd User manual, 2003)

Normal fibre separations in the probe head are a few tenths of a mm, consequently blood flow is measured in a tissue volume of typically 1mm3 or smaller. [...]

(c)

Haw 21a source

In a Laser Doppler blood flow Imager (LDI) the low intensity laser beam is scanned across a tissue surface in a raster fashion using a moving mirror. There is no direct contact with the tissue being assessed. The basic elements of the moorLDI are shown schematically in the following figure.

(d)

Haw 21b source

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[43.] Haw/Fragment 022 01

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Both large areas (a full torso) and small areas (part of a finger) can be scanned, enabling the blood flow to be mapped and colour coded images of the blood flow displayed. Regions of interest can be defined and statistical data can be calculated and recorded.

Single point measurements give a high temporal resolution (40Hz data rates are typical) enabling rapid blood flow changes to be recorded, whereas the laser Doppler imager can provide spatial information and has the ability to average blood flow measurements over large areas. Fibre optic systems can measure at tissue sites not easily accessible to a laser beam. For example measurements in brain tissue, mouth, gut, colon, muscle and bone.

5.3. The definition of perfusion units

The term commonly used to describe blood flow measured by the laser Doppler technique is ‘flux’: a quantity proportional to the product of the average speed of the blood cells and their number concentration (often referred to as blood volume). This is expressed in arbitrary ‘perfusion units’ and is calculated using the first moment of the power spectral density.

Both large areas (a full torso) and small areas (part of a finger) can be scanned enabling the blood flow to be mapped and colour coded images of the blood flow displayed. Regions of interest can be defined and statistical data calculated and recorded.

[Seite 3]

Single point measurements give a high temporal resolution (40Hz data rates are typical) enabling rapid blood flow changes to be recorded, whereas the laser Doppler imager can provide spatial information and has the ability to average blood flow measurements over large areas. Fibre optic systems can measure at tissue sites not easily accessible to a laser beam. For example measurements in brain tissue, mouth, gut, colon, muscle and bone.

[...]

Definitions

The term commonly used to describe blood flow measured by the laser Doppler technique is ‘flux’: a quantity proportional to the product of the average speed of the blood cells and their number concentration (often referred to as blood volume). This is expressed in arbitrary ‘perfusion units’ and is calculated using the first moment of the power spectral density.

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Cardiovascular diseases are the number one cause of death globally[104]. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.

104. Murray, C.J. and A.D. Lopez, Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet, 1997. 349(9063): p. 1436-42.

Cardiovascular diseases are the number one cause of death globally1. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.

1. World Health Organization. in Fact sheet No. 317 Feb. 2007 (World Health Organization, 2007) (http://www.who.int/mediacentre/factsheets/fs317/en/index.html).

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[45.] Haw/Fragment 023 19

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Connexin 37 and Connexin 40 (Cx37, Cx40) are the major gap junction proteins expressed in vascular endothelial cells[85-89]. These proteins are very dynamic, exhibiting rapid turnover times and variable expression patterns. Although the extent of combinations of different connexins within connexons and channels remains unclear, immunohistochemical and immunocytochemical studies demonstrate differential expression and localization patterns of both vascular connexins in endothelium, depending on species[97], vascular bed[98-100], and local hemodynamics[101].[...] For the microcirculation in vivo studies implicate Cx40 as the constitutive vascular gap junction protein across species [and vascular bed, playing an important role in coupling between cells in the vascular wall[78, 97-98], particularly in response to changes in tissue metabolic demand.]

78. de Wit, C., et al., Impaired conduction of vasodilation along arterioles in connexin40-deficient mice. Circ Res, 2000. 86(6): p. 649-55.

85. Bruzzone, R., et al., Connexin40, a component of gap junctions in vascular endothelium, is restricted in its ability to interact with other connexins. Mol Biol Cell, 1993. 4(1): p. 7-20.

86. Larson, D.M., C.C. Haudenschild, and E.C. Beyer, Gap junction messenger RNA expression by vascular wall cells. Circ Res, 1990. 66(4): p. 1074-80.

87. Little, T.L., E.C. Beyer, and B.R. Duling, Connexin 43 and connexin 40 gap junctional proteins are present in arteriolar smooth muscle and endothelium in vivo. Am J Physiol, 1995. 268(2 Pt 2): p. H729-39.

88. Reed, K.E., et al., Molecular cloning and functional expression of human connexin37, an endothelial cell gap junction protein. J Clin Invest, 1993. 91(3): p. 997-1004.

89. Van Rijen, H., et al., Gap junctions in human umbilical cord endothelial cells contain multiple connexins. Am J Physiol, 1997. 272(1 Pt 1): p. C117-30.

97. van Kempen, M.J. and H.J. Jongsma, Distribution of connexin37, connexin40 and connexin43 in the aorta and coronary artery of several mammals. Histochem Cell Biol, 1999. 112(6): p. 479-86. 98. Hill, C.E., et al., Heterogeneity in the distribution of vascular gap junctions and connexins: implications for function. Clin Exp Pharmacol Physiol, 2002. 29(7): p. 620-5.

99. Pepper, M.S., et al., Coupling and connexin 43 expression in microvascular and large vessel endothelial cells. Am J Physiol, 1992. 262(5 Pt 1): p. C1246-57.

100. Yeh, H.I., et al., Individual gap junction plaques contain multiple connexins in arterial endothelium. Circ Res, 1998. 83(12): p. 1248-63.

101. Gabriels, J.E. and D.L. Paul, Connexin43 is highly localized to sites of disturbed flow in rat aortic endothelium but connexin37 and connexin40 are more uniformly distributed. Circ Res, 1998. 83(6): p. 636-43.

Connexin 37, 40, and 43 (Cx37, Cx40, Cx43, respectively) are the major gap junction proteins expressed in vascular endothelial cells (7, 32, 34, 39, 45). These proteins are very dynamic, exhibiting rapid turnover times and variable expression patterns. [...]

Although the extent of combinations of different connexins within connexons and channels remains unclear, immunohistochemical and immunocytochemical studies demonstrate differential expression and localization patterns of all three vascular connexins in endothelium, depending on species (44), vascular bed (25, 37, 53), and local hemodynamics (21). In vivo studies implicate Cx40 as the constitutive vascular gap junction protein across species and vascular bed, playing an important role in coupling between cells in the vascular wall (44).


7. Bruzzone R, Haefliger JA, Gimlich RL, and Paul DL. Connexin40, a component of gap junctions in vascular endothelium, is restricted in its ability to interact with other connexins. Mol Biol Cell 4: 7–20, 1993.

21. Gabriels JE and Paul DL. Connexin43 is highly localized to sites of disturbed flow in rat aortic endothelium but connexin37 and connexin40 are more uniformly distributed. Circ Res 83: 636–643, 1998.

25. Hill CE, Rummery N, Hickey H, and Sandow SL. Heterogeneity in the distribution of vascular gap junctions and connexins: implications for function. Clin Exp Pharmacol Physiol 29: 620–625, 2002.

32. Larson DM, Haudenschild CC, and Beyer EC. Gap junction messenger RNA expression by vascular wall cells. Circ Res 66: 1074–1080, 1990.

34. Little TL, Beyer EC, and Duling BR. Connexin 43 and connexin 40 gap junctional proteins are present in arteriolar smooth muscle and endothelium in vivo. Am J Physiol Heart Circ Physiol 268: H729–H739, 1995.

37. Pepper MS, Montesano R, el Aoumari A, Gros D, Orci L, and Meda P. Coupling and connexin 43 expression in microvascular and large vessel endothelial cells. Am J Physiol Cell Physiol 262: C1246–C1257, 1992.

39. Reed KE, Westphale EM, Larson DM, Wang HZ, Veenstra RD, and Beyer EC. Molecular cloning and functional expression of human connexin37, an endothelial cell gap junction protein. J Clin Invest 91: 997–1004, 1993.

44. Van Kempen MJ and Jongsma HJ. Distribution of connexin37, connexin40 and connexin43 in the aorta and coronary artery of several mammals. Histochem Cell Biol 112: 479–486, 1999.

45. Van Rijen H, van Kempen MJ, Analbers LJ, Rook MB, van Ginneken AC, Gros D, and Jongsma HJ. Gap junctions in human umbilical cord endothelial cells contain multiple connexins. Am J Physiol Cell Physiol 272: C117–C130, 1997.

53. Yeh HI, Rothery S, Dupont E, Coppen SR, and Severs NJ. Individual gap junction plaques contain multiple connexins in arterial endothelium. Circ Res 83: 1248–1263, 1998.

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Der Text wird zum zweiten mal verwendet, siehe Fragment 017 10 und Fragment 019 01.


[46.] Haw/Fragment 025 02

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Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.
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[47.] Haw/Fragment 032 03

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The Doppler signal is linearly proportional to perfusion of the upper 200–300 μm of the skin[131]. Tissue perfusion is quantified in regions of interest (ROI) defined in the limbs relative to the contralateral, non-ligated side and can be displayed as color-coded images[132]. Perfusion measurements obtained from ROIs of thighs are confounded by fur, skin pigmentation and motion artifacts from the abdomen and have been shown not to correlate with limb perfusion[132]. We therefore take LDI measurements from the feet, which correlate with other measures of limb perfusion[18, 133].

18. Scholz, D., et al., Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol, 2002. 34(7): p. 775-87.

131. Jakobsson, A. and G.E. Nilsson, Prediction of sampling depth and photon pathlength in laser Doppler flowmetry. Med Biol Eng Comput, 1993. 31(3): p. 301-7.

132. Chalothorn, D., et al., Collateral density, remodeling, and VEGF-A expression differ widely between mouse strains. Physiol Genomics, 2007. 30(2): p. 179-91.

133. Helisch, A., et al., Impact of mouse strain differences in innate hindlimb collateral vasculature. Arterioscler Thromb Vasc Biol, 2006. 26(3): p. 520-6.

The Doppler signal is linearly proportional to perfusion of the upper 200–300 μm of the skin22. Tissue perfusion is quantified in regions of interest (ROI) defined in the limbs relative to the contralateral, non-ligated side and can be displayed as color-coded images23. Perfusion measurements obtained from ROIs of thighs are confounded by fur, skin pigmentation and motion artifacts from the abdomen and have been shown not to correlate with limb perfusion23. We therefore

[Seite 1739]

take LDI measurements from the feet, which correlate with other measures of limb perfusion15,24.


15. Scholz, D. et al. Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J. Mol. Cell. Cardiol. 34, 775–787 (2002).

22. Jakobsson, A. & Nilsson, G.E. Prediction of sampling depth and photon path length in laser Doppler flowmetry. Med. Biol. Eng. Comput. 31, 301–307 (1993).

23. Chalothorn, D., Clayton, J.A., Zhang, H., Pomp, D. & Faber, J.E. Collateral density, remodeling, and VEGF-A expression differ widely between mouse strains. Physiol. Genomics 30, 179–191 (2007).

24. Helisch, A. et al. Impact of mouse strain differences in innate hindlimb collateral vasculature. Arterioscler. Thromb. Vasc. Biol. 26, 520–526 (2006).

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Arteriogenesis (collateral vessel growth) is triggered by fluid shear stress in case of an arterial occlusion. It is an important focus in current cardiovascular research as it might provide new therapeutic opportunities. But the molecular mechanisms underlying arteriogenesis are not yet completely understood. Arteriogenesis (collateral vessel growth) is triggered by fluid shear stress in case of an arterial occlusion. It is an important focus in current cardiovascular research as it might provide new therapeutic opportunities. Although the molecular mechanisms underlying arteriogenesis are not yet completely understood, it has been shown that monocytes/macrophages and lymphocytes, in particular NK- and Tlymphocytes, play an important role in arteriogenesis.
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[49.] Haw/Fragment 044 05

KomplettPlagiat
Untersuchte Arbeit:
Seite: 44, Zeilen: 5-9, 11-16
Quelle: Figueroa and Duling 2009
Seite(n): 249, 260, Zeilen: 249: r. Spalte: 11 ff.; 260: l. Spalte: 25 ff.
Gap junctions play a multifaceted role in the vasculature that is essential in the control of gene expression, vascular development, and vascular function. However, the function of gap junctions in the vasculature does not depend only on the molecular selectivity or permeability of the different vascular connexin isoforms. [...] Although the participation of the gap junction in vascular function seems to be very complex, the development of connexin-knockout animals has been a great contribution to our understanding of how these proteins work in the vasculature.

In addition, connexin-mimetic peptides have been demonstrated to be an effective tool to dissect the participation of gap junctions in vascular function.

Gap junctions play a multifaceted role in the vasculature that is essential in the control of gene expression, vascular development, and vascular function. However, the function of gap junctions in the vasculature does not depend only on the molecular selectivity or permeability of the different vascular connexin isoforms.

[Seite 260]

Although the participation of the gap junction in vascular function seems to be very complex, the development of connexin-knockout animals has been a great contribution to our understanding of how these proteins work in the vasculature. In addition, connexin-mimetic peptides have demonstrated to be an effective tool to dissect the participation of gap junctions in vascular function.

Anmerkungen

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[50.] Haw/Fragment 045 03

Verschleierung
Untersuchte Arbeit:
Seite: 45, Zeilen: 3-7
Quelle: Limbourg et al 2009
Seite(n): 1737, Zeilen: abstract
Surgical ligation of the femoral artery at a specific site triggers arteriogenesis of small, pre-existing collateral arteries into functional conduit vessels proximally and ischemic angiogenesis distally. The vascular response to hind-limb ischemia can be readily evaluated by laser Doppler-based perfusion measurements, histological quantification of arteriogenesis and MicroCT imaging. Surgical ligation of the femoral artery at a specific site triggers arteriogenesis of small, pre-existing collateral arteries into functional conduit vessels proximally and ischemic angiogenesis distally. The vascular response to hind-limb ischemia can be readily evaluated by laser Doppler-based perfusion measurements, histological quantification of arteriogenesis and angiogenesis or whole-mount visualization of arteries in limb muscles.
Anmerkungen

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[51.] Haw/Fragment 045 28

BauernOpfer
Untersuchte Arbeit:
Seite: 45, Zeilen: 28-29
Quelle: Zagorchev et al 2010
Seite(n): 1, Zeilen: l. Spalte: 17 ff.
Studying vascular development or the mechanisms of neovascularisation (angiogenesis, arteriogenesis or vasculogenesis) and evaluating the effects of pro or antiangiogenic [strategies require complete and accurate analysis of the neoformed vascular network.] Studying vascular development or the mechanisms of neovascularisation (angiogenesis, arteriogenesis or vasculogenesis) and evaluating the effects of pro or antiangiogenic strategies require complete and accurate analysis of the neoformed vascular network.
Anmerkungen

Fortsetzung auf der nächsten Seite: Haw/Fragment 046 01


[52.] Haw/Fragment 046 01

BauernOpfer
Untersuchte Arbeit:
Seite: 46, Zeilen: 1-6
Quelle: Zagorchev et al 2010
Seite(n): 1, Zeilen: l. Spalte: 17 ff.
[Studying vascular development or the mechanisms of neovascularisation (angiogenesis, arteriogenesis or vasculogenesis) and evaluating the effects of pro or antiangiogenic] strategies require complete and accurate analysis of the neoformed vascular network. However, methods of assessment, such as histology with confocal or two-photon microscopy, laser Doppler, microangiography, fluorescent microspheres, magnetic resonance angiography, positron emission tomography, are not always precise or quantitative; they focus on a limited area of study, reveal capillary density primarily in 2 dimensions, and represent superficial blood flow[137].

137. Couffinhal, T., et al., Mouse model of angiogenesis. Am J Pathol, 1998. 152(6): p. 1667-79.

Studying vascular development or the mechanisms of neovascularisation (angiogenesis, arteriogenesis or vasculogenesis) and evaluating the effects of pro or antiangiogenic strategies require complete and accurate analysis of the neoformed vascular network. However, methods of assessment, such as histology with confocal or two-photon microscopy, laser Doppler, microangiography, fluorescent microspheres, magnetic resonance angiography, positron emission tomography, are not always precise or quantitative; they focus on a limited area of study, reveal capillary density primarily in 2 dimensions, and represent superficial blood flow (for details see review [1]).

1. Couffinhal T, Dufourcq P, Barandon L, Leroux L, Duplaa C: Mouse models to study angiogenesis in the context of cardiovascular diseases. Front Biosci 2009, 14:3310-3325.

Anmerkungen

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[53.] Haw/Fragment 047 15

KomplettPlagiat
Untersuchte Arbeit:
Seite: 47, Zeilen: 15-23
Quelle: Van Oostrom et al 2008
Seite(n): 1380, 1381, Zeilen: 1380: r. Spalte: 16 ff.; 1381: 1 ff.
Interestingly, Pipp et al.[44], demonstrated the importance of FSS in arteriogenesis by means of a porcine ischemic hindlimb model with extremely high levels of collateral flow and FSS. Normally, during the later phases of arteriogenesis, FSS decreases as the collateral diameter increases so that FSS normalizes. This drop in FSS acts as a signal to arrest proliferation and as a result, prevents further collateral growth before an optimal adaptation is reached. Pipp and colleagues [44] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic factor in collateral growth.

44. Pipp, F., et al., Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hindlimb. Arterioscler Thromb Vasc Biol, 2004. 24(9): p. 1664-8.

Interestingly, Pipp et al. [14] demonstrated the importance of FSS in arteriogenesis by means of a porcine ischemic hindlimb model with extremely high levels of collateral flow and FSS. Normally, during the later phases of arteriogenesis, FSS decreases as the collateral diameter increases so that FSS normalizes. This drop in FSS acts as a signal to arrest proliferation and as a result, prevents further collateral growth before an optimal adaptation

[Seite 1381]

is reached. Pipp and colleagues [14] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further, significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic power in collateral growth.


14. Pipp, F., Boehm, S., Cai, W. J., Adili, F., Ziegler, B., Karanovic, G., Ritter, R., Balzer, J., Scheler, C., Schaper, W., Schmitz-Rixen, T. (2004) Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler. Thromb. Vasc. Biol. 24, 1664–1668.

Anmerkungen

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Ein Teil des Fragments wird hier zum zweiten Mal verwendet: Fragment 006 21.


[54.] Haw/Fragment 049 03

KomplettPlagiat
Untersuchte Arbeit:
Seite: 49, Zeilen: 3-5
Quelle: Limbourg et al 2009
Seite(n): 1737, Zeilen: l. Spalte: 2ff
Cardiovascular diseases are the number one cause of death globally[104]. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.

104. Murray, C.J. and A.D. Lopez, Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet, 1997. 349(9063): p. 1436-42.

Cardiovascular diseases are the number one cause of death globally1. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.

1. World Health Organization. in Fact sheet No. 317 Feb. 2007 (World Health Organization, 2007) (http://www.who.int/mediacentre/factsheets/fs317/en/index.html).

Anmerkungen

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[55.] Haw/Fragment 050 03

KomplettPlagiat
Untersuchte Arbeit:
Seite: 50, Zeilen: 3-6
Quelle: Figueroa and Duling 2009
Seite(n): 260, Zeilen: l. Spalte: 25 ff.
Although the participation of the gap junction in vascular function seems to be very complex, the development of connexin-knockout animals has been a great contribution to our understanding of how these proteins work in the vasculature. Although the participation of the gap junction in vascular function seems to be very complex, the development of connexin- knockout animals has been a great contribution to our understanding of how these proteins work in the vasculature.
Anmerkungen

Ein Verweis auf die Quelle fehlt.

Die Passage wurde schon zuvor verwendet: Fragment 044 05.


[56.] Haw/Fragment 055 02

Verschleierung
Untersuchte Arbeit:
Seite: 55, Zeilen: 2-5
Quelle: Willems 2009
Seite(n): 3, Zeilen: 1 ff.
Arteriogenesis (collateral vessel growth) is triggered by fluid shear stress in case of an arterial occlusion. It is an important focus in current cardiovascular research as it might provide new therapeutic opportunities. But the molecular mechanisms underlying arteriogenesis are not yet completely understood. Arteriogenesis (collateral vessel growth) is triggered by fluid shear stress in case of an arterial occlusion. It is an important focus in current cardiovascular research as it might provide new therapeutic opportunities. Although the molecular mechanisms underlying arteriogenesis are not yet completely understood, it has been shown that monocytes/macrophages and lymphocytes, in particular NK- and Tlymphocytes, play an important role in arteriogenesis.
Anmerkungen

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Diese Passage wurde schon zuvor benutzt: Fragment 044 02.


[57.] Haw/Fragment 055 27

Verschleierung
Untersuchte Arbeit:
Seite: 55, Zeilen: 27-29
Quelle: Van Oostrom et al 2008
Seite(n): 1379, Zeilen: l. Spalte: 30 ff.
Cardiovascular diseases are the number one cause of death globally[104]. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients [who do not benefit from these treatment options.]

104. Murray, C.J. and A.D. Lopez, Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet, 1997. 349(9063): p. 1436-42.

In fact, cardiovascular disorders are currently the leading cause of death globally [1]. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients who do not benefit from these treatment options.

1. World Health Organization (February 2007) Factsheet 317.

Anmerkungen

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Dieser Abschnitt wird hier das zweite Mal verwertet, siehe Fragment 001 04.


[58.] Haw/Fragment 056 01

KomplettPlagiat
Untersuchte Arbeit:
Seite: 56, Zeilen: 1 ff. (komplett)
Quelle: Van Oostrom et al 2008
Seite(n): 1387, Zeilen: l. Spalte: 22 ff.
Identification of markers of collateral growth could help in determining patient prognosis and predicting therapy response and maybe even lead to new, proarteriogenic therapies. Development of preclinical animal models is needed to test these methods, as extreme caution needs to be taken when extrapolating research in mice to the clinical setting. This will also enable further investigation of mechanisms, e.g., signaling molecules involved in collateral artery growth, extending our knowledge, and possibilities in therapeutic application. Future research will therefore involve investigation of the mechanisms behind the individual response to arteriogenesis. Identification of markers of collateral growth could help in determining patient prognosis and predicting therapy response and maybe even lead to new, proarteriogenic therapies.

[...] Development of preclinical animal models (preferably large animal models such as pigs) is needed to test these methods, as extreme caution needs to be taken when extrapolating research in mice to the clinical setting. This will also enable further investigation of mechanisms, e.g., signaling molecules involved in collateral artery growth, extending our knowledge, and possibilities in therapeutic application.

Future research will therefore involve investigation of the mechanisms behind the individual response to arteriogenesis and its relation to growth factor and cell therapy for the development of novel, therapeutic strategies.

Anmerkungen

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Quellen

[1.] Quelle:Haw/Wikipedia Connexin 2010

Titel    Connexin
Verlag    (Wikipedia)
Datum    17. Dezember 2010
URL    http://en.wikipedia.org/w/index.php?title=Connexin&oldid=402804638

Literaturverz.   

nein
Fußnoten    nein


[2.] Quelle:Haw/Ebong et al 2006

Autor     Eno Essien Ebong, Sanghee Kim, Natacha DePaola
Titel    Flow regulates intercellular communication in HAEC by assembling functional Cx40 and Cx37 gap junctional channels
Zeitschrift    American Journal of Physiology - Heart and Circulatory Physiology
Ausgabe    290
Jahr    2006
Seiten    H2015–H2023
DOI    :10.1152/ajpheart.00204.2005
URL    http://ajpheart.physiology.org/content/ajpheart/290/5/H2015.full.pdf

Literaturverz.   

ja
Fußnoten    ja


[3.] Quelle:Haw/Van Oostrom et al 2008

Autor     Melany C. van Oostrom, Olivia van Oostrom, Paul H. A. Quax, Marianne C. Verhaar, Imo E. Hoefer
Titel    Insights into mechanisms behind arteriogenesis: what does the future hold?
Zeitschrift    Journal of Leukocyte Biology
Ausgabe    84
Datum    December 2008
Seiten    1379-1391
DOI    10.1189/jlb.0508281
URL    http://www.jleukbio.org/content/84/6/1379.full.pdf

Literaturverz.   

ja
Fußnoten    ja


[4.] Quelle:Haw/Figueroa and Duling 2009

Autor     Xavier F. Figueroa, Brian R. Duling
Titel    Gap Junctions in the Control of Vascular Function
Zeitschrift    Antioxidants & Redox Signalling
Ausgabe    11
Jahr    2009
Nummer    2
DOI    10.1089/ars.2008.2117
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2933153/pdf/ars.2008.2117.pdf

Literaturverz.   

nein
Fußnoten    nein


[5.] Quelle:Haw/Zagorchev et al 2010

Autor     Lyubomir Zagorchev, Pierre Oses, Zhen W Zhuang, Karen Moodie, Mary Jo Mulligan-Kehoe, Michael Simons, Thierry Couffinhal
Titel    Micro computed tomography for vascular exploration
Zeitschrift    Journal of Angiogenesis Research
Ausgabe    2
Jahr    2010
Nummer    7
URL    http://www.vascularcell.com/content/pdf/2040-2384-2-7.pdf

Literaturverz.   

ja
Fußnoten    ja


[6.] Quelle:Haw/Willems 2009

Autor     Sanne Willem
Titel    The potential role of monocytelymphocyte interaction in arteriogenesis
Ort    Utrecht
Jahr    2009
Anmerkung    Master Thesis (December 08-January 09) At the division of Heart and Lungs, Group of Experimental Cardiology Master Biology of Disease Utrecht University
URL    http://dspace.library.uu.nl/handle/1874/32027

Literaturverz.   

nein
Fußnoten    nein


[7.] Quelle:Haw/Limbourg et al 2009

Autor     Anne Limbourg, Thomas Korff, L Christian Napp, Wolfgang Schaper, Helmut Drexler, Florian P Limbourg
Titel    Evaluation of postnatal arteriogenesis and angiogenesis in a mouse model of hind-limb ischemia
Zeitschrift    Nature Protocols
Ausgabe    4
Jahr    2009
Seiten    1737-1748
URL    http://www.nature.com/nprot/journal/v4/n12/full/nprot.2009.185.html

Literaturverz.   

nein
Fußnoten    nein


[8.] Quelle:Haw/Schaper and Scholz 2003

Autor     Wolfgang Schaper, Dimitri Scholz
Titel    Factors Regulating Arteriogenesis
Zeitschrift    Arteriosclerosis, Thrombosis, and Vascular Biology
Herausgeber    American Heart Association
Ausgabe    23
Jahr    2003
Seiten    1143-1151
ISSN    1524-4636
DOI    10.1161/01.ATV.0000069625.11230.96
URL    http://atvb.ahajournals.org/content/23/7/1143.full.pdf

Literaturverz.   

ja
Fußnoten    ja


[9.] Quelle:Haw/Heil and Schaper 2004

Autor     Matthias Heil, Wolfgang Schaper
Titel    Influence of Mechanical, Cellular, and Molecular Factors on Collateral Artery Growth (Arteriogenesis)
Zeitschrift    Circulation Research
Ausgabe    95
Jahr    2004
Seiten    449-458
ISSN    1524-4571
DOI    10.1161/01.RES.0000141145.78900.44
URL    http://circres.ahajournals.org/content/95/5/449.full.pdf

Literaturverz.   

ja
Fußnoten    ja


[10.] Quelle:Haw/Buschmann and Schaper 1999

Autor     I. Buschmann, W. Schaper
Titel    Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth
Zeitschrift    News in physiological sciences
Ausgabe    14
Datum    June 1999
Seiten    121-125
URL    http://physiologyonline.physiology.org/content/nips/14/3/121.full.pdf

Literaturverz.   

ja
Fußnoten    ja


[11.] Quelle:Haw/Moor instruments 2006

Titel    Basic Theory and Operating Principles of Laser Doppler Blood Flow Monitoring and Imaging (LDF & LDI), Issue 1.
Herausgeber    Moor instruments
Jahr    2006
Anmerkung    Datierung über PDF File Properties
URL    http://www.moor.co.uk/ckfinder/userfiles/files/Moor_Laser_doppler_theory_Issue_1.pdf

Literaturverz.   

nein
Fußnoten    ja


[12.] Quelle:Haw/Dbouk et al 2009

Autor     Hashem A Dbouk, Rana M Mroue, Marwan E El-Sabban, Rabih S Talhouk
Titel    Connexins: a myriad of functions extending beyond assembly of gap junction channels
Zeitschrift    Cell Communication and Signaling
Ausgabe    7
Jahr    2009
Nummer    4
DOI    10.1186/1478-811X-7-4
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2660342/pdf/1478-811X-7-4.pdf

Literaturverz.   

ja
Fußnoten    ja


[13.] Quelle:Haw/Schaper 2009

Autor     Wolfgang Schaper
Titel    Collateral circulation Past and present
Zeitschrift    Basic Research in Cardiology
Verlag    Springer
Ausgabe    104
Jahr    2009
Seiten    5-21
DOI    10.1007/s00395-008-0760-x
URL    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2755790/pdf/395_2008_Article_760.pdf

Literaturverz.   

ja
Fußnoten    ja