Sprache: Englisch
Verlag: LAP LAMBERT Academic Publishing Feb 2012, 2012
ISBN 10: 3847341529 ISBN 13: 9783847341529
Anbieter: BuchWeltWeit Ludwig Meier e.K., Bergisch Gladbach, Deutschland
Taschenbuch. Zustand: Neu. Neuware -When compared to MTA cells, MTB-01 cells were susceptible to risedronateinduced apoptosis, had decreased ability to bind to risedronate-treated bone, and did not produce MMP-2 or MMP-9 proteases. MTA cells were less susceptible to risedronateinduced apoptosis and produced MMP-2. Additionally, adhesion of MTA cells to bone matrix was not diminished by risedronate treatment. Our results suggest that the nonresponsive nature of the MTA cell line may be due to MMP-2 production (possibly allowing ongoing destruction of risedronate-treated bone), continued adhesion to risedronate-treated bone matrix, and decreased susceptibility to risedronate-induced apoptosis. 128 pp. Englisch.
Sprache: Englisch
Verlag: LAP LAMBERT Academic Publishing, 2012
ISBN 10: 3847341529 ISBN 13: 9783847341529
Anbieter: preigu, Osnabrück, Deutschland
Taschenbuch. Zustand: Neu. Risedronate Effects on Bone Metastasis of Rat Mammary Tumor Cell Lines | Comparison of Effects of Risedronate on Bone Metastasis of Two Malignant Rat Mammary Tumor Cell Lines, MTA & MTB-01 | Kelli Boyd (u. a.) | Taschenbuch | 128 S. | Englisch | 2012 | LAP LAMBERT Academic Publishing | EAN 9783847341529 | Verantwortliche Person für die EU: preigu GmbH & Co. KG, Lengericher Landstr. 19, 49078 Osnabrück, mail[at]preigu[dot]de | Anbieter: preigu.
Sprache: Englisch
Verlag: LAP LAMBERT Academic Publishing, 2012
ISBN 10: 3847341529 ISBN 13: 9783847341529
Anbieter: Mispah books, Redhill, SURRE, Vereinigtes Königreich
EUR 138,46
Anzahl: 1 verfügbar
In den WarenkorbPaperback. Zustand: Like New. LIKE NEW. SHIPS FROM MULTIPLE LOCATIONS. book.
Sprache: Englisch
Verlag: LAP LAMBERT Academic Publishing, 2012
ISBN 10: 3847341529 ISBN 13: 9783847341529
Anbieter: moluna, Greven, Deutschland
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In den WarenkorbZustand: New. Dieser Artikel ist ein Print on Demand Artikel und wird nach Ihrer Bestellung fuer Sie gedruckt. Autor/Autorin: Boyd KelliDr. Boyd received her undergraduate and DVM degrees from Mississippi State University. She completed a residency and PhD program at the University of Georgia. Her expertise is in comparative pathology with a special intere.
Sprache: Englisch
Verlag: LAP LAMBERT Academic Publishing Feb 2012, 2012
ISBN 10: 3847341529 ISBN 13: 9783847341529
Anbieter: buchversandmimpf2000, Emtmannsberg, BAYE, Deutschland
Taschenbuch. Zustand: Neu. This item is printed on demand - Print on Demand Titel. Neuware -When compared to MTA cells, MTB-01 cells were susceptible to risedronateinduced apoptosis, had decreased ability to bind to risedronate-treated bone, and did not produce MMP-2 or MMP-9 proteases. MTA cells were less susceptible to risedronateinduced apoptosis and produced MMP-2. Additionally, adhesion of MTA cells to bone matrix was not diminished by risedronate treatment. Our results suggest that the nonresponsive nature of the MTA cell line may be due to MMP-2 production (possibly allowing ongoing destruction of risedronate-treated bone), continued adhesion to risedronate-treated bone matrix, and decreased susceptibility to risedronate-induced apoptosis.VDM Verlag, Dudweiler Landstraße 99, 66123 Saarbrücken 128 pp. Englisch.
Sprache: Englisch
Verlag: LAP LAMBERT Academic Publishing, 2012
ISBN 10: 3847341529 ISBN 13: 9783847341529
Anbieter: AHA-BUCH GmbH, Einbeck, Deutschland
Taschenbuch. Zustand: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - When compared to MTA cells, MTB-01 cells were susceptible to risedronateinduced apoptosis, had decreased ability to bind to risedronate-treated bone, and did not produce MMP-2 or MMP-9 proteases. MTA cells were less susceptible to risedronateinduced apoptosis and produced MMP-2. Additionally, adhesion of MTA cells to bone matrix was not diminished by risedronate treatment. Our results suggest that the nonresponsive nature of the MTA cell line may be due to MMP-2 production (possibly allowing ongoing destruction of risedronate-treated bone), continued adhesion to risedronate-treated bone matrix, and decreased susceptibility to risedronate-induced apoptosis.