The Experts below are selected from a list of 209094 Experts worldwide ranked by ideXlab platform
Jeanmarc Triscone - One of the best experts on this subject based on the ideXlab platform.
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influence of the Growth conditions on the laaio3 srtio3 interface electronic properties
EPL, 2010Co-Authors: Claudia Cancellieri, N Reyren, Stefano Gariglio, A D Caviglia, Alexandre Fete, Jeanmarc TrisconeAbstract:The effects of oxygen Pressure during the Growth of LaAlO3 on (001) SrTiO3, and of post-deposition annealing were investigated. While little influence on the structure was observed, the transport properties were found to depend on both Growth Pressure and annealing. For LaAlO3 layer thicknesses between 5 and 10 unit cells and Growth Pressures between 10− 4 and 10−2 mbar, the LaAlO3/SrTiO3 interfaces displayed similar metallic behavior with a sharp transition to a superconducting state. At an oxygen Pressure of 10− 6 mbar oxygen vacancies were clearly introduced and extended deep into the SrTiO3 crystal. These vacancies could be removed by post-deposition annealing in 0.2 bar of O2 at ~530 °C. At a Growth Pressure of 10− 4 mbar, the electronic properties of samples with ultra-thin LaAlO3 layers (2 to 3 unit cells thick) were found to depend markedly on the post-annealing step.
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Influence of the Growth conditions on the LaAIO3/SrTiO3 interface electronic properties
EPL (Europhysics Letters), 2010Co-Authors: Claudia Cancellieri, N Reyren, Stefano Gariglio, A D Caviglia, Alexandre Fete, Jeanmarc TrisconeAbstract:The effects of oxygen Pressure during the Growth of LaAlO3 on (001) SrTiO3, and of post-deposition annealing were investigated. While little influence on the structure was observed, the transport properties were found to depend on both Growth Pressure and annealing. For LaAlO3 layer thicknesses between 5 and 10 unit cells and Growth Pressures between 10− 4 and 10−2 mbar, the LaAlO3/SrTiO3 interfaces displayed similar metallic behavior with a sharp transition to a superconducting state. At an oxygen Pressure of 10− 6 mbar oxygen vacancies were clearly introduced and extended deep into the SrTiO3 crystal. These vacancies could be removed by post-deposition annealing in 0.2 bar of O2 at ~530 °C. At a Growth Pressure of 10− 4 mbar, the electronic properties of samples with ultra-thin LaAlO3 layers (2 to 3 unit cells thick) were found to depend markedly on the post-annealing step.
Audrey Claperon - One of the best experts on this subject based on the ideXlab platform.
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Mechanical induction of the tumorigenic b-catenin pathway by tumour Growth Pressure
Nature, 2015Co-Authors: Maria Elena Fernandez-sanchez, Elena María, Sandrine Barbier, Joanne Whitehead, Gaelle Bealle, Aude Michel, Heldmuth Latorre-ossa, Colette Rey, Laura Fouassier, Audrey ClaperonAbstract:The tumour microenvironment may contribute to tumorigenesis owing to mechanical forces such as fibrotic stiffness or mechanical Pressure caused by the expansion of hyper-proliferative cells 1,2. Here we explore the contribution of the mechanical Pressure exerted by tumour Growth onto non-tumorous adjacent epithe-lium. In the early stage of mouse colon tumour development in the Notch 1 Apc 1/1638N mouse model, we observed mechanistic Pressure stress in the non-tumorous epithelial cells caused by hyper-proliferative adjacent crypts overexpressing active Notch, which is associated with increased Ret and b-catenin signalling. We thus developed a method that allows the delivery of a defined mechanical Pressure in vivo, by subcutaneously inserting a magnet close to the mouse colon. The implanted magnet generated a magnetic force on ultra-magnetic liposomes, stabilized in the mesench-ymal cells of the connective tissue surrounding colonic crypts after intravenous injection. The magnetically induced Pressure quantitatively mimicked the endogenous early tumour Growth stress in the order of 1,200 Pa, without affecting tissue stiffness, as monitored by ultrasound strain imaging and shear wave elastography. The exertion of Pressure mimicking that of tumour Growth led to rapid Ret activation and downstream phosphorylation of b-catenin on Tyr654, imparing its interaction with the E-cadherin in adhe-rens junctions, and which was followed by b-catenin nuclear trans-location after 15 days. As a consequence, increased expression of b-catenin-target genes was observed at 1 month, together with crypt enlargement accompanying the formation of early tumorous aberrant crypt foci. Mechanical activation of the tumorigenic b-catenin pathway suggests unexplored modes of tumour propagation based on mechanical signalling pathways in healthy epithelial cells surrounding the tumour, which may contribute to tumour heterogeneity. To test the tumorous impact of early tumour Growth Pressure on non-tumorous epithelial tissues in vivo, apart from the mechanical stiffness characteristic of the microenvironment of late tumours 1-6
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Mechanical induction of the tumorigenic β-catenin pathway by tumour Growth Pressure
Nature, 2015Co-Authors: Maria Elena Fernandez-sanchez, Sandrine Barbier, Joanne Whitehead, Gaelle Bealle, Aude Michel, Heldmuth Latorre-ossa, Colette Rey, Laura Fouassier, Audrey Claperon, Laura BrulleAbstract:The tumour microenvironment may contribute to tumorigenesis owing to mechanical forces such as fibrotic stiffness or mechanical Pressure caused by the expansion of hyper-proliferative cells. Here we explore the contribution of the mechanical Pressure exerted by tumour Growth onto non-tumorous adjacent epithelium. In the early stage of mouse colon tumour development in the Notch(+)Apc(+/1638N) mouse model, we observed mechanistic Pressure stress in the non-tumorous epithelial cells caused by hyper-proliferative adjacent crypts overexpressing active Notch, which is associated with increased Ret and β-catenin signalling. We thus developed a method that allows the delivery of a defined mechanical Pressure in vivo, by subcutaneously inserting a magnet close to the mouse colon. The implanted magnet generated a magnetic force on ultra-magnetic liposomes, stabilized in the mesenchymal cells of the connective tissue surrounding colonic crypts after intravenous injection. The magnetically induced Pressure quantitatively mimicked the endogenous early tumour Growth stress in the order of 1,200 Pa, without affecting tissue stiffness, as monitored by ultrasound strain imaging and shear wave elastography. The exertion of Pressure mimicking that of tumour Growth led to rapid Ret activation and downstream phosphorylation of β-catenin on Tyr654, imparing its interaction with the E-cadherin in adherens junctions, and which was followed by β-catenin nuclear translocation after 15 days. As a consequence, increased expression of β-catenin-target genes was observed at 1 month, together with crypt enlargement accompanying the formation of early tumorous aberrant crypt foci. Mechanical activation of the tumorigenic β-catenin pathway suggests unexplored modes of tumour propagation based on mechanical signalling pathways in healthy epithelial cells surrounding the tumour, which may contribute to tumour heterogeneity.
Maria Elena Fernandez-sanchez - One of the best experts on this subject based on the ideXlab platform.
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Mechanical induction of the tumorigenic b-catenin pathway by tumour Growth Pressure
Nature, 2015Co-Authors: Maria Elena Fernandez-sanchez, Elena María, Sandrine Barbier, Joanne Whitehead, Gaelle Bealle, Aude Michel, Heldmuth Latorre-ossa, Colette Rey, Laura Fouassier, Audrey ClaperonAbstract:The tumour microenvironment may contribute to tumorigenesis owing to mechanical forces such as fibrotic stiffness or mechanical Pressure caused by the expansion of hyper-proliferative cells 1,2. Here we explore the contribution of the mechanical Pressure exerted by tumour Growth onto non-tumorous adjacent epithe-lium. In the early stage of mouse colon tumour development in the Notch 1 Apc 1/1638N mouse model, we observed mechanistic Pressure stress in the non-tumorous epithelial cells caused by hyper-proliferative adjacent crypts overexpressing active Notch, which is associated with increased Ret and b-catenin signalling. We thus developed a method that allows the delivery of a defined mechanical Pressure in vivo, by subcutaneously inserting a magnet close to the mouse colon. The implanted magnet generated a magnetic force on ultra-magnetic liposomes, stabilized in the mesench-ymal cells of the connective tissue surrounding colonic crypts after intravenous injection. The magnetically induced Pressure quantitatively mimicked the endogenous early tumour Growth stress in the order of 1,200 Pa, without affecting tissue stiffness, as monitored by ultrasound strain imaging and shear wave elastography. The exertion of Pressure mimicking that of tumour Growth led to rapid Ret activation and downstream phosphorylation of b-catenin on Tyr654, imparing its interaction with the E-cadherin in adhe-rens junctions, and which was followed by b-catenin nuclear trans-location after 15 days. As a consequence, increased expression of b-catenin-target genes was observed at 1 month, together with crypt enlargement accompanying the formation of early tumorous aberrant crypt foci. Mechanical activation of the tumorigenic b-catenin pathway suggests unexplored modes of tumour propagation based on mechanical signalling pathways in healthy epithelial cells surrounding the tumour, which may contribute to tumour heterogeneity. To test the tumorous impact of early tumour Growth Pressure on non-tumorous epithelial tissues in vivo, apart from the mechanical stiffness characteristic of the microenvironment of late tumours 1-6
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Mechanical induction of the tumorigenic β-catenin pathway by tumour Growth Pressure
Nature, 2015Co-Authors: Maria Elena Fernandez-sanchez, Sandrine Barbier, Joanne Whitehead, Gaelle Bealle, Aude Michel, Heldmuth Latorre-ossa, Colette Rey, Laura Fouassier, Audrey Claperon, Laura BrulleAbstract:The tumour microenvironment may contribute to tumorigenesis owing to mechanical forces such as fibrotic stiffness or mechanical Pressure caused by the expansion of hyper-proliferative cells. Here we explore the contribution of the mechanical Pressure exerted by tumour Growth onto non-tumorous adjacent epithelium. In the early stage of mouse colon tumour development in the Notch(+)Apc(+/1638N) mouse model, we observed mechanistic Pressure stress in the non-tumorous epithelial cells caused by hyper-proliferative adjacent crypts overexpressing active Notch, which is associated with increased Ret and β-catenin signalling. We thus developed a method that allows the delivery of a defined mechanical Pressure in vivo, by subcutaneously inserting a magnet close to the mouse colon. The implanted magnet generated a magnetic force on ultra-magnetic liposomes, stabilized in the mesenchymal cells of the connective tissue surrounding colonic crypts after intravenous injection. The magnetically induced Pressure quantitatively mimicked the endogenous early tumour Growth stress in the order of 1,200 Pa, without affecting tissue stiffness, as monitored by ultrasound strain imaging and shear wave elastography. The exertion of Pressure mimicking that of tumour Growth led to rapid Ret activation and downstream phosphorylation of β-catenin on Tyr654, imparing its interaction with the E-cadherin in adherens junctions, and which was followed by β-catenin nuclear translocation after 15 days. As a consequence, increased expression of β-catenin-target genes was observed at 1 month, together with crypt enlargement accompanying the formation of early tumorous aberrant crypt foci. Mechanical activation of the tumorigenic β-catenin pathway suggests unexplored modes of tumour propagation based on mechanical signalling pathways in healthy epithelial cells surrounding the tumour, which may contribute to tumour heterogeneity.
Annemiek J.m. Cornelissen - One of the best experts on this subject based on the ideXlab platform.
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Tissue Growth Pressure drives early blood flow in the chicken yolk sac
Developmental Dynamics, 2017Co-Authors: Raphaël Clément, Benjamin Mauroy, Annemiek J.m. CornelissenAbstract:BACKGROUND: Understanding how molecular and physical cues orchestrate vascular morphogenesis is a challenge for developmental biology. Only little attention has been paid to the impact of mechanical stress caused by tissue Growth on early blood distribution. Here we study the peripheral accumulation of blood in the chicken embryonic yolk sac, which precedes sinus vein formation. RESULTS: We report that blood accumulation starts before heart-induced blood circulation. We hypothesized that the driving force for the primitive blood flow is a Growth-induced gradient of tissue Pressure in the yolk sac mesoderm. Therefore, we studied embryos in which heart development was arrested after 2 days of incubation, and found that yolk sac Growth and blood peripheral accumulation still occurred. This suggests that tissue Growth is sufficient to initiate the flow and the formation of the sinus vein, whereas heart contractions are not required. We designed a simple mathematical model which makes explicit the Growth-induced Pressure gradient and the subsequent blood accumulation, and show that Growth can indeed account for the observed blood accumulation. CONCLUSIONS: This study shows that tissue Growth Pressure can drive early blood flow, and suggests that the mechanical environment, beyond hemodynamics, can contribute to vascular morphogenesis. Developmental Dynamics 246:573-584, 2017. © 2017 Wiley Periodicals, Inc.
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Tissue Growth Pressure drives early blood flow in the chicken yolk sac.
Developmental dynamics : an official publication of the American Association of Anatomists, 2017Co-Authors: Raphaël Clément, Benjamin Mauroy, Annemiek J.m. CornelissenAbstract:Background - Understanding how molecular and physical cues orchestrate vascular morphogenesis is a challenge for developmental biology. Only little attention has been paid to the impact of mechanical stress caused by tissue Growth on early blood distribution. Here we study the peripheral accumulation of blood in the chicken embryonic yolk sac, which precedes sinus vein formation. Results - We report that blood accumulation starts prior to heart-induced blood circulation. We hypothesized that the driving force for the primitive blood flow is a Growth-induced gradient of tissue Pressure in the yolk sac mesoderm. Therefore, we studied embryos in which heart development was arrested after two days of incubation, and found that yolk sac Growth and blood peripheral accumulation still occurred. This suggests that tissue Growth is sufficient to initiate the flow and the formation of the sinus vein, whereas heart contractions are not required. We designed a simple mathematical model which makes explicit the Growth-induced Pressure gradient and the subsequent blood accumulation, and show that Growth can indeed account for the observed blood accumulation. Conclusions - This study shows that tissue Growth Pressure can drive early blood flow, and suggests that the mechanical environment, beyond hemodynamics, can contribute to vascular morphogenesis. This article is protected by copyright. All rights reserved.
Claudia Cancellieri - One of the best experts on this subject based on the ideXlab platform.
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influence of the Growth conditions on the laaio3 srtio3 interface electronic properties
EPL, 2010Co-Authors: Claudia Cancellieri, N Reyren, Stefano Gariglio, A D Caviglia, Alexandre Fete, Jeanmarc TrisconeAbstract:The effects of oxygen Pressure during the Growth of LaAlO3 on (001) SrTiO3, and of post-deposition annealing were investigated. While little influence on the structure was observed, the transport properties were found to depend on both Growth Pressure and annealing. For LaAlO3 layer thicknesses between 5 and 10 unit cells and Growth Pressures between 10− 4 and 10−2 mbar, the LaAlO3/SrTiO3 interfaces displayed similar metallic behavior with a sharp transition to a superconducting state. At an oxygen Pressure of 10− 6 mbar oxygen vacancies were clearly introduced and extended deep into the SrTiO3 crystal. These vacancies could be removed by post-deposition annealing in 0.2 bar of O2 at ~530 °C. At a Growth Pressure of 10− 4 mbar, the electronic properties of samples with ultra-thin LaAlO3 layers (2 to 3 unit cells thick) were found to depend markedly on the post-annealing step.
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Influence of the Growth conditions on the LaAIO3/SrTiO3 interface electronic properties
EPL (Europhysics Letters), 2010Co-Authors: Claudia Cancellieri, N Reyren, Stefano Gariglio, A D Caviglia, Alexandre Fete, Jeanmarc TrisconeAbstract:The effects of oxygen Pressure during the Growth of LaAlO3 on (001) SrTiO3, and of post-deposition annealing were investigated. While little influence on the structure was observed, the transport properties were found to depend on both Growth Pressure and annealing. For LaAlO3 layer thicknesses between 5 and 10 unit cells and Growth Pressures between 10− 4 and 10−2 mbar, the LaAlO3/SrTiO3 interfaces displayed similar metallic behavior with a sharp transition to a superconducting state. At an oxygen Pressure of 10− 6 mbar oxygen vacancies were clearly introduced and extended deep into the SrTiO3 crystal. These vacancies could be removed by post-deposition annealing in 0.2 bar of O2 at ~530 °C. At a Growth Pressure of 10− 4 mbar, the electronic properties of samples with ultra-thin LaAlO3 layers (2 to 3 unit cells thick) were found to depend markedly on the post-annealing step.
