Browsing by Author "Sanhueza, C."

Now showing 1 - 16 of 16
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    Cross Talk between Adipose Tissue and Placenta in Obese and Gestational Diabetes Mellitus Pregnancies via Exosomes
    (2017) Jayabalan, N.; Nair, S.; Nuzhat, Z.; Rice, G.; Zúñiga, F.; Sobrevía Luarte, Luis Alberto; Leiva Mendoza, Andrea Alejandra; Sanhueza, C.; Gutiérrez, J.; Lappas, M.; Freeman, D.; Salomon, C.
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    Cross-sectional and longitudinal lipid determination studies in pregnant women reveal an association between increased maternal LDL cholesterol concentrations and reduced human umbilical vein relaxation
    (2015) Leiva Mendoza, Andrea Alejandra; Salsoso Rodríguez, M. Rocío; Saez, T.; Sanhueza, C.; Pardo, F.; Sobrevía Luarte, Luis Alberto
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    Effect of aparent cohesion from tree roots on the stability of natural slopes of Renaca dunes
    (PONTIFICIA UNIV CATOLICA CHILE, ESCUELA CONSTRUCCION CIVIL, 2012) Sanhueza, C.; Villavicencio, G.
    Several researches have shown that vegetation plays a key roll in preventing displacements of soil masses, particularly of surficial displacement of slopes. Thus, tree roots provide a reinforcement system that depends on its structure and distribution.
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    "Evaluation of the geotechnical behavior of Chilean volcanic soils as filter material for domestic water treatment"
    (PONTIFICIA UNIV CATOLICA CHILE, ESCUELA CONSTRUCCION CIVIL, 2011) Sanhueza, C.; Palma, J.; Valenzuela, P.; Araneda, O.; Calderon, K.
    Investigations carried out at Chile have determined that certain soils placed over the years as a product of the volcanic activity can be suitable for use as filter material in domestic wastewater purification. These soils have been studied by Universidad de Chile researchers, who have defined the main characteristics of the most important Chilean volcanic soils and, according to the properties studied (such as porosity, surface area and density, among others) have alleged that these materials exhibit water filter behaviour. As results of this research, first of all, the existing geotechnical information on Chilean volcanic soils has been complemented, such as hydraulic conductivity and, has been evaluating the influence design parameters, such as thickness of volcanic soil layers and the application rate of wastewater, in the purification of domestic wastewater.
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    Fetoplacental endothelial dysfunction in maternal hypercholesterolemia and obesity in pregnancy
    (2014) Pardo, F.; Silva Lagos, Luis Alfredo; Salsoso Rodríguez, M. Rocío; Saez, T.; Farías Jofré, Marcelo Enrique; Villalobos Labra, Roberto Esteban; Leiva Mendoza, Andrea Alejandra; Sanhueza, C.; Sobrevía Luarte, Luis Alberto
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    Human supraphysiological gestational weight gain and fetoplacental vascular dysfunction
    (2015) Pardo, F.; Silva, L.; Sáez, T.; Salsoso Rodríguez, M. Rocío; Gutiérrez, J.; Sanhueza, C.; Leiva Mendoza, Andrea Alejandra; Sobrevía Luarte, Luis Alberto
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    Insulin restores L-arginine transport requiring adenosine receptors activation in umbilical vein endothelium from late-onset preeclampsia
    (2015) Salsoso Rodríguez, M. Rocío; Guzman, E.; Saez, T.; Bugueno, K.; Ramirez, M.; Farías Jofré, Marcelo Enrique; Pardo, F.; Leiva Mendoza, Andrea Alejandra; Sanhueza, C.; Mate, A.; Vazquez, C.; Sobrevía Luarte, Luis Alberto
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    Insulin Reverses D-Glucose-Increased Nitric Oxide and Reactive Oxygen Species Generation in Human Umbilical Vein Endothelial Cells
    (2015) Gonzalez, M.; Rojas, S.; Avila. P.; Cabrera, L.; Villalobos Labra, Roberto Esteban; Palma, C.; Aguayo, C.; Pena, E.; Salsoso Rodríguez, M. Rocío; Leiva Mendoza, Andrea Alejandra; Sobrevía Luarte, Luis Alberto; Gallardo, V.; Guzman-Gutierrez, E.; Saez, T.; Sanhueza, C.; Pardo, F.
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    Insulin therapy and fetoplacental vascular function in gestational diabetes mellitus
    (2015) Sobrevía Luarte, Luis Alberto; Salsoso Rodríguez, M. Rocío; Saez, T.; Pardo, F.; Leiva Mendoza, Andrea Alejandra; Sanhueza, C.
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    Intracellular acidification increases adenosine transport in human umbilical vein endothelial cells
    (2017) Celis, N.; Araos, J.; Sanhueza, C.; Toledo, F.; Beltran, A.; Pardo, F.; Leiva Mendoza, Andrea Alejandra; Ramirez, M.; Sobrevía Luarte, Luis Alberto
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    Leptin promotes a more aggressive behavior of ovarian cancer cells : a potential explanation for a worse prognosis in obese ovarian cancer patients
    (2015) Cuello F., Mauricio; Kato Cardemil, Sumie Rode; Abarzúa Catalán, L.; Delpiano, A.; García, K.; Sanhueza, C.; Ibáñez Cáceres, Carolina; Brañes Yunusic, Jorge Antonio; Castellón E.; Owen, Gareth Ivor; Trigo, C.
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    Modulation of Intracellular pH in Human Ovarian Cancer
    (2016) Sanhueza, C.; Araos, J.; Naranjo, L.; Villalobos Labra, Roberto Esteban; Westermeier, F.; Salomon, C.; Beltran, A.; Ramirez, M.; Gutierrez, J.; Pardo, F.; Leiva, A.; Sobrevía Luarte, Luis Alberto
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    Nitric oxide and pH modulation in gynaecological cancer
    (2016) Naranjo, L.; Sanhueza, C.; Araos, J.; Barros Lamus, Eric Raúl; Subiabre Morales, Mario Enrique; Toledo, F.; Gutierrez, J.; Pardo, F.; Leiva Mendoza, Andrea Alejandra; Sobrevía Luarte, Luis Alberto; Chiarello, D.
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    Nitric Oxide is a Central Common Metabolite in Vascular Dysfunction Associated with Diseases of Human Pregnancy
    (2016) Leiva Mendoza, Andrea Alejandra; Fuenzalida Saavedra, Bárbara; Barros Lamus, Eric Raúl; Sobrevia, B.; Salsoso Rodríguez, M. Rocío; Saez, T.; Villalobos Labra, Roberto Esteban; Silva Lagos, Luis Alfredo; Chiarello, I.; Toledo, F.; Gutierrez, J.; Sanhueza, C.; Pardo, F.; Sobrevía Luarte, Luis Alberto
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    Snowpack retaining techniques in the avalanche starting zones
    (PONTIFICIA UNIV CATOLICA CHILE, ESCUELA CONSTRUCCION CIVIL, 2010) Castro, D.; Jose Pedro Mery, J P; Aravena, R.; Sanhueza, C.
    Snow avalanches are events often involving serious risk to human beings and goods due to their destructive power This is why effective control measures are required to mitigate the risk for human settlements, goods and services on mountain slopes or at the foot of avalanche ways. This article summarizes the different structural systems and techniques used nationally and internationally to support and stabilize the snowpack in avalanche starting zones. These measures act by reducing the pressures originated by the creeping and sliding of the snowpack. While the current state of the art and the control systems implementation have been mainly developed in Europe, the prevention measures by modern supporting structures have been carried out in Chile since the 80s.
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    The twisted survivin connection to angiogenesis
    (2015) Sanhueza, C.
    Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.Abstract Survivin, a member of the inhibitor of apoptosis family of proteins (IAPs) that controls cell division, apoptosis, metastasis and angiogenesis, is overexpressed in essentially all human cancers. As a consequence, the gene/protein is considered an attractive target for cancer treatment. Here, we discuss recent findings related to the regulation of survivin expression and its role in angiogenesis, particularly in the context of hypoxia. We propose a novel role for survivin in cancer, whereby expression of the protein in tumor cells promotes VEGF synthesis, secretion and angiogenesis. Mechanistically, we propose the existence of a positive feed-back loop involving PI3-kinase/Akt activation and enhanced β-Catenin-TCF/LEF-dependent VEGF expression followed by secretion. Finally, we elaborate on the possibility that this mechanism operating in cancer cells may contribute to enhanced tumor vascularization by vasculogenic mimicry together with conventional angiogenesis.