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    • Mayo 2014 - Abril 2016
    Ejecutado

    Caracterización de la vía Hippo en el ovario de la tijereta Forficula auricularia (L) como mecanismo celular regulador de crecimiento de un tejido

    [vc_section el_class="container mx-auto align-items-center circle--pattern" css=".vc_custom_1648956589196{padding-top: 3rem !important;}"][vc_row el_class="pb-5"][vc_column][vc_wp_custommenu nav_menu="6"][uoh_breadcrumb_component automatic_breadcrumb="true"][uoh_title_component title_dropdown="big" title_decorator="true"]{{title}}[/uoh_title_component][vc_column_text css=""]El proyecto busca establecer a la tijereta como insecto modelo para estudios de oogénesis y caracterizar una vía de señalización celular fundamental en el tamaño de un órgano. Además de establecer técnicas de silenciamiento génico en este organismo.[/vc_column_text][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649209804184{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5"][vc_row el_class="container mx-auto align-items-center p-md-0 pt-5"][vc_column el_class="p-0"][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649210787516{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5 pb-md-5"][vc_row el_class="container mx-auto align-items-center"][vc_column][/vc_column][/vc_row][/vc_section]
    Investigador/a Responsable
    • Mayo 2014 - Mayo 2017
    Ejecutado

    Transitividad y agentividad: el principio de gradualidad para la explicación semántico-discursiva de los procesos. Un enfoque sistémico-funcional

    [vc_section el_class="container mx-auto align-items-center circle--pattern" css=".vc_custom_1648956589196{padding-top: 3rem !important;}"][vc_row el_class="pb-5"][vc_column][vc_wp_custommenu nav_menu="6"][uoh_breadcrumb_component automatic_breadcrumb="true"][uoh_title_component title_dropdown="big" title_decorator="true"]{{title}}[/uoh_title_component][vc_column_text css=""][/vc_column_text][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649209804184{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5"][vc_row el_class="container mx-auto align-items-center p-md-0 pt-5"][vc_column el_class="p-0"][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649210787516{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5 pb-md-5"][vc_row el_class="container mx-auto align-items-center"][vc_column][/vc_column][/vc_row][/vc_section]
    Co-Investigador/a
    • Abril 2014 - Mayo 2015
    FinalizadoThe Rufford Small Grants

    What Can Reveal the Tree Rings of Nothofagus Macrocarpa about the Conservation State of the Mediterranean Deciduous Forest of Central Chile?

    [vc_section el_class="container mx-auto align-items-center circle--pattern" css=".vc_custom_1648956589196{padding-top: 3rem !important;}"][vc_row el_class="pb-5"][vc_column][vc_wp_custommenu nav_menu="6"][uoh_breadcrumb_component automatic_breadcrumb="true"][uoh_title_component title_dropdown="big" title_decorator="true"]{{title}}[/uoh_title_component][vc_column_text css=""]El objetivo del proyecto es evaluar la dinámica de crecimiento y la variabilidad genética de las poblaciones remanentes de N. macrocarpa y su vulnerabilidad al cambio climático. Para ello, realizaremos muestreos y trabajos de campo en cinco áreas de estudio en la zona central de Chile utilizando técnicas clásicas de dendrocronología y genética forestal. Los resultados generados permitirán destacar el estado de conservación del bosque mediterráneo caducifolio, caracterizado por la especie endémica N. Macrocarpa. De esta manera, podríamos entender y evaluar la degradación histórica que ha afectado a este bosque, que a pesar de su actual estado de conservación aún tendría un rol ecológico clave en Chile central. Además, nuestros resultados podrían ser utilizados en la toma de decisiones públicas para la conservación y restauración ecológica de este ecosistema, considerando que Chile está pasando por un momento de discusión, modificación e implementación de sus leyes forestales.[/vc_column_text][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649209804184{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5"][vc_row el_class="container mx-auto align-items-center p-md-0 pt-5"][vc_column el_class="p-0"][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649210787516{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5 pb-md-5"][vc_row el_class="container mx-auto align-items-center"][vc_column][/vc_column][/vc_row][/vc_section]
    Investigador/a Responsable
    • Fondecyt No. 1141303
    • Marzo 2014 - Noviembre 2026
    FinalizadoAgencia Nacional de Investigación y Desarrollo - ANID
    Co-Investigador/a
    • Marzo 2014 - Diciembre 2024
    En Ejecución

    Centro Avanzado de Enfermedades Crónicas (ACCDiS)

    [vc_section el_class="container mx-auto align-items-center circle--pattern" css=".vc_custom_1648956589196{padding-top: 3rem !important;}"][vc_row el_class="pb-5"][vc_column][vc_wp_custommenu nav_menu="6"][uoh_breadcrumb_component automatic_breadcrumb="true"][uoh_title_component title_dropdown="big" title_decorator="true"]{{title}}[/uoh_title_component][vc_column_text css=""][/vc_column_text][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649209804184{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5"][vc_row el_class="container mx-auto align-items-center p-md-0 pt-5"][vc_column el_class="p-0"][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649210787516{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5 pb-md-5"][vc_row el_class="container mx-auto align-items-center"][vc_column][/vc_column][/vc_row][/vc_section]
    Co-Investigador/a
    • CNPq No 014/2010
    • Marzo 2014 - Diciembre 2017
    FinalizadoConselho Nacional de Desenvolvimento Científico e Tecnológico

    Characterization of Brazilian soybean germplasm by genotyping, and genome wide association mapping of genes and QTLs for agronomic traits

    [vc_section el_class="container mx-auto align-items-center circle--pattern" css=".vc_custom_1648956589196{padding-top: 3rem !important;}"][vc_row el_class="pb-5"][vc_column][vc_wp_custommenu nav_menu="6"][uoh_breadcrumb_component automatic_breadcrumb="true"][uoh_title_component title_dropdown="big" title_decorator="true"]{{title}}[/uoh_title_component][vc_column_text css=""]NA[/vc_column_text][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649209804184{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5"][vc_row el_class="container mx-auto align-items-center p-md-0 pt-5"][vc_column el_class="p-0"][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649210787516{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5 pb-md-5"][vc_row el_class="container mx-auto align-items-center"][vc_column][/vc_column][/vc_row][/vc_section]
    Co-Investigador/a
    • Marzo 2014
    Ejecutado

    Herramientas para fortalecer la formación de profesores de educación básica basadas en experiencias de enseñanza de la matemática en aula

    [vc_section el_class="container mx-auto align-items-center circle--pattern" css=".vc_custom_1648956589196{padding-top: 3rem !important;}"][vc_row el_class="pb-5"][vc_column][vc_wp_custommenu nav_menu="6"][uoh_breadcrumb_component automatic_breadcrumb="true"][uoh_title_component title_dropdown="big" title_decorator="true"]{{title}}[/uoh_title_component][vc_column_text css=""]Fondef IT13I10005 Investigadora responsable Salomé Martínez[/vc_column_text][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649209804184{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5"][vc_row el_class="container mx-auto align-items-center p-md-0 pt-5"][vc_column el_class="p-0"][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649210787516{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5 pb-md-5"][vc_row el_class="container mx-auto align-items-center"][vc_column][/vc_column][/vc_row][/vc_section]
    Co-Investigador/a
    • 11201336
    • Marzo 2014 - Febrero 2018
    AdjudicadoCorporación de Fomento de la Producción - CORFO

    Asthma is a chronic disease that affects young children starting mostly in the first years of life; with a high prevalence across countries globally. In Santiago, Chile, the prevalence of asthma among children 6-7 and 13-14 years of age is 11% and 15%, respectively; and for recurrent wheezing during the first year of life is as high as 22%. Asthma is the fourth most common cause of disability-adjusted life years for children aged 10–14 yrs and an important cause of reduced quality of life and exercise tolerance, higher rates of school absenteeism and hospitalization. A recent study done in Santiago reports that 30.4% of all infants visits to the emergency department presented with wheezing and wheezing exacerbations accounted for 8.4% hospital admission. Treatment of asthma currently focuses in reducing symptoms; however the morbidity remains high due to limited curative options and the unresolved etiology of asthma. There are no well-established methods or diagnostic tools to indentify the risk to develop asthma, and the current accepted practice base the diagnosis on parental or self-reported symptoms. One of the most accepted tools to predict asthma early in the infancy was developed by our team (the Asthma Predictive Index); and has been incorporated in most asthma early diagnosis guidelines globally. However, there is growing evidence supporting that beside genetic inheritance, maternal health during gestation represents an important factor conditioning the risk of asthma in the offspring. Thus a better understanding of pathogenesis of asthma in the neonatal period throughout uncovering the mechanisms that explain the associations between fetal life cues with asthma would contribute to an early prevention and treatment. Immune function plays a central role in the development of asthma, but the relative contribution of different immune cell types (i.e. mast cells, eosinophils, lymphocytes, neutrophils and monocytes/macrophages) to this disease is still under examination. Nonetheless, it is clear that asthma presents an altered expression of pro-inflammatory molecules (IL-12, TNF-α) and anti-inflammatory mediators (IL-10, IL-4). Notably, modulation of M1-M2 polarization of monocytes and macrophages seems to be crucial for the development of altered immune response in asthma, and this process would be tightly regulated by epigenetic mechanisms (i.e. DNA methylation, histone modifications). Numerous clinical and epidemiological studies have underlined the detrimental or beneficial role of nutritional factors in complex inflammation-related disorders such as allergy and asthma. It is now progressively better established that most of this risk is influenced in the very early stages of development, by a process of “early life programming” in which epigenetic mechanisms will actively participates. Remarkably, maternal obesity during gestation associates with increased plasma levels of TNF-α at birth, and a 4-fold increased risk of asthma in the offspring. Also growing data show that epigenetic mechanisms exert an important control on the altered immune function observed in autoimmune and inflammatory controlling the expression of key genes. However, whether maternal obesity during pregnancy influences the immune function and the risk of asthma in the offspring throughout epigenetic mechanisms has not been addressed. In this context we propose that “Maternal obesity during pregnancy increases the risk of developing asthma in the offspring by an epigenetic-mediated programming of the inflammatory response in monocytes. This programmed inflammatory response is characterized by a higher expression of pro-inflammatory molecules (IL-12, TNF-α) along with a lower expression of anti-inflammatory mediators (IL-10, IL-4Rα) which occurs due to changes in the methylation status of the promoter regions of these immune response- key genes”. Studying a cohort of 400 children (0–3 years old) born from mother with or without obesity during pregnancy this proposal will address whether: a) the increased risk of asthma in children born from obese mother can be observed at 3 years of life; b) the increased asthma risk in these children associates with an altered immune reactivity in monocytes at birth; and c) the altered immune reactivity in monocytes occurs along with changes in the DNA methylation status at the promoter regions of asthma-related genes. This study would reveal new molecular markers contributing to early diagnosis of asthma during childhood, as well as establish the real effects of epigenetic mechanisms modeling the immune function and responses at long term.
    Co-Investigador/a
    • Marzo 2014 - Febrero 2018
    Adjudicado

    Fondecyt Regular 1141195 – Early risk of asthma in children exposed to in-utero maternal obesity. An epigenetic-mediated programming of immune function

    [vc_section el_class="container mx-auto align-items-center circle--pattern" css=".vc_custom_1648956589196{padding-top: 3rem !important;}"][vc_row el_class="pb-5"][vc_column][vc_wp_custommenu nav_menu="6"][uoh_breadcrumb_component automatic_breadcrumb="true"][uoh_title_component title_dropdown="big" title_decorator="true"]{{title}}[/uoh_title_component][vc_column_text css=""]Asthma is a chronic disease that affects young children starting mostly in the first years of life; with a high prevalence across countries globally. In Santiago, Chile, the prevalence of asthma among children 6-7 and 13-14 years of age is 11% and 15%, respectively; and for recurrent wheezing during the first year of life is as high as 22%. Asthma is the fourth most common cause of disability-adjusted life years for children aged 10–14 yrs and an important cause of reduced quality of life and exercise tolerance, higher rates of school absenteeism and hospitalization. A recent study done in Santiago reports that 30.4% of all infants visits to the emergency department presented with wheezing and wheezing exacerbations accounted for 8.4% hospital admission. Treatment of asthma currently focuses in reducing symptoms; however the morbidity remains high due to limited curative options and the unresolved etiology of asthma. There are no well-established methods or diagnostic tools to indentify the risk to develop asthma, and the current accepted practice base the diagnosis on parental or self-reported symptoms. One of the most accepted tools to predict asthma early in the infancy was developed by our team (the Asthma Predictive Index); and has been incorporated in most asthma early diagnosis guidelines globally. However, there is growing evidence supporting that beside genetic inheritance, maternal health during gestation represents an important factor conditioning the risk of asthma in the offspring. Thus a better understanding of pathogenesis of asthma in the neonatal period throughout uncovering the mechanisms that explain the associations between fetal life cues with asthma would contribute to an early prevention and treatment. Immune function plays a central role in the development of asthma, but the relative contribution of different immune cell types (i.e. mast cells, eosinophils, lymphocytes, neutrophils and monocytes/macrophages) to this disease is still under examination. Nonetheless, it is clear that asthma presents an altered expression of pro-inflammatory molecules (IL-12, TNF-α) and anti-inflammatory mediators (IL-10, IL-4). Notably, modulation of M1-M2 polarization of monocytes and macrophages seems to be crucial for the development of altered immune response in asthma, and this process would be tightly regulated by epigenetic mechanisms (i.e. DNA methylation, histone modifications). Numerous clinical and epidemiological studies have underlined the detrimental or beneficial role of nutritional factors in complex inflammation-related disorders such as allergy and asthma. It is now progressively better established that most of this risk is influenced in the very early stages of development, by a process of “early life programming” in which epigenetic mechanisms will actively participates. Remarkably, maternal obesity during gestation associates with increased plasma levels of TNF-α at birth, and a 4-fold increased risk of asthma in the offspring. Also growing data show that epigenetic mechanisms exert an important control on the altered immune function observed in autoimmune and inflammatory controlling the expression of key genes. However, whether maternal obesity during pregnancy influences the immune function and the risk of asthma in the offspring throughout epigenetic mechanisms has not been addressed. In this context we propose that “Maternal obesity during pregnancy increases the risk of developing asthma in the offspring by an epigenetic-mediated programming of the inflammatory response in monocytes. This programmed inflammatory response is characterized by a higher expression of pro-inflammatory molecules (IL-12, TNF-α) along with a lower expression of anti-inflammatory mediators (IL-10, IL-4Rα) which occurs due to changes in the methylation status of the promoter regions of these immune response- key genes”. Studying a cohort of 400 children (0–3 years old) born from mother with or without obesity during pregnancy this proposal will address whether: a) the increased risk of asthma in children born from obese mother can be observed at 3 years of life; b) the increased asthma risk in these children associates with an altered immune reactivity in monocytes at birth; and c) the altered immune reactivity in monocytes occurs along with changes in the DNA methylation status at the promoter regions of asthma-related genes. This study would reveal new molecular markers contributing to early diagnosis of asthma during childhood, as well as establish the real effects of epigenetic mechanisms modeling the immune function and responses at long term.[/vc_column_text][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649209804184{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5"][vc_row el_class="container mx-auto align-items-center p-md-0 pt-5"][vc_column el_class="p-0"][/vc_column][/vc_row][/vc_section][vc_section css=".vc_custom_1649210787516{background-color: #f6faff !important;}" el_class="p-md-0 pt-md-5 pb-md-5"][vc_row el_class="container mx-auto align-items-center"][vc_column][/vc_column][/vc_row][/vc_section]
    Co-Investigador/a
    • 11140576.
    • Marzo 2014 - Marzo 2016
    FinalizadoAgencia Nacional de Investigación y Desarrollo - ANID

    Proyecto FIV. Facultad de Ciencias Veterinarias y Pecuarias. Universidad de Chile. Investigador Responsable
    Co-Investigador/a