Proyectos

[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=""]Estudio que involucra el estudio de la via Wnt en la regulación de vias metabolicas en el contexto de la Enfermedad de Alzheimer[/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]

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Conocimientos, actitudes y prácticas relacionadas con el cáncer cervical en Monteagudo rural, Bolivia.

Latin America is home to an estimated 600 million people, the majority of whom live in severe economic deprivation and political instability. While mental illness and substance use problems (MISUP) in Latin America account for approximately a tenth of the world's total burden of the disease, very few individuals receive adequate treatment. 18 million Latin Americans are reported to be facing unemployment, eviction, and homelessness as a result of mental disorders. Untreated MISUP are a major public health issue as they can lead to long-term disability, impaired functioning, caregiver burden, and ultimately premature death. Given the prevalence of such issues in Latin America, an effort to address health equity and accessibility to mental health services is warranted. Research regarding mental health service use in Latin America is scarce, with even fewer studies focusing on barriers to accessibility such as stigma and discrimination. The goal for this project is to share key insights among Latin American countries to better understand factors that inhibit access to mental health services. Funding for a 3-day meeting bringing together key stakeholders from Chile, Canada, Peru, Bolivia and Argentina who are actively addressing these issues will serve three objectives: 1. Dissemination of Research - Disseminating findings from anti-stigma projects in Chile, Peru and Canada detailing challenges within their health systems, impact of interventions and opportunities to further research in this area. 2. Information Gathering - Exploring research studies concerning factors that prevent access to mental health care in Bolivia and Argentina to extract key insights from each approach. 3. Collaboration - Developing new, relevant and collaborative regional projects, research and interventions addressing accessibility to mental health services.

Latin America is home to an estimated 600 million people, the majority of whom live in severe economic deprivation and political instability. While mental illness and substance use problems (MISUP) in Latin America account for approximately a tenth of the world's total burden of the disease, very few individuals receive adequate treatment. 18 million Latin Americans are reported to be facing unemployment, eviction, and homelessness as a result of mental disorders. Untreated MISUP are a major public health issue as they can lead to long-term disability, impaired functioning, caregiver burden, and ultimately premature death. Given the prevalence of such issues in Latin America, an effort to address health equity and accessibility to mental health services is warranted. Research regarding mental health service use in Latin America is scarce, with even fewer studies focusing on barriers to accessibility such as stigma and discrimination. The goal for this project is to share key insights among Latin American countries to better understand factors that inhibit access to mental health services. Funding for a 3-day meeting bringing together key stakeholders from Chile, Canada, Peru, Bolivia and Argentina who are actively addressing these issues will serve three objectives: 1. Dissemination of Research - Disseminating findings from anti-stigma projects in Chile, Peru and Canada detailing challenges within their health systems, impact of interventions and opportunities to further research in this area. 2. Information Gathering - Exploring research studies concerning factors that prevent access to mental health care in Bolivia and Argentina to extract key insights from each approach. 3. Collaboration - Developing new, relevant and collaborative regional projects, research and interventions addressing accessibility to mental health services.

As a scientist in Chile, I have been focused on understanding the mechanisms underlying fetal vascular dysfunction associated with altered fetal growth with a special interest in impaired fetal growth and epigenetic regulation. Fetal growth restriction (FGR), commonly defined by a weight below the 10th percentile is associated with increased perinatal morbidity and mortality with an incidence of 3 to 10% of all live births1, 2. Therefore, FGR remains at the forefront of basic science and clinical investigation, as it poses a significant problem on every nation’s wealth and health. Adverse conditions in complicated pregnancy known to induce FGR include reductions in fetal oxygenation or chronic fetal hypoxia3. Several studies in humans have established that high altitude pregnancy reduces fetal growth 4-6. Further, several studies in mammalian animal models of hypoxic pregnancy have also reported a significant effect in slowing fetal growth7. However, since most high altitude populations are also impoverished with a high prevalence of maternal undernutrition and since hypoxic exposure of mammalian animals during pregnancy can reduce maternal food intake7, the partial contributions of fetal under-nutrition versus fetal under-oxygenation in promoting FGR remain uncertain. The Giussani group at the University of Cambridge have combined the chick embryo model with hypoxic incubation to isolate the direct effects of chronic fetal hypoxia in promoting FGR. This group has shown that incubation at high altitude of fertilized eggs laid by sea level hens leads to FGR. Conversely, incubation at sea level of fertilized eggs laid by high altitude hens that normally show FGR completely recovered fetal growth. Importantly, incubation at high altitude of fertilized eggs laid by sea level with oxygen supplementation also prevented FGR8. Recent studies by the Cambridge group have also reported that isobaric rather than hypobaric chronic fetal hypoxia also leads to FGR in the chick embryo9. Further, they have reported that FGR as a result of isolated chronic fetal hypoxia is associated with significant oxidative stress and endothelial dysfunction in fetal peripheral circulations. Treatment of chick embryos during hypoxic incubation with the antioxidant melatonin rescued the endothelial dysfunction in peripheral circulations by the end of the incubation period. The mechanisms involved included reduced oxidative stress, enhanced antioxidant capacity, restored vascular endothelial growth factor expression and increased NO bioavailability9. Combined, therefore, studies by the Cambridge group have isolated a direct effect of hypoxia in promoting FGR and fetal endothelial dysfunction independent of effects at the level of the placenta or the mother and suggest that antioxidant therapy may also have a direct protective effect on the fetus. These findings are of particular interest to me because my research group in Chile has recently established a guinea pig experimental model of FGR. This is by progressive bilateral occlusion of the uterine arteries during the second half of gestation that gradually increases placental vascular resistance10, 11. Using this guinea pig model, we have recently shown that FGR induces epigenetic programming of eNOS expression in the fetal endothelium, which is prevented by a maternal treatment with N-acetylcysteine11. However, whether the effects of increased placental vascular resistance on the fetal epigenetic programming of eNOS expression is due to fetal under-nutrition versus fetal under-oxygenation in this model of FGR again remains uncertain. Therefore, the aim of my research proposal is to use the Cambridge chick embryo model of FGR as a result of hypoxic incubation to isolate the direct effects of chronic fetal hypoxia on epigenetic regulation promoting fetal vascular dysfunction. This would be the first step to enable better identification of potential targets for clinical intervention designed to protect the developing fetal circulation in pregnancy complicated by FGR and chronic fetal hypoxia.

As a scientist in Chile, I have been focused on understanding the mechanisms underlying fetal vascular dysfunction associated with altered fetal growth with a special interest in impaired fetal growth and epigenetic regulation. Fetal growth restriction (FGR), commonly defined by a weight below the 10th percentile is associated with increased perinatal morbidity and mortality with an incidence of 3 to 10% of all live births1, 2. Therefore, FGR remains at the forefront of basic science and clinical investigation, as it poses a significant problem on every nation’s wealth and health. Adverse conditions in complicated pregnancy known to induce FGR include reductions in fetal oxygenation or chronic fetal hypoxia3. Several studies in humans have established that high altitude pregnancy reduces fetal growth 4-6. Further, several studies in mammalian animal models of hypoxic pregnancy have also reported a significant effect in slowing fetal growth7. However, since most high altitude populations are also impoverished with a high prevalence of maternal undernutrition and since hypoxic exposure of mammalian animals during pregnancy can reduce maternal food intake7, the partial contributions of fetal under-nutrition versus fetal under-oxygenation in promoting FGR remain uncertain. The Giussani group at the University of Cambridge have combined the chick embryo model with hypoxic incubation to isolate the direct effects of chronic fetal hypoxia in promoting FGR. This group has shown that incubation at high altitude of fertilized eggs laid by sea level hens leads to FGR. Conversely, incubation at sea level of fertilized eggs laid by high altitude hens that normally show FGR completely recovered fetal growth. Importantly, incubation at high altitude of fertilized eggs laid by sea level with oxygen supplementation also prevented FGR8. Recent studies by the Cambridge group have also reported that isobaric rather than hypobaric chronic fetal hypoxia also leads to FGR in the chick embryo9. Further, they have reported that FGR as a result of isolated chronic fetal hypoxia is associated with significant oxidative stress and endothelial dysfunction in fetal peripheral circulations. Treatment of chick embryos during hypoxic incubation with the antioxidant melatonin rescued the endothelial dysfunction in peripheral circulations by the end of the incubation period. The mechanisms involved included reduced oxidative stress, enhanced antioxidant capacity, restored vascular endothelial growth factor expression and increased NO bioavailability9. Combined, therefore, studies by the Cambridge group have isolated a direct effect of hypoxia in promoting FGR and fetal endothelial dysfunction independent of effects at the level of the placenta or the mother and suggest that antioxidant therapy may also have a direct protective effect on the fetus. These findings are of particular interest to me because my research group in Chile has recently established a guinea pig experimental model of FGR. This is by progressive bilateral occlusion of the uterine arteries during the second half of gestation that gradually increases placental vascular resistance10, 11. Using this guinea pig model, we have recently shown that FGR induces epigenetic programming of eNOS expression in the fetal endothelium, which is prevented by a maternal treatment with N-acetylcysteine11. However, whether the effects of increased placental vascular resistance on the fetal epigenetic programming of eNOS expression is due to fetal under-nutrition versus fetal under-oxygenation in this model of FGR again remains uncertain. Therefore, the aim of my research proposal is to use the Cambridge chick embryo model of FGR as a result of hypoxic incubation to isolate the direct effects of chronic fetal hypoxia on epigenetic regulation promoting fetal vascular dysfunction. This would be the first step to enable better identification of potential targets for clinical intervention designed to protect the developing fetal circulation in pregnancy complicated by FGR and chronic fetal hypoxia.