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=""]Proyecto de investigación básica en procesos de arrastre estocásticos.[/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]

During the last decades, compelling evidence shows how the context in which early life takes place impinges risk or protection for later development of non-communicable chronic diseases. In this regard, impaired fetal growth, as occur in the fetal growth restriction (FGR), leads to a higher risk for later cardiovascular diseases, an effect that would be mediated by accelerated aging at molecular, structural, and functional levels. FGR remains a leading cause of perinatal morbidity and mortality, affecting ~10% of pregnancies, but ranging from 5 to 25% depending on the population surveyed, with a higher prevalence among pregnant women of low socioeconomic status. In the clinic, FGR is normally defined by a fetal weight below the 10th percentile, however, new evidence shows that impaired intrauterine growth may affect several neonates born over the 10th percentile, especially late in pregnancy, which may be missed from the perinatal survey for preventing adverse outcomes. This points out the need for further studies to improve the understanding and identification of altered fetal growth trajectories and their consequences on vascular function. Studies in the placenta show that FGR vascular dysfunction is also found at birth in chorionic and umbilical arteries. We have demonstrated the presence of functional and molecular markers (e.g. vasodilator mediators and epigenetic changes) of endothelial dysfunction in human FGR umbilical and chorionic vessels, findings that have been further confirmed by comparing systemic and umbilical arteries in guinea pigs and chicken FGR models. These traits suggest that umbilical artery endothelial cells (HUAEC), in complement with approaches in animal models, can be used as a surrogate to explore the vascular programming within the fetus, however, their translation to clinical preventive applications for promoting healthy aging deserves further studies. It worth noting that fetal reduced oxygen supply (fetal hypoxia) and altered blood flow patterns (e.g. shear stress) are key clinical markers in the FGR, independently of the constraints leading to impaired growth, and both factors exert a tight control of vascular development and function across life. However, how these key stimuli interact and impose an epigenetic program on the endothelial function remains elusive. This proposal will focus on the crosstalk between hypoxia and shear stress that results in the endothelial programming related to impaired fetal growth, and the molecular mechanisms that mediate the vascular responses to these stimuli. Furthermore, we will address if these molecular markers may allow detecting early vascular aging in FGR subjects beyond the 10th centile cutoff. We hypothesize that “Impaired fetal growth conditions are associated with epigenetic programming of aging- and mechanosensing-related miRNAs and transcripts in the endothelium, which can be triggered by the confluence of altered flow patterns and hypoxia resulting in molecular and structural pro-hypertensive biomechanical vascular properties”. This hypothesis will be addressed by three General Objectives (GO) involving ex vivo, in vitro, and in vivo observational and mechanistic approaches: GO1 To demonstrate, in HUAEC, whether late FGR results in epigenetic changes related to the regulation of vascular aging and the expression of mechanosensing mechanisms involved in the endothelial-dependent relaxation, and their relationship with general prenatal parameters of vascular health. GO1 will be performed by recruiting HUAEC samples from late FGR and control pregnancies, to assess transcriptomic and DNA methylation analyses that will be crossed with prenatal clinical data. GO2 To study, in vivo, whether hypoxia and shear stress differentially regulate mechanosensing pathways involved in the endothelial-dependent relaxation and their relationship with the in vivo and ex vivo vascular properties (e.g. functional and biomechanical). GO2 will be performed in chicken embryos exposed to hypoxia and treated with agents targeting mechanosensing pathways, in which wall shear stress will be determined by Ultrasound Localization Microscopy, with complementary functional, structural, and molecular analyses. GO 3. To study, in cultured HUAEC, whether stimuli related to impaired fetal growth converge in the regulation of mechanosensing- and aging-related transcripts and miRNA, contributing to the cellular programming of endothelial dysfunction. GO3 will be performed in HUAEC exposed, in vitro, to sustained hypoxia and diverse flow patterns (shear stress), in which target DNA methylation, miRNA, transcripts, and proteins will be assessed. Our expected outcome is to improve the knowledge about the endothelial epigenetic programming after FGR in humans and enhance the characterization of the shear stress patterns and mechanisms associated with chronic fetal hypoxia. These effects will be isolated by studying, in vivo, hypoxic chicken embryos and, in vitro, cultured HUAEC exposed to FGR-like flow patterns. This project is not only relevant to uncover the developmental mechanisms that determine short- and long-term vascular dysfunction but also to open potential approaches for preventing, diagnosing, and treating FGR-pregnancies.

[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=""]During the last decades, compelling evidence shows how the context in which early life takes place impinges risk or protection for later development of non-communicable chronic diseases. In this regard, impaired fetal growth, as occur in the fetal growth restriction (FGR), leads to a higher risk for later cardiovascular diseases, an effect that would be mediated by accelerated aging at molecular, structural, and functional levels. FGR remains a leading cause of perinatal morbidity and mortality, affecting ~10% of pregnancies, but ranging from 5 to 25% depending on the population surveyed, with a higher prevalence among pregnant women of low socioeconomic status. In the clinic, FGR is normally defined by a fetal weight below the 10th percentile, however, new evidence shows that impaired intrauterine growth may affect several neonates born over the 10th percentile, especially late in pregnancy, which may be missed from the perinatal survey for preventing adverse outcomes. This points out the need for further studies to improve the understanding and identification of altered fetal growth trajectories and their consequences on vascular function. Studies in the placenta show that FGR vascular dysfunction is also found at birth in chorionic and umbilical arteries. We have demonstrated the presence of functional and molecular markers (e.g. vasodilator mediators and epigenetic changes) of endothelial dysfunction in human FGR umbilical and chorionic vessels, findings that have been further confirmed by comparing systemic and umbilical arteries in guinea pigs and chicken FGR models. These traits suggest that umbilical artery endothelial cells (HUAEC), in complement with approaches in animal models, can be used as a surrogate to explore the vascular programming within the fetus, however, their translation to clinical preventive applications for promoting healthy aging deserves further studies. It worth noting that fetal reduced oxygen supply (fetal hypoxia) and altered blood flow patterns (e.g. shear stress) are key clinical markers in the FGR, independently of the constraints leading to impaired growth, and both factors exert a tight control of vascular development and function across life. However, how these key stimuli interact and impose an epigenetic program on the endothelial function remains elusive. This proposal will focus on the crosstalk between hypoxia and shear stress that results in the endothelial programming related to impaired fetal growth, and the molecular mechanisms that mediate the vascular responses to these stimuli. Furthermore, we will address if these molecular markers may allow detecting early vascular aging in FGR subjects beyond the 10th centile cutoff. We hypothesize that “Impaired fetal growth conditions are associated with epigenetic programming of aging- and mechanosensing-related miRNAs and transcripts in the endothelium, which can be triggered by the confluence of altered flow patterns and hypoxia resulting in molecular and structural pro-hypertensive biomechanical vascular properties”. This hypothesis will be addressed by three General Objectives (GO) involving ex vivo, in vitro, and in vivo observational and mechanistic approaches: GO1 To demonstrate, in HUAEC, whether late FGR results in epigenetic changes related to the regulation of vascular aging and the expression of mechanosensing mechanisms involved in the endothelial-dependent relaxation, and their relationship with general prenatal parameters of vascular health. GO1 will be performed by recruiting HUAEC samples from late FGR and control pregnancies, to assess transcriptomic and DNA methylation analyses that will be crossed with prenatal clinical data. GO2 To study, in vivo, whether hypoxia and shear stress differentially regulate mechanosensing pathways involved in the endothelial-dependent relaxation and their relationship with the in vivo and ex vivo vascular properties (e.g. functional and biomechanical). GO2 will be performed in chicken embryos exposed to hypoxia and treated with agents targeting mechanosensing pathways, in which wall shear stress will be determined by Ultrasound Localization Microscopy, with complementary functional, structural, and molecular analyses. GO 3. To study, in cultured HUAEC, whether stimuli related to impaired fetal growth converge in the regulation of mechanosensing- and aging-related transcripts and miRNA, contributing to the cellular programming of endothelial dysfunction. GO3 will be performed in HUAEC exposed, in vitro, to sustained hypoxia and diverse flow patterns (shear stress), in which target DNA methylation, miRNA, transcripts, and proteins will be assessed. Our expected outcome is to improve the knowledge about the endothelial epigenetic programming after FGR in humans and enhance the characterization of the shear stress patterns and mechanisms associated with chronic fetal hypoxia. These effects will be isolated by studying, in vivo, hypoxic chicken embryos and, in vitro, cultured HUAEC exposed to FGR-like flow patterns. This project is not only relevant to uncover the developmental mechanisms that determine short- and long-term vascular dysfunction but also to open potential approaches for preventing, diagnosing, and treating FGR-pregnancies.[/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]

[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 asociar exposiciones ambientales, alimentarias y genéticas con la enfermedad renal crónica de causa idiopática en la Cohorte del Maule MAUCO, Molina, Chile[/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]

[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=""]During the last decades, compelling evidence shows how the context in which early life takes place impinges risk or protection for later development of non-communicable chronic diseases. In this regard, impaired fetal growth, as occur in the fetal growth restriction (FGR), leads to a higher risk for later cardiovascular diseases, an effect that would be mediated by accelerated aging at molecular, structural, and functional levels. FGR remains a leading cause of perinatal morbidity and mortality, affecting ~10% of pregnancies, but ranging from 5 to 25% depending on the population surveyed, with a higher prevalence among pregnant women of low socioeconomic status. In the clinic, FGR is normally defined by a fetal weight below the 10th percentile, however, new evidence shows that impaired intrauterine growth may affect several neonates born over the 10th percentile, especially late in pregnancy, which may be missed from the perinatal survey for preventing adverse outcomes. This points out the need for further studies to improve the understanding and identification of altered fetal growth trajectories and their consequences on vascular function. Studies in the placenta show that FGR vascular dysfunction is also found at birth in chorionic and umbilical arteries. We have demonstrated the presence of functional and molecular markers (e.g. vasodilator mediators and epigenetic changes) of endothelial dysfunction in human FGR umbilical and chorionic vessels, findings that have been further confirmed by comparing systemic and umbilical arteries in guinea pigs and chicken FGR models. These traits suggest that umbilical artery endothelial cells (HUAEC), in complement with approaches in animal models, can be used as a surrogate to explore the vascular programming within the fetus, however, their translation to clinical preventive applications for promoting healthy aging deserves further studies. It worth noting that fetal reduced oxygen supply (fetal hypoxia) and altered blood flow patterns (e.g. shear stress) are key clinical markers in the FGR, independently of the constraints leading to impaired growth, and both factors exert a tight control of vascular development and function across life. However, how these key stimuli interact and impose an epigenetic program on the endothelial function remains elusive. This proposal will focus on the crosstalk between hypoxia and shear stress that results in the endothelial programming related to impaired fetal growth, and the molecular mechanisms that mediate the vascular responses to these stimuli. Furthermore, we will address if these molecular markers may allow detecting early vascular aging in FGR subjects beyond the 10th centile cutoff. We hypothesize that “Impaired fetal growth conditions are associated with epigenetic programming of aging- and mechanosensing-related miRNAs and transcripts in the endothelium, which can be triggered by the confluence of altered flow patterns and hypoxia resulting in molecular and structural pro-hypertensive biomechanical vascular properties”. This hypothesis will be addressed by three General Objectives (GO) involving ex vivo, in vitro, and in vivo observational and mechanistic approaches: GO1 To demonstrate, in HUAEC, whether late FGR results in epigenetic changes related to the regulation of vascular aging and the expression of mechanosensing mechanisms involved in the endothelial-dependent relaxation, and their relationship with general prenatal parameters of vascular health. GO1 will be performed by recruiting HUAEC samples from late FGR and control pregnancies, to assess transcriptomic and DNA methylation analyses that will be crossed with prenatal clinical data. GO2 To study, in vivo, whether hypoxia and shear stress differentially regulate mechanosensing pathways involved in the endothelial-dependent relaxation and their relationship with the in vivo and ex vivo vascular properties (e.g. functional and biomechanical). GO2 will be performed in chicken embryos exposed to hypoxia and treated with agents targeting mechanosensing pathways, in which wall shear stress will be determined by Ultrasound Localization Microscopy, with complementary functional, structural, and molecular analyses. GO 3. To study, in cultured HUAEC, whether stimuli related to impaired fetal growth converge in the regulation of mechanosensing- and aging-related transcripts and miRNA, contributing to the cellular programming of endothelial dysfunction. GO3 will be performed in HUAEC exposed, in vitro, to sustained hypoxia and diverse flow patterns (shear stress), in which target DNA methylation, miRNA, transcripts, and proteins will be assessed. Our expected outcome is to improve the knowledge about the endothelial epigenetic programming after FGR in humans and enhance the characterization of the shear stress patterns and mechanisms associated with chronic fetal hypoxia. These effects will be isolated by studying, in vivo, hypoxic chicken embryos and, in vitro, cultured HUAEC exposed to FGR-like flow patterns. This project is not only relevant to uncover the developmental mechanisms that determine short- and long-term vascular dysfunction but also to open potential approaches for preventing, diagnosing, and treating FGR-pregnancies.[/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]

[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=""]This project aims to analyze the dressing discursive-material entanglements and the political effects of apparel design on fat people. From new materialisms and posthumanisms, the body-wardrobe relationship may be thought in a continuum (Braidotti, 2015): discursive and material issues are articulated and intertwined in design (Bari, 2019; Coleman, 2008; Hekman, 2014, 2010). In this sense, apparel design is not limited to garment shapes, but as an activity or practice that installs a way of being in the world. In other words, this can be understood as a becoming, which is also material, discursive, bodily and technological. Studying clothing, as a practice, from design allows us to investigate a way of being in/with the world or worldings in which a diversity of matters occur (Haraway, 2008) that are not limited only to the constitution of the self through the use of garments. We seek to articulate the way of becoming human through design and clothing and overcome the construction of inequities and the need to reformulate design based on these dynamics. Investigating the design and clothing of the fat body overcomes the opposition between body/being and appearance. Rather, they are entangled issues (Bari, 2019) where, to name a few, not only the body and clothing are articulated, but also networks (Forlano, 2017), accessories (Merrill and Filstrup, 2013), technologies and environmental issues (Forlano, 2017). From this perspective, the human/non-human distinction is outweighed: dressing is not the action of choosing objects to wear, but a doing where things that are constituted as a network or phenomenon (Barad, 2007) in which entities and relationships have multiple forms, where objects do things. This has significant implications for the study of the fat body, as it is not only that there are no clothes which allow a diversity of possible identities, but that both fat and apparel design are constantly made in dressing: they are part of a worlding that goes away creating openly and critically in which discrimination and violence emerge but where other worldings are possible (Forlano, 2017). This research comprises a post-qualitative epistemological approach (Lather and St. Pierre, 2013), characterized by the speculative commitment of the research team which focuses on what is done, rather than what is, developing latent possibilities of what is being investigated and avoiding the logic based on the representation. Lather (2013) refers to this as QUAL 4.0; a work technique which is focused on becoming, carrying out innovative material practices in research that allow knowledge production in a different way. The project is designed in three modules: (i) Garments ethnographies (we seek to document practices, objects, agencies, bodies, technologies and apparel, among others, that are entangled in fat people apparel design and dressing), (ii) Focus groups (aim to document discriminatory practices in relation to the "being fat" experience and (iii) Design of a collection (the purpose is to intervene the entanglements where the fat body and clothing intra-act). Three kind of results are expected: (i) Fat discrimination has been widely documented in English-speaking countries; however, we do not have data on Chile. This project aims to produce information and situated knowledge about fat discrimination. (ii) It is expected to articulate different disciplines such as socialpsychology, so ciology and design in a transdisciplinary and novel relationship. And (iii) as part of the research we expect to intervene the reality we are studying. This is, the design of a clothing collection will be made with a co-participatory strategy as praxis (Lather, 1986), as a form of action and participation.[/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]

[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=""]The NetForSur project will evaluate the vulnerability of forests to climate change along a latitudinal gradient in the Andes Cordillera; to achieve this goal, we will build a research network including 4 countries (Argentina, Chile, France, Peru) to develop synergies using similar methodologies in dendroecology, ecophysiology and remote sensing. The results will complete worldwide inventories of forest dieback and to propose updating of the species status in national and international red lists. Obj 1 : We will assess the level of forest decline and tree mortality in the Andes Cordillera, through a bibliographic analysis including published and grey literature, since many studies are not yet available in international literature or only in Spanish. We will seek to identify the species at stake, the significance of decline in symptoms and surface area affected, the abiotic events associated to the decline and the mechanisms underlying the observed decline. Obj 2: The growth dynamics of endangered, declining or protected tree species will be analyzed. We will use a common methodology to study tree growth response to climate change, building a database to share existing data in dendro-ecology and field stand monitoring over the whole latitudinal gradient, and over local environmental gradients. We will explore several remote sensing tools to upscale the analyses at landscape and regional. Obj 3: Our third objective is to evaluate the ecophysiological adaptive strategies to climate change of endangered or declining tree species (Araucaria araucana, Austrocedrus chilensis, Nothofagus spp, Polylepis spp.). We will set up a common methodology to study tree ecophysiology, measuring adaptive traits characteristic of plant response to abiotic stress (hydraulic traits, energy dissipation traits) associating lab-measured species-specific traits and field based ecophysiological campaigns. Obj 4: Tree mortality risk will be assessed using model simulations associated to current and future climatic conditions using the SUREAU ecophysiological model. It will be adapted to local species and environmental conditions of the Andean Cordillera, and parameterized using data from objectives 2 and 3. Mortality risks predicted by the model will be evaluated in front of decline estimated in the field. Model simulations will be further considered under climate change scenario. Obj 5: A major goal will be to build a long-term research network on forest adaptation to climate change. The collaboration, data sharing and methodology integration will focus on strengthening the international network between all countries in a formalized framework such as 2RI (https://www.inrae.fr/en/2ri-international-research-networks), and to visualize other calls in conjunction with the project to develop and disseminate new joint results on the adaptation of forests to climate change.[/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]

[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=""]En el emergente campo de investigación sobre la identificación de factores de vulnerabilidad para el desarrollo de patología ansiosa, destaca la incorporación de los procesos de generalización del miedo condicionado. La generalización es una característica de las personas ansiosas, en tanto el foco del miedo se vuelve excesivo y se extiende a situaciones que no son amenazantes (i.e. sobregeneralización). Así, variaciones individuales en el proceso de generalización explicarían estos resultados, Alternativamente, se ha propuesto a un fallo en la inhibición del miedo como mecanismo para explicar la sobregeneralización. Tan importante como aprender a temer a una amenaza, es aprender a no tener miedo ante señales de seguridad (i.e., inhibir). Un número de experimentos ha demostrado evidencia sugerente, pero no sustantiva, de propiedades inhibitorias de señales de seguridad en la generalización del miedo en humanos. Los estudios de miedo condicionado, que incluyen medidas de generalización o inhibición, típicamente por separado, proveen un modelo traslacional completo de la ansiedad, abarcando desde su etiología hasta las recaídas luego del tratamiento, permitiendo una comprensión teórica de sus mecanismos subyacentes, y una contribución práctica en la identificación de parámetros para mejorar el tratamiento -basado en la extinción- y reducir así las recaídas. En base a esta relevancia traslacional, es necesario estudiar las diferencias individuales en mecanismos de aprendizaje y su relación con la vulnerabilidad para el desarrollo de la ansiedad (vulnerabilidad ansiosa). En particular, el presente proyecto se interesa en dos procesos: generalización e inhibición del miedo. En la literatura actual, existen cuatro problemas importantes respecto a la evaluación de mecanismos inhibitorios y de la generalización como procesos alternativos para explicar las respuestas excesivas de miedo. 1) Los estudios no incluyen medidas tradicionales de inhibición. 2) No se ha caracterizado el tipo de proceso inhibitorio que participaría en la sobregeneralización. 3) El tercer problema es de índole teórico: existe la posibilidad de que la inhibición sea parte del proceso de generalización (Spence, 1936). Desde esta teoría, no es necesario proponer a la inhibición como alternativa a la generalización del miedo en humanos, en tanto los dos procesos por separado amenazan la parsimonia. La idea básica es que, al establecer discriminaciones -lo opuesto a generalizar- entre señales de amenaza y de seguridad, los sujetos aprenden ambas. De la primera, las calves de amenaza, aprenden una tendencia excitatoria, mientras que, de las señales de seguridad, se adquiere un aprendizaje de tipo inhibitorio. También, las evaluaciones de esta cuestión en la literatura son insuficientes, no existiendo estudios con mediciones independientes de la generalizaciestimón e inhibición. 4) Tampoco existen estudios sistemáticos que evalúen los procesos de generalización e inhibición luego de la adquisición, extinción y situaciones de recaídas. Cada una de estas etapas tiene importancia traslacional en tanto modelan la etiología, el tratamiento y la potencial recaída después del tratamiento en trastornos de ansiedad. Frente a esta problemática, nos preguntamos si en el aprendizaje discriminativo de miedo en la población adulta ¿la generalización y la inhibición contribuyen, de manera separada o como un único mecanismo, en las distintas etapas (adquisición, extinción y recaídas)? ¿Cuál es la relación que tienen estos mecanismos con la vulnerabilidad ansiosa? Para responder a esta pregunta diseñamos 3 líneas de experimentos. En la línea 1 buscamos determinar si manipulaciones que afectan la inhibición producen un efecto sobre la generalización. En la línea 2 buscamos determinar si manipulaciones que afectan la generalización producen un efecto sobre la inhibición. En la línea 3 buscamos determinar si manipulaciones que afectan la inhibición y la generalización interactúan en sus efectos de generalización e inhibitorios. En cada experimento, las manipulaciones son tratadas como variables independientes que generan distintos grupos. Los participantes proveerán respuestas en múltiples medidas de inhibición y generalización en las distintas fases de adquisición, extinción y recaída luego de la extinción. Antes de comenzar el experimento, los participantes proveen respuestas de cuestionarios para evaluar la vulnerabilidad ansiosa. Estos datos permitirán evaluar la relación que tienen los efectos inhibitorios y de generalización con la vulnerabilidad ansiosa. Se espera que 1) los resultados apoyen la teoría de Spence y 2) que se observe más generalización y menos inhibición en sujetos más ansiosos. Este último resultado sería evidencia a favor de que esta variación en los mecanismos de aprendizaje contribuiría a la vulnerabilidad para el desarrollo de sintomatología ansiosa.[/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]

[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=""]La estocástica (entendida como la unión entre la estadística y probabilidad) se ha establecido como un componente necesario para desenvolverse eficazmente en la era de la información. Esta situación, ha generado un movimiento de reforma curricular en torno a su enseñanza en la escuela, a la que se han sumado un gran número de países. En este contexto, el éxito de las nuevas directrices curriculares depende fuertemente de la formación de quienes tienen la tarea de su implementación, los profesores de matemática. Con ello, emerge el problema de que muchos docentes consideran que no están bien preparados para enseñar estadística ni para afrontar las dificultades de sus estudiantes. En consecuencia, nos planteamos que las mayores problemáticas relativas al conocimiento del contenido y la enseñanza de la estocástica en profesores pueden ser abordadas reorientando su formación inicial. En esta nueva mirada, es necesario considerar el desarrollo de habilidades vinculadas con las tareas profesionales del estadístico y con un fuerte apoyo tecnológico. Esta perspectiva se ha sintetizado en nuevos currículos centrados en la inferencia a través de la simulación computacional (SBI por Simulation-Based introduction to Inference) basadas en técnicas de re-muestreo (repeated sampling), procedimientos que consideran la repetición reiterada de los procesos de muestreo. Objetivos Asumiendo el modelo de Conocimiento didáctico-matemáticos del profesor como marco teórico de esta investigación, nos planteamos analizar el desarrollo de los conocimientos didáctico-matemáticos de los futuros profesores de educación media en relación a la enseñanza de la estocástica a través de enfoques progresivos de lo informal a lo formal. Meta que se articula en torno a cinco metas parciales relativas a: (1) Analizar la pertinencia y adecuación de centrar el currículo de estocástica en la inferencia, basados en la simulación computacional; (2) Diseñar módulos de enseñanza para introducir progresivamente las ideas claves en la formación del profesorado; (3) Explorar los resultados de la implementación de los módulos diseñados en futuros profesores de matemática; (4) Explorar los conocimientos meta-didácticos de los futuros profesores al valorar la idoneidad didáctica de algunas secuencias diseñadas para ser utilizadas en el ámbito escolar; (5) Analizar los conocimientos didáctico-matemáticos sobre la estocástica en los futuros profesores de matemática durante una asignatura de enseñanza de la estocástica[/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]

[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=""]En el emergente campo de investigación sobre la identificación de factores de vulnerabilidad para el desarrollo de patología ansiosa, destaca la incorporación de los procesos de generalización del miedo condicionado. La generalización es una característica de las personas ansiosas, en tanto el foco del miedo se vuelve excesivo y se extiende a situaciones que no son amenazantes (i.e. sobregeneralización). Así, variaciones individuales en el proceso de generalización explicarían estos resultados, Alternativamente, se ha propuesto a un fallo en la inhibición del miedo como mecanismo para explicar la sobregeneralización. Tan importante como aprender a temer a una amenaza, es aprender a no tener miedo ante señales de seguridad (i.e., inhibir). Un número de experimentos ha demostrado evidencia sugerente, pero no sustantiva, de propiedades inhibitorias de señales de seguridad en la generalización del miedo en humanos. Los estudios de miedo condicionado, que incluyen medidas de generalización o inhibición, típicamente por separado, proveen un modelo traslacional completo de la ansiedad, abarcando desde su etiología hasta las recaídas luego del tratamiento, permitiendo una comprensión teórica de sus mecanismos subyacentes, y una contribución práctica en la identificación de parámetros para mejorar el tratamiento -basado en la extinción- y reducir así las recaídas. En base a esta relevancia traslacional, es necesario estudiar las diferencias individuales en mecanismos de aprendizaje y su relación con la vulnerabilidad para el desarrollo de la ansiedad (vulnerabilidad ansiosa). En particular, el presente proyecto se interesa en dos procesos: generalización e inhibición del miedo. En la literatura actual, existen cuatro problemas importantes respecto a la evaluación de mecanismos inhibitorios y de la generalización como procesos alternativos para explicar las respuestas excesivas de miedo. 1) Los estudios no incluyen medidas tradicionales de inhibición. 2) No se ha caracterizado el tipo de proceso inhibitorio que participaría en la sobregeneralización. 3) El tercer problema es de índole teórico: existe la posibilidad de que la inhibición sea parte del proceso de generalización (Spence, 1936). Desde esta teoría, no es necesario proponer a la inhibición como alternativa a la generalización del miedo en humanos, en tanto los dos procesos por separado amenazan la parsimonia. La idea básica es que, al establecer discriminaciones -lo opuesto a generalizar- entre señales de amenaza y de seguridad, los sujetos aprenden ambas. De la primera, las calves de amenaza, aprenden una tendencia excitatoria, mientras que, de las señales de seguridad, se adquiere un aprendizaje de tipo inhibitorio. También, las evaluaciones de esta cuestión en la literatura son insuficientes, no existiendo estudios con mediciones independientes de la generalizaciestimón e inhibición. 4) Tampoco existen estudios sistemáticos que evalúen los procesos de generalización e inhibición luego de la adquisición, extinción y situaciones de recaídas. Cada una de estas etapas tiene importancia traslacional en tanto modelan la etiología, el tratamiento y la potencial recaída después del tratamiento en trastornos de ansiedad. Frente a esta problemática, nos preguntamos si en el aprendizaje discriminativo de miedo en la población adulta ¿la generalización y la inhibición contribuyen, de manera separada o como un único mecanismo, en las distintas etapas (adquisición, extinción y recaídas)? ¿Cuál es la relación que tienen estos mecanismos con la vulnerabilidad ansiosa? Para responder a esta pregunta diseñamos 3 líneas de experimentos. En la línea 1 buscamos determinar si manipulaciones que afectan la inhibición producen un efecto sobre la generalización. En la línea 2 buscamos determinar si manipulaciones que afectan la generalización producen un efecto sobre la inhibición. En la línea 3 buscamos determinar si manipulaciones que afectan la inhibición y la generalización interactúan en sus efectos de generalización e inhibitorios. En cada experimento, las manipulaciones son tratadas como variables independientes que generan distintos grupos. Los participantes proveerán respuestas en múltiples medidas de inhibición y generalización en las distintas fases de adquisición, extinción y recaída luego de la extinción. Antes de comenzar el experimento, los participantes proveen respuestas de cuestionarios para evaluar la vulnerabilidad ansiosa. Estos datos permitirán evaluar la relación que tienen los efectos inhibitorios y de generalización con la vulnerabilidad ansiosa. Se espera que 1) los resultados apoyen la teoría de Spence y 2) que se observe más generalización y menos inhibición en sujetos más ansiosos. Este último resultado sería evidencia a favor de que esta variación en los mecanismos de aprendizaje contribuiría a la vulnerabilidad para el desarrollo de sintomatología ansiosa.[/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]