Project acronym Acclimatize
Project Hypothalamic mechanisms of thermal homeostasis and adaptation
Researcher (PI) Jan SIEMENS
Host Institution (HI) UNIVERSITATSKLINIKUM HEIDELBERG
Call Details Consolidator Grant (CoG), LS5, ERC-2017-COG
Summary Mammalian organisms possess the remarkable ability to maintain internal body temperature (Tcore) within a narrow range close to 37°C despite wide environmental temperature variations. The brain’s neural “thermostat” is made up by central circuits in the hypothalamic preoptic area (POA), which orchestrate peripheral thermoregulatory responses to maintain Tcore. Thermogenesis requires metabolic fuel, suggesting intricate connections between the thermoregulatory centre and hypothalamic circuits controlling energy balance. How the POA detects and integrates temperature and metabolic information to achieve thermal balance is largely unknown. A major question is whether this circuitry could be harnessed therapeutically to treat obesity.
We have recently identified the first known molecular temperature sensor in thermoregulatory neurons of the POA, transient receptor potential melastatin 2 (TRPM2), a thermo-sensitive ion channel. I aim to use TRPM2 as a molecular marker to gain access to and probe the function of thermoregulatory neurons in vivo. I propose a multidisciplinary approach, combining local, in vivo POA temperature stimulation with optogenetic circuit-mapping to uncover the molecular and cellular logic of the hypothalamic thermoregulatory centre and to assess its medical potential to counteract metabolic syndrome.
Acclimation is a beneficial adaptive process that fortifies thermal responses upon environmental temperature challenges. Thermoregulatory neuron plasticity is thought to mediate acclimation. Conversely, maladaptive thermoregulatory changes affect obesity. The cell-type-specific neuronal plasticity mechanisms underlying these changes within the POA, however, are unknown.
Using ex-vivo slice electrophysiology and in vivo imaging, I propose to characterize acclimation- and obesity-induced plasticity of thermoregulatory neurons. Ultimately, I aim to manipulate thermoregulatory neuron plasticity to test its potential counter-balancing effect on obesity.
Summary
Mammalian organisms possess the remarkable ability to maintain internal body temperature (Tcore) within a narrow range close to 37°C despite wide environmental temperature variations. The brain’s neural “thermostat” is made up by central circuits in the hypothalamic preoptic area (POA), which orchestrate peripheral thermoregulatory responses to maintain Tcore. Thermogenesis requires metabolic fuel, suggesting intricate connections between the thermoregulatory centre and hypothalamic circuits controlling energy balance. How the POA detects and integrates temperature and metabolic information to achieve thermal balance is largely unknown. A major question is whether this circuitry could be harnessed therapeutically to treat obesity.
We have recently identified the first known molecular temperature sensor in thermoregulatory neurons of the POA, transient receptor potential melastatin 2 (TRPM2), a thermo-sensitive ion channel. I aim to use TRPM2 as a molecular marker to gain access to and probe the function of thermoregulatory neurons in vivo. I propose a multidisciplinary approach, combining local, in vivo POA temperature stimulation with optogenetic circuit-mapping to uncover the molecular and cellular logic of the hypothalamic thermoregulatory centre and to assess its medical potential to counteract metabolic syndrome.
Acclimation is a beneficial adaptive process that fortifies thermal responses upon environmental temperature challenges. Thermoregulatory neuron plasticity is thought to mediate acclimation. Conversely, maladaptive thermoregulatory changes affect obesity. The cell-type-specific neuronal plasticity mechanisms underlying these changes within the POA, however, are unknown.
Using ex-vivo slice electrophysiology and in vivo imaging, I propose to characterize acclimation- and obesity-induced plasticity of thermoregulatory neurons. Ultimately, I aim to manipulate thermoregulatory neuron plasticity to test its potential counter-balancing effect on obesity.
Max ERC Funding
1 902 500 €
Duration
Start date: 2018-09-01, End date: 2023-08-31
Project acronym ACCUPOL
Project Unlimited Growth? A Comparative Analysis of Causes and Consequences of Policy Accumulation
Researcher (PI) Christoph KNILL
Host Institution (HI) LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN
Call Details Advanced Grant (AdG), SH2, ERC-2017-ADG
Summary ACCUPOL systematically analyzes an intuitively well-known, but curiously under-researched phenomenon: policy accumulation. Societal modernization and progress bring about a continuously growing pile of policies in most political systems. At the same time, however, the administrative capacities for implementation are largely stagnant. While being societally desirable in principle, ever-more policies hence may potentially imply less in terms of policy achievements. Whether or not policy accumulation remains at a ‘sustainable’ rate thus crucially affects the long-term output legitimacy of modern democracies.
Given this development, the central focus of ACCUPOL lies on three questions: Do accumulation rates vary across countries and policy sectors? Which factors mitigate policy accumulation? And to what extent is policy accumulation really associated with an increasing prevalence of implementation deficits? In answering these questions, ACCUPOL radically departs from established research traditions in public policy.
First, the project develops new analytical concepts: Rather than relying on individual policy change as the unit of analysis, we consider policy accumulation to assess the growth of policy portfolios over time. In terms of implementation, ACCUPOL takes into account the overall prevalence of implementation deficits in a given sector instead of analyzing the effectiveness of individual implementation processes.
Second, this analytical innovation also implies a paradigmatic theoretical shift. Because existing theories focus on the analysis of individual policies, they are of limited help to understand causes and consequences of policy accumulation. ACCUPOL develops a novel theoretical approach to fill this theoretical gap.
Third, the project provides new empirical evidence on the prevalence of policy accumulation and implementation deficits focusing on 25 OECD countries and two key policy areas (social and environmental policy).
Summary
ACCUPOL systematically analyzes an intuitively well-known, but curiously under-researched phenomenon: policy accumulation. Societal modernization and progress bring about a continuously growing pile of policies in most political systems. At the same time, however, the administrative capacities for implementation are largely stagnant. While being societally desirable in principle, ever-more policies hence may potentially imply less in terms of policy achievements. Whether or not policy accumulation remains at a ‘sustainable’ rate thus crucially affects the long-term output legitimacy of modern democracies.
Given this development, the central focus of ACCUPOL lies on three questions: Do accumulation rates vary across countries and policy sectors? Which factors mitigate policy accumulation? And to what extent is policy accumulation really associated with an increasing prevalence of implementation deficits? In answering these questions, ACCUPOL radically departs from established research traditions in public policy.
First, the project develops new analytical concepts: Rather than relying on individual policy change as the unit of analysis, we consider policy accumulation to assess the growth of policy portfolios over time. In terms of implementation, ACCUPOL takes into account the overall prevalence of implementation deficits in a given sector instead of analyzing the effectiveness of individual implementation processes.
Second, this analytical innovation also implies a paradigmatic theoretical shift. Because existing theories focus on the analysis of individual policies, they are of limited help to understand causes and consequences of policy accumulation. ACCUPOL develops a novel theoretical approach to fill this theoretical gap.
Third, the project provides new empirical evidence on the prevalence of policy accumulation and implementation deficits focusing on 25 OECD countries and two key policy areas (social and environmental policy).
Max ERC Funding
2 359 000 €
Duration
Start date: 2018-10-01, End date: 2023-09-30
Project acronym activeFly
Project Circuit mechanisms of self-movement estimation during walking
Researcher (PI) M Eugenia CHIAPPE
Host Institution (HI) FUNDACAO D. ANNA SOMMER CHAMPALIMAUD E DR. CARLOS MONTEZ CHAMPALIMAUD
Call Details Starting Grant (StG), LS5, ERC-2017-STG
Summary The brain evolves, develops, and operates in the context of animal movements. As a consequence, fundamental brain functions such as spatial perception and motor control critically depend on the precise knowledge of the ongoing body motion. An accurate internal estimate of self-movement is thought to emerge from sensorimotor integration; nonetheless, which circuits perform this internal estimation, and exactly how motor-sensory coordination is implemented within these circuits are basic questions that remain to be poorly understood. There is growing evidence suggesting that, during locomotion, motor-related and visual signals interact at early stages of visual processing. In mammals, however, it is not clear what the function of this interaction is. Recently, we have shown that a population of Drosophila optic-flow processing neurons —neurons that are sensitive to self-generated visual flow, receives convergent visual and walking-related signals to form a faithful representation of the fly’s walking movements. Leveraging from these results, and combining quantitative analysis of behavior with physiology, optogenetics, and modelling, we propose to investigate circuit mechanisms of self-movement estimation during walking. We will:1) use cell specific manipulations to identify what cells are necessary to generate the motor-related activity in the population of visual neurons, 2) record from the identified neurons and correlate their activity with specific locomotor parameters, and 3) perturb the activity of different cell-types within the identified circuits to test their role in the dynamics of the visual neurons, and on the fly’s walking behavior. These experiments will establish unprecedented causal relationships among neural activity, the formation of an internal representation, and locomotor control. The identified sensorimotor principles will establish a framework that can be tested in other scenarios or animal systems with implications both in health and disease.
Summary
The brain evolves, develops, and operates in the context of animal movements. As a consequence, fundamental brain functions such as spatial perception and motor control critically depend on the precise knowledge of the ongoing body motion. An accurate internal estimate of self-movement is thought to emerge from sensorimotor integration; nonetheless, which circuits perform this internal estimation, and exactly how motor-sensory coordination is implemented within these circuits are basic questions that remain to be poorly understood. There is growing evidence suggesting that, during locomotion, motor-related and visual signals interact at early stages of visual processing. In mammals, however, it is not clear what the function of this interaction is. Recently, we have shown that a population of Drosophila optic-flow processing neurons —neurons that are sensitive to self-generated visual flow, receives convergent visual and walking-related signals to form a faithful representation of the fly’s walking movements. Leveraging from these results, and combining quantitative analysis of behavior with physiology, optogenetics, and modelling, we propose to investigate circuit mechanisms of self-movement estimation during walking. We will:1) use cell specific manipulations to identify what cells are necessary to generate the motor-related activity in the population of visual neurons, 2) record from the identified neurons and correlate their activity with specific locomotor parameters, and 3) perturb the activity of different cell-types within the identified circuits to test their role in the dynamics of the visual neurons, and on the fly’s walking behavior. These experiments will establish unprecedented causal relationships among neural activity, the formation of an internal representation, and locomotor control. The identified sensorimotor principles will establish a framework that can be tested in other scenarios or animal systems with implications both in health and disease.
Max ERC Funding
1 500 000 €
Duration
Start date: 2017-11-01, End date: 2022-10-31
Project acronym AIR-NB
Project Pre-natal exposure to urban AIR pollution and pre- and post-Natal Brain development
Researcher (PI) Jordi Sunyer
Host Institution (HI) FUNDACION PRIVADA INSTITUTO DE SALUD GLOBAL BARCELONA
Call Details Advanced Grant (AdG), LS7, ERC-2017-ADG
Summary Air pollution is the main urban-related environmental hazard. It appears to affect brain development, although current evidence is inadequate given the lack of studies during the most vulnerable stages of brain development and the lack of brain anatomical structure and regional connectivity data underlying these effects. Of particular interest is the prenatal period, when brain structures are forming and growing, and when the effect of in utero exposure to environmental factors may cause permanent brain injury. I and others have conducted studies focused on effects during school age which could be less profound. I postulate that: pre-natal exposure to urban air pollution during pregnancy impairs foetal and postnatal brain development, mainly by affecting myelination; these effects are at least partially mediated by translocation of airborne particulate matter to the placenta and by placental dysfunction; and prenatal exposure to air pollution impairs post-natal brain development independently of urban context and post-natal exposure to air pollution. I aim to evaluate the effect of pre-natal exposure to urban air pollution on pre- and post-natal brain structure and function by following 900 pregnant women and their neonates with contrasting levels of pre-natal exposure to air pollutants by: i) establishing a new pregnancy cohort and evaluating brain imaging (pre-natal and neo-natal brain structure, connectivity and function), and post-natal motor and cognitive development; ii) measuring total personal exposure and inhaled dose of air pollutants during specific time-windows of gestation, noise, paternal stress and other stressors, using personal samplers and sensors; iii) detecting nanoparticles in placenta and its vascular function; iv) modelling mathematical causality and mediation, including a replication study in an external cohort. The expected results will create an impulse to implement policy interventions that genuinely protect the health of urban citizens.
Summary
Air pollution is the main urban-related environmental hazard. It appears to affect brain development, although current evidence is inadequate given the lack of studies during the most vulnerable stages of brain development and the lack of brain anatomical structure and regional connectivity data underlying these effects. Of particular interest is the prenatal period, when brain structures are forming and growing, and when the effect of in utero exposure to environmental factors may cause permanent brain injury. I and others have conducted studies focused on effects during school age which could be less profound. I postulate that: pre-natal exposure to urban air pollution during pregnancy impairs foetal and postnatal brain development, mainly by affecting myelination; these effects are at least partially mediated by translocation of airborne particulate matter to the placenta and by placental dysfunction; and prenatal exposure to air pollution impairs post-natal brain development independently of urban context and post-natal exposure to air pollution. I aim to evaluate the effect of pre-natal exposure to urban air pollution on pre- and post-natal brain structure and function by following 900 pregnant women and their neonates with contrasting levels of pre-natal exposure to air pollutants by: i) establishing a new pregnancy cohort and evaluating brain imaging (pre-natal and neo-natal brain structure, connectivity and function), and post-natal motor and cognitive development; ii) measuring total personal exposure and inhaled dose of air pollutants during specific time-windows of gestation, noise, paternal stress and other stressors, using personal samplers and sensors; iii) detecting nanoparticles in placenta and its vascular function; iv) modelling mathematical causality and mediation, including a replication study in an external cohort. The expected results will create an impulse to implement policy interventions that genuinely protect the health of urban citizens.
Max ERC Funding
2 499 992 €
Duration
Start date: 2018-09-01, End date: 2023-08-31
Project acronym ARMOR-T
Project Armoring multifunctional T cells for cancer therapy
Researcher (PI) Sebastian Kobold
Host Institution (HI) LUDWIG-MAXIMILIANS-UNIVERSITAET MUENCHEN
Call Details Starting Grant (StG), LS7, ERC-2017-STG
Summary Adoptive T cell therapy (ACT) is a powerful approach to treat even advanced cancer diseases where poor prognosis calls for innovative treatments. However ACT is critically limited by insufficient T cell infiltration into the tumor, T cell activation at the tumor site and local T cell suppression. Few advances have been made in the field to tackle these limitations besides increasing T cell activation. My group has focussed on these unaddressed issues but came to realise that tackling these one by one will not be sufficient. I have developed a panel of unpublished chemokine receptors and innovative modular antibody-activated receptors which have the potential to overcome the limitations of ACT against solid tumors. This ground-breaking portfolio places my group in the unique position to address combination of synergistic receptors and enable cellular therapies in previously unsuccessful indications. My project will provide the rationale for provision of an effective cancer treatment. The goal is to develop the next generation of ACT through T cell engineering both by forced expression of migratory and activating receptors and simultaneous deletion of immune suppressive molecules by gene editing. ARMOR-T will provide the basis for further preclinical and clinical development of a pioneering cellular product devoid of the limitations of available products to date. I will prove 1) synergy between migratory and modular activating receptors, 2) feasibility to integrate gene editing into a T cell expansion protocol, 3) synergy between gene editing, migratory and modular receptors and 4) efficacy, safety and mode of action. The main work of the project will be carried out in models of pancreatic cancer. The ARMOR-T platform will subsequently be translated to other cancer entities where response to ACT is likely such as melanoma, breast or colon cancer, providing less toxic and more effective therapies to otherwise untreatable disease.
Summary
Adoptive T cell therapy (ACT) is a powerful approach to treat even advanced cancer diseases where poor prognosis calls for innovative treatments. However ACT is critically limited by insufficient T cell infiltration into the tumor, T cell activation at the tumor site and local T cell suppression. Few advances have been made in the field to tackle these limitations besides increasing T cell activation. My group has focussed on these unaddressed issues but came to realise that tackling these one by one will not be sufficient. I have developed a panel of unpublished chemokine receptors and innovative modular antibody-activated receptors which have the potential to overcome the limitations of ACT against solid tumors. This ground-breaking portfolio places my group in the unique position to address combination of synergistic receptors and enable cellular therapies in previously unsuccessful indications. My project will provide the rationale for provision of an effective cancer treatment. The goal is to develop the next generation of ACT through T cell engineering both by forced expression of migratory and activating receptors and simultaneous deletion of immune suppressive molecules by gene editing. ARMOR-T will provide the basis for further preclinical and clinical development of a pioneering cellular product devoid of the limitations of available products to date. I will prove 1) synergy between migratory and modular activating receptors, 2) feasibility to integrate gene editing into a T cell expansion protocol, 3) synergy between gene editing, migratory and modular receptors and 4) efficacy, safety and mode of action. The main work of the project will be carried out in models of pancreatic cancer. The ARMOR-T platform will subsequently be translated to other cancer entities where response to ACT is likely such as melanoma, breast or colon cancer, providing less toxic and more effective therapies to otherwise untreatable disease.
Max ERC Funding
1 636 710 €
Duration
Start date: 2018-03-01, End date: 2023-02-28
Project acronym ARTTOUCH
Project Generating artificial touch: from the contribution of single tactile afferents to the encoding of complex percepts, and their implications for clinical innovation
Researcher (PI) Rochelle ACKERLEY
Host Institution (HI) CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS
Call Details Consolidator Grant (CoG), LS5, ERC-2017-COG
Summary Somatosensation encompass a wide range of processes, from feeling touch to temperature, as well as experiencing pleasure and pain. When afferent inputs are degraded or removed, such as in neuropathies or amputation, exploring the world becomes extremely difficult. Chronic pain is a major health issue that greatly diminishes quality of life and is one of the most disabling and costly conditions in Europe. The loss of a body part is common due to accidents, tumours, or peripheral diseases, and it has instantaneous effects on somatosensory functioning. Treating such disorders entails detailed knowledge about how somatosensory signals are encoded. Understanding these processes will enable the restoration of healthy function, such as providing real-time, naturalistic feedback in prostheses. To date, no prosthesis currently provides long-term sensory feedback, yet accomplishing this will lead to great quality of life improvements. The present proposal aims to uncover how basic tactile processes are encoded and represented centrally, as well as how more complex somatosensation is generated (e.g. wetness, pleasantness). Novel investigations will be conducted in humans to probe these mechanisms, including peripheral in vivo recording (microneurography) and neural stimulation, combined with advanced brain imaging and behavioural experiments. Preliminary work has shown the feasibility of the approach, where it is possible to visualise the activation of single mechanoreceptive afferents in the human brain. The multi-disciplinary approach unites detailed, high-resolution, functional investigations with actual sensations generated. The results will elucidate how basic and complex somatosensory processes are encoded, providing insights into the recovery of such signals. The knowledge gained aims to provide pain-free, efficient diagnostic capabilities for detecting and quantifying a range of somatosensory disorders, as well as identifying new potential therapeutic targets.
Summary
Somatosensation encompass a wide range of processes, from feeling touch to temperature, as well as experiencing pleasure and pain. When afferent inputs are degraded or removed, such as in neuropathies or amputation, exploring the world becomes extremely difficult. Chronic pain is a major health issue that greatly diminishes quality of life and is one of the most disabling and costly conditions in Europe. The loss of a body part is common due to accidents, tumours, or peripheral diseases, and it has instantaneous effects on somatosensory functioning. Treating such disorders entails detailed knowledge about how somatosensory signals are encoded. Understanding these processes will enable the restoration of healthy function, such as providing real-time, naturalistic feedback in prostheses. To date, no prosthesis currently provides long-term sensory feedback, yet accomplishing this will lead to great quality of life improvements. The present proposal aims to uncover how basic tactile processes are encoded and represented centrally, as well as how more complex somatosensation is generated (e.g. wetness, pleasantness). Novel investigations will be conducted in humans to probe these mechanisms, including peripheral in vivo recording (microneurography) and neural stimulation, combined with advanced brain imaging and behavioural experiments. Preliminary work has shown the feasibility of the approach, where it is possible to visualise the activation of single mechanoreceptive afferents in the human brain. The multi-disciplinary approach unites detailed, high-resolution, functional investigations with actual sensations generated. The results will elucidate how basic and complex somatosensory processes are encoded, providing insights into the recovery of such signals. The knowledge gained aims to provide pain-free, efficient diagnostic capabilities for detecting and quantifying a range of somatosensory disorders, as well as identifying new potential therapeutic targets.
Max ERC Funding
1 223 639 €
Duration
Start date: 2019-01-01, End date: 2023-12-31
Project acronym ASA
Project Understanding Statehood through Architecture: a comparative study of Africa's state buildings
Researcher (PI) Julia Catherine GALLAGHER
Host Institution (HI) SCHOOL OF ORIENTAL AND AFRICAN STUDIES ROYAL CHARTER
Call Details Consolidator Grant (CoG), SH2, ERC-2017-COG
Summary The project will develop a new ethnography of statehood through architecture. It goes beyond conventional approaches to statehood, which describe states as an objectively existing set of tools used to run a country, and critical approaches that understand them as discursive constructs. Instead, this research understands statehood as a result of the relationship between functions and symbols, and will read it through an innovative new methodology, namely a study of state architecture.
The study will focus on state buildings in Africa. African statehood, uncertain and often ambiguous, in many cases profoundly shaped by colonial heritages and post-colonial relationships, is reflected in classical-colonial, modernist-nationalist and post-modern or vernacular styles of architecture. African state buildings reveal the complex interplay of ideas, activities and relationships that together constitute an often uncomfortable statehood. They symbolise the state, embodying and projecting ideas of it through their aesthetics; they enable its concrete functions and processes; and they reveal what citizens think about the state in the ways they describe and negotiate them.
The study is comparative, multi-layered and interdisciplinary. It focuses on seven countries (South Africa, Tanzania, DR Congo, Ethiopia, Ghana, Côte d’Ivoire and Guinea Bissau), exploring politics and statehood on domestic, regional and international levels, and drawing on theory and methods from political science, history, sociology, art and architecture theory. It employs innovative ethnographic methods, including the collection and display of photographs in interactive exhibitions staged in Africa to explore the ways citizens think about and use state buildings.
This project will provide an innovative reading of how African statehood is expressed and how it looks and feels to African citizens. In doing this, it will make a distinctive new contribution to understanding how statehood works everywhere.
Summary
The project will develop a new ethnography of statehood through architecture. It goes beyond conventional approaches to statehood, which describe states as an objectively existing set of tools used to run a country, and critical approaches that understand them as discursive constructs. Instead, this research understands statehood as a result of the relationship between functions and symbols, and will read it through an innovative new methodology, namely a study of state architecture.
The study will focus on state buildings in Africa. African statehood, uncertain and often ambiguous, in many cases profoundly shaped by colonial heritages and post-colonial relationships, is reflected in classical-colonial, modernist-nationalist and post-modern or vernacular styles of architecture. African state buildings reveal the complex interplay of ideas, activities and relationships that together constitute an often uncomfortable statehood. They symbolise the state, embodying and projecting ideas of it through their aesthetics; they enable its concrete functions and processes; and they reveal what citizens think about the state in the ways they describe and negotiate them.
The study is comparative, multi-layered and interdisciplinary. It focuses on seven countries (South Africa, Tanzania, DR Congo, Ethiopia, Ghana, Côte d’Ivoire and Guinea Bissau), exploring politics and statehood on domestic, regional and international levels, and drawing on theory and methods from political science, history, sociology, art and architecture theory. It employs innovative ethnographic methods, including the collection and display of photographs in interactive exhibitions staged in Africa to explore the ways citizens think about and use state buildings.
This project will provide an innovative reading of how African statehood is expressed and how it looks and feels to African citizens. In doing this, it will make a distinctive new contribution to understanding how statehood works everywhere.
Max ERC Funding
1 870 665 €
Duration
Start date: 2018-09-01, End date: 2023-08-31
Project acronym ASSESS
Project Episodic Mass Loss in the Most Massive Stars: Key to Understanding the Explosive Early Universe
Researcher (PI) Alceste BONANOS
Host Institution (HI) NATIONAL OBSERVATORY OF ATHENS
Call Details Consolidator Grant (CoG), PE9, ERC-2017-COG
Summary Massive stars dominate their surroundings during their short lifetimes, while their explosive deaths impact the chemical evolution and spatial cohesion of their hosts. After birth, their evolution is largely dictated by their ability to remove layers of hydrogen from their envelopes. Multiple lines of evidence are pointing to violent, episodic mass-loss events being responsible for removing a large part of the massive stellar envelope, especially in low-metallicity galaxies. Episodic mass loss, however, is not understood theoretically, neither accounted for in state-of-the-art models of stellar evolution, which has far-reaching consequences for many areas of astronomy. We aim to determine whether episodic mass loss is a dominant process in the evolution of the most massive stars by conducting the first extensive, multi-wavelength survey of evolved massive stars in the nearby Universe. The project hinges on the fact that mass-losing stars form dust and are bright in the mid-infrared. We plan to (i) derive physical parameters of a large sample of dusty, evolved targets and estimate the amount of ejected mass, (ii) constrain evolutionary models, (iii) quantify the duration and frequency of episodic mass loss as a function of metallicity. The approach involves applying machine-learning algorithms to existing multi-band and time-series photometry of luminous sources in ~25 nearby galaxies. Dusty, luminous evolved massive stars will thus be automatically classified and follow-up spectroscopy will be obtained for selected targets. Atmospheric and SED modeling will yield parameters and estimates of time-dependent mass loss for ~1000 luminous stars. The emerging trend for the ubiquity of episodic mass loss, if confirmed, will be key to understanding the explosive early Universe and will have profound consequences for low-metallicity stars, reionization, and the chemical evolution of galaxies.
Summary
Massive stars dominate their surroundings during their short lifetimes, while their explosive deaths impact the chemical evolution and spatial cohesion of their hosts. After birth, their evolution is largely dictated by their ability to remove layers of hydrogen from their envelopes. Multiple lines of evidence are pointing to violent, episodic mass-loss events being responsible for removing a large part of the massive stellar envelope, especially in low-metallicity galaxies. Episodic mass loss, however, is not understood theoretically, neither accounted for in state-of-the-art models of stellar evolution, which has far-reaching consequences for many areas of astronomy. We aim to determine whether episodic mass loss is a dominant process in the evolution of the most massive stars by conducting the first extensive, multi-wavelength survey of evolved massive stars in the nearby Universe. The project hinges on the fact that mass-losing stars form dust and are bright in the mid-infrared. We plan to (i) derive physical parameters of a large sample of dusty, evolved targets and estimate the amount of ejected mass, (ii) constrain evolutionary models, (iii) quantify the duration and frequency of episodic mass loss as a function of metallicity. The approach involves applying machine-learning algorithms to existing multi-band and time-series photometry of luminous sources in ~25 nearby galaxies. Dusty, luminous evolved massive stars will thus be automatically classified and follow-up spectroscopy will be obtained for selected targets. Atmospheric and SED modeling will yield parameters and estimates of time-dependent mass loss for ~1000 luminous stars. The emerging trend for the ubiquity of episodic mass loss, if confirmed, will be key to understanding the explosive early Universe and will have profound consequences for low-metallicity stars, reionization, and the chemical evolution of galaxies.
Max ERC Funding
1 128 750 €
Duration
Start date: 2018-09-01, End date: 2023-08-31
Project acronym Asterochronometry
Project Galactic archeology with high temporal resolution
Researcher (PI) Andrea MIGLIO
Host Institution (HI) THE UNIVERSITY OF BIRMINGHAM
Call Details Consolidator Grant (CoG), PE9, ERC-2017-COG
Summary The Milky Way is a complex system, with dynamical and chemical substructures, where several competing processes such as mergers, internal secular evolution, gas accretion and gas flows take place. To study in detail how such a giant spiral galaxy was formed and evolved, we need to reconstruct the sequence of its main formation events with high (~10%) temporal resolution.
Asterochronometry will determine accurate, precise ages for tens of thousands of stars in the Galaxy. We will take an approach distinguished by a number of key aspects including, developing novel star-dating methods that fully utilise the potential of individual pulsation modes, coupled with a careful appraisal of systematic uncertainties on age deriving from our limited understanding of stellar physics.
We will then capitalise on opportunities provided by the timely availability of astrometric, spectroscopic, and asteroseismic data to build and data-mine chrono-chemo-dynamical maps of regions of the Milky Way probed by the space missions CoRoT, Kepler, K2, and TESS. We will quantify, by comparison with predictions of chemodynamical models, the relative importance of various processes which play a role in shaping the Galaxy, for example mergers and dynamical processes. We will use chrono-chemical tagging to look for evidence of aggregates, and precise and accurate ages to reconstruct the early star formation history of the Milky Way’s main constituents.
The Asterochronometry project will also provide stringent observational tests of stellar structure and answer some of the long-standing open questions in stellar modelling (e.g. efficiency of transport processes, mass loss on the giant branch, the occurrence of products of coalescence / mass exchange). These tests will improve our ability to determine stellar ages and chemical yields, with wide impact e.g. on the characterisation and ensemble studies of exoplanets, on evolutionary population synthesis, integrated colours and thus ages of galaxies.
Summary
The Milky Way is a complex system, with dynamical and chemical substructures, where several competing processes such as mergers, internal secular evolution, gas accretion and gas flows take place. To study in detail how such a giant spiral galaxy was formed and evolved, we need to reconstruct the sequence of its main formation events with high (~10%) temporal resolution.
Asterochronometry will determine accurate, precise ages for tens of thousands of stars in the Galaxy. We will take an approach distinguished by a number of key aspects including, developing novel star-dating methods that fully utilise the potential of individual pulsation modes, coupled with a careful appraisal of systematic uncertainties on age deriving from our limited understanding of stellar physics.
We will then capitalise on opportunities provided by the timely availability of astrometric, spectroscopic, and asteroseismic data to build and data-mine chrono-chemo-dynamical maps of regions of the Milky Way probed by the space missions CoRoT, Kepler, K2, and TESS. We will quantify, by comparison with predictions of chemodynamical models, the relative importance of various processes which play a role in shaping the Galaxy, for example mergers and dynamical processes. We will use chrono-chemical tagging to look for evidence of aggregates, and precise and accurate ages to reconstruct the early star formation history of the Milky Way’s main constituents.
The Asterochronometry project will also provide stringent observational tests of stellar structure and answer some of the long-standing open questions in stellar modelling (e.g. efficiency of transport processes, mass loss on the giant branch, the occurrence of products of coalescence / mass exchange). These tests will improve our ability to determine stellar ages and chemical yields, with wide impact e.g. on the characterisation and ensemble studies of exoplanets, on evolutionary population synthesis, integrated colours and thus ages of galaxies.
Max ERC Funding
1 958 863 €
Duration
Start date: 2018-04-01, End date: 2023-03-31
Project acronym AstroNeuroCrosstalk
Project Astrocyte-Neuronal Crosstalk in Obesity and Diabetes
Researcher (PI) Cristina GARCÍA CÁCERES
Host Institution (HI) HELMHOLTZ ZENTRUM MUENCHEN DEUTSCHES FORSCHUNGSZENTRUM FUER GESUNDHEIT UND UMWELT GMBH
Call Details Starting Grant (StG), LS5, ERC-2017-STG
Summary Despite considerable efforts aimed at prevention and treatment, the prevalence of obesity and type 2 diabetes has increased at an alarming rate worldwide over recent decades. Given the urgent need to develop safe and efficient anti-obesity drugs, the scientific community has to intensify efforts to better understand the mechanisms involved in the pathogenesis of obesity. Based on human genome-wide association studies and targeted mouse mutagenesis models, it has recently emerged that the brain controls most aspects of systemic metabolism and that obesity may be a brain disease. I have recently shown that like neurons, astrocytes also respond to circulating nutrients, and they cooperate with neurons to efficiently regulate energy metabolism. So far, the study of brain circuits controlling energy balance has focused on neurons, ignoring the presence and role of astrocytes. Importantly, our studies were the first to describe that exposure to a high-fat, highsugar (HFHS) diet triggers hypothalamic astrogliosis prior to significant body weight gain, indicating a potentially important role in promoting obesity. Overall, my recent findings suggest a novel model in which astrocytes are actively involved in the central nervous system (CNS) control of metabolism, likely including active crosstalk between astrocytes and neurons. To test this hypothetical model, I propose to develop a functional understanding of astroglia-neuronal communication in the CNS control of metabolism focusing on: 1) dissecting the ability of astrocytes to release gliotransmitters to neurons, 2) assessing how astrocytes respond to neuronal activity, and 3) determining if HFHS-induced astrogliosis interrupts this crosstalk and contributes to the development of obesity and type 2 diabetes. These studies aim to uncover the molecular underpinnings of astrocyte-neuron inputs regulating metabolism in health and disease so as to
inspire and enable novel therapeutic strategies to fight diabetes and obesity.
Summary
Despite considerable efforts aimed at prevention and treatment, the prevalence of obesity and type 2 diabetes has increased at an alarming rate worldwide over recent decades. Given the urgent need to develop safe and efficient anti-obesity drugs, the scientific community has to intensify efforts to better understand the mechanisms involved in the pathogenesis of obesity. Based on human genome-wide association studies and targeted mouse mutagenesis models, it has recently emerged that the brain controls most aspects of systemic metabolism and that obesity may be a brain disease. I have recently shown that like neurons, astrocytes also respond to circulating nutrients, and they cooperate with neurons to efficiently regulate energy metabolism. So far, the study of brain circuits controlling energy balance has focused on neurons, ignoring the presence and role of astrocytes. Importantly, our studies were the first to describe that exposure to a high-fat, highsugar (HFHS) diet triggers hypothalamic astrogliosis prior to significant body weight gain, indicating a potentially important role in promoting obesity. Overall, my recent findings suggest a novel model in which astrocytes are actively involved in the central nervous system (CNS) control of metabolism, likely including active crosstalk between astrocytes and neurons. To test this hypothetical model, I propose to develop a functional understanding of astroglia-neuronal communication in the CNS control of metabolism focusing on: 1) dissecting the ability of astrocytes to release gliotransmitters to neurons, 2) assessing how astrocytes respond to neuronal activity, and 3) determining if HFHS-induced astrogliosis interrupts this crosstalk and contributes to the development of obesity and type 2 diabetes. These studies aim to uncover the molecular underpinnings of astrocyte-neuron inputs regulating metabolism in health and disease so as to
inspire and enable novel therapeutic strategies to fight diabetes and obesity.
Max ERC Funding
1 499 938 €
Duration
Start date: 2018-01-01, End date: 2022-12-31
