Project acronym QITBOX
Project Quantum Information Theory with black BOXes
Researcher (PI) Antonio Acín
Host Institution (HI) FUNDACIO INSTITUT DE CIENCIES FOTONIQUES
Call Details Consolidator Grant (CoG), PE2, ERC-2013-CoG
Summary "With QITBOX we aim to develop a novel device-independent framework for quantum information processing. In this framework, devices are seen as black boxes that only receive inputs and produce outputs. Our main objective is to understand what can and cannot be done for information processing using only the observed correlations among the devices. We will structure our effort along three main research lines: (i) Characterization of quantum correlations: the general objective will be to characterize those correlations that are possible among quantum devices; (ii) Protocols based on correlations: the general objective will be to understand how quantum correlations can be exploited in order to construct relevant information protocols and (iii) Applications to physical setups: here the previous results to concrete physical setups will be applied, such as the quantum-optical realizations of the protocols or the study of the non-local properties of many-body systems. The expected results of QITBOX are: (i) Novel methods for the characterization of quantum correlations, (ii) Improved or novel device-independent protocols, (iii) Proposals for feasible experimental implementations of these protocols and (iv) Novel methods for the study of many-body systems based on correlations. QITBOX is a highly-interdisciplinary project with implications in Physics, Mathematics, Computer Science and Engineering. The execution of the planned research work will provide a unifying framework for a Quantum Information Theory with black BOXes (hence the acronym). Such a framework will bring quantum information processing to an unprecedented level of abstraction, in which information protocols and primitives are defined without any reference to the internal physical working of the devices. This, in turn, will lead to much more robust practical implementations of quantum information protocols, closing the mismatch between theoretical requirements and experimental realisations."
Summary
"With QITBOX we aim to develop a novel device-independent framework for quantum information processing. In this framework, devices are seen as black boxes that only receive inputs and produce outputs. Our main objective is to understand what can and cannot be done for information processing using only the observed correlations among the devices. We will structure our effort along three main research lines: (i) Characterization of quantum correlations: the general objective will be to characterize those correlations that are possible among quantum devices; (ii) Protocols based on correlations: the general objective will be to understand how quantum correlations can be exploited in order to construct relevant information protocols and (iii) Applications to physical setups: here the previous results to concrete physical setups will be applied, such as the quantum-optical realizations of the protocols or the study of the non-local properties of many-body systems. The expected results of QITBOX are: (i) Novel methods for the characterization of quantum correlations, (ii) Improved or novel device-independent protocols, (iii) Proposals for feasible experimental implementations of these protocols and (iv) Novel methods for the study of many-body systems based on correlations. QITBOX is a highly-interdisciplinary project with implications in Physics, Mathematics, Computer Science and Engineering. The execution of the planned research work will provide a unifying framework for a Quantum Information Theory with black BOXes (hence the acronym). Such a framework will bring quantum information processing to an unprecedented level of abstraction, in which information protocols and primitives are defined without any reference to the internal physical working of the devices. This, in turn, will lead to much more robust practical implementations of quantum information protocols, closing the mismatch between theoretical requirements and experimental realisations."
Max ERC Funding
1 487 505 €
Duration
Start date: 2014-01-01, End date: 2019-12-31
Project acronym RSHEALTH
Project Investigating the causes and consequences of replication stress in mammalian health
Researcher (PI) Oscar Fernandez-Capetillo Ruiz
Host Institution (HI) FUNDACION CENTRO NACIONAL DE INVESTIGACIONES ONCOLOGICAS CARLOS III
Call Details Consolidator Grant (CoG), LS3, ERC-2013-CoG
Summary "DNA damage (DD) is the cause of several diseases, including cancer, and it is also linked to the organ decline that arises in ageing. Yet, the contribution of different sources of DD to these processes is not understood. Sources of DD such as chromosome breaks, eroded telomeres or oxidative stress are been heavily investigated. For establishing my group, I decided to focus on a source of DD that arises every time a cell replicates its DNA, and which is known as replication stress (RS). In short, RS stands for the excessive accumulation of single-stranded DNA at replication forks that, due to its recombinogenic nature, can initiate genomic rearrangements. Consistently, RS is now known to be a key source of genomic instability in human tumors. In mammalian cells, a signalling cascade initiated by ATR and Chk1 kinases suppresses RS. Unfortunately, the essential nature of these kinases significantly limited the study of the RS-response in mammals. In the initial years of our lab we have developed several tools that facilitate the study of RS in mammals. These include a cellular system where ATR can be activated at will, potent and selective ATR inhibitors, and mice with reduced or increased levels of ATR and Chk1 kinases. These tools have allowed us to start exploring how RS impacts on cancer and ageing, as well as to investigate the potential of targeting ATR for cancer therapy. Yet, the field of RS is still poorly developed, and many basic questions are still in the need of answers.
This application outlines a plan for our research in the next five years, and explains how I propose to investigate RS at molecular, cellular and animal levels. Whereas I plan to capitalize on the tools (published and unpublished) that we have generated within the last few years, I also propose several innovative strategies for the study of the RS-response in mammals. This grant would allow us to consolidate our still young group as a solid laboratory for the study of RS in mammals."
Summary
"DNA damage (DD) is the cause of several diseases, including cancer, and it is also linked to the organ decline that arises in ageing. Yet, the contribution of different sources of DD to these processes is not understood. Sources of DD such as chromosome breaks, eroded telomeres or oxidative stress are been heavily investigated. For establishing my group, I decided to focus on a source of DD that arises every time a cell replicates its DNA, and which is known as replication stress (RS). In short, RS stands for the excessive accumulation of single-stranded DNA at replication forks that, due to its recombinogenic nature, can initiate genomic rearrangements. Consistently, RS is now known to be a key source of genomic instability in human tumors. In mammalian cells, a signalling cascade initiated by ATR and Chk1 kinases suppresses RS. Unfortunately, the essential nature of these kinases significantly limited the study of the RS-response in mammals. In the initial years of our lab we have developed several tools that facilitate the study of RS in mammals. These include a cellular system where ATR can be activated at will, potent and selective ATR inhibitors, and mice with reduced or increased levels of ATR and Chk1 kinases. These tools have allowed us to start exploring how RS impacts on cancer and ageing, as well as to investigate the potential of targeting ATR for cancer therapy. Yet, the field of RS is still poorly developed, and many basic questions are still in the need of answers.
This application outlines a plan for our research in the next five years, and explains how I propose to investigate RS at molecular, cellular and animal levels. Whereas I plan to capitalize on the tools (published and unpublished) that we have generated within the last few years, I also propose several innovative strategies for the study of the RS-response in mammals. This grant would allow us to consolidate our still young group as a solid laboratory for the study of RS in mammals."
Max ERC Funding
1 997 819 €
Duration
Start date: 2014-03-01, End date: 2019-02-28
Project acronym SEARCHLIGHT
Project A new communication paradigm for future very high speed wireless networks
Researcher (PI) Joerg Carsten Widmer
Host Institution (HI) FUNDACION IMDEA NETWORKS
Call Details Consolidator Grant (CoG), PE7, ERC-2013-CoG
Summary "Due to the tremendous growth in mobile devices such as smartphones, tablet PCs, and laptops over the past years, a larger and larger fraction of Internet traffic is delivered wirelessly. Dealing with this vast increase in traffic is one of the most important challenges for future wireless networks. State-of-the-art wireless communication already operates close to Shannon capacity. The only viable option to further increase data rates is to use high bandwidth channels in the very high frequency part of the radio spectrum. However, this spectrum suffers from high attenuation and signal absorption, restricting communication primarily to line-of-sight (LOS) scenarios. This in turn requires a radical rethinking of wireless networking. We envision that future wireless networks will consist of many highly directional LOS channels for communication between access points (APs) and end devices. Such an environment is extremely dynamic, in particular for mobile devices. At the same time, such channels experience very little interference and resources that would otherwise be used to handle interference can now be used to further increase achievable data rates.
We propose to build a wireless network architecture that maintains directional LOS channels between several APs and (mobile) end devices. Data is transmitted via all of these channels and end device uses multiple antennas to receive and decode several such data streams simultaneously. The main complexity of the design lies in the selection of APs as well as the beamforming directions of their antennas, given the large number of end devices that future wireless networks will have to support. To speed up this decision process, the system maintains a map of the radio environment and learns likely sequences of beamforming patterns and APs. This further allows to intelligently switch off APs to improve energy efficiency. We believe that such a design is the key element for the scalability of future wireless networks."
Summary
"Due to the tremendous growth in mobile devices such as smartphones, tablet PCs, and laptops over the past years, a larger and larger fraction of Internet traffic is delivered wirelessly. Dealing with this vast increase in traffic is one of the most important challenges for future wireless networks. State-of-the-art wireless communication already operates close to Shannon capacity. The only viable option to further increase data rates is to use high bandwidth channels in the very high frequency part of the radio spectrum. However, this spectrum suffers from high attenuation and signal absorption, restricting communication primarily to line-of-sight (LOS) scenarios. This in turn requires a radical rethinking of wireless networking. We envision that future wireless networks will consist of many highly directional LOS channels for communication between access points (APs) and end devices. Such an environment is extremely dynamic, in particular for mobile devices. At the same time, such channels experience very little interference and resources that would otherwise be used to handle interference can now be used to further increase achievable data rates.
We propose to build a wireless network architecture that maintains directional LOS channels between several APs and (mobile) end devices. Data is transmitted via all of these channels and end device uses multiple antennas to receive and decode several such data streams simultaneously. The main complexity of the design lies in the selection of APs as well as the beamforming directions of their antennas, given the large number of end devices that future wireless networks will have to support. To speed up this decision process, the system maintains a map of the radio environment and learns likely sequences of beamforming patterns and APs. This further allows to intelligently switch off APs to improve energy efficiency. We believe that such a design is the key element for the scalability of future wireless networks."
Max ERC Funding
1 719 960 €
Duration
Start date: 2014-04-01, End date: 2019-03-31
Project acronym SYSPHARMAD
Project A systems pharmacology approach to the discovery of novel therapeutics in Alzheimer´s disease
Researcher (PI) Patricio Aloy Calaf
Host Institution (HI) FUNDACIO INSTITUT DE RECERCA BIOMEDICA (IRB BARCELONA)
Call Details Consolidator Grant (CoG), LS2, ERC-2013-CoG
Summary Alzheimer´s disease (AD) is the most common form of dementia, with over 35 million people suffering from it worldwide, and it constitutes a personal and societal tragedy of immense proportions. Fifty years of intense research have revealed many key elements of the biology of this neurodegenerative disorder. However, our understanding of the molecular bases of the disease is still very limited, and the available medical treatments for AD are purely symptomatic and hardly effective. It is now clear that the modulation of a single target is unlikely to yield the desired outcome, and we should move from gene-centric to network-centric therapeutic strategies. In addition, we should focus on early (asymptomatic) phases of AD, before the brain damage is irreversible, and the identification of molecular biomarkers to monitor the response of patients is paramount.
Accordingly, the main objective of our proposal is the identification of novel biomarkers in AD to monitor the onset and progression of the pathology from very early stages, and to discover combinations of drug targets and chemical compounds able to modify the biology of the disease. We will first run proteomics and transcriptomics experiments, in AD mouse models, to reveal the organization of proteins and genes that are up- or down-regulated at different ages and AD stages, and their potential translocation into/out of mitochondria. We will then construct the AD-associated network, incorporating clinical data, which we will use as a framework for the integration and analyses of the –omics data collected. We will transform the static data snapshots, corresponding to the different AD stages, into a dynamic model able to explain the progression of the disease, providing hints as to the best strategies to monitor and modulate AD evolution. We will finally design and validate a systems pharmacology strategy, based on concerted multi-target perturbations with small molecules, to modify the biology of the disease.
Summary
Alzheimer´s disease (AD) is the most common form of dementia, with over 35 million people suffering from it worldwide, and it constitutes a personal and societal tragedy of immense proportions. Fifty years of intense research have revealed many key elements of the biology of this neurodegenerative disorder. However, our understanding of the molecular bases of the disease is still very limited, and the available medical treatments for AD are purely symptomatic and hardly effective. It is now clear that the modulation of a single target is unlikely to yield the desired outcome, and we should move from gene-centric to network-centric therapeutic strategies. In addition, we should focus on early (asymptomatic) phases of AD, before the brain damage is irreversible, and the identification of molecular biomarkers to monitor the response of patients is paramount.
Accordingly, the main objective of our proposal is the identification of novel biomarkers in AD to monitor the onset and progression of the pathology from very early stages, and to discover combinations of drug targets and chemical compounds able to modify the biology of the disease. We will first run proteomics and transcriptomics experiments, in AD mouse models, to reveal the organization of proteins and genes that are up- or down-regulated at different ages and AD stages, and their potential translocation into/out of mitochondria. We will then construct the AD-associated network, incorporating clinical data, which we will use as a framework for the integration and analyses of the –omics data collected. We will transform the static data snapshots, corresponding to the different AD stages, into a dynamic model able to explain the progression of the disease, providing hints as to the best strategies to monitor and modulate AD evolution. We will finally design and validate a systems pharmacology strategy, based on concerted multi-target perturbations with small molecules, to modify the biology of the disease.
Max ERC Funding
1 296 000 €
Duration
Start date: 2014-04-01, End date: 2019-03-31
Project acronym TensionControl
Project Multiscale regulation of epithelial tension
Researcher (PI) Xavier Trepat Guixer
Host Institution (HI) FUNDACIO INSTITUT DE BIOENGINYERIA DE CATALUNYA
Call Details Consolidator Grant (CoG), LS3, ERC-2013-CoG
Summary Throughout development and adult life, the growth and remodelling of living tissues is determined by a complex interplay between chemical and physical cues. Among such physical cues, mechanical tension is emerging as central regulator of cellular fate and function. To explain tension regulation, current research emphasizes molecular mechanisms at an ever increasing level of detail. How these local mechanisms are integrated to give rise to global patterns of tissue tension is unknown, however. The goal of this project is to provide a multiscale understanding of tension regulation within epithelial cell monolayers. We propose two pairs of competing mechanisms for tension regulation: fluidization vs. reinforcement and cell division vs. apoptosis. These competing mechanisms are inherently multiscale in the sense that they span and couple multiple levels of tissue organization, from the local actomyosin contraction to the multicellular rearrangement. For each of these competing mechanisms we plan to study how local processes and interactions give rise to global tensional patterns. To do this, we propose to develop an integrated experimental setup to map and perturb monolayer tension at different length scales. We expect this project to unveil the repertoire of mechanisms that epithelial tissues use to regulate their tension and dynamics.
Summary
Throughout development and adult life, the growth and remodelling of living tissues is determined by a complex interplay between chemical and physical cues. Among such physical cues, mechanical tension is emerging as central regulator of cellular fate and function. To explain tension regulation, current research emphasizes molecular mechanisms at an ever increasing level of detail. How these local mechanisms are integrated to give rise to global patterns of tissue tension is unknown, however. The goal of this project is to provide a multiscale understanding of tension regulation within epithelial cell monolayers. We propose two pairs of competing mechanisms for tension regulation: fluidization vs. reinforcement and cell division vs. apoptosis. These competing mechanisms are inherently multiscale in the sense that they span and couple multiple levels of tissue organization, from the local actomyosin contraction to the multicellular rearrangement. For each of these competing mechanisms we plan to study how local processes and interactions give rise to global tensional patterns. To do this, we propose to develop an integrated experimental setup to map and perturb monolayer tension at different length scales. We expect this project to unveil the repertoire of mechanisms that epithelial tissues use to regulate their tension and dynamics.
Max ERC Funding
1 981 761 €
Duration
Start date: 2015-01-01, End date: 2019-12-31
Project acronym TRANSRIGHTS
Project Gender citizenship and sexual rights in Europe: transgender lives from a transnational perspective
Researcher (PI) Sofia Isabel Da Costa D'aboim Inglez
Host Institution (HI) INSTITUTO DE CIENCIAS SOCIAIS
Call Details Consolidator Grant (CoG), SH2, ERC-2013-CoG
Summary "The TRANSRIGHTS project investigates transgender lives and the institutional apparatus that frames them. Rather than focusing exclusively on self displayed identities, four lines of inquiry will be developed. Firstly, gender politics and sexual rights are analyzed as the opposition between politics of equality and of difference is unable to provide answers for the inclusion of trans-people. Secondly, by comparing the lives of trans-people in five European countries – Portugal, France, United Kingdom, the Netherlands and Sweden – we wish to attain an overview of how institutional frameworks impact on these lives. Thirdly, our approach will take into account the immigration of trans-individuals to Europe, whether in search for recognition or as a way of survival often leading to sex work. Fourthly, by comparing different countries, different groups of transgender people, different forms of attaining inclusion or dealing with exclusion, different conceptions of gender citizenship and sexual rights, we wish not only to gain a deeper understanding of societal change and its impact on the lives of transgender individuals, but also to identify the gaps between policies and rights and the categories actually mobilized for self-identification. Such a task implies examining the voices of trans-people, the effect of policies on the materiality of lives as well as conceptualizations of selfhood that do not necessarily confine to the European context. Project outputs will contribute to the fields of gender, sexuality and citizenship by providing a grounded theoretical debate, discussing the gender categories of citizenship. Trans-people are a heterogeneous group that represents one of the most challenging boundaries for framing this debate within and beyond Europe. The voices of trans-people are essential to avoid an excessive reduction of lives to institutional categories, whether from the institutional apparatus, the LGBT movements or the social sciences."
Summary
"The TRANSRIGHTS project investigates transgender lives and the institutional apparatus that frames them. Rather than focusing exclusively on self displayed identities, four lines of inquiry will be developed. Firstly, gender politics and sexual rights are analyzed as the opposition between politics of equality and of difference is unable to provide answers for the inclusion of trans-people. Secondly, by comparing the lives of trans-people in five European countries – Portugal, France, United Kingdom, the Netherlands and Sweden – we wish to attain an overview of how institutional frameworks impact on these lives. Thirdly, our approach will take into account the immigration of trans-individuals to Europe, whether in search for recognition or as a way of survival often leading to sex work. Fourthly, by comparing different countries, different groups of transgender people, different forms of attaining inclusion or dealing with exclusion, different conceptions of gender citizenship and sexual rights, we wish not only to gain a deeper understanding of societal change and its impact on the lives of transgender individuals, but also to identify the gaps between policies and rights and the categories actually mobilized for self-identification. Such a task implies examining the voices of trans-people, the effect of policies on the materiality of lives as well as conceptualizations of selfhood that do not necessarily confine to the European context. Project outputs will contribute to the fields of gender, sexuality and citizenship by providing a grounded theoretical debate, discussing the gender categories of citizenship. Trans-people are a heterogeneous group that represents one of the most challenging boundaries for framing this debate within and beyond Europe. The voices of trans-people are essential to avoid an excessive reduction of lives to institutional categories, whether from the institutional apparatus, the LGBT movements or the social sciences."
Max ERC Funding
1 262 943 €
Duration
Start date: 2014-09-01, End date: 2019-08-31
