Project acronym BEEHIVE
Project Bridging the Evolution and Epidemiology of HIV in Europe
Researcher (PI) Christopher Fraser
Host Institution (HI) THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Call Details Advanced Grant (AdG), LS2, ERC-2013-ADG
Summary The aim of the BEEHIVE project is to generate novel insight into HIV biology, evolution and epidemiology, leveraging next-generation high-throughput sequencing and bioinformatics to produce and analyse whole-genomes of viruses from approximately 3,000 European HIV-1 infected patients. These patients have known dates of infection spread over the last 25 years, good clinical follow up, and a wide range of clinical prognostic indicators and outcomes. The primary objective is to discover the viral genetic determinants of severity of infection and set-point viral load. This primary objective is high-risk & blue-skies: there is ample indirect evidence of polymorphisms that alter virulence, but they have never been identified, and it is not known how easy they are to discover. However, the project is also high-reward: it could lead to a substantial shift in the understanding of HIV disease.
Technologically, the BEEHIVE project will deliver new approaches for undertaking whole genome association studies on RNA viruses, including delivering an innovative high-throughput bioinformatics pipeline for handling genetically diverse viral quasi-species data (with viral diversity both within and between infected patients).
The project also includes secondary and tertiary objectives that address critical open questions in HIV epidemiology and evolution. The secondary objective is to use viral genetic sequences allied to mathematical epidemic models to better understand the resurgent European epidemic amongst high-risk groups, especially men who have sex with men. The aim will not just be to establish who is at risk of infection, which is known from conventional epidemiological approaches, but also to characterise the risk factors for onwards transmission of the virus. Tertiary objectives involve understanding the relationship between the genetic diversity within viral samples, indicative of on-going evolution or dual infections, to clinical outcomes.
Summary
The aim of the BEEHIVE project is to generate novel insight into HIV biology, evolution and epidemiology, leveraging next-generation high-throughput sequencing and bioinformatics to produce and analyse whole-genomes of viruses from approximately 3,000 European HIV-1 infected patients. These patients have known dates of infection spread over the last 25 years, good clinical follow up, and a wide range of clinical prognostic indicators and outcomes. The primary objective is to discover the viral genetic determinants of severity of infection and set-point viral load. This primary objective is high-risk & blue-skies: there is ample indirect evidence of polymorphisms that alter virulence, but they have never been identified, and it is not known how easy they are to discover. However, the project is also high-reward: it could lead to a substantial shift in the understanding of HIV disease.
Technologically, the BEEHIVE project will deliver new approaches for undertaking whole genome association studies on RNA viruses, including delivering an innovative high-throughput bioinformatics pipeline for handling genetically diverse viral quasi-species data (with viral diversity both within and between infected patients).
The project also includes secondary and tertiary objectives that address critical open questions in HIV epidemiology and evolution. The secondary objective is to use viral genetic sequences allied to mathematical epidemic models to better understand the resurgent European epidemic amongst high-risk groups, especially men who have sex with men. The aim will not just be to establish who is at risk of infection, which is known from conventional epidemiological approaches, but also to characterise the risk factors for onwards transmission of the virus. Tertiary objectives involve understanding the relationship between the genetic diversity within viral samples, indicative of on-going evolution or dual infections, to clinical outcomes.
Max ERC Funding
2 499 739 €
Duration
Start date: 2014-04-01, End date: 2019-03-31
Project acronym BESTDECISION
Project "Behavioural Economics and Strategic Decision Making: Theory, Empirics, and Experiments"
Researcher (PI) Vincent Paul Crawford
Host Institution (HI) THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Call Details Advanced Grant (AdG), SH1, ERC-2013-ADG
Summary "I will study questions of central microeconomic importance via interwoven theoretical, empirical, and experimental analyses, from a behavioural perspective combining standard methods with assumptions that better reflect evidence on behaviour and psychological insights. The contributions of behavioural economics have been widely recognized, but the benefits of its insights are far from fully realized. I propose four lines of inquiry that focus on how institutions interact with cognition and behaviour, chosen for their potential to reshape our understanding of important questions and their synergies across lines.
The first line will study nonparametric identification and estimation of reference-dependent versions of the standard microeconomic model of consumer demand or labour supply, the subject of hundreds of empirical studies and perhaps the single most important model in microeconomics. It will allow such studies to consider relevant behavioural factors without imposing structural assumptions as in previous work.
The second line will analyze history-dependent learning in financial crises theoretically and experimentally, with the goal of quantifying how market structure influences the likelihood of a crisis.
The third line will study strategic thinking experimentally, using a powerful new design that links subjects’ searches for hidden payoff information (“eye-movements”) much more directly to thinking.
The fourth line will significantly advance Myerson and Satterthwaite’s analyses of optimal design of bargaining rules and auctions, which first went beyond the analysis of given institutions to study what is possible by designing new institutions, replacing their equilibrium assumption with a nonequilibrium model that is well supported by experiments.
The synergies among these four lines’ theoretical analyses, empirical methods, and data analyses will accelerate progress on each line well beyond what would be possible in a piecemeal approach."
Summary
"I will study questions of central microeconomic importance via interwoven theoretical, empirical, and experimental analyses, from a behavioural perspective combining standard methods with assumptions that better reflect evidence on behaviour and psychological insights. The contributions of behavioural economics have been widely recognized, but the benefits of its insights are far from fully realized. I propose four lines of inquiry that focus on how institutions interact with cognition and behaviour, chosen for their potential to reshape our understanding of important questions and their synergies across lines.
The first line will study nonparametric identification and estimation of reference-dependent versions of the standard microeconomic model of consumer demand or labour supply, the subject of hundreds of empirical studies and perhaps the single most important model in microeconomics. It will allow such studies to consider relevant behavioural factors without imposing structural assumptions as in previous work.
The second line will analyze history-dependent learning in financial crises theoretically and experimentally, with the goal of quantifying how market structure influences the likelihood of a crisis.
The third line will study strategic thinking experimentally, using a powerful new design that links subjects’ searches for hidden payoff information (“eye-movements”) much more directly to thinking.
The fourth line will significantly advance Myerson and Satterthwaite’s analyses of optimal design of bargaining rules and auctions, which first went beyond the analysis of given institutions to study what is possible by designing new institutions, replacing their equilibrium assumption with a nonequilibrium model that is well supported by experiments.
The synergies among these four lines’ theoretical analyses, empirical methods, and data analyses will accelerate progress on each line well beyond what would be possible in a piecemeal approach."
Max ERC Funding
1 985 373 €
Duration
Start date: 2014-04-01, End date: 2019-03-31
Project acronym Coupled gene circuit
Project Dynamics, noise, and coupling in gene circuit modules
Researcher (PI) James Charles Wallace Locke
Host Institution (HI) THE CHANCELLOR MASTERS AND SCHOLARS OF THE UNIVERSITY OF CAMBRIDGE
Call Details Starting Grant (StG), LS2, ERC-2013-StG
Summary Cells must integrate output from multiple genetic circuits in order to correctly control cellular processes. Despite much work characterizing regulation in these circuits, how circuits interact to control global cellular programs remains unclear. This is particularly true given that recent research at the single cell level has revealed that genetic circuits often generate variable or stochastic regulation dynamics. In this proposal we will use a multi-disciplinary approach, combining modelling and time-lapse microscopy, to investigate how cells can robustly integrate signals from multiple dynamic genetic circuits. In particular we will answer the following questions: 1) What types of dynamic signal encoding strategies are available for the cell? 2) What are the benefits of dynamic gene activation, whether stochastic or oscillatory, to the cell? 3) How do cells couple and integrate output from diverse gene modules despite the noise and variability observed in gene circuit dynamics?
We will study these questions using 2 key model systems. In Aim 1, we will examine stochastic pulse regulation dynamics and coupling between alternative sigma factors in B. subtilis. Our preliminary data has revealed that multiple B. subtilis sigma factors stochastically pulse under stress. We will look for evidence of any coupling or interactions between these stochastic pulse circuits. This system will serve as a model for how a cell uses stochastic pulsing to control diverse cellular processes. In Aim 2, we will examine coupling between a deterministic oscillator, the circadian clock, and multiple other key pathways in Cyanobacteria. We will examine how the cell can dynamically couple multiple cellular processes using an oscillating signal. This work will provide an excellent base for Aim 3, in which we will use synthetic biology approaches to develop ‘bottom up’ tests of generation of novel dynamic coupling strategies.
Summary
Cells must integrate output from multiple genetic circuits in order to correctly control cellular processes. Despite much work characterizing regulation in these circuits, how circuits interact to control global cellular programs remains unclear. This is particularly true given that recent research at the single cell level has revealed that genetic circuits often generate variable or stochastic regulation dynamics. In this proposal we will use a multi-disciplinary approach, combining modelling and time-lapse microscopy, to investigate how cells can robustly integrate signals from multiple dynamic genetic circuits. In particular we will answer the following questions: 1) What types of dynamic signal encoding strategies are available for the cell? 2) What are the benefits of dynamic gene activation, whether stochastic or oscillatory, to the cell? 3) How do cells couple and integrate output from diverse gene modules despite the noise and variability observed in gene circuit dynamics?
We will study these questions using 2 key model systems. In Aim 1, we will examine stochastic pulse regulation dynamics and coupling between alternative sigma factors in B. subtilis. Our preliminary data has revealed that multiple B. subtilis sigma factors stochastically pulse under stress. We will look for evidence of any coupling or interactions between these stochastic pulse circuits. This system will serve as a model for how a cell uses stochastic pulsing to control diverse cellular processes. In Aim 2, we will examine coupling between a deterministic oscillator, the circadian clock, and multiple other key pathways in Cyanobacteria. We will examine how the cell can dynamically couple multiple cellular processes using an oscillating signal. This work will provide an excellent base for Aim 3, in which we will use synthetic biology approaches to develop ‘bottom up’ tests of generation of novel dynamic coupling strategies.
Max ERC Funding
1 499 571 €
Duration
Start date: 2014-02-01, End date: 2019-01-31
Project acronym DEVOCHROMO
Project Chromosome structure and genome organization in early mammalian development
Researcher (PI) Peter Fraser
Host Institution (HI) THE BABRAHAM INSTITUTE
Call Details Advanced Grant (AdG), LS2, ERC-2013-ADG
Summary "The spatial organization of the genome inside the cell nucleus is tissue-specific and has been linked to several nuclear processes including gene activation, gene silencing, genomic imprinting, gene co-regulation, genome maintenance, DNA replication, DNA repair, chromosomal translocations and X chromosome inactivation. In fact, just about any nuclear/genome function has a spatial component that has been implicated in its control. We know surprisingly little about chromosome conformation and spatial organization or how they are established. The extent to which they are a cause or consequence of genome functions are current topics of considerable debate, however emerging data from my group and many other groups world-wide indicate that nuclear location and organization are drivers of genome functions, which in cooperation with other features including epigenetic marks, non-coding RNAs and trans-factor binding bring about genome control. Thus, genome spatial organization can be considered on a par with other epigenetic features that together contribute to overall genome control. The classical paradigm of early mammalian development arguably represents the most dramatic and yet least understood process of genome reprogramming, where a single cell undergoes a series of divisions to ultimately give rise to the hundreds of different cell types found in a mature organism. Study of pre-implantation embryo development is hindered by the very nature of the life form, composed of extremely low cell numbers at each stage, which severely limits the options for investigation. My lab has recently developed a novel technique called single cell Hi-C, which has the power to detect tens of thousands of simultaneous chromatin contacts from a single cell. In this application I propose to apply this technology to study chromosome structure and genome organization during mouse pre-implantation development along with single cell transcriptome analyses from the same cells."
Summary
"The spatial organization of the genome inside the cell nucleus is tissue-specific and has been linked to several nuclear processes including gene activation, gene silencing, genomic imprinting, gene co-regulation, genome maintenance, DNA replication, DNA repair, chromosomal translocations and X chromosome inactivation. In fact, just about any nuclear/genome function has a spatial component that has been implicated in its control. We know surprisingly little about chromosome conformation and spatial organization or how they are established. The extent to which they are a cause or consequence of genome functions are current topics of considerable debate, however emerging data from my group and many other groups world-wide indicate that nuclear location and organization are drivers of genome functions, which in cooperation with other features including epigenetic marks, non-coding RNAs and trans-factor binding bring about genome control. Thus, genome spatial organization can be considered on a par with other epigenetic features that together contribute to overall genome control. The classical paradigm of early mammalian development arguably represents the most dramatic and yet least understood process of genome reprogramming, where a single cell undergoes a series of divisions to ultimately give rise to the hundreds of different cell types found in a mature organism. Study of pre-implantation embryo development is hindered by the very nature of the life form, composed of extremely low cell numbers at each stage, which severely limits the options for investigation. My lab has recently developed a novel technique called single cell Hi-C, which has the power to detect tens of thousands of simultaneous chromatin contacts from a single cell. In this application I propose to apply this technology to study chromosome structure and genome organization during mouse pre-implantation development along with single cell transcriptome analyses from the same cells."
Max ERC Funding
2 401 393 €
Duration
Start date: 2014-02-01, End date: 2019-01-31
Project acronym EMF-FEIM
Project Empirical Macro-Finance and the Financial Economics of Insurance Markets
Researcher (PI) Ralph Koijen
Host Institution (HI) LONDON BUSINESS SCHOOL
Call Details Starting Grant (StG), SH1, ERC-2013-StG
Summary "My project consists of two lines of work. 1.Empirical Macro-Finance: Asset prices are informative about the macro-economic risks that matter to investors and about the welfare costs of economic fluctuations. However, recent empirical evidence suggests that leading asset pricing models cannot explain how risks are priced across maturities in equity markets, which is a key input to measuring the costs of business cycles. An analysis of what leading models miss will vastly improve our understanding of how the real economy and asset prices are related. Also, by expanding our empirical evidence about the term structure of equity to the firm-level, I plan to study how investment decisions relate to asset prices. My goal is to measure the firms' incentives to invest and how this impacts economic growth more broadly.
2.Financial Economics of Insurance Markets: Households in Europe and the US can choose from a wide variety of insurance products that insure health and mortality risks. Choosing between these products is no easy task and the costs from sub-optimal insurance choices are estimated to be large. My plan is to develop a comprehensive life-cycle theory of insurance choice that accounts for family structure, risk factors such as labor income and housing, and different institutional settings across countries. I also plan to study the supply side of insurance markets. The traditional view is that insurance prices are driven by life-cycle demand or informational frictions. However, as is clear from evidence during the financial crisis, insurance companies are in fact financial institutions. If financial constraints bind, it may affect insurance prices and ultimately consumers' welfare. My goal is to understand how financial frictions affect insurance companies. A policy implication of my research may be that the private supply of insurance is an imperfect substitute for public supply as insurance companies face different incentives and constraints than the government."
Summary
"My project consists of two lines of work. 1.Empirical Macro-Finance: Asset prices are informative about the macro-economic risks that matter to investors and about the welfare costs of economic fluctuations. However, recent empirical evidence suggests that leading asset pricing models cannot explain how risks are priced across maturities in equity markets, which is a key input to measuring the costs of business cycles. An analysis of what leading models miss will vastly improve our understanding of how the real economy and asset prices are related. Also, by expanding our empirical evidence about the term structure of equity to the firm-level, I plan to study how investment decisions relate to asset prices. My goal is to measure the firms' incentives to invest and how this impacts economic growth more broadly.
2.Financial Economics of Insurance Markets: Households in Europe and the US can choose from a wide variety of insurance products that insure health and mortality risks. Choosing between these products is no easy task and the costs from sub-optimal insurance choices are estimated to be large. My plan is to develop a comprehensive life-cycle theory of insurance choice that accounts for family structure, risk factors such as labor income and housing, and different institutional settings across countries. I also plan to study the supply side of insurance markets. The traditional view is that insurance prices are driven by life-cycle demand or informational frictions. However, as is clear from evidence during the financial crisis, insurance companies are in fact financial institutions. If financial constraints bind, it may affect insurance prices and ultimately consumers' welfare. My goal is to understand how financial frictions affect insurance companies. A policy implication of my research may be that the private supply of insurance is an imperfect substitute for public supply as insurance companies face different incentives and constraints than the government."
Max ERC Funding
1 077 765 €
Duration
Start date: 2013-10-01, End date: 2018-09-30
Project acronym ESCQUMA
Project Exploring Strongly Correlated Quantum Matter
with Cold Excited Atoms
Researcher (PI) Igor Walter Lesanovsky
Host Institution (HI) THE UNIVERSITY OF NOTTINGHAM
Call Details Starting Grant (StG), PE3, ERC-2013-StG
Summary The understanding of quantum matter in and out of equilibrium is among the biggest challenges of modern physics. Despite decades of research fundamental questions, such as the precise
workings behind rather ubiquitous materials such as high temperature superconductors are still unresolved. At the same time there is a new generation of experiments approaching which realises and probes quantum matter with novel and exotic interactions at an unprecedented level of precision. This has already highlighted new avenues of research but also demands for radically new theoretical approaches which lie outside the scope of just a single traditional physical discipline. Novel and in particular multidisciplinary lines of thinking are required to tackle this immense challenge. Such new research will not solely be delivering invaluable insights into currently unresolved problems but rather form a new basis for the understanding of quantum matter from a multidisciplinary perspective. This will open up new horizons for fundamental research and at the same time will pave the way for future technologies and materials which rely on non-equilibrium phenomena or quantum matter. This research proposal takes on this challenge by setting up a broad theoretical research programme which is multipronged and multidisciplinary and which directly connects to the most recent research efforts in ultra cold atomic physics. Here currently a step change is taking place where new experiments explore strongly correlated quantum physics within gases of excited atoms – so-called Rydberg atoms. Exploiting this unique moment we will develop a framework for the description of the equilibrium and non-equilibrium properties of these complex and very versatile quantum systems. This system-specific research approach has the advantage that theoretical predictions can be verified experimentally and applied in practice almost immediately, leading to research attacking the frontiers of current knowledge.
Summary
The understanding of quantum matter in and out of equilibrium is among the biggest challenges of modern physics. Despite decades of research fundamental questions, such as the precise
workings behind rather ubiquitous materials such as high temperature superconductors are still unresolved. At the same time there is a new generation of experiments approaching which realises and probes quantum matter with novel and exotic interactions at an unprecedented level of precision. This has already highlighted new avenues of research but also demands for radically new theoretical approaches which lie outside the scope of just a single traditional physical discipline. Novel and in particular multidisciplinary lines of thinking are required to tackle this immense challenge. Such new research will not solely be delivering invaluable insights into currently unresolved problems but rather form a new basis for the understanding of quantum matter from a multidisciplinary perspective. This will open up new horizons for fundamental research and at the same time will pave the way for future technologies and materials which rely on non-equilibrium phenomena or quantum matter. This research proposal takes on this challenge by setting up a broad theoretical research programme which is multipronged and multidisciplinary and which directly connects to the most recent research efforts in ultra cold atomic physics. Here currently a step change is taking place where new experiments explore strongly correlated quantum physics within gases of excited atoms – so-called Rydberg atoms. Exploiting this unique moment we will develop a framework for the description of the equilibrium and non-equilibrium properties of these complex and very versatile quantum systems. This system-specific research approach has the advantage that theoretical predictions can be verified experimentally and applied in practice almost immediately, leading to research attacking the frontiers of current knowledge.
Max ERC Funding
1 492 000 €
Duration
Start date: 2014-01-01, End date: 2018-12-31
Project acronym EVOCAN
Project Why do cancers occur where they do? A genetic and evolutionary approach
Researcher (PI) Ian Phlip Mark Tomlinson
Host Institution (HI) THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Call Details Advanced Grant (AdG), LS2, ERC-2013-ADG
Summary "Tumorigenesis is a form of somatic evolution, a topical subject given the advent of cancer genome sequencing. However, we contend that some features of Darwinian evolution have been neglected when cancer is studied, as have some aspects of evolution that are special to cancers. For example, tumours comprise an expanding population of cells, cancers must occur within a normal human lifespan, and genotypes detrimental to growth of the tumour as a whole may be selected. These factors may render invalid the classical model in which successive mutations with large advantages arise and spread through the tumour in selective sweeps. To incorporate these neglected features and to test how tumorigenesis depends on factors such as mutation rate, selection and size constraints, we shall set up a comprehensive model of tumour growth incorporating cell birth, death, division and mutation parameters. We shall examine specific aspects of cancer-as-evolution in mice. By marking mutant clones using fluorescent proteins, we can track them and see how they persist, spread and die. We shall also determine the mutation profiles and genetic diversity of mutant clones and whole tumours in mice and humans using next-generation sequencing. Specific experiments will determine: (i) the fate of new advantageous clones arising in an existing tumour; (ii) whether new disadvantageous clones can persist in tumours; (iii) whether apparently maladaptive traits for tumour growth, such as suppressing the growth of competitors, can be selected; (iv) why do housekeeper gene mutations cause cancer in specific sites; (v) can cancer cells have too much genomic instability; and (vi) whether all cancers develop owing to driver mutations with big effects, or are there “mini-drivers” of tumorigenesis? There will be continual cross-talk between the experimental and modelling work. The results of the project will enhance our basic understanding of tumorigenesis and suggest strategies for anticancer therapy."
Summary
"Tumorigenesis is a form of somatic evolution, a topical subject given the advent of cancer genome sequencing. However, we contend that some features of Darwinian evolution have been neglected when cancer is studied, as have some aspects of evolution that are special to cancers. For example, tumours comprise an expanding population of cells, cancers must occur within a normal human lifespan, and genotypes detrimental to growth of the tumour as a whole may be selected. These factors may render invalid the classical model in which successive mutations with large advantages arise and spread through the tumour in selective sweeps. To incorporate these neglected features and to test how tumorigenesis depends on factors such as mutation rate, selection and size constraints, we shall set up a comprehensive model of tumour growth incorporating cell birth, death, division and mutation parameters. We shall examine specific aspects of cancer-as-evolution in mice. By marking mutant clones using fluorescent proteins, we can track them and see how they persist, spread and die. We shall also determine the mutation profiles and genetic diversity of mutant clones and whole tumours in mice and humans using next-generation sequencing. Specific experiments will determine: (i) the fate of new advantageous clones arising in an existing tumour; (ii) whether new disadvantageous clones can persist in tumours; (iii) whether apparently maladaptive traits for tumour growth, such as suppressing the growth of competitors, can be selected; (iv) why do housekeeper gene mutations cause cancer in specific sites; (v) can cancer cells have too much genomic instability; and (vi) whether all cancers develop owing to driver mutations with big effects, or are there “mini-drivers” of tumorigenesis? There will be continual cross-talk between the experimental and modelling work. The results of the project will enhance our basic understanding of tumorigenesis and suggest strategies for anticancer therapy."
Max ERC Funding
2 500 000 €
Duration
Start date: 2014-09-01, End date: 2019-08-31
Project acronym FRICTIONS
Project Frictions in the Financial System
Researcher (PI) Péter Kondor
Host Institution (HI) LONDON SCHOOL OF ECONOMICS AND POLITICAL SCIENCE
Call Details Starting Grant (StG), SH1, ERC-2013-StG
Summary "The financial crisis, since its start in 2008 has exposed enormous fractures both in the financial architecture and in the structure of the global economy. Although with some notable exceptions, the magnitude of the events caught the finance profession largely by surprise. Clearly, we have to understand better the institutional mechanism channeling savings towards the best uses of capital, and to what extent this mechanism can sometimes fail. The projects in this proposal will push the boundaries of our knowledge in this direction.
I suggest a dual approach to achieve this goal. First, we have to improve our understanding of which frictions are the crucial impediments of the efficient functioning of markets. As this approach focuses on particular markets in isolation, I call this the micro approach. I propose three projects within this approach: trading and information diffusion in OTC markets, the crowdedness in limits-to-arbitrage, and the interaction of political uncertainty and sovereign bond prices.
Second, from the frictions emerging from the micro approach, we have to select the ones which determine the aggregate liquidity fluctuations in the economy. I use this concept in a broad sense; referring to the changing efficiency with which the financial system allocates resources across investment opportunities. As this approach focuses on the functionality of the financial system as a whole, I call this the macro approach. I propose two projects within this approach. The first project focuses on the determinants of the differences in the financial architecture of different economies. It builds a novel framework to study the dynamics of the financial sector of an economy. The second project studies the role of shadow banking in the fluctuation of aggregate liquidity. In particular, this project concentrates on the fluctuation of the efficiency of private liquidity creation as the state of the economy changes."
Summary
"The financial crisis, since its start in 2008 has exposed enormous fractures both in the financial architecture and in the structure of the global economy. Although with some notable exceptions, the magnitude of the events caught the finance profession largely by surprise. Clearly, we have to understand better the institutional mechanism channeling savings towards the best uses of capital, and to what extent this mechanism can sometimes fail. The projects in this proposal will push the boundaries of our knowledge in this direction.
I suggest a dual approach to achieve this goal. First, we have to improve our understanding of which frictions are the crucial impediments of the efficient functioning of markets. As this approach focuses on particular markets in isolation, I call this the micro approach. I propose three projects within this approach: trading and information diffusion in OTC markets, the crowdedness in limits-to-arbitrage, and the interaction of political uncertainty and sovereign bond prices.
Second, from the frictions emerging from the micro approach, we have to select the ones which determine the aggregate liquidity fluctuations in the economy. I use this concept in a broad sense; referring to the changing efficiency with which the financial system allocates resources across investment opportunities. As this approach focuses on the functionality of the financial system as a whole, I call this the macro approach. I propose two projects within this approach. The first project focuses on the determinants of the differences in the financial architecture of different economies. It builds a novel framework to study the dynamics of the financial sector of an economy. The second project studies the role of shadow banking in the fluctuation of aggregate liquidity. In particular, this project concentrates on the fluctuation of the efficiency of private liquidity creation as the state of the economy changes."
Max ERC Funding
1 122 883 €
Duration
Start date: 2013-12-01, End date: 2018-11-30
Project acronym HIGEN
Project ADVANCED STATISTICAL METHODS FOR HIGH-DIMENSIONAL GENETIC STUDIES
Researcher (PI) Jonathan Lawrence Marchini
Host Institution (HI) THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Call Details Consolidator Grant (CoG), LS2, ERC-2013-CoG
Summary "Statistical methods play a central role in the field of modern genetics. New technologies are driving an explosion of high-dimensional datasets that will sustain a continuing need for new methods, theory and computationally efficient software. My proposal has two parts that will address the statistical challenges and creation of resources at the frontier of the science in this area. The methods development will be driven by, and applied to, several cutting-edge datasets in the fields of human disease genetics, population genetics and plant and animal breeding, guaranteeing impact on exciting scientific questions.
The first part concerns a wide circle of ideas around haplotype estimation, genotype imputation and analysis of sequencing data. The overarching aim is to provide a suite of methods that can estimate haplotypes and impute genotypes in a unified and computationally efficient manner. In addition, we will work to create a reference set of haplotypes from tens of thousands of European and worldwide samples that will form a central resource for human disease and population genetic studies.
The second part concerns the development of models for high-dimensional phenotypic data in genome-wide association studies. This is poorly developed area of human disease genetics with great potential for methods development and wide ranging applications."
Summary
"Statistical methods play a central role in the field of modern genetics. New technologies are driving an explosion of high-dimensional datasets that will sustain a continuing need for new methods, theory and computationally efficient software. My proposal has two parts that will address the statistical challenges and creation of resources at the frontier of the science in this area. The methods development will be driven by, and applied to, several cutting-edge datasets in the fields of human disease genetics, population genetics and plant and animal breeding, guaranteeing impact on exciting scientific questions.
The first part concerns a wide circle of ideas around haplotype estimation, genotype imputation and analysis of sequencing data. The overarching aim is to provide a suite of methods that can estimate haplotypes and impute genotypes in a unified and computationally efficient manner. In addition, we will work to create a reference set of haplotypes from tens of thousands of European and worldwide samples that will form a central resource for human disease and population genetic studies.
The second part concerns the development of models for high-dimensional phenotypic data in genome-wide association studies. This is poorly developed area of human disease genetics with great potential for methods development and wide ranging applications."
Max ERC Funding
1 627 906 €
Duration
Start date: 2014-06-01, End date: 2019-05-31
Project acronym HISKNOWL
Project Using Historical Quasi-Experiments to Understand the Knowledge Economy
Researcher (PI) Fabian Waldinger
Host Institution (HI) LONDON SCHOOL OF ECONOMICS AND POLITICAL SCIENCE
Call Details Starting Grant (StG), SH1, ERC-2013-StG
Summary This proposal covers three research strands at the intersection of innovation economics, economic history, and labour economics.
In project A I will investigate how the number of entrepreneurs at the city level affects city growth. As the number of entrepreneurs in a city is likely to be endogenous I identify the causal effect of entrepreneurs using the exodus of Jewish entrepreneurs from German cities during the Nazi era. As different German cities were affected to varying extents by the exodus of Jewish entrepreneurs I can investigate how entrepreneurs affect local GDP and employment in the long-run. Furthermore, I will analyse which types of entrepreneurs matter (e.g. bankers versus manufacturers) because different cities lost Jewish entrepreneurs in different professions.
In project B we will analyse how increases in the availability of secondary schools in Germany affect the number of talented people (such as scientists, parliamentarians or entrepreneurs) who originate from certain cities. To analyse the causal effect of secondary school availability we study large expansions in the number of schools in Germany that lowered the cost of attending an academic-track school for children in some locations, in particular for students in rural areas. Furthermore, we will investigate how the school curriculum and how single-sex versus mixed-sex education affect the production of talent.
In project C we investigate the role of open science for the accumulation of knowledge. To investigate the causal effect of open science on the productivity of scientists we will investigate the exclusion of scientists from the losing Central Powers (e.g. Germany) from the international scientific community after WWI. As the exclusion affected scientists in different scientific fields and countries very differently we can identify the role of open science for the number of published articles by a certain scientist and how quickly she cites important work by foreign scientists.
Summary
This proposal covers three research strands at the intersection of innovation economics, economic history, and labour economics.
In project A I will investigate how the number of entrepreneurs at the city level affects city growth. As the number of entrepreneurs in a city is likely to be endogenous I identify the causal effect of entrepreneurs using the exodus of Jewish entrepreneurs from German cities during the Nazi era. As different German cities were affected to varying extents by the exodus of Jewish entrepreneurs I can investigate how entrepreneurs affect local GDP and employment in the long-run. Furthermore, I will analyse which types of entrepreneurs matter (e.g. bankers versus manufacturers) because different cities lost Jewish entrepreneurs in different professions.
In project B we will analyse how increases in the availability of secondary schools in Germany affect the number of talented people (such as scientists, parliamentarians or entrepreneurs) who originate from certain cities. To analyse the causal effect of secondary school availability we study large expansions in the number of schools in Germany that lowered the cost of attending an academic-track school for children in some locations, in particular for students in rural areas. Furthermore, we will investigate how the school curriculum and how single-sex versus mixed-sex education affect the production of talent.
In project C we investigate the role of open science for the accumulation of knowledge. To investigate the causal effect of open science on the productivity of scientists we will investigate the exclusion of scientists from the losing Central Powers (e.g. Germany) from the international scientific community after WWI. As the exclusion affected scientists in different scientific fields and countries very differently we can identify the role of open science for the number of published articles by a certain scientist and how quickly she cites important work by foreign scientists.
Max ERC Funding
733 621 €
Duration
Start date: 2013-11-01, End date: 2018-09-30
