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 CarnoMorph
Project The Evolution and Development of Complex Morphologies
Researcher (PI) Enrico Coen
Host Institution (HI) JOHN INNES CENTRE
Call Details Advanced Grant (AdG), LS3, ERC-2012-ADG_20120314
Summary Plant and animal organs display a remarkable diversity of shapes. A major challenge in developmental and evolutionary biology is to understand how this diversity of forms is generated. Recent advances in imaging, computational modelling and genomics now make it possible to address this challenge effectively for the first time. Leaf development is a particularly tractable system because of its accessibility to imaging and preservation of connectivity during growth. Leaves also display remarkable diversity in shape and form, with perhaps the most complex form being the pitcher-shaped (epiascidiate) leaves of carnivorous plants. This form has evolved four times independently, raising the question of whether its seeming complexity may have arisen through simple modulations in underlying morphogenetic mechanisms. To test this hypothesis, I aim to develop a model system for carnivorous plants based on Utricularia gibba (humped bladderwort), which has the advantage of having one of the smallest genomes known in plants (~2/3 the size of the Arabidopsis genome) and small transparent pitcher-shaped leaves amenable to imaging. I will use this system to define the morphogenetic events underlying the formation of pitcher-shaped leaves and their molecular genetic control. I will also develop and apply computational modelling to explore hypotheses that may account for the development of U. gibba bladders and further test these hypotheses experimentally. In addition, I will investigate the relationship between U. gibba bladder development and species with simpler leaf shapes, such as Arabidopsis, or species where the epiascidiate form has evolved independently. Taken together, these studies should show how developmental rules elucidated in current model systems might be extended and built upon to account for the diversity and complexity of tissue forms, integrating evo-devo approaches with a mechanistic understanding of morphogenesis.
Summary
Plant and animal organs display a remarkable diversity of shapes. A major challenge in developmental and evolutionary biology is to understand how this diversity of forms is generated. Recent advances in imaging, computational modelling and genomics now make it possible to address this challenge effectively for the first time. Leaf development is a particularly tractable system because of its accessibility to imaging and preservation of connectivity during growth. Leaves also display remarkable diversity in shape and form, with perhaps the most complex form being the pitcher-shaped (epiascidiate) leaves of carnivorous plants. This form has evolved four times independently, raising the question of whether its seeming complexity may have arisen through simple modulations in underlying morphogenetic mechanisms. To test this hypothesis, I aim to develop a model system for carnivorous plants based on Utricularia gibba (humped bladderwort), which has the advantage of having one of the smallest genomes known in plants (~2/3 the size of the Arabidopsis genome) and small transparent pitcher-shaped leaves amenable to imaging. I will use this system to define the morphogenetic events underlying the formation of pitcher-shaped leaves and their molecular genetic control. I will also develop and apply computational modelling to explore hypotheses that may account for the development of U. gibba bladders and further test these hypotheses experimentally. In addition, I will investigate the relationship between U. gibba bladder development and species with simpler leaf shapes, such as Arabidopsis, or species where the epiascidiate form has evolved independently. Taken together, these studies should show how developmental rules elucidated in current model systems might be extended and built upon to account for the diversity and complexity of tissue forms, integrating evo-devo approaches with a mechanistic understanding of morphogenesis.
Max ERC Funding
2 499 997 €
Duration
Start date: 2013-06-01, End date: 2018-05-31
Project acronym ColonCan
Project Targeting downstream effectors of Wnt signaling in colorectal cancer
Researcher (PI) Owen James Sansom
Host Institution (HI) BEATSON INSTITUTE FOR CANCER RESEARCH LBG
Call Details Starting Grant (StG), LS3, ERC-2012-StG_20111109
Summary Colorectal cancer (CRC) is one of the most common cancers of the western world. The underlying initiating mutation for the majority of CRC is within the Adenomatous Polyposis Coli (Apc) gene. The APC protein performs an important role in controlling the levels of Wnt signalling by targeting beta-catenin for degradation. Loss of the APC protein leads to the activation of Wnt signaling target genes such as c-Myc which is required for phenotypes causes by Apc loss.
However, despite the clear importance of APC loss and deregulated Wnt signalling, additional events are required for the development of CRC such as KRAS and P53 mutations.The impact of these changes on the development of CRC and response to therapy is not well understood. Furthermore, identification and testing of potential novel targets and therapies is hampered by lack of a preclinical model that faithfully recapitulates the course of the human disease.
This proposal has two aims:
1. Assess the impact of cooperating mutations with Apc and assess how they alter sensitivities of
Apc deficient cells.
2. Develop mouse models of invasive and metastatic colorectal cancer that recapitulate the human disease.
We will use ‘state of the art’ methodologies to identify the changes in signaling output conferred by these cooperating mutations. Genetic mouse models of invasive and metastatic colorectal cancers will be generated through the acquisition of additional mutations and genomic instability.
These studies will produce predictions on therapeutic combinations that will be tested in mouse models in vitro and in vivo that may identify new treatment regimens for patients with late stage CRC.
Summary
Colorectal cancer (CRC) is one of the most common cancers of the western world. The underlying initiating mutation for the majority of CRC is within the Adenomatous Polyposis Coli (Apc) gene. The APC protein performs an important role in controlling the levels of Wnt signalling by targeting beta-catenin for degradation. Loss of the APC protein leads to the activation of Wnt signaling target genes such as c-Myc which is required for phenotypes causes by Apc loss.
However, despite the clear importance of APC loss and deregulated Wnt signalling, additional events are required for the development of CRC such as KRAS and P53 mutations.The impact of these changes on the development of CRC and response to therapy is not well understood. Furthermore, identification and testing of potential novel targets and therapies is hampered by lack of a preclinical model that faithfully recapitulates the course of the human disease.
This proposal has two aims:
1. Assess the impact of cooperating mutations with Apc and assess how they alter sensitivities of
Apc deficient cells.
2. Develop mouse models of invasive and metastatic colorectal cancer that recapitulate the human disease.
We will use ‘state of the art’ methodologies to identify the changes in signaling output conferred by these cooperating mutations. Genetic mouse models of invasive and metastatic colorectal cancers will be generated through the acquisition of additional mutations and genomic instability.
These studies will produce predictions on therapeutic combinations that will be tested in mouse models in vitro and in vivo that may identify new treatment regimens for patients with late stage CRC.
Max ERC Funding
1 499 045 €
Duration
Start date: 2012-11-01, End date: 2017-10-31
Project acronym DMEA
Project The Dynamics of Migration and Economic Adjustment
Researcher (PI) Christian Dustmann
Host Institution (HI) UNIVERSITY COLLEGE LONDON
Call Details Advanced Grant (AdG), SH1, ERC-2012-ADG_20120411
Summary The research proposed here is concerned with the dynamics of immigrant impacts and the process of economic adaptation in receiving societies. The immigration process is inherently dynamic: many new immigrants return home within a short time; and those that remain undergo a long term series of investments and behavioural changes that gradually alter the way that they interact with the economy of the receiving country. Moreover, in the longer run the presence of immigrants affects the choices of firms over new technology investments, and the choices of native workers over schooling and occupations. Thus simple static frameworks provide an incomplete and even potentially misleading perspective for understanding modern immigration patterns. The point of departure for this proposed research is the recognition that we need to reformulate the analysis of immigrant impacts in a fully dynamic framework, acknowledging the inter-temporal choices of immigrants, firms, and native workers and the ways that these three groups of agents interact over a longer horizon. Our approach involves treating immigration as a dynamic shock, where the dynamics relates to the different agents involved: immigrants, who change their position in the native skill distribution over time as a result of their life-cycle decisions; firms, who react by adjusting their technologies, product mix, and their involvement with institutions and regulatory environment; and native workers, who adjust by changing their career plans. Our work will combine highly innovative theoretical perspectives with state-of-the-art empirical analyses exploiting unique policy experiments and exceptional data sources, merging longitudinal administrative population data with data from firm and individual surveys. This agenda will enable us to construct a comprehensive picture of the adjustment process in response to immigration and open new horizons for future research on the impact of immigration in a dynamic framework.
Summary
The research proposed here is concerned with the dynamics of immigrant impacts and the process of economic adaptation in receiving societies. The immigration process is inherently dynamic: many new immigrants return home within a short time; and those that remain undergo a long term series of investments and behavioural changes that gradually alter the way that they interact with the economy of the receiving country. Moreover, in the longer run the presence of immigrants affects the choices of firms over new technology investments, and the choices of native workers over schooling and occupations. Thus simple static frameworks provide an incomplete and even potentially misleading perspective for understanding modern immigration patterns. The point of departure for this proposed research is the recognition that we need to reformulate the analysis of immigrant impacts in a fully dynamic framework, acknowledging the inter-temporal choices of immigrants, firms, and native workers and the ways that these three groups of agents interact over a longer horizon. Our approach involves treating immigration as a dynamic shock, where the dynamics relates to the different agents involved: immigrants, who change their position in the native skill distribution over time as a result of their life-cycle decisions; firms, who react by adjusting their technologies, product mix, and their involvement with institutions and regulatory environment; and native workers, who adjust by changing their career plans. Our work will combine highly innovative theoretical perspectives with state-of-the-art empirical analyses exploiting unique policy experiments and exceptional data sources, merging longitudinal administrative population data with data from firm and individual surveys. This agenda will enable us to construct a comprehensive picture of the adjustment process in response to immigration and open new horizons for future research on the impact of immigration in a dynamic framework.
Max ERC Funding
1 129 428 €
Duration
Start date: 2013-06-01, End date: 2018-05-31
Project acronym DROPFAT
Project Biogenesis of lipid droplets and lipid homeostasis
Researcher (PI) Pedro Nuno Chaves Simoes De Carvalho
Host Institution (HI) THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD
Call Details Starting Grant (StG), LS3, ERC-2012-StG_20111109
Summary Organisms and cells face a myriad of environmental changes with periods of nutrient surplus and shortage. It is therefore not surprising that in all kingdoms of life, cells have evolved the means to store energy and thereby minimize the effects of environmental fluctuations. While the capability for energy storage has obvious advantages, deregulated energy accumulation can also be detrimental and is the hallmark of many diseases such as obesity.
In most cells energy is stored as neutral lipids in a dedicated cellular compartment, the lipid droplets (LDs). LDs are found in virtually every eukaryotic cell and play a central role in cellular lipid and energy metabolism. Despite their ubiquitous presence and importance, the physiology of LDs is poorly understood. LDs are composed of a single lipid layer and therefore distinct from all other cellular compartments. How do LDs originate at the endoplasmic reticulum (ER) and what is the machinery involved? How is the size, number and the storage capacity of the LDs regulated? How are specific proteins and lipids targeted to LDs? Addressing these questions is fundamental for understanding the “life cycle” of LDs and for a global picture of the cellular energy homeostasis.
The main goal of this proposal is to reveal the molecular mechanisms controlling neutral lipid dynamics and their storage in LDs. We will focus specifically on the role of the endoplasmic reticulum in the biogenesis of LDs. First, we will identify the ER protein complexes required for LD formation and regulation. Second, we will develop an assay to dissect the targeting of proteins to LDs. Finally, we will develop a cell-free system that recapitulates the biogenesis of LDs in vitro. Altogether, our strategy constitutes a systematic, in-depth analysis of LD dynamics and will lead to significant insight on the mechanisms of cellular energy storage. Our findings will likely offer a better understanding of human pathologies such as obesity and lipodistrophies
Summary
Organisms and cells face a myriad of environmental changes with periods of nutrient surplus and shortage. It is therefore not surprising that in all kingdoms of life, cells have evolved the means to store energy and thereby minimize the effects of environmental fluctuations. While the capability for energy storage has obvious advantages, deregulated energy accumulation can also be detrimental and is the hallmark of many diseases such as obesity.
In most cells energy is stored as neutral lipids in a dedicated cellular compartment, the lipid droplets (LDs). LDs are found in virtually every eukaryotic cell and play a central role in cellular lipid and energy metabolism. Despite their ubiquitous presence and importance, the physiology of LDs is poorly understood. LDs are composed of a single lipid layer and therefore distinct from all other cellular compartments. How do LDs originate at the endoplasmic reticulum (ER) and what is the machinery involved? How is the size, number and the storage capacity of the LDs regulated? How are specific proteins and lipids targeted to LDs? Addressing these questions is fundamental for understanding the “life cycle” of LDs and for a global picture of the cellular energy homeostasis.
The main goal of this proposal is to reveal the molecular mechanisms controlling neutral lipid dynamics and their storage in LDs. We will focus specifically on the role of the endoplasmic reticulum in the biogenesis of LDs. First, we will identify the ER protein complexes required for LD formation and regulation. Second, we will develop an assay to dissect the targeting of proteins to LDs. Finally, we will develop a cell-free system that recapitulates the biogenesis of LDs in vitro. Altogether, our strategy constitutes a systematic, in-depth analysis of LD dynamics and will lead to significant insight on the mechanisms of cellular energy storage. Our findings will likely offer a better understanding of human pathologies such as obesity and lipodistrophies
Max ERC Funding
1 475 282 €
Duration
Start date: 2013-02-01, End date: 2018-01-31
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 FRICTIONS
Project Financial Frictions
Researcher (PI) Lasse Heje Pedersen
Host Institution (HI) COPENHAGEN BUSINESS SCHOOL
Call Details Starting Grant (StG), SH1, ERC-2012-StG_20111124
Summary "Financial economics is at a crossroads: Academics are struggling to redefine the theory of finance and practitioners and regulators to restructure the financial industry. The current financial crisis will have significant impact on how we regulate financial markets and how we manage risk in companies and financial institutions. It will continue to inspire an intense discussion and research agenda over the next decade in academics, in industry, and among financial regulators and a central focus will be the role of frictions in financial markets. Nowhere are these issues more pertinent than in Europe right now.
To take up the challenge presented by this crossroad of financial economics, my research project seeks to contribute to the knowledge of financial frictions and what to do about them. FRICTIONS will explore how financial frictions affect asset prices and the economy, and the implications of frictions for financial risk management, the optimal regulation, and the conduct of monetary policy.
Whereas economists have traditionally focused on the assumption of perfect markets, a growing body of evidence is leading to a widespread recognition that markets are plagued by significant financial frictions. FRICTIONS will model key financial frictions such as leverage constraints, margin requirements, transaction costs, liquidity risk, and short sale constraints. The objective is to develop theories of the origins of these frictions, study how these frictions change over time and across markets, and, importantly, how they affect the required return on assets and the economy.
The project will test these theories using data from global equity, bond, and derivative markets. In particular, the project will measure these frictions empirically and study the empirical effect of frictions on asset returns and economic dynamics. The end result is an empirically-validated model of economic behavior subject to financial frictions that yields qualitative and quantitative insights."
Summary
"Financial economics is at a crossroads: Academics are struggling to redefine the theory of finance and practitioners and regulators to restructure the financial industry. The current financial crisis will have significant impact on how we regulate financial markets and how we manage risk in companies and financial institutions. It will continue to inspire an intense discussion and research agenda over the next decade in academics, in industry, and among financial regulators and a central focus will be the role of frictions in financial markets. Nowhere are these issues more pertinent than in Europe right now.
To take up the challenge presented by this crossroad of financial economics, my research project seeks to contribute to the knowledge of financial frictions and what to do about them. FRICTIONS will explore how financial frictions affect asset prices and the economy, and the implications of frictions for financial risk management, the optimal regulation, and the conduct of monetary policy.
Whereas economists have traditionally focused on the assumption of perfect markets, a growing body of evidence is leading to a widespread recognition that markets are plagued by significant financial frictions. FRICTIONS will model key financial frictions such as leverage constraints, margin requirements, transaction costs, liquidity risk, and short sale constraints. The objective is to develop theories of the origins of these frictions, study how these frictions change over time and across markets, and, importantly, how they affect the required return on assets and the economy.
The project will test these theories using data from global equity, bond, and derivative markets. In particular, the project will measure these frictions empirically and study the empirical effect of frictions on asset returns and economic dynamics. The end result is an empirically-validated model of economic behavior subject to financial frictions that yields qualitative and quantitative insights."
Max ERC Funding
1 307 160 €
Duration
Start date: 2013-01-01, End date: 2017-12-31
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 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
Project acronym HSCnicheIVM
Project In vivo imaging of haematopoietic stem cells in their natural niches to uncover cellular and molecular dynamics regulating self-renewal
Researcher (PI) Cristina Lo Celso
Host Institution (HI) IMPERIAL COLLEGE OF SCIENCE TECHNOLOGY AND MEDICINE
Call Details Starting Grant (StG), LS3, ERC-2013-StG
Summary Haematopoietic stem cells (HSC) reside in the bone marrow, from where they maintain immune cells, erythrocytes and platelets. To function correctly, they depend on their localisation within highly specialised niches, where cell-cell and -matrix interactions as well as medium- and long-range molecular signals are integrated to instruct them to either remain quiescent, or to generate progeny that will maintain both the stem cell pool and the differentiated lineages. Studies based on HSC transplantation assays have identified several signalling pathways and bone marrow cell types as regulators of HSC function; however the full picture of the cellular and molecular components of the HSC niche remains elusive because of lack of direct observation over time. HSC subpopulations have been identified based on their proliferative behaviour and it is likely that either migration between different microenvironments or transient modifications of the niche structure mediate changes in HSC fate in response to perturbations such as infection or leukaemia development.
I pioneered the combination of confocal and two-photon microscopy to visualise single HSC and their progeny within the bone marrow of live mice and here I propose to combine advanced microscopy techniques with multi-colour genetic lineage marking and highly sensitive expression profiling to track HSC and their clonal progeny in vivo in real time and to study the cellular and molecular composition of their niches during steady state and when responding to infection and leukaemia development. This work will uncover whether functionally distinct HSC subpopulations reside in anatomically distinct niches or rather all HSC niches are in principle equivalent, but change over time to mediate changes in HSC fate balance. The results obtained will provide a comprehensive picture of HSC niche dynamics, which will be critical for the development of regenerative medicine approaches based on in vivo or ex vivo expansion of HSC.
Summary
Haematopoietic stem cells (HSC) reside in the bone marrow, from where they maintain immune cells, erythrocytes and platelets. To function correctly, they depend on their localisation within highly specialised niches, where cell-cell and -matrix interactions as well as medium- and long-range molecular signals are integrated to instruct them to either remain quiescent, or to generate progeny that will maintain both the stem cell pool and the differentiated lineages. Studies based on HSC transplantation assays have identified several signalling pathways and bone marrow cell types as regulators of HSC function; however the full picture of the cellular and molecular components of the HSC niche remains elusive because of lack of direct observation over time. HSC subpopulations have been identified based on their proliferative behaviour and it is likely that either migration between different microenvironments or transient modifications of the niche structure mediate changes in HSC fate in response to perturbations such as infection or leukaemia development.
I pioneered the combination of confocal and two-photon microscopy to visualise single HSC and their progeny within the bone marrow of live mice and here I propose to combine advanced microscopy techniques with multi-colour genetic lineage marking and highly sensitive expression profiling to track HSC and their clonal progeny in vivo in real time and to study the cellular and molecular composition of their niches during steady state and when responding to infection and leukaemia development. This work will uncover whether functionally distinct HSC subpopulations reside in anatomically distinct niches or rather all HSC niches are in principle equivalent, but change over time to mediate changes in HSC fate balance. The results obtained will provide a comprehensive picture of HSC niche dynamics, which will be critical for the development of regenerative medicine approaches based on in vivo or ex vivo expansion of HSC.
Max ERC Funding
1 699 724 €
Duration
Start date: 2013-12-01, End date: 2018-11-30