280 research outputs found

    Policy-induced Internal Migration: An Empirical Investigation of the Canadian Case

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    We investigate the influence of public policy on interprovincial migration in Canada using new aggregated migration data for 1974-1996, the longest period studied so far. We consider the consequences of regional variation in a variety of policies, and also investigate the effects of certain extraordinary events in Quebec and in the Atlantic provinces. The results indicate that while the changing bias in the unemployment insurance system may have induced some people to move to the relatively high unemployment Atlantic region, the resulting flows are likely too small to have altered regional unemployment rates. In contrast, political events in Quebec in the 1970's and the closing of the cod fishery in 1992 appear to be associated with large changes in migration patterns.migration, regional disparity, public policy, unemployment insurance, conditional logit, taxation data

    Growth and the Environment in Canada: An Empirical Analysis

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    Standard reduced form models are estimated for Canada to examine the relationships between real per capita GDP and four measures of environmental degradation. Of the four chosen measures of environmental degradation, only concentrations of carbon monoxide appear to decline in the long run with increases in real per capita income. The data used in the reduced form models are also tested for the presence of unit roots and for the existence of cointegration between each of the measures of environmental degradation and per capita income. Unit root tests indicate nonstationarity in logs of the measures of environmental degradation and per capita income. The Engle-Granger test and the maximum eigenvalue test suggest that per capita income and the measures of environmental degradation are not cointegrated, or that a long-term relationship between the variables does not exist. Causality tests also indicate a bi-directional causality, rather than a uni-directional causality, from income to the environment. The results suggest that Canada does not have the luxury of being able to grow out of its environmental problems. The implication is that to prevent further environmental degradation, Canada requires concerted policies and incentives to reduce pollution intensity per unit of output across sectors, to shift from more to less pollution-producing-outputs and to lower the environmental damage associated with aggregate consumption.environment, economic growth, Canada

    What do we Know about the Relationship between Regionalized Aspects of the Unemployment Insurance System and Internal Migration in Canada?

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    The purpose of this paper is to critically review the past four decades of empirical research on the relationship between internal migration and regional variation in the generosity of Canada’s unemployment insurance system. It has long been argued that because the Canadian insurance system is more generous towards people who live in relatively disadvantaged regions, it retards the out-migration that is part of the market process, thereby slowing economic development and contributing to the persistence of regional inequality in earned incomes. The survey shows, however, that there is no evidence in the empirical literature that regional variation in the generosity of the insurance system has altered internal migration patterns in Canada in a substantial manner.regional variation in unemployment insurance generosity, internal migration, interprovincial migration, earned income, comprehensive income differentials, index of insurance generosity, labour market attachment, conditional logit model

    Policy-induced internal migration : an empirical investigation of the Canadian case

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    We investigate the influence of public policy on interprovincial migration in Canada using new aggregated migration data for 1974-1996, the longest period studied so far. We consider the consequences of regional variation in a variety of policies, and also investigate the effects of certain extraordinary events in Quebec and in the Atlantic provinces. The results indicate that while the changing bias in the unemployment insurance system may have induced some people to move to the relatively high unemployment Atlantic region, the resulting flows are likely too small to have altered regional unemployment rates. In contrast, political events in Quebec in the 1970's and the closing of the cod fishery in 1992 appear to be associated with large changes in migration patterns

    Policy-Induced Migration in Canada: An Empirical Study

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    We investigate the influence of public policy on interregional migration in Canada using new interprovincial migration data constructed from personal income tax files for the years 1974 to 1996. We consider the consequences for gross and net migration flows of regional variation in employment insurance, provincial social assistance, personal income taxes and public spending of different types, and we compare the effects of these policies to the impacts on migration of wages, employment prospects and moving costs. We also conduct a preliminary investigation of the migration consequences of certain extraordinary political events in Quebec and of the closing of the cod fishery in Newfoundland. Unemployment insurance is an especially important and well documented source of income for many people, and regional variation in the generosity of the insurance system over the last three decades has been substantial. The results suggest that while increasing the generosity of the system in high unemployment regions may have induced more migration to the Atlantic region than would otherwise have occurred, the resulting changes in gross flows are probably not large and have had, at most, small effects on average provincial unemployment rates. A variety of other interesting results is also provided

    Human adipose derived stromal/stem cells (hASCs) protect against STZ-induced hyperglycemia; analysis of hASC-derived paracrine effectors

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    Adipose-derived stromal/stem cells (ASCs) ameliorate hyperglycemia in rodent models of islet transplantation and autoimmune diabetes, yet the precise human ASC (hASC)-derived factors responsible for these effects remain largely unexplored. Here, we show that systemic administration of hASCs improved glucose tolerance, preserved β cell mass, and increased β cell proliferation in streptozotocin-treated nonobese diabetic/severe combined immunodeficient mice. Coculture experiments combining mouse or human islets with hASCs demonstrated that islet viability and function were improved by hASCs following prolonged culture or treatment with proinflammatory cytokines. Analysis of hASC-derived factors revealed vascular endothelial growth factor and tissue inhibitor of metalloproteinase 1 (TIMP-1) to be highly abundant factors secreted by hASCs. Notably, TIMP-1 secretion increased in the presence of islet stress from cytokine treatment, while TIMP-1 blockade was able to abrogate in vitro prosurvival effects of hASCs. Following systemic administration by tail vein injection, hASCs were detected in the pancreas and human TIMP-1 was increased in the serum of injected mice, while recombinant TIMP-1 increased viability in INS-1 cells treated with interleukin-1beta, interferon-gamma, and tumor necrosis factor alpha. In aggregate, our data support a model whereby factors secreted by hASCs, such as TIMP-1, are able to mitigate against β cell death in rodent and in vitro models of type 1 diabetes through a combination of local paracrine as well as systemic effects

    Coenzyme Q Metabolism Is Disturbed in High Fat Diet-Induced Non Alcoholic Fatty Liver Disease in Rats

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    Oxidative stress is believed to be a major contributory factor in the development of non alcoholic fatty liver disease (NAFLD), the most common liver disorder worldwide. In this study, the effects of high fat diet-induced NAFLD on Coenzyme Q (CoQ) metabolism and plasma oxidative stress markers in rats were investigated. Rats were fed a standard low fat diet (control) or a high fat diet (57% metabolizable energy as fat) for 18 weeks. The concentrations of total (reduced + oxidized) CoQ9 were increased by >2 fold in the plasma of animals fed the high fat diet, while those of total CoQ10 were unchanged. Reduced CoQ levels were raised, but oxidized CoQ levels were not, thus the proportion in the reduced form was increased by about 75%. A higher percentage of plasma CoQ9 as compared to CoQ10 was in the reduced form in both control and high fat fed rats. Plasma protein thiol (SH) levels were decreased in the high fat-fed rats as compared to the control group, but concentrations of lipid hydroperoxides and low density lipoprotein (LDL) conjugated dienes were unchanged. These results indicate that high fat diet-induced NAFLD in rats is associated with altered CoQ metabolism and increased protein, but not lipid, oxidative stress

    Community Health Environment Scan Survey (CHESS): a novel tool that captures the impact of the built environment on lifestyle factors

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    Background: Novel1 1This study was performed on behalf of the Community Interventions for Health (CIH) collaboration. efforts and accompanying tools are needed to tackle the global burden of chronic disease. This paper presents an approach to describe the environments in which people live, work, and play. Community Health Environment Scan Survey (CHESS) is an empirical assessment tool that measures the availability and accessibility, of healthy lifestyle options lifestyle options. CHESS reveals existing community assets as well as opportunities for change, shaping community intervention planning efforts by focusing on community-relevant opportunities to address the three key risk factors for chronic disease (i.e. unhealthy diet, physical inactivity, and tobacco use). Methods: The CHESS tool was developed following a review of existing auditing tools and in consultation with experts. It is based on the social-ecological model and is adaptable to diverse settings in developed and developing countries throughout the world. Results: For illustrative purposes, baseline results from the Community Interventions for Health (CIH) Mexico site are used, where the CHESS tool assessed 583 food stores and 168 restaurants. Comparisons between individual-level survey data from schools and community-level CHESS data are made to demonstrate the utility of the tool in strategically guiding intervention activities. Conclusion: The environments where people live, work, and play are key factors in determining their diet, levels of physical activity, and tobacco use. CHESS is the first tool of its kind that systematically and simultaneously examines how built environments encourage/discourage healthy eating, physical activity, and tobacco use. CHESS can help to design community interventions to prevent chronic disease and guide healthy urban planning

    Signaling from β1- and β2-adrenergic receptors is defined by differential interactions with PDE4

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    β1- and β2-adrenergic receptors (βARs) are highly homologous, yet they play clearly distinct roles in cardiac physiology and pathology. Myocyte contraction, for instance, is readily stimulated by β1AR but not β2AR signaling, and chronic stimulation of the two receptors has opposing effects on myocyte apoptosis and cell survival. Differences in the assembly of macromolecular signaling complexes may explain the distinct biological outcomes. Here, we demonstrate that β1AR forms a signaling complex with a cAMP-specific phosphodiesterase (PDE) in a manner inherently different from a β2AR/β-arrestin/PDE complex reported previously. The β1AR binds a PDE variant, PDE4D8, in a direct manner, and occupancy of the receptor by an agonist causes dissociation of this complex. Conversely, agonist binding to the β2AR is a prerequisite for the recruitment of a complex consisting of β-arrestin and the PDE4D variant, PDE4D5, to the receptor. We propose that the distinct modes of interaction with PDEs result in divergent cAMP signals in the vicinity of the two receptors, thus, providing an additional layer of complexity to enforce the specificity of β1- and β2-adrenoceptor signaling
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