246 research outputs found
Equity and growth in developing countries : old and new perspectives on the policy issues
No full textThe"stylized fact"that distribution must get worse with economic growth in poor countries before it can get better turns out not to be a fact at all. Growth's effects on inequality can go either way and are contingent on several other factors. The authors found no sign in the new cross-country data they assembled that growth has any systematic impact on inequality. Possibly measurement errors confound the true relationship, but they think it more likely that the relationship between growth and distribution is not as simple as some theories have held. Since distribution does not worsen, growth reduces absolute poverty. Indeed, absolute poverty measures typically respond quite elastically to growth, and the benefits are certainly not confined to those near typical poverty lines. Of course, one cannot say that growth always benefits the poor or that none of the poor lose from pro-growth policy reform. Only aggregate effects are studied. But for 17 of the 20 countries for which they assemble quite good data (from at least two surveys since the mid-1980s), the mean and the proportion of people living below $1 a day moved in opposite directions. The gains to poor people from a distribution-neutral growth process will tend to be lower, the higher the extent of initial inequality. A smaller share of total income must imply a smaller absolute gain from a given increment to total income. Compensatory direct interventions can be important, provided they are integrated into a framework of fiscal and monetary discipline. The evidence does not suggest that growth is always distribution-neutral, and it would be wrong to conclude that changes in distribution are of little consequence. The point is not that distribution is irrelevant or that it never changes, but that its changes are roughly uncorrelated with economic growth. There is no intrinsic tradeoff between long-run aggregate efficiency and overall equity. Policies aimed at helping the poor accumulate productive assets--especially policies to improve schooling, health, and nutrition--when adopted in a relatively nondistorted framework, are important instruments for achieving higher growth.Services&Transfers to Poor,Environmental Economics&Policies,Economic Conditions and Volatility,Health Monitoring&Evaluation,Public Health Promotion,Achieving Shared Growth,Inequality,Governance Indicators,Safety Nets and Transfers,Rural Poverty Reduction
Cognitive psychology and mathematics education: Reflections on the past and the future
No full textIt has been well over a decade since I wrote the book, Mathematics education: Models and processes (1995), along with my co-author, Graeme S. Halford. A good deal of what we wrote is still relevant to mathematics education today, as I indicate in this article. But there have been many significant developments in the intervening years that have impacted on our discipline and indicate future directions for our field. I address some of these developments here. Issues of Continued Significance Proponents of the period of Meaningful Learning (19030s and 1940s) advocated the development of mathematical learning with understanding, with William Brownell (e.g., 1945) emphasizing the importance of students appreciating and understanding the structure of mathematics. His recommendations are still highly relevant today: mathematics is the study of structure (Lesh & English, 2005). As highlighted in the National Council of Teachers of Mathematics ’ Principles and Standards for School Mathematics (NCTM 2000), students need to learn mathematics with understanding by actively building new knowledge from existing knowledge and experience. The curriculum must be “more than a collection of activities: it must be coherent, focused on important mathematics, and well articulated across the grades ” (p. 14)
The impact of labor market regulations
No full textThe authors investigate the impact of labor market regulations in settings where compliance is incomplete. They review some stylized facts about labor market behavior, present an analytical model that may explain such behavior, and provide a checklist for assessing the distortionary impact of a regulation such as the minimum wage. They take as their starting point the limited evidence about the distortionary effects of such regulations and argue that there may be natural limits on the efficiency losses engendered by labor market regulations. First, the regulations may not be binding at market equilibrium. For example, minimum wages may be set so low that they are ineffective. Second, even if they are binding, the relevant elasticities of supply and demand may be so low that the regulations have little impact on efficiency. Third, even if the regulations are binding and elasticities are sizable, compliance may be low. The authors argue that the likelihood of compliance will be greatest when the regulations are binding and the relevant elasticities are sizable. That is, if the distortionary costs of regulations are not rendered insignificant by the first two reasons, then the returns to noncompliance will be high and, other things being equal, employers will evade or avoid the regulations, thereby minimizing the imact on efficiency. The argument rests on profit maximization subject to a hard budget constraint. Public enterprises, which are not concerned only with profit maximization and often have softer budget constraints than the private sector, may be more willing to conform to profit-reducing regulations, but in this case the authors argue that compliance may reduce already-existing efficiency losses.Environmental Economics&Policies,Health Monitoring&Evaluation,Labor Policies,Public Health Promotion,Banks&Banking Reform,Health Monitoring&Evaluation,Banks&Banking Reform,Municipal Financial Management,Poverty Assessment,Environmental Economics&Policies
Impact of obesity on cardiovascular disease
No full textObesity is associated with increased risk of cardiovascular disease (CVD), heart failure, diabetes, cancer, and ultimately all-cause mortality. Obesity is causally related to dyslipidemia, hypertension, and diabetes, all strong CVD risk factors, and so causally related to CVD risk. In fact, a substantial part of the risk imparted by obesity on CVD outcomes operates via traditional risk factors. Obese men are almost twice as likely and women almost two and half times as likely to develop hypertension. Obese individuals are around 50% more likely to have a stroke and have around 6–12 times higher risks of developing type 2 diabetes compared to those with a normal BMI.
Obesity is also linked to greater risk for development of heart failure. Yet, there appears to be an obesity paradox in established heart failure such that the risk of death is lower in overweight and mildly obese individuals than in those with normal weight. Such observations are likely partially driven by reverse causality whereby disease-specific issues drive weight loss rather than higher weight per se being protective.
While obesity is most commonly defined by BMI, the importance of body fat distribution and markers such as waist circumference, waist: hip ratio, visceral and ectopic fat volumes are becoming better appreciated. The concept of harmful fat distribution is therefore topical and recent evidence suggest those who can store more fat subcutaneously (and so delay their ectopic depot expansions until much heavier) have lesser diabetes and cardiovascular risks. This paradigm may also largely explain men’s greater risks for both chronic conditions at similar BMI’s to women.
Trials of weight loss add strong support for causal links between adiposity and CVD; for example, the best evidence suggests that losing around 1 kg reduces SBP by around 1 mmHg. Weight loss also improves lipid profiles with reduced total cholesterol, LDL-cholesterol, and in particular triglyceride levels. Weight loss of around 5 kg reduces the risk of obese individuals progressing to impaired glucose tolerance and type 2 diabetes. In those with type 2 diabetes, 5 to <10% intentional weight loss is associated with 3.5 times increased odds of obtaining a 0.5% reduction in HbA1c. Not surprisingly, substantial weight loss has been associated with significantly lower mortality from several causes.
This chapter will show how the best epidemiological evidence, using methods to lessen the impact of reverse causality, supports strong graded links between adiposity and CVD. It will also examine and explain the apparent obesity paradox of heart failure. The chapter will then describe the effect on CVD outcomes of robust lifestyle and surgical intervention studies and trials. Finally, we will also explain how genetics data have helped support causal associations between increasing BMI and CVD, including understanding better the causal links between regional adiposity and CVD.
In conclusion, several lines of evidence, including observational, trial, and genetic, collectively support causal links between obesity, cardiovascular morbidity and mortality, and all-cause mortality
Impact of Obesity on Cardiovascular Disease
No full textObesity is associated with increased risk of cardiovascular disease (CVD), heart failure, diabetes, cancer, and ultimately all-cause mortality. Obesity is causally related to dyslipidemia, hypertension, and diabetes, all strong CVD risk factors, and so causally related to CVD risk. In fact, a substantial part of the risk imparted by obesity on CVD outcomes operates via traditional risk factors. Obese men are almost twice as likely and women almost two and half times as likely to develop hypertension. Obese individuals are around 50% more likely to have a stroke and have around 6–12 times higher risks of developing type 2 diabetes compared to those with a normal BMI.
Obesity is also linked to greater risk for development of heart failure. Yet, there appears to be an obesity paradox in established heart failure such that the risk of death is lower in overweight and mildly obese individuals than in those with normal weight. Such observations are likely partially driven by reverse causality whereby disease-specific issues drive weight loss rather than higher weight per se being protective.
While obesity is most commonly defined by BMI, the importance of body fat distribution and markers such as waist circumference, waist: hip ratio, visceral and ectopic fat volumes are becoming better appreciated. The concept of harmful fat distribution is therefore topical and recent evidence suggest those who can store more fat subcutaneously (and so delay their ectopic depot expansions until much heavier) have lesser diabetes and cardiovascular risks. This paradigm may also largely explain men’s greater risks for both chronic conditions at similar BMI’s to women.
Trials of weight loss add strong support for causal links between adiposity and CVD; for example, the best evidence suggests that losing around 1 kg reduces SBP by around 1 mmHg. Weight loss also improves lipid profiles with reduced total cholesterol, LDL-cholesterol, and in particular triglyceride levels. Weight loss of around 5 kg reduces the risk of obese individuals progressing to impaired glucose tolerance and type 2 diabetes. In those with type 2 diabetes, 5 to <10% intentional weight loss is associated with 3.5 times increased odds of obtaining a 0.5% reduction in HbA1c. Not surprisingly, substantial weight loss has been associated with significantly lower mortality from several causes.
This chapter will show how the best epidemiological evidence, using methods to lessen the impact of reverse causality, supports strong graded links between adiposity and CVD. It will also examine and explain the apparent obesity paradox of heart failure. The chapter will then describe the effect on CVD outcomes of robust lifestyle and surgical intervention studies and trials. Finally, we will also explain how genetics data have helped support causal associations between increasing BMI and CVD, including understanding better the causal links between regional adiposity and CVD.
In conclusion, several lines of evidence, including observational, trial, and genetic, collectively support causal links between obesity, cardiovascular morbidity and mortality, and all-cause mortality
Agricultural trade liberalization in the Uruguay Round : one step forward, one step back?
No full textAfter evaluating the Uruguay Round's impact on agriculture and border protection in the next decade, the author concludes that while there was significant reform of the rules - particularly the conversion of nontariff barriers into tariffs and the reduction and binding of all tariffs - in practice, trade will probably be liberalized less than expected. The objective of the Round was to reverse protectionism and remove trade distortions. This may not be achieved in practice, at least not until further reductions are carried out in future rounds of negotiations. The major exception to this conclusion is in high-income Asian countries, where protection for major commodities will be significantly reduced. The tariffication and binding of all tariffs on agricultural products represents a significant step forward. Liberalization is implicit because countries are prohhibited from arbitrarily raising tariffs to new higher levels. But many of the newly established tariffs are so high in many countries as to effectively prohibit trade. Patterns of liberalization vary considerably by commodity and by country. Generally, the extent of liberalization was diminished by binding tariffs to the base period of 1986-88, when border protection was at a high point. In most OECD countries, this was worsened by"dirty tariffication:"the new base tariffs offered even greater protection than the nontariff barriers they replaced. Even after the commitments to tariff reductions in the Round, the ad valorem measure of the final binding tariffs will remain higher than the average rate of protection in 1982-93. A number of developing countries in East Asia, Latin America, and the Middle East chose to lock in prior liberalization efforts on some products. But for most commodities, there will be little actual liberalization, since most developing countries chose to bind their tariffs at a maximum level. Even when countries reduced already-bound rates, bound tariffs remained significantly higher than current applied rates, giving countries the flexibility to raise tariffs later. The high level of bound tariffs may allow countries to apply variable tariffs below the bound level, thus failing to stabilize tariffs and improve market access. Moreover, the Round did not touch many of the worst distortions in developing countries, such as import subsidies, export taxes, state-trading monopolies, and domestic policies that implicitly tax agriculture.Trade Policy,Environmental Economics&Policies,Economic Theory&Research,Export Competitiveness,Rules of Origin,Trade Policy,Rules of Origin,TF054105-DONOR FUNDED OPERATION ADMINISTRATION FEE INCOME AND EXPENSE ACCOUNT,Environmental Economics&Policies,Economic Theory&Research
Xanthine oxidase inhibition for the treatment of stroke disease: a novel therapeutic approach
No full textNo abstract available
Cytokine pathways driving diverse tissue pathologies in rheumatoid arthritis
No full textRheumatoid arthritis is a complex systemic disorder characterised primarily by articular inflammation and destruction with associated functional loss and reduced quality of life. RA is also associated with extra-articular disease e.g. of the lung with potentially devastating clinical consequences. The critical importance of co-morbidities, and consequent multi-morbidity, in determining outcomes in RA has now been recognised, not least as novel therapeutics have emerged with attendant increased life expectancy. The primary role of cytokine networks in mediating RA pathogenesis was established in extensive pre-clinical and clinical trials and in the adoption of cytokine targeted therapeutics in clinical care over three decades. Herein we briefly review those pivotal cytokine pathways that are associated with RA articular disease, and extend these insights to include extra-articular RA and its common co-morbidities
Weighing in on obesity and psoriatic arthritis – time to move beyond association to robust randomised trials
No full textAlmost one in two individuals with psoriatic arthritis (PsA) are now living with obesity. Obesity increases the risk of developing PsA, worsens disease activity, pain and fatigue, impairs treatment response, and amplifies the risk of many cardiometabolic comorbidities already more prevalent in PsA. Despite the increasing evidence for the pathogenic role of obesity in PsA, current treatment focuses on immune mediated therapies, with limited attention to tackling excess adiposity. Residual pain and disease activity in PsA can in turn adversely impact physical activity, leading to a cycle of further weight gain and worse disease activity. Preliminary evidence from dietary interventions in patients with PsA and obesity suggests weight loss of ≥5% body weight can improve disease activity, holding promise for potentially even better improvements with newer pharmacological anti-obesity therapies, such as incretin-based weight loss medicines, which result in average weight losses of 15-20%. In this narrative review, we provide an overview of the adverse impacts of obesity in PsA and discuss weight loss therapies now available to help address this. We highlight the urgent need for robust randomised controlled trials of weight loss therapies in patients with PsA and obesity to determine their clinical and cost effectiveness in PsA management and to inform where these are best implemented in the disease course and treatment pathway
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