In order to be competitive, telecommunications service providers need new technologies that facilitate the rapid introduction of new services and resolve the problems how to use the services safely. This paper introduces a network platform based on mobile agent and provides a security mechanism based on zero knowledge proof in the mobile communication system. In this way, service providers can provide the new services rapidly, expediently and safely.
This paper discusses the nature of the paradigm shift that will be accelerated as the next-generation Internet (NGI) pervades society. First, we define the NGI society as one in which the network is so ubiquitous that no one will be conscious of connecting with it. Then we investigate trends and expectations of current NGI research and development projects worldwide. Secondly, we have performed comprehensive questionnaire-based market research into new technologies. This reveals that Japan can be expected to create global markets by developing NGI applications in home-electronic appliances, mobile assistants, transportation systems, and animation games. Furthermore, we generalize the discussion on the nature of the paradigm shift as follows. Although modern western rationalism produced the astonishing growth of the industrialized countries in the 19th-20th centuries, this approach alone no longer offers the prospect of much further advance. The 21st century paradigm for science and technology, for social, economic and governmental systems, and for industrial structures and working styles will necessarily shift towards autonomous and cooperative decentralization. The Internet is a decentralized computer system that is operated autonomously and cooperatively by individuals and small organizations. The NGI will further accelerate this paradigm shift. We conclude that this approach is essentially similar to the traditional oriental philosophy of harmony, and urge that it should be adopted in positioning Japan within the global, information-oriented network society of the 21st century.
Decentralization is commonly championed as a means for achieving equity. To date, however, there has been little discussion of the mechanisms underlying this relationship, and several of the few empirical investigations that have addressed the topic have found the converse; that decentralization has exacerbated inequalities. This article examines the performance and equity in financing of the Honduras Ministry of Health's (MOH) decentralized user fee system. The MOH of Honduras established a national user fee policy in 1989. It provided a framework of rules and regulations and decentralized administration of the system to the regional offices. A survey conducted under the auspices of this study provided detailed information about the structures and operations of MOH user fee systems. The survey revealed that the systems vary markedly by region, creating horizontal inequities, and that they have numerous other shortcomings. The average price of a consultation is low, US dollars 0.16, and revenues have consistently equalled just 2% of MOH expenditures. The systems' administrative costs are equal to 67% of their revenues. Eliminating the user fee systems in all but the national and regional hospitals would actually save money and/or enable the MOH to provide more care. Average consultation prices are highest in health posts, intermediate in centres and lowest in the national hospitals, thereby encouraging the inappropriate use of the MOH's pyramidal referral system and fostering MOH inefficiency. Fee levels and exemption practices are horizontally and vertically inequitable. The likelihood of paying for an ambulatory visit is highest at a health post, 89%, and lowest at a hospital, 49%. Individuals from the poorest one-fifth of households are the most likely to have to pay for care. Honduras' experience demonstrates that a decentralized user fee system is not necessarily equitable, and that, more generally, the gains that can be realized from decentralizing user fee systems are not automatic. They must be anticipated, planned for and cultivated by a well-designed and well-implemented initiative that is not a single, one-time event, but rather a dynamic, on-going enterprise.
Most economists agree that new investments in highways at this point in time in the United States have little impact on overall growth in output. New highways play a more important role in shifting economic activities among places, drawing jobs from other locations into the highway corridors, a phenomenon known as negative spillovers. The objective of this dissertation is two-fold, to examine the proposal to decentralize highway finance, which aims to solve the financial responsibility mismatch problem that stems from economic spillovers of highways, and to test the hypothesis of economic spillovers of highway investment at the metropolitan level. First, to better understand how spillovers influence the highway investment decision, the theoretical framework from the interjurisdictional tax competition literature is borrowed to model governments' investment behaviors. Numerical simulations show that decentralized local governments, which independently maximize output in their own jurisdiction, may engage in wasteful investments in highways with the presence of spillovers. Second, to shed more light on the spatial detail of economic spillovers, empirical tests of the spillover hypothesis are conducted at the metropolitan level, with census tracts as the unit of observation. The results of the quasi-experiment reveal census tract employment growth patterns that confirm the existence of negative spillovers caused by the opening of the Interstate 105 in 1993. The benefiting area, which grew substantially after the highway was opened, is limited to a long narrow corridor around the highway, while nearby locations outside the corridor experienced slow growth relative to the rest of the metropolitan area after controlling for various factors. Together, these results suggest that although negative spillovers are present at the metropolitan level, decentralizing highway finance may not be an effective policy to deal with the financial responsibility mismatch problem. Highway finance should remain centralized within metropolitan areas, and regional governing bodies should pay special attention to the distributional impact of highway projects.
Vertical fiscal imbalance, decentralized responsibility of spending with centralized financing, creates a common pool problem with spending pressure towards central funds. A model of decentralized government spending under vertical fiscal imbalance is developed, and the importance of national political characteristics for internalization of costs and spending level is investigated in an econometric analysis of Norway during 1880â1990. We argue that in a parliamentary democracy, the internalization of costs is influenced by the party fragmentation of parliament. This is confirmed by the econometric analysis using a Herfindahl index as a measure of fragmentation and political strength.
Small hydropower (SHP), a renewable and non polluting energy, could participate in the sustainable development of humanity. As a mature industry, SHP is a decentralized energy. It's also a wonderful economic development tool for rural countries, poor areas or for millions of people in the world who have not yet access to electricity. Nevertheless obstacles are too many to increase SHP, i.e. : poor financing capacity in foreign countries, environmental lobbies in Europe and in France...
Over the last 15 yr, genes responsible for hundreds of inherited human diseases have been identified, enabling clinical diagnosis and the potential for therapeutic intervention. Until very recently, however, success has been limited to so-called monogenic disorders, diseases in which mutation of a single gene is both necessary and sufficient to cause disease in any given individual. Because such mutations are strictly co-inherited with disease, it is possible to use linkage analysis to identify their chromosomal location by analyzing which of a genome-wide set of markers segregates with disease in families. Genes contained within such linked regions become positional âcandidatesâ and are next examined for mutations in affected individuals. For any such candidate gene, proof of causality typically depends on two additional lines of evidence. First, the putative causal changes should be found only in affected individuals. Second, one hopes for a âsmoking gunââthat the disease-associated mutations are obviously deleterious to protein function (due to truncation or deletion of a coding region or alteration of a highly conserved residue). Success is typically declared when these criteria are all satisfied: the putative disease gene 1) is located in a chromosomal region that co-segregates with disease in affected families, 2) contains multiple independent mutations that are perfectly associated with disease status in the families, and 3) whose characteristics obviously alter protein function. Most common diseases are strongly influenced by inheritance, but, to date, relatively few genes have been identified that are responsible for familial clustering of these diseases. Success has been elusive because common diseases are almost all complex disorders, where multiple genes and environmental factors collaborate to cause disease. Because no single gene segregates tightly with disease, it has proven very difficult to confidently localize putative disease genes to chromosomal locations. For this reason, optimistic gene hunters have leapt directly to the latter stage of examining candidate genes for mutations that show association to disease. Typically, however, these candidate genes are based on a biological hypothesis, rather than chromosomal position relative to a linkage study. Association studies can, in theory, succeed where linkage fails, because association can offer much greater statistical power (1), thus providing a rationale for circumventing linkage analysis. But several problems bedevil such association studies. First, it is expected that the causal mutations are neither necessary nor sufficient to cause disease. That is, some people will have the mutation but not disease, and others will have disease without a causal mutation of that gene. Because of this imperfect correlation, association studies must compare the frequencies of a putative causal mutation in individuals with disease and in appropriate controls. If the mutation is found at a statistically significant higher frequency in affected individuals, the mutation is said to be associated with disease. However, determining appropriate thresholds of significance is challenging because the a priori likelihood that any given candidate gene plays a role in disease is unknown, but certainly low (in following up a solid linkage peak, one at least begins with the knowledge that one or more genes in the region is responsible for the disease). In addition, these more subtle genetic risk factors need not be premature stop codons or protein truncation mutants. Rather, they may be innocuous to the scientistâs eye and yet cause disease by altering the in vivo regulation, expression, stability, activity, or interactions of the encoded protein. Because of these and other difficulties (see, for example, Ref. 2), it is important that association studies be performed and scrutinized carefully, especially when different investigators reach different conclusions as to whether mutations or genetic variation in a gene is associated with disease. Here, we discuss the relevant points in light of a report in this issue questioning the relationship of mutations in the MC4R gene and severe obesity (3). Most association studies have focused on a common genetic variation: by convention, common genetic variants (or polymorphisms) are those for which two or more alleles each exist in 1% or more of the population at large. There are many practical advantages to studying common variants. Because they are present at high frequency, common variants can be discovered in any modest sized group of individuals. This facilitates cataloging of common variants. Over the last 3 yr, millions of common human sequence variants have been identified and placed in databases (4). Moreover, because strong correlations are typically observed between neighboring variants (linkage disequilibrium), most common variations in the genome can be tested for a role in disease using a subset of carefully chosen âtagâ single nucleotide polymorphisms (see Ref. 5 and references therein). Finally, testing common variants for association to disease is technically straightforward. The frequencies of each variant can be accurately estimated in modest sized collections of patients with and without the disease. Of course, there is no reason to presume that the mutations responsible for common diseases will themselves be common. Certainly, many rare monogenic disorders are due to a heterogeneous collection of variants that are individually very rare. In thinking about the allele spectrum of common diseases, it is important to consider both the overall characteristics of human genetic variation and the particular evolutionary features of each disease (6). The characteristic features of human genetic variation have been well described (see Ref. 4 and references therein). Numerically, rare variants outnumber common variants, but the vast majority of variant alleles in the population (heterozygosity) are attributable to the small number of common variants. Thus, for disease phenotypes that had a neutral effect on human evolutionary fitness, the spectrum of alleles causing disease should resemble this overall patternâmost of the genetic burden of disease in the population will be due to common variants. In contrast, where disease was disadvantageous from an evolutionary perspective (e.g. diseases that are lethal in childhood), rare variants will predominate, because variants that lower reproductive fitness generally do not drift up to high frequency. Finally, disease phenotypes that experienced balancing selection (e.g. sickle cell disease, where disease is balanced by resistance to malaria in carriers) or that may even have been evolutionarily advantageous (as has been proposed for obesity under the thrifty gene hypothesis) should be due to variants that are even more common than those found throughout the genome as a whole. Given the speculative nature of such evolutionary hypotheses, as well as the experience from rare monogenic disorders, there has been great attention to the importance of studying rare genetic variants for a role in common disease (see, for example, Ref. 6). However, studying rare variants introduces important methodological challenges. First, investigators must discover the variants in each of their populations, often by directly resequencing affected individuals. Moreover, because they are rare, much larger samples must be examined before an accurate estimate of frequency can be obtained for the comparison of cases and controls. In making such comparisons, it is critical that controls be scrutinized for variation in the exact same manner as cases, because resequencing only of cases leads to a significant problem called ascertainment bias. In brief, sequencing a large group of individuals will nearly always identify a particular collection of vanishingly rare variants (including missense variants) that will be absent from any second collection of individuals that is tested. Thus, finding a few rare, apparently deleterious mutations in affected individuals does not signify a role in disease, unless controls have been examined with the same intensity as have cases, and the preferential presence of variants in affected individuals is strong and statistically convincing. In fact, the statistical analysis of rare variation almost always requires that collections of different rare variants be considered as a group, because no individual variant is sufficiently common to permit an accurate assessment of its frequency in realistically sized disease or control populations. It is important that the grouping of rare variants not be done post hoc in a subjective (and, therefore, potentially biased) manner. Rather, the grouping must be on the basis of obvious sequence characteristics (e.g. all missense variants, all nonsense and frameshift mutations, etc.), or on the basis of a valid functional assay. To avoid a biased assignment of functional importance to variants identified in affected individuals, such a functional assay should be developed and validated independently of the results of association analysis. Despite these additional challenges, association testing of rare and common variants is fundamentally similar. Once a relevant common variant âor group of rare variantsâis identified, the frequency of variants must be rigorously compared in affected individuals and in controls. The choice of a threshold for declaring a significant association has been a matter of some debate. The P value for differences in frequencies between affected individuals and controls reflects the likelihood of observing an association by chance if the true frequency were the same in both groups. This obviously is not equivalent, however, to the likelihood that the experimenterâs hypothesis of association is in error, because this latter calculation requires knowledge of the a priori probability that the variant in question was associated with disease. In most such studies, this prior probability is extremely lowâthere are hundreds of candidate genes, each of which contains a hundred or more commonly varying sites; moreover, many causal genes will not be obvious candidates, and the entire genome contains 10 million common variants and many more rare variants. In this Bayesian framework, the P values for most association studies are not low enough to meet a conservative threshold for declaring significance that minimizes type 1 errors (false positive studies). Thus, a single report of association is almost always inadequate to prove causation. Rather, replication, preferably in multiple independent studies, is required. However, consistent replication of associations has been difficult to achieve. Indeed, a review of associations between common variants and disease found that the vast majority of such associations have not been consistently reproduced (2). The possible reasons for the inconsistency include false positives due to type 1 error, false positives due to population stratification, false negatives due to lack of power in potential replication studies, and true differences between study populations (e.g. different phenotypes, or different environmental or genetic modifiers). These explanations probably all contribute to the lack of reproducibility and are relevant to both studies of individual common variants and of grouped rare variants. However, to interpret an association that has not been consistently replicated, it is important to try to distinguish which of these explanations is truly relevant to that particular association. Lack of power for true associations with modest effects can clearly contribute to inconsistent replication. For example, several studies failed to detect an association of the Pro12Ala variant with type 2 diabetes and concluded that no such role was likely to exist. In fact, this PPARG variant has a much lower relative risk (1.25-fold) than was initially estimated, and consequently many studies were underpowered to detect the true effect of the allele on diabetes risk (7). To assess power, then, the range of genetic effects that are consistent with the negative data should be compared with the genetic effect estimated by considering all of the previous studies together. In this context, Jacobson et al. (3) report in this journal their failure to replicate the previously described association of rare functional variants in the MC4R gene with morbid human obesity. MC4R was originally implicated in obesity by mouse studies (see, for example, Ref. 8); two groups then independently identified severely obese individuals (one in each study) with a frameshift mutation in the MC4R gene (9, 10). Several additional studies subsequently found at least 34 additional missense or frameshift mutations in MC4R in obese individuals, but no functional missense variants were identified in control individuals who were resequenced (see Refs. 18â24 in Ref. 3). It is worth noting that there are three somewhat common missense variants that are present at approximately equal frequencies in obese and nonobese individuals (Val103Ile, Thr112Met, and Ile251Leu). These variants have been distinguished from the putative functional variants because they do not affect MC4R function in in vitro tests (11, 12). If these common variants were included in statistical analysis, they would swamp out any signal due to the rarer, apparently functional mutations. Thus, the statistical arguments in favor of association rely critically on the relevance of the in vitro assay used to assess protein function. In total, at least 34 putative functional MC4R mutations have been identified in 1187 obese individuals (2.9% frequency) as compared with zero in 827 controls. Nearly all of the obese individuals who were found to carry mutations are either severely morbidly obese [body mass index (BMI),50] or had onset of obesity in childhood or early adolescence. However, some carriers and relatives were identified who also carry MC4R mutations but have less severe phenotypes (12). These findings led to the hypothesis that mutations in MC4R might be a common cause of morbid obesity (12). It was the intent of Jacobson et al. (3) to test this hypothesis. To study the role of MC4R mutations in obesity, they resequenced the MC4R gene in over 200 obese white subjects and 47 obese black subjects, plus a similar number of controls. None of the previously described putative functional variants were identified. Three new missense variants were identified, each in one black control (Ile102Thr, Phe202Leu, and Asn240Ser). Unfortunately, no functional evaluation of these variants was performed. In addition, one frameshift mutation leading to a predicted premature termination codon was discovered in an obese white female. The authors interpret these data as failing to replicate the previous findings of a high rate of MC4R mutations in obese individuals. To evaluate whether the authors have failed to replicate the previous finding, or have simply asked a different question, we consider below each of the main possible explanations for the failure to replicate: false negative study (inadequate power), a falsely positive original report, and true differences between study populations. Jacobson et al. (3) state that they can strongly reject the hypothesis that mutations in MC4R account for 4% of cases of obesity, with 80â85% power in blacks and greater than 99.9% power in whites. These arguments are based on not having observed any of the previously reported functional variants. However, the spectrum of variants that can affect MC4R function is apparently quite diverse (few or none of the functional variants have been identified independently in separate studies), so the expectation should be that most functional variants in MC4R would be novel. Indeed, Jacobson et al. (3) did discover one such variant (the frameshift mutation, although they did not test it for function in vitro). Thus, a more appropriate interpretation of their data is that they identified one apparently functional mutation in approximately 200 unrelated obese white individuals and 47 obese black individuals. Furthermore, 4% is the highest estimate of MC4R mutations in the literature (12). A more appropriate figure to test would be 2.9% (the estimate from all available data), and even this value may be too high because some of the rare missense changes identified in obese individuals do not impair function in vitro (see Ref. 12) and, thus, may not represent functional MC4R mutations. What range of frequencies of MC4R mutations could be consistent with the data in Jacobson et al. (3)? Given the observation of one mutation in 200 individuals, the 95% confidence interval for the frequency of MC4R mutations is quite wide; values from 0.12â2.75% are all consistent with the data. Even if the data from blacks and whites are pooled, the 95% confidence interval extends from 0.1â2.2%; the data from blacks alone are actually consistent with mutation frequencies as high as 7% in this population. If power is set at a more conservative 80%, the data can reject frequencies of mutations greater than 1.5% in whites, 3.3% in blacks, and 1.2% in the pooled sample. Although the confidence intervals are wide, the data are apparently inconsistent with the 2.9% frequency of mutations found in previous studies. Thus, additional explanations are required other than inadequate power of the current study. The second possibility is that the previous studies were false positives: all of the functional variants were found in the obese individuals by chance or due to a biased selection of which variants were considered functional. However, this explanation also seems unlikely. The P value for finding 34 functional variants in 1187 obese individuals but no functional variants in 827 controls is under 10â6. In addition, many of the variants are obviously deleterious, and there is no reason to suspect that the functional assay is biased. Thus, one must consider the possibility that the authors of the present study may have asked a different question than that posed before, specifically that the populations used in previous studies and the populations used in Jacobson et al. (3) are in some way fundamentally different from each other. The possibility of differences in populations seems quite plausible if one compares the characteristics of the populations used in previous studies with those of the obese individuals in this most recent study. In previous studies, almost all MC4R carriers were found among severely obese individuals (BMI, >50) and/or individuals with early-onset obesity (usually in childhood). By contrast, only 42% of the white individuals in the study by Jacobson et al. (3) had early-onset obesity (childhood or adolescence), and less than 10% had a BMI greater than 50. If one only considers these approximately 100 subjects in the study, there is no longer 80% power to reject a mutation frequency of 2.9%, although the estimate of the frequency (now 1% rather than 0.5%) is still much lower than the 2.9% estimated by previous studies. However, a potentially more important conclusion is suggested from these data: Jacobson et al. (3) observe no MC4R mutations in 100 individuals with a BMI under 50 and onset of obesity in adulthood. Indeed, the only other studies to examine populations not selected or enriched for severe or early-onset obesity also failed to find mutations in MC4R despite screening 90 individuals (13, 14). This suggests that although MC4R mutation might be a rare (2â3%) but significant cause of early-onset or severe obesity, it is likely to be a less common cause of obesity in the general population. This could be explained (post hoc) by invoking the possible selective disadvantage of relatively penetrant alleles that cause severe, early-onset obesity (where rare MC4R mutations are observed) compared with the less easily predicted evolutionary history of the more common form of the disease. How can one reconcile this apparent absence of MC4R mutations in cases of less severe obesity with the fact that some relatives of severely affected probands carry MC4R mutations but have milder obesity (12)? Shouldnât some of these relatives have turned up in the studies of âtypicalâ obesity? The answer probably lies in the fact that there are many, many more people with typical obesity than there are relatives of MC4R carriers. This theory predicts that if one studied people with mild obesity who had a relative with severe or early-onset obesity, it would be possible to enrich for carriers of MC4R mutations. This dichotomy is reminiscent of the situation for BRCA1 and breast cancer, where mutations are found at appreciable frequencies in highly familial cases, early-onset cases, or women with multiple cancers. Where family members of such women are tested, carriers with later onset breast cancer (or no cancer at all) are found at appreciable when more typical cases of breast cancer are BRCA1 mutations are found at much lower the current study many of the important in association studies of genetic variants and disease. is because prior of true association are low and, thus, all genetic associations a high of failure to replicate can be due to many possible explanations false positive studies and type 1 Lack of power to modest effects and different phenotypes of patients in different collections can both contribute to apparent among studies. Moreover, genetic variants both rare and common are to a role in most diseases, but their relative in any given are to Given the of resequencing and the of grouping rare variants and an of the hypothesis is even for candidate rare variants such as are found in MC4R will no a great about and the in which human can be by severe genetic rare variants also out to much of the population burden of disease is an important question that will for some to mass
Open access
Genetic Associations and Epidemiology
Genetic Mapping and Diversity in Plants and Animals
ABSTRACT This paper asks how well different organizational structures perform in terms of generating information about investment projects and allocating capital to these projects. A decentralized approachâwith small, singleâmanager firmsâis most likely to be attractive when information about projects is âsoftâ and cannot be credibly transmitted. In contrast, large hierarchies perform better when information can be costlessly âhardenedâ and passed along inside the firm. The model can be used to think about the consequences of consolidation in the banking industry, particularly the documented tendency for mergers to lead to declines in smallâbusiness lending.
Argumentation is receiving an increasing attention as a technique for practical and uncertain reasoning underlying the realization of intelligent autonomous agents. Since a decentralized organization has been proposed by several authors as an appropriate paradigm for the design of agent architectures, we propose in this article, a distributed approach to argumentation, in which several independent asynchronous processes carry out argumentation activity, by exploiting local information only. The final result of this process is the computation of the defeat status of the arguments: we devise a general distributed algorithm, which does not rely on any specific notion of defeat between arguments. The issue of coordination has been explicitly tackled by ensuring the property of self-stabilization for the algorithm. A proof of its correctness, as well as an analysis of its complexity, is provided.
This paper reviews the economic rationale for and against decentralization with particular attention to the organization and delivery of education. The paper frames the overview within the standard efficiency-equity trade off and highlights the increasingly important role of incentive mechanisms, accountability, and citizens' participation. The discussion then turns to the issues that are specific to decentralizing education, including the pros and cons of financing schools from local taxes, and a taxonomy and description of institutional arrangements around the world. A brief review of evaluation studies of decentralization reforms in education concludes the paper.
The impact of local government spending on output growth is estimated using a panel of Brazilian municipalities during 1985â1994. Attention is focused on three expenditure categories, housing/urbanization, health/sanitation, and transport services, which are expected to be growth-enhancing, and their sources of finance (local taxes, intergovernmental transfers, and borrowing). The determinants of these spending categories are also examined. The size of the municipality, measured by the resident population, is shown to affect government spending nonlinearly. This is a contribution to the recent empirical literature on the linkages between decentralized government spending, public finances, and economic growth at the local, rather than national, level.
In Oscar Wilde's Portrait of WH we have an essay on the exigencies of interpretation presented to us as though it were a melodramatic murder mystery. As Scott Wilson describes it: After an opening discussion about Art as the realization of personality beyond and its ethical demands, Lord Erskine tells the story of his dead friend Cyril Graham, who devised a theory about the young man of Shakespeare's sonnets. Graham, an effeminate boy player of Shakespeare's roles at Trinity, decided that the Mr. WH of the sonnets must have been, like him, a boy player on Shakespeare's stage called Willy [sic] Hughes. Graham assembles what he believes is convincing textual evidence for his theory and attempts to persuade Erskine who, while accepting the internal evidence, will not be converted until he has seen external proof of the boy's existence. Graham provides a miniature painting. It is exposed as a fake, a simulacrum, and he shoots himself, substituting the reality of his own life and death for that of Willy Hughes. (231-232) Wilde's endlessly interpretable tale points to, among other things, the impossibility of ever really knowing the difference between the fake and the real--even in a situation in which the end result is a death caused by the illusion of evidence. In addition to raising questions about what we might now call post-structuralist hermeneutics, Wilde also warns that the mistaking of the fake for the (and vice versa) can have a material effect. The essays for this special issue investigate just what is at stake in the idea of the real as defined by the artists and thinkers of the Victorian era. Rather than approaching the dichotomy of realism vs. artificiality as it is usually defined for the period--that is, realism vs. any number of complementary binary terms such as neo-mediaevalism, Hellenism, etc.--I would like to call into question just how stable such a binary really was. That is, Victorians were always extremely invested in the fake--even in the authenticity of fakery, such as Eugene Emmanuel Viollet-le-Duc's Gothic designs for Notre Dame de Paris or A. C. Swinburne's invented rural dialects in which he would write the epics of a region and recite them to the people living there who were convinced that he had indeed uncovered a real poem. If so much of Victorian culture was based upon the elaborate creation of simulacra--whether Pre-Raphaelitism or the legends of Tannhauser and Arthur--then why do we persist in seeing the Victorian period as the height of realism, and how might we explain how that period managed to derive so much pleasure from the inability to tell the fake from the real? If the origins of modernism are in the Victorian period, then it behooves us to understand also how postmodernism can trace some of its own origins to the dyadic quality of the Victorian pleasure in simulacra. As clearly obsessed with finding origins as the Victorians were, they seemed always to re-create the past in a form that expressed more about their anxieties about the future (or the present) than it did a clear understanding of even the immediate past. In a similar attempt to turn away from modernism and back toward history, the postmodern artist is often not interested in the past as material reality but as the quotation of a style--a temporal fragment that metonymically stands in for an entire era but may go no deeper than the glossy surface of a label. The extent to which Victorian writers manipulated the surfaces of commodification--and were likewise taken over by them in their own interest in the question of origins and authenticity--is what this volume attempts to explore. The Victorians knew they had the opportunity to be mythmakers, and they took this role on with all the earnestness they could muster; that more was going on than (sometimes) met the eye is proof that the Victorians themselves could be lost in the dizzying simulacra that their culture produced. âŠ
Abstract The development field is currently dominated by two powerful and interconnected ideas: the idea of participation, and the idea of a bottom-up approach. The idea of participation emphasizes the process of development, and claims that development is more likely to be successful if as many as possible of its beneficiaries are actively involved in improving their own conditions. The bottom-up approachâwhich has a parallel in fiscal decentralization in public financeâmaintains that the beneficiaries should choose democratically the means and objectives of the development strategies that concern them.
INTRODUCTION Decentralization of government seems to be one of the intellectual darlings of public finance in the 1990s, just as direct consumption-based taxation in its various guises (e.g., the expenditure tax, the tax on consumed income, the flat tax, the X-tax, and the simplified alternative tax) was the darling of the 1980s. More important, many countries are considering decentralization-or have actually embarked on a policy of decentralization. The question of tax assignment-which level of government should tax what in a decentralized system-is an important aspect of the literature of fiscal decentralization. Unfortunately, some of those responsible for decentralization policy, especially in less developed countries (LDCs) and countries in transition from socialism, are not always thinking clearly about issues of tax assignment and are not taking due cognizance of international experience. At best they may make choices that are sub-optimal; at worst, they run the risk of repeating mistakes other countries have made-mistakes transition countries and LDCs can ill afford to make. These risks are aggravated by the fact that the literature is always not clear on some issues.
Escalating costs of the pension system is forcing the Indian Government to reevaluate the formal programmes that provide social security to employees. The government has so far received three official reports (namely, OASIS, IRDA and Bhattacharya), which have examined the issue and suggested several measures to provide a safety net to the aging population. This paper examines the recommendations made in these reports and analyses the potential effects of them. It is organized around five policy questions: 1. Should the reformed system create individual (funded defined-contribution) accounts, or should it remain a single collective fund with a defined-benefit formula? The changeover involves a larger public policy choice issue: who should ultimately bear the risk? Should employees/retirees shoulder those risks alone arising from variations in asset yields and unexpected changes in longevity, or should these risks be shared more broadly across participants, if not society? Choice would depend upon to which group the individual belongs. Financially successful people may believe in individual ownership and choice, while low wage earners may want assured returns because they do not have other resources to fall back upon. Unfortunately most Indians, unlike those in many other countries, are in the latter category which cannot bear any risk, more so in the old age. 2. If individual accounts are adopted, should the reformed system move toward private and decentralized collection of contributions, management of investments, and payment of annuities, or should these functions be administered by a public agency? In privately managed funds, associated problems would be intermediation costs, agency problem (principal-agent fiduciary relationship), and greatly increased costs to administer the plan. Several studies across the world have shown that periodic fee may look deceptively low but, over longer time horizons, the cumulative effect can be dramatic, sometimes reducing the benefits by 30 to 50 per cent. 3. Should fund managers of retirement savings be allowed to invest in a diversified portfolio that includes stocks and private bonds? In recent years equity investments, particularly index investing, have become a favoured strategy. Index funds are subject to tracking error, and being loaded with few big stocks, there are much higher risks in index investing than people perceive. Over the period, real annual return on index funds may be more, but people retire only once. Equity markets are highly volatile and go through long periods of feasts and famine. Guarantees would have to be provided in the form of minimum return or providing minimum basic pension on retirement. World bank studies show that government ends up acquiring conjectural liabilities wherever a pension system based on private providers is mandated. How would that be different from the present system where a government agency (EPFO) provides retirement benefits? 4. Should the government move toward advance funding of its pension obligations for its employees, or should these obligations continue to be financed on pay-as-you-go basis? Studies have shown that a simultaneous implementation of funded, diversified, individual accounts is not a "free lunch" once you properly account for existing unfounded obligations and risk. The Bhattacharya Committees estimates show that the government would have to pay out more on account of pensions to its employees for the next 38 years before the new scheme starts showing reduced government expenditure. These amounts do not include the tax foregone by the government on the employees contribution. Several assumptions have been made about the scheme, which the committee hopes would remain valid and that the future governments would behave responsibly. The proposed scheme does not consider intermediation costs and agency risks; in fact, the committee presumes that agents would behave more responsibly than principals. 5. What should be the level of government fiscal support in the form of tax subsidy, foregone tax collections, grants, administrative costs incurred by its agencies, and level of assumed contingent liabilities in case the government guarantees minimum pension? The crucial question is: how much and to whom is this subsidy accruing? Are beneficiaries of the proposed system the ones who need subsidy? Tax treatment of pension is a critical policy choice. A generous tax treatment may promote savings but may be costly in terms of revenue foregone. Apparently, an exercise in balancing is necessary. The priority should, therefore, be putting in place a policy vision and road map with specific goals in relation to pre-determined milestones. These should include a tax financed and means-tested system for lower income groups. If government cannot afford it, then it has no moral or political justification to even consider providing further tax benefits to privileged income groups. If there are no government funds for the first pillar in the World Bank recommended multipillar system, the third pillar should remain out of policy discussions. Emphasis should be on strengthening the second pillar. Suggested reforms neither enhance efficiency nor make the social security system more equitable. It would only privatize the gains while costs and risk for the government would increase considerably. It would only help well-off segment of society in availing more tax concessions. Present problem in the government pension system is due to successive governments behaving like Santa Clauses ignoring the cost to exchequer. Fund managers would not be able to solve these problems. Specific fiscal and other measures for implementing a feasible and viable pension system in Indian conditions have also been suggested in the paper.
Social assistance as the technique providing means-tested income guaranteed financed by general taxation in Spain is composed by different benefits. There is not a only one policy, but different measures oriented to different groups of population and organised by different public administrations. During the last two decades, the different levels of public administration have implemented a set of benefits, which observed together can considered as the Spanish âsafety netâ. The main lines of this development has been: a) fragmented in different protection systems (unemployment, pensions, social services), b) subsidiary of the development of these systems and c) decentralized in different levels of public administration (mainly in regional level, i.e. Autonomous Communities).
This paper studies optimal earnings taxation in a three period life cycle model where the taxes raised to finance an exogenous amount of public expenditure are allowed to be differentiated across ages. Agents choose their level of education when young and their age of retirement when old. We first look at the problem of optimal taxation when the young can borrow and then turn to the case where young face borrowing constraints. It is shown that, without borrowing constraints, a first best optimum can be decentralized by setting a zero tax rate in the third period and a first period tax lower than the second one.\nWith the borrowing constraint, the government may not be able restore intertemporal efficiency in which case a zero tax rate when old may not be optimal.
An optimal linear world income tax that maximizes a border-neutral social welfare function provides a drastic reduction in world consumption inequality, dropping the Gini coefficient from 0.69 to 0.25. In contrast, an optimal decentralized (i.e., within countries) redistribution has a miniscule effect on world income inequality. Thus, the traditional public finance concern about the excess burden of redistribution cannot explain why there is so little world redistribution.