483 research outputs found
The Harrod-Balassa-Samuelson Effect: A Survey of Empirical Evidence
No full textThe paper surveys empirical evidence on the Harrod-Balassa-Samuelson effect. The survey encompasses the published empirical work on the phenomenon since its (re)discovery in 1964. In total, 58 empirical papers are examined within a specialized analytical framework. The body of empirical evidence is synthesized through four major elements. The analysis starts with the ongoing controversy related to the name of the theory. This is followed by a presentation of the evolution of the theoretical and econometric model. It ends with an analysis of the results of the surveyed empirical studies. Results of the survey indicate that growing body of evidence definitely points towards professional rethinking about the significance of the Harrod-Balassa-Samuelson effect.Harrod Balassa Samuelson effect, real exchange rate, purchasing power parity, productivity
The Political Economy of Textbook Writing: Paul Samuelson and the making of the first ten Editions of Economics (1945-1976)
No full textOver the past two decades, numerous contributions to the history of economics have tried to assess Paul Samuelson’s political positioning by tracing it in the subsequent editions of his famous textbook Economics. This literature, however, has provided no consensus about the location of Samuelson’s political ideas. While some authors believe that Samuelson has always had inclinations toward interventionism, others conclude that he more often acted as a pro-business advocate. The purpose of this paper is not to argue for one of these two interpretations but to depict the making of Economics itself as a political process. By ‘political’ it is not meant the conduct of party politics but the many political elements that a textbook author has to take into account if he wants to be published and favorably received. I argue that the “middle of the road” stance that Samuelson adopted in the book was consciously constructed by the MIT economist, with the help of his home institution and his publishing company, McGraw-Hill, to ensure both academic freedom and the success of the book. The reason for which the stance developed is related to pre-McCarthyist right-wing criticisms of the textbook and how Samuelson and the MIT department had to endure the pressures from members of the Corporation (MIT’s Board of Trustees), who tried to prevent the publication of the textbook and threatened Samuelson’s tenure at MIT as soon as 1947 – when early manuscripts were circulated. As a result, it was decided in accordance with both the Corporation and McGraw-Hill that the Readings volume would be published to balance conflicting ideas about state intervention. Following these early criticisms, the making of the subsequent editions relied on a network of instructors and referees all over the US in order to make it as successful and consensual as possible. This seemed to work quite well in the 1950s and for a good portion of the 1960s, until Economics became victim of its own success and was seen, in an ironical twist of fate, as a right wing text by younger, radical economists. From now on, Samuelson will try to have his book sent as often as possible to the radicals for referring process, with mixed results. Eventually, the book became criticized from both its left and its right.Paul Samuelson, Economics, Textbook, Politics, Economic Education
The Balassa-Samuelson Effect in 'East & West'. Differences and Similarities
No full textBased on two detailed Balassa-Samuelson (BS) studies, Wagner and Hlouskova (2004) for eight Central Eastern European countries (CEECs) and Wagner and Doytchinov (2004) for ten Western European countries (WECs), this study assesses the differences and similarities of the BS effect between these two country groups. The econometric results show that the BS effect may have been overestimated in previous studies due to application of inappropriate first generation panel cointegration methods. When appropriately quantified, the BS effect itself explains RER movements respectively inflation differentials only to a small extent. However, extended BS relationships that include additional variables allow for an adequate modelling of inflation. Based on the comparative analysis we draw some conclusions for monetary policy in the future enlarged Euro Area.Balassa-Samuelson effect, Central and Eastern Europe, Western Europe, Non-stationary panels, Inflation simulations
El legado de Samuelson. La preferencia revelada
No full textThe prolific work of the recently deceased Paul A. Samuelson makes a significant contribution to several areas of economic theory. He was awarded the 1970 Nobel Prize in Economics for doing more than any other contemporary economist to raise the level of scientific analysis in economic theory. He is also well-known as the author of several influential textbooks which are among all-time best-sellers. Although it is not easy to highlight only one of his contributions, over seventy years ago his revealed preference analysis opened a fertile field of research that went beyond the scope of consumer theory, thus creating a bridge that leads to reconciling economic theory with other social sciences.La fecunda obra del recientemente fallecido Paul A. Samuelson contiene aportaciones significativas en muy diversas áreas de la teoría económica. Premio Nobel de Economía en 1970 por contribuir activamente a elevar el nivel de análisis de la ciencia económica, es también conocida su labor divulgativa como autor de varios manuales que figuran entre los libros de texto universitarios más vendidos de la historia. Aunque no es fácil destacar una de sus contribuciones por encima de las demás, su teoría de la preferencia revelada abrió hace más de setenta años un fértil campo de investigación que ha sobrepasado el ámbito de la teoría del consumidor, estableciendo un puente que conduce a la reconciliación de la teoría económica con otras ciencias sociales
Real Convergence, Price Level Convergence and Inflation Differentials in Europe
No full textThis paper provides a comprehensive review of the factors that can cause price levels to diverge and which are at the root of different inflation rates in Europe including the EU-27. Among others, we study the structural and cyclical factors influencing market and non-marketbased service, house and goods prices, and we summarise some stylised facts emerging from descriptive statistics. Subsequently, we set out the possible mismatches between price level convergence and inflation rates. Having described in detail the underlying economic factors, we proceed to demonstrate the relative importance of these factors on observed inflation rates first in an accounting framework and then by relying on panel estimations. Our estimation results provide the obituary notice for the Balassa-Samuelson effect. Nevertheless, we show that other factors related to economic convergence may push up inflation rates in transition economies. Cyclical effects and regulated prices are found to be important drivers of inflation rates in an enlarged Europe. House prices matter to some extent in the euro area, whereas the exchange rate plays a prominent (but declining) role in transition economies.price level, inflation, Balassa-Samuelson, tradables, house prices, regulated prices, Europe, transition
Developmental expression and gene regulation of mouse cholecystokinin.
No full textThe gastrointestinal tract is a major site for production and release of peptide hormones. Several of these peptides are also found in the brain. My research focused on cholecystokinin (CCK), a regulatory peptide that is expressed in endocrine cells in the intestine and in neurons in the brain. I examined the pattern of CCK gene expression during prenatal mouse development by analysis of a mouse strain in which expression of the normal CCK gene was replaced by the bacterial lacZ reporter gene. Early expression (E8.5--14.5) was limited to neuronal lineages; endocrine expression began later (E15.5). Expression in the neural tube and neural crest was observed on embryonic days 8.5--9.5 (E8.5--9.5). In the fetal intestine, beta-galactosidase activity was detected transiently in a subpopulation of developing enteric neurons (from E10.5 through E15.5) and later in developing enteroendocrine cells (from E15.5 through birth). This expression is earlier and more extensive than previously reported, suggesting that CCK expression may be an early marker of subpopulations of gastrointestinal endocrine cells and neurons. To further understand the importance of CCK as a signaling molecule in development, I cloned and sequenced the gene for the CCK-B/gastrin receptor, and showed that both the CCK-A and CCK-B/gastrin receptors are expressed in embryos as early as E10.5. This suggests that CCK signaling may be established early in mouse development. To identify DNA sequences regulating expression of the CCK gene, I generated transgenic mice using a 6 kb CCK genomic fragment linked to the lacZ gene. Analysis of beta-galactosidase activity showed that the transgene exhibited correct tissue-specific expression, with activity present in intestine and brain, but not in liver and stomach. In the small intestine, only one of the three lines tested showed expression in CCK-expressing endocrine cells. These results suggest that although the minimal cis-regulatory elements necessary for appropriate CCK expression in endocrine cells are localized within 5 kb of the transcriptional start site, other important elements must be located outside this region.PhDBiological SciencesCellular biologyGeneticsMolecular biologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/132404/2/9963832.pd
Mouse models of cholecystokinin deficiency: Effects on the exocrine pancreas.
No full textUtilizing genetically deficient mice, I tested the hypothesis that cholecystokinin (CCK) is required for pancreatic growth and function. I examined the Cpe\sp{fat} mouse strain as a potential CCK-deficient model. This mutant contains a point mutation in the carboxypeptidase E (CPE) gene, abolishing enzyme activity. Because many regulatory peptides require caboxypeptidase activity for biosynthesis, I proposed that the Cpe\sp{fat} mouse would be CCK-deficient. Analysis of CCK processing revealed a 10-fold decrease in neural CCK, while intestinal endocrine cells maintained normal CCK concentrations by increasing peptide synthesis. Gastrin biosynthesis in stomach endocrine cells closely resembles intestinal endocrine cell CCK processing, suggesting the presence of an endocrine-specific biosynthetic regulatory mechanism, not present in neuronal CCK synthesis. Although, normal CCK and gastrin processing requires CPE, the Cpe\sp{fat} mouse is not completely CCK deficient. In contrast, the Cck\sp{LacZ} mouse, generated by gene targeting in embryonic stem cells, is a complete CCK null mutant. This mouse provides a better model to address the physiological requirement for CCK. Analysis of the Cck\sp{LacZ} mouse revealed that CCK is not required for pancreatic development, or protein induced pancreatic hypertrophy and enzyme content. I cloned and sequenced the gene for the pancreatic CCK receptor (CCKAR) and showed that Cck\sp{LacZ} mice express functional CCKAR at normal levels. Pancreatic acinar cells from CCK-deficient mice respond to physiological CCK doses, indicating that CCKAR expression is not dependant upon the presence of ligand. The studies presented in this dissertation have led to the novel finding that CCK is not required for pancreatic growth, or adaption to dietary changes, suggesting that redundant mechanisms compensate for lack of CCK. Initial analysis of compensatory mechanisms revealed that although gastrin is closely related to CCK, it does not appear to compensate for CCK. Somatostatin, a general inhibitor of pancreatic secretion and growth, is decreased in the intestine of Cck\sp{LacZ} mice. Thus, decreasing inhibitory signals to the pancreas may be one compensatory change to maintain a functional pancreas. The Cck\sp{LacZ} mouse model will be useful in future studies to examine other physiological regulators of the exocrine pancreas and previously overlooked regulatory pathways.PhDAnimal PhysiologyBiological SciencesCellular biologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/131461/2/9909922.pd
Transcriptional regulators promoting enteroendocrine cell differentiation from multipotential progenitors.
No full textThe intestine is one of the largest endocrine organs. Little is known about the mechanisms regulating intestinal endocrine cell differentiation. Loss-of-function mouse models have been used to conclude that the basic helix loop-helix transcription factors Neurogenin 3 (Neurog3) and neurogenic differentiation factor 1 (Neurod1) are required for the differentiation of intestinal endocrine cells. In this study, we investigated whether these two transcription factors are sufficient to promote endocrine cell differentiation in the intestine. We used a transgenic mouse approach to direct intestine-specific expression of Neurog3 or Neurod1 using the villin gene promoter to drive transgene overexpression. Vil-Neurog3 and Vil-Neurod1 transgenic founder intestines were analyzed at late embryonic development (E18.5 and E17.5, respectively) and transgenic lines were generated for analysis of the adult intestine. We showed that Neurog3 is sufficient to promote endocrine cell differentiation in the developing intestine. The total number of secretory cells was unchanged in Vil-Neurog3 transgenic embryos; as a result the increase in endocrine cells was countered by a decrease in goblet cell numbers. This finding suggested the existence of a bipotential secretory progenitor that could give rise to endocrine or goblet cells, with Neurog3 expression promoting endocrine cell fate. In contrast to the activity in embryos, transgenic expression of Neurog3 in adults was not associated with increased endocrine cell numbers demonstrating that expression in fully differentiated cells could not promote transdifferentiation to the endocrine lineage. Analysis of Vil-Neurod1 transgenic founder embryos or adult lines showed that there was no increase in endocrine cell numbers or endocrine marker expression. However, gene expression of its downstream target, secretin, was upregulated in the adult. These results lead us to conclude that Neurod1 alone is not sufficient to change the fate of progenitor cells to promote endocrine cell development, but it is sufficient to activate secretin gene expression. Consequently, regulation of endocrine gene expression might not be sufficient to change the fate of an epithelial cell into the endocrine cell lineage. This study contributes to our understanding of the molecular factors that regulate endocrine cell differentiation and enhances our knowledge about lineage relationships in the intestinal epithelium.PhDAnimal PhysiologyBiological SciencesCellular biologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/127021/2/3305029.pd
Investigation of the roles of gastrin and histamine in gastric acid secretion using genetically engineered mouse models.
No full textThe primary objective of this research was to investigate the roles of gastrin and histamine in the regulation of acid secretion using genetically engineered mouse models. Previously, gastrin-deficient mice were shown to have an in vivo impairment in acid secretion. The first aim of this project was to test whether the reduction in acid secretion in gastrin-deficient mice was due to an intrinsic defect in parietal cells. Using purified parietal cells and isolated glands, calcium responses and in vitro acid accumulation were analyzed. Surprisingly, calcium levels and acid accumulation were enhanced in comparison to controls, suggesting that gastrin is not required for parietal cells to secrete acid but that it is essential for normal in vivo acid levels. An increase in parietal cell number and a decrease in parietal cell size were also detected, emphasizing the role for gastrin in regulating mucosal cell growth. The second aim was to test whether the alterations in gastrin-deficient mice were age-dependent, since changes in the acid secretory system had been reported with age. While an increase in parietal cell number and mucosal proliferation were detected in young gastrin-deficient mice, these changes were not observed in older mice. Interestingly, acid levels significantly increased with age in both controls and gastrin-deficient mice. The age-dependent alterations in the mutant mice suggested that an early compensatory effect existed that served to counteract low acid levels by increasing parietal cell number. The third aim was to engineer a novel transgenic mouse with elevated parietal cell cAMP levels to investigate the consequences of constitutive stimulation of this signaling pathway in the acid secretory system. Preliminary analysis indicated no alterations in basal acid content; however, plasma gastrin levels were significantly reduced, suggesting that elevated parietal cell CAMP may upregulate acid secretion. In addition, gastric morphology was altered in aged transgenic mice, indicating that long-term elevation of cAMP may result in the loss of parietal cells. In summary, the genetically engineered mouse models utilized in this thesis have allowed the opportunity to investigate the independent affects of gastrin and histamine signaling on the normal regulation of the gastric acid secretory system.PhDAnimal PhysiologyBiological SciencesMolecular biologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/132000/2/3057961.pd
New Results in an Old Framework: Comment on Samuelson and Modigliani
No full textThe Author in this article replies to a paper written by Professor Samuelson and Professor Modigliani on the implications of the results which emerged from his 1962 article ("Rate of Profit and Income Distribution in relation to the Rate of Economic Growth", in The Review of Economic Studies, 1961-62, vol.29, pp.267-279.). Their paper has one unfortunate drawback: it was written with the aim of defending a specific theory. As such, the authors were compelled to fit the new results within the rigid constraints of a preconceived framework. The restrictive consequences of such an approach underlie all their attempts to generalize. One of Professors Samuelson and Modigliani's main preoccupations is with defending the theory of the marginal productivity of capital. As is well known, this theory relies on a series of assumptions, which have been the subject of wide disagreement among economists.
Now, however, a new result has been reached. Whether one makes or does not make such assumptions, whether one believes in the existence of something called the "marginal productivity of capital", or not, the long run equilibrium rate of profit -with only one proviso- turns out to be determined according to the simple relation which is entirely independent of those assumptions. This result has come as such a surprise to Professors Samuelson and Modigliani that they have called it a "paradox” and stated that nonetheless, the marginal productivity theory is not " incompatible" in explaining the long run rate of profit by making the necessary assumptions that it requires. Thus, the rate of profit in the long run determines what the marginal productivity of capital is going to be. The Author finds these arguments unconvincing since marginal productivity is a concept, which was invented in order to explain the rate of profit
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