Ethics and the economics of Adam Smith and J.S. Mill: On the moral significance of classical economics.

This work examines some of the effects that developments in economic theory might have had on concepts of economic justice that are associated with it. Classical economics, as represented by Adam Smith and J.S. Mill is a good example of models of general equilibrium where moral responsibility cannot be evaded. Indeed, in the ethical analysis of these models- conducted by the same people who suggested them- the role of desert was prominent. Contrary to the general belief that classical economists advocated natural liberty for its moral goodness as much as for its economic efficiency, analysis by desert reveals a serious moral inadequacy of natural liberty. This, in turn, may explain the discrepancy between the received view and the fact that the works of classical economists are sometimes full with moral apprehensions about natural liberty. To reach such conclusions there is a need to re-interpret the works of Smith and Mill at both levels of economics and ethics. The bulk of this work is devoted to that purpose. A new interpretation of Smith's ethics is being offered. It is based on the consistency of human character and on the existence of some 'rationalistic' considerations in his work. Such an interpretation offers an alternative (and more comprehensive) solution to what became to be known as the Adam Smith's problem (old and new). Also, the application of his moral theory to the analysis of actions implies that a correlation must exist between intention and consequences. Thus the moral significance of the proposed spill-over of beneficence derived from the 'invisible hand' mechanism, is questioned. A new interpretation of Smith's economic follows where 'pre-market demand' relates the capitalists' decisions on saving to equilibrium prices. A distinction that has a moral significance is then being drawn between 'market-price' and 'natural price'. The study of Mill's methodology serves as a foundation to interpret some apparent contradictions in his moral theory (the relationship between Utilitarianism and Liberty). Ethology, which is the theory of character formation plays a major role in it. Coupled with Mill's theories of Free-will and Individuality, it is possible to establish a solution to the problems of Utilitarianism and Liberty without expanding the concept of utility. Similar principles are then introduced to Mill's discussion of economic justice. The principle of individuality is being presented in the form of Mill's principle of 'proportional remuneration'. A discussion of his theories of property follows and then, the question of the meaning of 'proportional remuneration' is being put forward. Before, however, an exposition of Mill's economic model in the framework of 'cost of production' general equilibrium is being offered. Then, the principle of proportional remuneration is being investigated. It is also related to a much wider question of the role and meaning of the labour theory of value in classical economics. (Abstract shortened by UMI.)

Increased glycation and oxidative damage to apolipoprotein B100 of LDL cholesterol in patients with type 2 diabetes and effect of metformin

OBJECTIVE The aim of this study was to investigate whether apolipoprotein B100 of LDL suffers increased damage by glycation, oxidation, and nitration in patients with type 2 diabetes, including patients receiving metformin therapy. RESEARCH DESIGN AND METHODS For this study, 32 type 2 diabetic patients and 21 healthy control subjects were recruited; 13 diabetic patients were receiving metformin therapy (median dose: 1.50 g/day). LDL was isolated from venous plasma by ultracentrifugation, delipidated, digested, and analyzed for protein glycation, oxidation, and nitration adducts by stable isotopic dilution analysis tandem mass spectrometry. RESULTS Advanced glycation end product (AGE) content of apolipoprotein B100 of LDL from type 2 diabetic patients was higher than from healthy subjects: arginine-derived AGE, 15.8 vs. 5.3 mol% (P < 0.001); and lysine-derived AGE, 2.5 vs. 1.5 mol% (P < 0.05). Oxidative damage, mainly methionine sulfoxide residues, was also increased: 2.5 vs. 1.1 molar equivalents (P < 0.001). 3-Nitrotyrosine content was decreased: 0.04 vs. 0.12 mol% (P < 0.05). In diabetic patients receiving metformin therapy, arginine-derived AGE and methionine sulfoxide were lower than in patients not receiving metformin: 19.3 vs. 8.9 mol% (P < 0.01) and 2.9 vs. 1.9 mol% (P < 0.05), respectively; 3-nitrotyrosine content was higher: 0.10 vs. 0.03 mol% (P < 0.05). Fructosyl-lysine residue content correlated positively with fasting plasma glucose. Arginine-derived AGE residue contents were intercorrelated and also correlated positively with methionine sulfoxide. CONCLUSIONS Patients with type 2 diabetes had increased arginine-derived AGEs and oxidative damage in apolipoprotein B100 of LDL. This was lower in patients receiving metformin therapy, which may contribute to decreased oxidative damage, atherogenicity, and cardiovascular disease

Monoclonal antibody detects Ag polymorphism of apolipoprotein B

AbstractA monoclonal antibody (MB-19) was used to investigate the polymorphism of apolipoprotein B in a large family and in unrelated subjects. Apolipoprotein B was shown to exhibit high-, intermediate- or low-affinitybinding to this antibody. Thus, MB-19 bound strongly to the Ag(c) epitope, an Ag antigenic domain previously characterized by human antisera, while it bound only weakly to the allelic epitope Ag(g). It proved therefore useful for the detection of the two corresponding allelic apoB species designated apoBc (high-affinity binding) and apoBg (low-affinity binding), and for confirming their co-dominant transmission. Intermediate binding resulted from the presence of a mixture of both apoB populations in heterozygous subjects

Mycophenolate Mofetil Decreases Atherosclerotic Lesion Size by Depression of Aortic T-Lymphocyte and Interleukin-17–Mediated Macrophage Accumulation

ObjectivesThis study tested whether immunosuppression with mycophenolate mofetil (MMF) inhibits atherosclerosis development in apolipoprotein-E–deficient (Apoe−/−) mice and investigated the mechanism.BackgroundChronic vascular inflammation involving both innate and adaptive immunity is central in the development of atherosclerosis, but immunosuppressive treatment is not uniformly beneficial. The immunosuppressive MMF targets lymphocyte proliferation by inhibiting inosine-monophosphate dehydrogenase.MethodsYoung and aged Apoe−/− mice were treated with 30 mg/kg daily MMF during 12 and 3 weeks of a high-fat diet, respectively. Aortic lesion size and composition was investigated by histology and flow cytometry; soluble inflammatory mediators were investigated by enzyme-linked immunosorbent assay.ResultsMacroscopic and histologic aortic atherosclerotic lesions were significantly decreased in both MMF-treated groups. While systemic immunoglobulin G directed against low-density lipoproteins was not significantly altered, the T-cell cytokine interleukin (IL)-17 was significantly reduced in plasma of MMF-treated mice and supernatants from their aortas after T-cell stimulation. The MMF treatment decreased aortic αβ T-cell receptor+ lymphocyte proliferation and cell numbers. Also, aortic contents of CD11b+CD11c+ cells and their proliferation were reduced in MMF-treated Apoe−/− mice. The IL-17 supplementation restored the number of proliferating aortic CD11b+CD11c+ cells in MMF-treated mice. The IL-17 receptor A was highly expressed on circulating monocytes that are macrophage progenitors. Genetic deletion of IL-17 receptor A or IL-17A reduced inflammatory peritoneal CD11b+CD11c+ macrophage accumulation.ConclusionsThe lymphocyte-directed immunosuppressant MMF that curbs IL-17 production was a successful antiatherosclerotic treatment. Our data delineate a role for IL-17 in CD11b+CD11c+ cell accumulation