Did Pareto discover income and substitution effects? On an interpretation suggested by Hutchison

Terence Hutchison (1953) has argued that in his Manual of Political Economy Vilfredo Pareto provided a verbal, non-mathematical description of income and substitution effects. Hutchison's claim on Pareto''s behalf is important since it would move the date of the discovery of the concept (if not the mathematical proof) of separate income and substitution effects back from 1915 to the 1906 publication of the original Italian language version of the Manual, and would reassign priority for the discovery from Slutsky to Pareto. This note reexamines this claim of Hutchison''s, and shows that in fact it is mistaken. Pareto did not actually discuss income and substitution effects as they are now understood. Rather, in the passage which Hutchison cites, Pareto was discussing the impact of a change in income, not prices, on quantities demand.

Linearity, Slutsky symmetry, and a conjecture of Hicks

Hicks (1956) conjectured that Slutsky symmetry should hold for discrete as well as infinitesimal price changes if demand functions are globally linear. This paper proves this conjecture using the LES utility function and the Slutsky compensation for price changes. More importantly, in sharp contrast to previous doubts expressed by Hicks, Samuelson and others, this paper provides the first formal demonstration that compensated cross price effects can indeed be symmetric for discrete changes in prices.

Quasi-linear peferences with Auspitz-Lieben-Pareto complementarity

I show that if preferences are quasi-linear (non-linear in goods x1, …, xn but linear in xn+1) and the sub-utility function defined over [x1, …, xn] is strongly concave and exhibits Auspitz-Lieben-Pareto complementarity, then goods x1-xn must be gross and compensated complements for each other and xn+1 must be a compensated substitute for all other goods. Also, an increase in its price of xn+1 must reduce the demand for goods x1-xn. The effects of uncompensated changes in the prices of goods x1-xn on the demand for good xn+1 vary predictably with income.Auspitz-Lieben-Pareto complementarity

Evolutionary Dynamics and Optimization: Neutral Networks as Model-Landscapes for RNA Secondary-Structure Folding-Landscapes

We view the folding of RNA-sequences as a map that assigns a pattern of base pairings to each sequence, known as secondary structure. These preimages can be constructed as random graphs (i.e. the neutral networks associated to the structure $s$). By interpreting the secondary structure as biological information we can formulate the so called Error Threshold of Shapes as an extension of Eigen's et al. concept of an error threshold in the single peak landscape. Analogue to the approach of Derrida & Peliti for a of the population on the neutral network. On the one hand this model of a single shape landscape allows the derivation of analytical results, on the other hand the concept gives rise to study various scenarios by means of simulations, e.g. the interaction of two different networks. It turns out that the intersection of two sets of compatible sequences (with respect to the pair of secondary structures) plays a key role in the search for ''fitter'' secondary structures.Comment: 20 pages, uuencoded compressed postscript-file, Proc. of ECAL '95 conference, to appear., email: chris @ imb-jena.d

Insulin-Like Growth Factor II (IGF-II) Is More Potent Than IGF-I in Stimulating Cortisol Secretion from Cultured Bovine Adrenocortical Cells: Interaction with the IGF-I Receptor and IGF-Binding Proteins

Although the stimulating effect of insulin-like growth factor I (IGF-I) on adrenal steroidogenesis has been well established, the role of IGF-II in the adult adrenal gland remains unknown. We, therefore, investigated the effect of recombinant human IGF-II on cortisol and cAMP synthesis from adult bovine adrenocortical cells. IGF-II, time and dose dependently, stimulated basal cortisol secretion maximally 3-fold. In combination with ACTH, IGF-II (13 nM) synergistically increased cortisol secretion from 1-fold (10(-8) M ACTH) to 28-fold of untreated control levels. In contrast, IGF-I at equimolar concentrations did not show an effect on basal cortisol secretion, and in combination with ACTH elicited a significant weaker stimulatory effect than IGF-II (22-fold increase). The synergistic effect of IGF-II on ACTH-promoted cortisol secretion was paralleled by accumulation of cAMP in the culture medium. Although both IGF receptors are present in adult bovine adrenocortical cells, the effect of IGF-II seems to be mediated through interaction with the IGF-I receptor, as [Arg54,55]IGF-II, which only binds to the IGF-I receptor, was equipotent to native IGF-II, whereas [Leu27]IGF-II, which preferentially binds to the type II IGF receptor, did not show any effect. By Western ligand blotting, four different molecular forms of IGF-binding proteins (IGFBPs) were identified in conditioned medium of bovine adrenocortical cells with apparent molecular masses of 39-44, 34, 29, and 24 kilodaltons. ACTH treatment increased the abundance of all binding proteins, on the average, 2.3-fold, except for the 29-kDa band, which was predominantly induced 6.8-fold. Additionally, [des1-3]IGF-I, a truncated IGF variant that exhibits only minimal binding to IGFBPs, was significant more potent than IGF-I and elicited the same maximum stimulatory effect on cortisol secretion as IGF-II and [des1-6]IGF-II. In conclusion, these results demonstrate that 1) IGF-II stimulates basal as well as ACTH-induced cortisol secretion from bovine adrenocortical cells more potently than IGF-I; 2) this effect is mediated through interaction of IGF-II with the IGF-I receptor; 3) bovine adrenocortical cells synthesize various IGFBPs that are induced differentially by ACTH; and 4) IGFBPs apparently play a modulatory role in IGF-induced stimulation of adrenal steroidogenesis. Therefore, bovine adult adrenocortical cells provide a useful tissue culture model in which the interactions among locally produced IGFs, IGFBPs, and the IGF-I receptor can be evaluated

Weimar – a Personal Tribute

Weimar is a relatively small town in the centre of Germany. Around 1552 it became the capital of the small Herzogtum Sachsen-Weimar (Principality Saxony-Weimar), from 1741 until 1918 the capital of the (still relatively small) Principality – since 1815 Grand Principality – (Groß-) Herzogtum Sachsen-Weimar-Eisenach (Saxony-Weimar-Eisenach). After World War I all monarchic structures in Germany were abandoned, the democratic Free State of Thuringia was founded in 1920, and Weimar became its capital until 1950. Despite its moderate size, Weimar managed to gain a cultural profile that extended and still extends far beyond the borders of the (Grand-) Principality, even beyond Germany. The foundations were laid in the 18th and early 19th century, connected to writers and pilosophers like Christoph Martin Wieland, Johann Wolfgang von Goethe, Johann Gottfried von Herder, and Friedrich von Schiller who all lived and worked in Weimar. In the late 19th and early 20th century more writers, musicians and artists contributed to Weimar’s reputation, e.g. Franz Liszt, Richard Strauss, Hugo von Hofmannsthal, Harry Graf Kessler, Henry van de Velde, Edvard Munch, Walter Gropius, Paul Klee, Oskar Schlemmer, Wassily Kandinsky, Lyonel Feininger. In politics, Weimar played ambiguous roles between a comparatively liberal (Grand) Principality, the birth place of the first democratic state in Germany (Weimar Republic), turning “brown” (National-Socialist) from the late 1920s, Communist after World War II, democratic again after the German re-unification in 1990. Weimar is a very special, even intriguing place. This book tries to convey its aura by telling its story from the early beginnings in the 16th century until today, with a main focus on the last three centuries – embedded into pan-German, even pan-European developments

Low-degree Cohomology of Integral Specht Modules

We introduce a way of describing cohomology of the symmetric groups with coefficients in Specht modules over Z or F_p. We study i-th-degree cohomology for i in {0,1,2}. The focus lies on the isomorphism type of second-degree cohomology of integral Specht modules. Unfortunately, only in few cases can we determine this exactly. In many cases we obtain only some information about the prime divisors of the cohomology group's order. The most important tools we use are the Zassenhaus algorithm, the Branching Rules, Bockstein type homomorphisms, and the results from [Burichenko et al., 1996].Comment: 25 page

ACE-inhibition prevents postischemic coronary leukocyte adhesion and leukocyte-dependent reperfusion injury

Objective: Polymorphonuclear leukocytes (PMN), retained in the microvascular bed, can contribute to postischemic myocardial reperfusion injury. Since a beneficial effect of ACE-inhibition on reperfusion injury has been reported, we investigated the impact of cilazaprilat on PMN dependent reperfusion injury in isolated guinea pig hearts. Methods: Hearts (n=5 per group) were subjected to 15 min of ischemia. Immediately thereafter, a bolus of PMN was injected into the coronary system. External heart work (EHW) and total cardiac nitric oxide release were measured. For microscopic evaluation, hearts received rhodamine 6G labelled PMN after ischemia, were arrested 5 min later and further perfused with FITC dextran (0.1%). Localization of retained PMN was assessed by fluorescence microscopy. Leukocyte activation was studied by FACS analysis of the adhesion molecule CD11b before and after coronary passage of the PMN. The ACE-inhibitor cilazaprilat (Cila, 2 μM) and the NO-synthase inhibitor nitro-L-arginine (NOLAG, 10 μM) were used to modulate nitric oxide formation of the heart. Results: Postischemic EHW recovered to 67±5% (controls) and 64±6% (Cila) of the preischemic value. Addition of PMN severely depressed recovery of EHW (39±2%) and NO release (39±6% of the preischemic value). Simultaneously, ischemia led to a substantial increase in postcapillary PMN adhesion (from 21±5 to 172±27 PMN/mm² surface) and CD11b-expression of the recovered PMN (3-fold). Cila attenuated postischemic PMN adhesion (83±52 PMN/mm²) and activation of PMN, whereas it improved recovery of work performance (64±4%) and NO release (65±4%) in the presence of PMN. Conversely, NOLAG increased PMN adhesion (284±40 PMN/mm²) and myocardial injury. We conclude that ACE-inhibition prevents leukocyte dependent reperfusion injury mainly by inhibition of postcapillary leukocyte adhesion. The effect may be mediated by NO, given the proadhesive effect of NOLAG