Collusion in growing and shrinking markets: empirical evidence from experimental duopolies

We study collusive behaviour in experimental duopolies that compete in prices under dynamic demand conditions. In one treatment the demand grows at a constant rate. In the other treatment the demand declines at another constant rate. The rates are chosen so that the evolution of the demand in one case is just the reverse in time than the one for the other case. We use a box-design demand function so that there are no issues of finding and co-ordinating on the collusive price. Contrary to game-theoretic reasoning, our results show that collusion is significantly larger when the demand shrinks than when it grows. We conjecture that the prospect of rapidly declining profit opportunities exerts a disciplining effect on firms that facilitates collusion and discourages deviation.

Location models for ceding market share and shrinking services

New location models are presented here for exploring the reduction of facilities in aregion. The first of these models considers firms ceding market share to competitorsunder situations of financial exigency. The goal of this model is to cede the leastmarket share, i.e., retain as much of the customer base as possible while sheddingcostly outlets. The second model considers a firm essentially without competition thatmust shrink it services for economic reasons. This firm is assumed to close outlets sothat the degradation of service is limited. An example is offered within a competitiveenvironment to demonstrate the usefulness of this modeling approach.

Comparative effects of oleoyl-estrone and a specific b3-adrenergic agonist (CL316, 243) on the expression of genes involved in energy metabolism of rat white adipose tissue

Background: The combination of oleoyl-estrone (OE) and a selective b3-adrenergic agonist (B3A; CL316,243) treatment in rats results in a profound and rapid wasting of body reserves (lipid). Methods: In the present study we investigated the effect of OE (oral gavage) and/or B3A (subcutaneous constant infusion) administration for 10 days to overweight male rats, compared with controls, on three distinct white adipose tissue (WAT) sites: subcutaneous inguinal, retroperitoneal and epididymal. Tissue weight, DNA (and, from these values cellularity), cAMP content and the expression of several key energy handling metabolism and control genes were analyzed and computed in relation to the whole site mass. Results: Both OE and B3A significantly decreased WAT mass, with no loss of DNA (cell numbers). OE decreased and B3A increased cAMP. Gene expression patterns were markedly different for OE and B3A. OE tended to decrease expression of most genes studied, with no changes (versus controls) of lipolytic but decrease of lipogenic enzyme genes. The effects of B3A were widely different, with a generalized increase in the expression of most genes, including the adrenergic receptors, and, especially the uncoupling protein UCP1. Discussion: OE and B3A, elicit widely different responses in WAT gene expression, end producing similar effects, such as shrinking of WAT, loss of fat, maintenance of cell numbers. OE acted essentially on the balance of lipolysislipogenesis and the blocking of the uptake of substrates; its decrease of synthesis favouring lipolysis. B3A induced a shotgun increase in the expression of most regulatory systems in the adipocyte, an effect that in the end favoured again the loss of lipid; this barely selective increase probably produces inefficiency, which coupled with the increase in UCP1 expression may help WAT to waste energy through thermogenesis. Conclusions: There were considerable differences in the responses of the three WAT sites. OE in general lowered gene expression and stealthily induced a substrate imbalance. B3A increasing the expression of most genes enhanced energy waste through inefficiency rather than through specific pathway activation. There was not a synergistic effect between OE and B3A in WAT, but their combined action increased WAT energy waste.

Semiquantitative RT-PCR measurement of gene expression in rat tissues including a correction for varying cell size and number

Background: Current methodology of gene expression analysis limits the possibilities of comparison between cells/tissues of organs in which cell size and/or number changes as a consequence of the study (e.g. starvation). A method relating the abundance of specific mRNA copies per cell may allow direct comparison or different organs and/or changing physiological conditions. Methods: With a number of selected genes, we analysed the relationship of the number of bases and the fluorescence recorded at a present level using cDNA standards. A lineal relationship was found between the final number of bases and the length of the transcript. The constants of this equation and those of the relationship between fluorescence and number of bases in cDNA were determined and a general equation linking the length of the transcript and the initial number of copies of mRNA was deduced for a given pre-established fluorescence setting. This allowed the calculation of the concentration of the corresponding mRNAs per g of tissue. The inclusion of tissue RNA and the DNA content per cell, allowed the calculation of the mRNA copies per cell. Results: The application of this procedure to six genes: Arbp, cyclophilin, ChREBP, T4 deiodinase 2, acetyl-CoA carboxylase 1 and IRS-1, in liver and retroperitoneal adipose tissue of food-restricted rats allowed precise measures of their changes irrespective of the shrinking of the tissue, the loss of cells or changes in cell size, factors that deeply complicate the comparison between changing tissue conditions. The percentage results obtained with the present methods were essentially the same obtained with the delta-delta procedure and with individual cDNA standard curve quantitative RT-PCR estimation. Conclusion: The method presented allows the comparison (i.e. as copies of mRNA per cell) between different genes and tissues, establishing the degree of abundance of the different molecular species tested.

Massive consumption of gelatinous plankton by Mediterranean apex predators

Stable isotopes of carbon and nitrogen were used to test the hypothesis that stomach content analysis has systematically overlooked the consumption of gelatinous zooplankton by pelagic mesopredators and apex predators. The results strongly supported a major role of gelatinous plankton in the diet of bluefin tuna (Thunnus thynnus), little tunny (Euthynnus alletteratus), spearfish (Tetrapturus belone) and swordfish (Xiphias gladius). Loggerhead sea turtles (Caretta caretta) in the oceanic stage and ocean sunfish (Mola mola) also primarily relied on gelatinous zooplankton. In contrast, stable isotope ratios ruled out any relevant consumption of gelatinous plankton by bluefish (Pomatomus saltatrix), blue shark (Prionace glauca), leerfish (Lichia amia), bonito (Sarda sarda), striped dolphin (Stenella caerueloalba) and loggerhead sea turtles (Caretta caretta) in the neritic stage, all of which primarily relied on fish and squid. Fin whales (Balaenoptera physalus) were confirmed as crustacean consumers. The ratios of stable isotopes in albacore (Thunnus alalunga), amberjack (Seriola dumerili), blue butterfish (Stromaeus fiatola), bullet tuna (Auxis rochei), dolphinfish (Coryphaena hyppurus), horse mackerel (Trachurus trachurus), mackerel (Scomber scombrus) and pompano (Trachinotus ovatus) were consistent with mixed diets revealed by stomach content analysis, including nekton and crustaceans, but the consumption of gelatinous plankton could not be ruled out completely. In conclusion, the jellyvorous guild in the Mediterranean integrates two specialists (ocean sunfish and loggerhead sea turtles in the oceanic stage) and several opportunists (bluefin tuna, little tunny, spearfish, swordfish and, perhaps, blue butterfish), most of them with shrinking populations due to overfishing.