Bertrand Oligopoly And Factors Markets With Scarcity And Price Controls

In an earlier article, we reported the results of a classroom experiment simulating price competition in an oligopoly with differentiated goods. That study raised some questions that we were unable to address at that time. For this current study, we have adapted the experiment to further explore the effects of scarcity in the input markets, and to study the effects of price controls in these markets. We find that scarcity in an input market has the expected directional effect on prices in both input and output markets, but not necessarily the magnitude expected; we further find that price controls have only some of the effects expected. In the current experiment, we increased the number of rounds of the game to allow more opportunity for convergence to a stable outcome, and to allow for three distinct phases of the game: initial rounds in which inputs were abundantly available, subsequent rounds in which one input’s supply was dramatically reduced, and final rounds in which a price floor was established on the one input which remained abundant. As expected, firms played Nash/Bertrand strategies in the early rounds. However, the shock caused by reducing the availability of capital took many rounds for full adjustment, with both output prices and the equilibrium rental rate of capital rising consistently and gradually toward their projected equilibria over ten rounds, although even then capital prices did not rise enough to absorb all firm profits. Surprisingly, establishing a minimum wage did not have the anticipated effect of balancing payments between labor and capital; instead, the minimum wage completely disrupted the trend of an increasing rental price of capital and reduced it to zero, while creating volatility in profits without consistently eliminating them. Overall, we find that most of our anticipated results ultimately obtain, but adjustments to variations in market conditions are neither immediate nor perfectly consistent with the predictions of theory

Experiments In Bertrand Competition With Factor Markets

We present a classroom experiment which introduces product differentiation and factor markets into the traditional Bertrand framework.  We find that student behavior converges toward the market outcomes predicted by theory.  We also find that the experiment enhances student understanding of Bertrand price competition in a market with product differentiation and factor markets, and also appears to increase student satisfaction

Contemporary management of cancer of the oral cavity

Oral cancer represents a common entity comprising a third of all head and neck malignant tumors. The options for curative treatment of oral cavity cancer have not changed significantly in the last three decades; however, the work up, the approach to surveillance, and the options for reconstruction have evolved significantly. Because of the profound functional and cosmetic importance of the oral cavity, management of oral cavity cancers requires a thorough understanding of disease progression, approaches to management and options for reconstruction. The purpose of this review is to discuss the most current management options for oral cavity cancers

TRY plant trait database – enhanced coverage and open access

Plant traits - the morphological, anatomical, physiological, biochemical and phenological characteristics of plants - determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait‐based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits - almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Characterization and modulation of EDHF-mediated relaxations in the rat isolated superior mesenteric arterial bed

1. We have used the isolated, buffer-perfused, mesenteric arterial bed of the rat (preconstricted with methoxamine or 60 mM K(+)) to characterize nitric oxide (NO)-independent vasorelaxation which is thought to be mediated by the endothelium-derived hyperpolarizing factor (EDHF). 2. The muscarinic agonists carbachol, acetylcholine (ACh) and methacholine caused dose-related relaxations in preconstricted preparations with ED(50) values of 0.18±0.04 nmol (n=8), 0.05±0.02 nmol (n=6) and 0.26±0.16 nmol (n=5), respectively. In the same preparations N(G)-nitro-L-arginine methyl ester (L-NAME, 100 μM) significantly (P<0.05) decreased the potency of all the agents (ED(50) values in the presence of L-NAME: carbachol, 0.66±0.11 nmol; ACh, 0.28±0.10 nmol; methacholine, 1.97±1.01 nmol). The maximal relaxation to ACh was also significantly (P<0.05) reduced (from 85.3±0.9 to 73.2±3.7%) in the presence of L-NAME. The vasorelaxant effects of carbachol were not significantly altered by the cyclo-oxygenase inhibitor indomethacin (10 μM; n=4). 3. The K(+) channel blocker, tetraethylammonium (TEA, 10 mM) also significantly (P<0.001) reduced both the potency of carbachol (ED(50)=1.97±0.14 nmol in presence of TEA) and the maximum relaxation (R(max)=74.6±3.2% in presence of TEA, P<0.05, n=3). When TEA was added in the presence of L-NAME (n=4), there was a further significant (P<0.001) decrease in the potency of carbachol (ED(50)=22.4±13.5 nmol) relative to that in the presence of L-NAME alone, and R(max) was also significantly (P<0.05) reduced (74.6±4.2%). The ATP-sensitive K(+) channel inhibitor, glibenclamide (10 μM), had no effect on carbachol-induced relaxation (n=9). 4. High extracellular K(+) (60 mM) significantly (P<0.01) reduced the potency of carbachol (n=5) by 5 fold (ED(50): control, 0.16±0.04 nmol; high K(+), 0.88±0.25 nmol) and the R(max) was also significantly (P<0.01) reduced (control, 83.4±2.7%; high K(+), 40.3±9.2%). The residual vasorelaxation to carbachol in the presence of high K(+) was abolished by L-NAME (100 μM; n=5). In preparations preconstricted with high K(+), the potency of sodium nitroprusside was not significantly different from that in preparations precontracted with methoxamine, though the maximal response was reduced (62.4±3.4% high K(+), n=7; 83.1±3.1% control, n=7). 5. In the presence of the cytochrome P450 inhibitor, clotrimazole (1 μM, n=5 and 10 μM, n=4), the dose-response curve to carbachol was significantly shifted to the right 2 fold (P<0.05) and 4 fold (P<0.001) respectively, an effect which was further enhanced in the presence of L-NAME. R(max) was significantly (P<0.01) reduced by the presence of 10 μM clotrimazole alone, being 86.9±2.5% in its absence and 61.8±7.8% in its presence (n=6). 6. In the presence of the cell permeable analogue of cyclic GMP, 8-bromo cyclic GMP (6 μM), the inhibitory effects of L-NAME on carbachol-induced relaxation were substantially enhanced (ED(50): L-NAME alone, 0.52±0.11 nmol, n=5; L-NAME+8-bromo cyclic GMP, 1.42±0.28 nmol, n=7. R(max): L-NAME alone, 82.2±2.4%; L-NAME+8-bromo cyclic GMP, 59.1±1.8%. P<0.001). These results suggest that the magnitude of the NO-independent component of vasorelaxation is reduced when functional cyclic GMP levels are maintained, suggesting that basal NO (via cyclic GMP) may modulate EDHF activity and, therefore, on loss of basal NO production the EDHF component of endothelium-dependent relaxations becomes functionally greater. 7. The present investigation demonstrates that muscaranic receptor-induced vasorelaxation in the rat mesenteric arterial bed is mediated by both NO-dependent and independent mechanisms. The L-NAME-insensitive mechanism, most probably occurs via activation of a K(+) conductance and shows the characteristics of EDHF-mediated responses. Finally, the results demonstrate that EDHF activity may become upregulated on inhibition of NO production and this may compensate for the loss of NO