The location model with two periods of price competition

Game Theory;Location Theory;Nash Equilibrium;Price Competition

Spatial competition with intermediated matching

This paper analyzes the spatial competition in commission fees between two match makers. These match makers serve as middlemen between buyers and sellers who are located uniformly on a circle. The profits of the match makers are determined by their respective market sizes. A limited willingness to pay is incorporated by means of reservation prices. If the fraction of buyers and sellers is unequal, the match makers are willing to subsidize the short side of the market, while the long side is exploited completely, provided reservation prices are sufficiently high. Competition is then concentrated entirely on the short side. When reservation prices are low, two local monopolies will emerge.Matching;Price Competition;Intermediation;Microeconometrics;microeconomics

Spatial competition with intermediated matching

Matching;Price Competition;Intermediation;Microeconometrics

The Location Model with Reservation Prices

In this paper, we analyze a variant of the standard Hotelling model of spatial competition where firms first choose locations along the line and then, given these locations, compete in prices.Consumers have a finite reservation price and incur a quadratic transportation cost.We show that there exists a unique subgame perfect Nash equilibrium with identical prices for the location-then-price game if the reservation price is sufficiently high.In that case the degree of differentiation is nondecreasing in the reservation price, for differentiation relaxes price competition.If the reservation price is lower, there is a continuum of subgame perfect Nash equilibria due to the fact that firms may act as local monopolists and the other firm's location choice becomes of less importance.All equilibria yield the same profit, however

On the Existence of Unique Equilibria in Location Models

In this paper, we study a two-stage location-then-price game where consumers are distributed piecewise uniformly, each piece being referred to as an interval.Although the firms face a coordination problem, it is obvious that, for any given locations and prices, there is a unique indifferent consumer.So only the exact interval in which the indifferent consumer is located may be uncertain for the firms.Therefore, we encompass the firms with beliefs about the interval in which the indifferent consumer is located.Given their beliefs, the firms' expected profit functions are quasi-concave.We consider the situation where firms first choose beliefs and then maximize the corresponding expected profit in two stages as a psychological game.We show that there exists a unique psychological equilibrium for this game, which consists of a subgame perfect Nash equilibrium for the two-stage game given certain beliefs, and of beliefs such that the equilibrium outcome is consistent with these beliefs.This equilibrium outcome is found easily by applying a coordination argument.

Neuroinflammation, microglia and the cell biology of Alzheimer's Disease

The pathology of Alzheimer’s disease (AD) is characterised by progressive accumulation of misfolded proteins, which form senile plaques and neurofibrillary tangles, and chronic inflammation in the brain associated with inflammatory mediators by the activation of innate immune responses. There has been considerable interest in the role of neuroinflammation in directly contributing to the progression of AD. Studies in mice and humans have identified a role for microglial cells, the resident innate immune cells of the CNS, in AD. Activated microglia are a key hallmark of the disease and the secretion of pro-inflammatory cytokines by microglia may result in a positive feedback loop between neurons and microglia, resulting in ongoing low-grade inflammation and associated neurotoxicity. The underlying mechanisms however are poorly understood. Here the role of microglia was investigated, especially their link to ApoE – the strongest risk factor for late onset Alzheimer’s disease – and the relationship between microglia, neurons and neuroinflammation. Target replacement mice were used, where the human ApoE2, ApoE3 or ApoE4 allele replaces the mouse ApoE allele. Microglia were activated in a two- step setup. Initially cells were primed with LPS, followed by a secondary stimulus, such as ATP or Aβ. The system was used to characterise the cytokines secreted by activated microglia and to assess the impact of conditioned medium from stimulated and Aβ treated microglia on neuronal morphology. The first results Chapter (Chapter 3) established the system – mouse microglia were isolated from brains of neonatal mice and characterised by CD11b staining. Microglia from all three ApoE genotypes were directly compared and the data from ELISA and mass spectrometry revealed an enhanced pro- inflammatory response by ApoE4 microglia and the least efficient at internalizing amyloid β. Chapter 4 analysed the impact of conditional medium from the microglia ApoE variants on neurons and the results showed an ApoE-dependent effect on dendrite morphology. Conditioned media from immunostimulated and Aβ microglia were incubated with cortical neurons from wt animals. Both the dendrite length and number of dendrites were significantly reduced in neurons treated with conditioned medium from ApoE4 microglia. TNFα was identified as a major cytokine and was responsible for modifying neuron morphology in cell assays. Neutralising the cytokine, with an anti-TNFα antibody abrogated the majority of morphological changes induced by the conditioned media from activated microglia. Hence the data suggests that TNFα may have a major role in mediating neuroinflammation. The third results Chapter (Chapter 5) compared aspects of macrophage function with microglia. Here it was shown, that microglia do not require SNX5 for macropinocytosis, and most likely utilise peripheral mediated macropinocytosis as the main form of macropinocytic internalisation. A major finding was the ability of sodium chloride to augment a pro-inflammatory response not only by immunostimulated macrophages by also microglia. Inhibition of the p38 MAPK signalling pathway partially ameliorated the NaCl- induced inflammatory responses in both macrophages and microglia, together with high levels of secreted IL-1β, indicating activation of the NLRP3 inflammasome. Overall the studies highlight a role for ApoE4 allele to promote an enhanced inflammatory response by microglia cells

Non-uniformities in spatial location models

Location Theory;Demand;General Equilibrium;Location Models;management science