Competitive reaction to entry is an important issue in the marketing and economics areas. The monopolistic incumbent of a market often faces competitive entry if the market is profitable. This is a common issue that often occurs in the market transition from monopoly to competition. The entrant not only enters the market, but also wants to signal to tell consumers his quality level. The incumbent's reaction is also a signal to the consumers. Thus, how should the incumbent do? The paper "Response to Competitive Entry: A Rationale for Delayed Defensive Reaction" which is written by Ajay Kalra, Surendra Rajiv and Kannan Srinivasan (1998) and published in Marketing Science provides a completed and clear explanation of this issue. They claim that the incumbent would delay the defensive reaction to the competitive entry under information asymmetry. But it is still incorrect. Hence, we want to provide a revision to support that delayed defensive reaction is really a rational response to competitive entry, and explain this issue correctly and logically. We analyze the strategic interactions of the incumbent and the entrants which were omitted previously. Finally, we would obtain the conclusion that is also supporting this point of view¡G delayed defensive reaction is really a rational response to competitive. And it is really a Nash equilibrium, no firms would deviate.

Background: Although several neurophysiological models have been proposed for panic disorder with agoraphobia (PD/AG), there is limited evidence from functional magnetic resonance imaging (fMRI) studies on key neural networks in PD/AG. Fear conditioning has been proposed to represent a central pathway for the development and maintenance of this disorder; however, its neural substrates remain elusive. The present study aimed to investigate the neural correlates of fear conditioning in PD/AG patients. Method: The blood oxygen level-dependent (BOLD) response was measured using fMRI during a fear conditioning task. Indicators of differential conditioning, simple conditioning and safety signal processing were investigated in 60 PD/AG patients and 60 matched healthy controls. Results: Differential conditioning was associated with enhanced activation of the bilateral dorsal inferior frontal gyrus (IFG) whereas simple conditioning and safety signal processing were related to increased midbrain activation in PD/AG patients versus controls. Anxiety sensitivity was associated positively with the magnitude of midbrain activation. Conclusions: The results suggest changes in top-down and bottom-up processes during fear conditioning in PD/AG that can be interpreted within a neural framework of defensive reactions mediating threat through distal (forebrain) versus proximal (midbrain) brain structures. Evidence is accumulating that this network plays a key role in the aetiopathogenesis of panic disorder.