A Man-Machine Competitive Game: A Naval Duel

The research reported here is the development of a man-machine game in which the competitors are the captain of a submarine and the commander of an opposing task force. This naval game has been implemented and tested in the Problem Solving Facility of the University of Pennsylvania under Contract NOnr 551(48) sponsored by the Methodology Division, Office of Naval Research. The broad objective of this research has been to experiment with and develop a man-machine framework in which an executive, scientist or engineer may employ strategies and tactics in an operational environment. A complete functional description of the game will be given in this report. This chapter provides an overview of the game and cites its salient characteristics. Chapter 2 presents the game through a play-by-play record of one competitor in an actual duel. Chapter 3 presents the various aspects of the Problem Solving methodology and developed tactics by means of three annotated duels. This also illustrates the versatility of the game and demonstrates the competitors\u27 capability to interact with the computer. Chapter 4 summarizes our research to date and lists planned refinements to the game. Additional documentation of the game structure is provided in the appendices

Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation

Background: The neuroinflammatory response following traumatic brain injury (TBI) is known to be a key secondary injury factor that can drive ongoing neuronal injury. Despite this, treatments that have targeted aspects of the inflammatory pathway have not shown significant efficacy in clinical trials. Main body: We suggest that this may be because classical inflammation only represents part of the story, with activation of neurogenic inflammation potentially one of the key initiating inflammatory events following TBI. Indeed, evidence suggests that the transient receptor potential cation channels (TRP channels), TRPV1 and TRPA1, are polymodal receptors that are activated by a variety of stimuli associated with TBI, including mechanical shear stress, leading to the release of neuropeptides such as substance P (SP). SP augments many aspects of the classical inflammatory response via activation of microglia and astrocytes, degranulation of mast cells, and promoting leukocyte migration. Furthermore, SP may initiate the earliest changes seen in blood-brain barrier (BBB) permeability, namely the increased transcellular transport of plasma proteins via activation of caveolae. This is in line with reports that alterations in transcellular transport are seen first following TBI, prior to decreases in expression of tight-junction proteins such as claudin-5 and occludin. Indeed, the receptor for SP, the tachykinin NK1 receptor, is found in caveolae and its activation following TBI may allow influx of albumin and other plasma proteins which directly augment the inflammatory response by activating astrocytes and microglia. Conclusions: As such, the neurogenic inflammatory response can exacerbate classical inflammation via a positive feedback loop, with classical inflammatory mediators such as bradykinin and prostaglandins then further stimulating TRP receptors. Accordingly, complete inhibition of neuroinflammation following TBI may require the inhibition of both classical and neurogenic inflammatory pathways.Frances Corrigan, Kimberley A. Mander, Anna V. Leonard and Robert Vin