This paper describes the design and implementation of an imaging protocol for mobile phones. This protocol enables a user to transfer content from a mobile phone to various display devices (e.g. projector) and control content presentation (e.g. display, forward , backward, etc.) by the same mobile phone, via various network interfaces (e.g. WLAN, Bluetooth, USB and IrDA). Using the proposed protocol, a mobile phone user can realize a content presentation equivalent to that possible with a PC. To ensure interoperability with existing display devices, we set a gateway between the mobile phone and the display devices. The gateway outputs the commands accepted by the device selected to allow the mobile phone user to control the device transparently.
To investigate myocardial interstitial noradrenaline (NA) kinetics during activation of systemic sympathetic nerves, we applied a dialysis technique to the left ventricle of anaesthetised cats and monitored myocardial interstitial NA levels during 6-min occlusion of the inferior vena cava (IVC). Dialysis probes were implanted in the left ventricular wall, and dialysate NA levels as an index of myocardial interstitial NA levels, were measured with high-performance liquid chromatographic-electrochemical detection. During IVC occlusion, dialysate NA levels progressively increased from 110 +/- 17 pmol L-1 in the control and reached 620 +/- 160 pmol L-1 at 4-6 min of IVC occlusion. Local administration of omega-conotoxin GVIA at 10 microM decreased the control dialysate NA level to 35 +/- 0.2 pmol L-1. The IVC occlusion induced increase in dialysate NA was suppressed only at 0-2 min of IVC occlusion. Intravenous injection of omega-conotoxin GVIA (10 micrograms kg-1) did not increase the dialysate NA levels during IVC occlusion. Local administration of desipramine at 100 microM increased the control dialysate NA level to 900 +/- 73 pmol L-1. The IVC occlusion induced progressive increase in dialysate NA was augmented at 2-6 min of IVC occlusion. These results suggest that the early increase in myocardial interstitial NA levels is mainly caused by neuronal release of NA from cardiac sympathetic nerve terminals, and that extraction from the circulation and neuronal NA uptake contribute to changes in myocardial interstitial NA levels after a delay of several minutes.
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