These results identify a sensitive method to track in vivo leukocyte localization and specifically demonstrate that lymphocyte localization is altered in both traumatic and nontraumatic models of inflammation.
Canine skeletal muscle was heated with a single microwave antenna within a brachytherapy catheter driven at 2000 MHz. The radial, steady-state temperature distribution was measured with and without air cooling of the antenna, as produced by room temperature air flowing in the catheter at 7.5 l/min. The axial temperature distribution was also measured with air cooling. In the antenna junction plane the area heated to a given temperature increased by a factor of four with air cooling when the same antenna temperature was enforced. With the same maximum temperature enforced, the area would increase by a factor of 2.5 with air cooling. The axial temperature distribution was not compromised by air cooling.
A prototype adaptive automatic control algorithm was implemented to regulate temperatures measured at several points in a tumour by adjusting the power applied to several ultrasound transducers. The goal was to control the temperatures under the elements of a mosaic applicator individually without any priori knowledge of which probes are under which elements. The control algorithm was devised for clinical applications where the position of each probe with respect to the heat sources is difficult to determine precisely. Instead, the program 'learns' the relationship between the inputs (power levels) and the outputs (temperatures) automatically. Based on the observed transfer function relating the power at m sources to the temperatures n probes, where n and m are not necessarily the same, a new method was used to implement a feedback controller. This method simplifies the design of the controller for a multiple-input/multiple-output (MIMO) system, while taking into account the coupling that may exist between the various elements of the system. As a result of using an adaptive scheme, the regulator continuously tracks changes in the system, such as blood flow variations or patient motion, by modifying its control parameters. The algorithm performance has been tested in simulations as well as experiments in dog thigh and a perfused kidney model.
The purpose of this study was to examine if ATP-MgCl2, an agent that protects against acute cisplatin toxicity in vitro, protected against cisplatin toxicity in vivo. Baseline renal function measurements were obtained on dogs (n = 12) and rats (n = 20) on day -1. Dogs were given 90 mg m-2 cisplatin (n = 5), 90 mg m-2 cisplatin and 50 mumol kg-1 ATP-MgCl2 (n = 5), or 90 mg m-2 cisplatin and 150 mumol kg-1 ATP-MgCl2 (n = 2), in a slow bolus i.v. injection on day 0. Rats were given 4 mg kg-1 cisplatin i.p. (n = 6) and 25 mumol kg ATP-MgCl2 (n = 8) i.v. or 4 mg kg-1 cisplatin i.p. and 25 mumol kg-1 ATP-MgCl2 (n = 6) i.v. on day 0. Renal function was assessed on a routine basis for 14 days. All dogs had significantly decreased creatinine clearance following cisplatin administration. There were no significant differences in renal function tests between groups of dogs. One dog given 50 mumol kg-1 ATP-MgCl2 and both dogs given 150 mumol kg-1 ATP-MgCl2 in addition to cisplatin developed acute anuric renal failure and were euthanatized prior to completion of the study. Rats given 4 mg kg-1 cisplatin and 25 mumol kg-1 ATP-MgCl2 had significantly increased blood urea nitrogen and serum creatinine after drug administration, compared to rats given cisplatin alone. The results indicated that ATP-MgCl2 worsened in vivo cisplatin renal toxicity in the dog and rat.
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