Posture of the unconscious patient.
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Biomedical subjects
Publications and source records attributed to W J Atkinson.
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Needle-shaped thermoseeds have been manufactured from an alloy consisting of 70.4% nickel and 29.6% copper. The magnetic properties of the alloy were measured at various temperatures and from this the heating power produced by a thermoseed exposed to an electromagnetic induction field was computed as a function of the seed temperature. Calorimetric measurements were also performed. From these data, temperature distributions in simple tumor models assumed to be heated by an array of nickel-copper implants were computed. It was found that the nickel-copper implants produce substantially better temperature homogeneity than readily available constant power seeds, especially in tumors with unpredictable rates of blood perfusion or when the implant arrangement is not perfectly regular. Since such conditions are likely to be present in actual patients, the nickel-copper implants should be very useful in clinical hyperthermia.
We used the calcium-sensitive fluorescent indicator quin 2 to monitor changes in cytosolic free calcium concentration ([Ca2+]i) associated with angiotensin II receptor activation in cultured vascular smooth muscle cells isolated from rat aorta. Resting [Ca2+]i in unstimulated vascular smooth muscle cells was 198 +/- 7 nM. Angiotensin II induced concentration-dependent rapid increases in [Ca2+]i (threshold congruent to 10(-11) M; effective concentration, 50% congruent to 5 X 10(-10) M; maximum congruent to 10(-8) M); the rate of increase in [Ca2+]i also appeared to be concentration dependent. The angiotensin II-induced changes were completely blocked by the angiotensin II receptor antagonist [Sar1, Ile8]-angiotensin II. In the presence of extracellular calcium, 10(-8) M angiotensin II induced an increase in [Ca2+]i that reached peak values of five to six times the resting levels within 15 seconds, followed by a gradual decline to a plateau at two to three times the resting level. When EGTA was added to chelate external calcium, the angiotensin II-induced increases in peak [Ca2+]i were attenuated and the plateau phase was abolished. These data show that (1) quin 2 can be used in cultured vascular smooth muscle cells to study changes in calcium homeostasis induced by angiotensin II, and (2) angiotensin II acts on cultured vascular smooth muscle cells to cause a rapid increase in [Ca2+]i that appears to depend on both the mobilization of intracellular calcium and the influx of extracellular calcium.