| 1. |
- Risenfors, M, et al.
(författare)
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Early treatment with thrombolysis and betablockade in suspected acute myocardial infarction : results from the TEAHAT Study
- 1991
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Ingår i: Journal of Internal Medicine. - : Wiley-Blackwell Publishing Ltd.. - 0954-6820 .- 1365-2796. ; 734:suppl 1, s. 35-42
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Tidskriftsartikel (refereegranskat)abstract
- Independent trials of early administration of beta-blockers and thrombolytic agents have shown beneficial effects on both short- and long-term prognoses in acute myocardial infarction (AMI). The effects of a combination of the two strategies have not been thoroughly documented. Three hundred and fifty-two patients, of less than 75 years of age, with chest pain indicative of AMI, and onset less than 2 h and 45 min before first examination, were randomized to treatment with rt-PA or placebo. All patients without contraindication were given intravenous metoprolol 15 mg acutely and then 200 mg orally daily. Treatment was started either at the prehospital stage or in hospital. Thirty-seven per cent of patients had contraindications to beta-blockade, the most frequent of which were heart rate less than 60 beats min-1 and hypotension. The remaining 63% were given intravenous beta-blockade. No side-effects of metoprolol, alone or in combination with rt-PA, were observed during the prehospital phase. Overall, toleration of the treatment was good. Reduction in enzymatically estimated infarct size by rt-PA was more pronounced in patients who were also treated with metoprolol (41%, P less than 0.001) than in those with contraindications to beta-blockade (15%, NS). Patients who were also treated with metoprolol also had a lower incidence of Q-wave infarctions, congestive heart failure and ventricular fibrillation than those who were not given intravenous beta-blockade. In conclusion, toleration of intravenous administration of rt-PA and metoprolol was good, and this was also the case in the prehospital phase.
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| 2. |
- Bengtsson, Stefan, 1961, et al.
(författare)
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Silicon on aluminum nitride structures formed by wafer bonding
- 1994
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Ingår i: 1994 IEEE International SOI Conference Proceedings. ; , s. 35-
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Tidskriftsartikel (refereegranskat)abstract
- This paper deals with the use of reactively sputtered aluminum nitride (AlN) films as insulators for Bond and Etch-back Silicon-On-Insulator (BESOI) materials. In SOI-applications where high power is dissipated in the silicon SOI-film the low thermal conductivity of the buried silicon dioxide layer may cause a temperature rise in the silicon film detrimentally affecting the device performance. An attractive alternative would be to replace the silicon dioxide of the SOI structure with another material, like diamond, silicon carbide or aluminum nitride. The thermal conductivity of AlN is considerably larger than that of Si02. This paper presents results on how sputter deposition of AlN may be combined with wafer bonding for the creation of highly thermally conductive SOI structures
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| 3. |
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| 4. |
- Holte, J, et al.
(författare)
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Enhanced early insulin response to glucose in relation to insulin resistance in women with polycystic ovary syndrome and normal glucose tolerance.
- 1994
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Ingår i: Journal of Clinical Endocrinology and Metabolism. - : The Endocrine Society. - 0021-972X .- 1945-7197. ; 78:5, s. 1052-8
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Tidskriftsartikel (refereegranskat)abstract
- Insulin secretion in response to iv glucose and insulin sensitivity (euglycemic hyperinsulinemic clamp) were evaluated in 49 women with polycystic ovary syndrome (PCOS) [body mass index (BMI), 17.6-37.2 kg/m2] and 42 control subjects (BMI, 18.8-38.1 kg/m2). Seven women with PCOS exhibited glucose intolerance with subnormal insulin secretion. Compared with control subjects, women with PCOS and normal glucose tolerance had an increased (36-56%) insulin increment, not explained by insulin resistance, and over the whole range of BMI. In contrast, insulin sensitivity was similar in women with PCOS and control subjects at BMI 21 kg/m2, but showed a more pronounced decline with increasing BMI in women with PCOS, who had 35% and 70% lower insulin sensitivities at BMI 28 and 35 kg/m2, respectively. After adjusting for truncal-abdominal sc fat distribution, which was more pronounced in the women with PCOS, the two groups had similar insulin sensitivity over the entire range of BMI (P = 0.9), whereas the difference in insulin increment was insignificant after adjusting for the free androgen index (testosterone x 100/sex hormone binding globulin; P = 0.16). Hemoglobin A1C levels were lower in women with PCOS than in the control subjects. It is concluded that the early insulin response to glucose was increased in women with PCOS, not accounted for by insulin resistance, closely associated to the increased androgenicity, and present also at low-normal BMI. In contrast, insulin resistance was seen only at higher BMI levels and was largely determined by the increased truncal-abdominal fat mass in PCOS.
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| 5. |
- Mannheimer, C, et al.
(författare)
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Effects of spinal cord stimulation in angina pectoris induced by pacing and possible mechanisms of action.
- 1993
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Ingår i: BMJ (Clinical research ed.). - 0959-8138. ; 307:6902, s. 477-80
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Tidskriftsartikel (refereegranskat)abstract
- To investigate the effects of spinal cord stimulation on myocardial ischaemia, coronary blood flow, and myocardial oxygen consumption in angina pectoris induced by atrial pacing.The heart was paced to angina during a control phase and treatment with spinal cord stimulation. Blood samples were drawn from a peripheral artery and the coronary sinus.Multidisciplinary pain centre, department of medicine, Ostra Hospital, and Wallenberg Research Laboratory, Sahlgrenska Hospital, Gothenburg, Sweden.Twenty patients with intractable angina pectoris, all with a spinal cord stimulator implanted before the study.Spinal cord stimulation increased patients' tolerance to pacing (p < 0.001). At the pacing rate comparable to that producing angina during the control recording, myocardial lactate production during control session turned into extraction (p = 0.003) and, on the electrocardiogram, ST segment depression decreased, time to ST depression increased, and time to recovery from ST depression decreased (p = 0.01; p < 0.05, and p < 0.05, respectively). Spinal cord stimulation also reduced coronary sinus blood flow (p = 0.01) and myocardial oxygen consumption (p = 0.02). At the maximum pacing rate during treatment, all patients experienced anginal pain. Myocardial lactate extraction reverted to production (p < 0.01) and the magnitude and duration of ST segment depression increased to the same values as during control pacing, indicating that myocardial ischaemia during treatment with spinal cord stimulation gives rise to anginal pain.Spinal cord stimulation has an anti-anginal and anti-ischaemic effect in severe coronary artery disease. These effects seem to be secondary to a decrease in myocardial oxygen consumption. Furthermore, myocardial ischemia during treatment gives rise to anginal pain. Thus, spinal cord stimulation does not deprive the patient of a warning signal.
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