This paper focuses on a new definition of urbanization trends by investigating the concept of a fuzzy urban boundary (UB) that assigns different membership levels to urbanized aggregates based on a proposed composite index. The research work builds on this logic to investigate a new approach in defining urbanized areas by compounding the characteristics of the fuzzy density of an urban agglomeration with land use variation and intensity of economic activity. Spatial overlaying capabilities of geographic information system (GIS) are used to model the urbanization trend in the case study of Greater Beirut. The UB is defined using a multispectral high resolution visible (HRV) Satellite Pour L'observation de la Terre (SPOT) satellite image. The challenges of urban modelling using satellite images are addressed through an investigative approach in cartographic feature extraction and delineation of the urban agglomeration. This entails image treatment of the spot HRV image, defining internal characteristics of the urban agglomeration and constructing spatially continuous socio-economic data sets that can be combined with the digital remotely sensed image.Key words: fuzzy logic, GIS, remote sensing, spatial urban modelling, urban boundary, urbanization trends.

We conducted this study on 15 chronic haemodialysis patients to evaluate the efficacy of i.v. calcitriol over a 1-year period in the treatment of severe secondary hyperparathyroidism (HPT), in particular its effect on bone mineral density (BMD) and parathyroid gland mass. Mean age was 39 ± 11.9 (20-65) years and dialysis duration was 58 ± 3 (19-130) months, i.v. calcitriol was given at a dose of 1 µg post-dialysis 3 times/week for 3 weeks; the dose was then adjusted to maintain the total serum calcium at less than 2.88 mmol/l. The maximum dose was 3 µg 3 times/week. Serum calcium (Ca) and phosphorus (P) were determined prior to treatment, then weekly for 6 weeks and every 2 weeks thereafter. Skeletal survey, dual photon densitometry and parathyroid ultrasound (US) were done prior to treatment and after 1 year. Bone biopsy was done in 10 patients at the beginning of treatment. There was a significant reduction (p < 0.01) in pre-treatment mid-region serum parathyroid hormone (PTH) from 1,476 ± 895 to 489 ± 485 P mol/l, as well as alkaline phosphatase (p < 0.04) from 236.5 ± 221 to 116.3 ± 49 U/l. This was without a significant increase in serum Ca (2.15 ± 0.25 to 2.44 ± 0.26 mmol/l, p = 0.08). Three patients had recurrent hypercalcaemia which responded to reduction of Ca in dialysate. There was a significant increase in BMD over the spine from 1.071 ± 0.25 to 1.159 ± 0.22 g/cm² (p < 0.003) with a percent increase of 9.3 ± 8.9% as well as over the femoral neck from 0.834 ± 0.002 to 0.89 ± 0.09 g/ cm² (p < 0.001) with a percent increase of 7.45 ± 6.81%. Five patients had enlarged parathyroid glands by US and in 3 of these, there was a significant reduction to normal with treatment. Bone biopsy was done in 10 patients. Six patients had predominant hyperparathyroid bone disease and 4 had mixed uraemic osteodystrophy. In conclusion, long-term i.v. treatment with calcitriol is effective in the treatment of severe secondary HPT. PTH decreased without a significant increase in serum Ca. BMD also increases during this therapy.

We have studied the effect of the intravenous administration of the following drugs on ventricular refractoriness in 35 experiments in open chested beagle dogs: atenolol 0.2 mg X kg-1; nadolol 0.05 mg X kg-1; oxprenolol 0.2 mg X kg-1; pindolol 0.04 mg X kg-1; propranolol 0.2 mg X kg-1; sotalol 0.6 mg X kg-1 and timolol 0.1 mg X kg-1. The animals were anaesthetised with chloralose and urethane. Measurements were made of left ventricular epicardial monophasic action potentials (MAP) (n = 35) and the left ventricular paced evoked response (PER) (n = 25) at a fixed paced cycle length of between 220 and 310 ms. The animals were initially beta-blocked with iv pindolol or propranolol and the drug under study then administered iv 10 min later. The results were as follows: (control and post drug administration) MAP: nadolol 151 +/- 12 SD to 172 +/- 13 SD (p less than 0.001); oxprenolol 153 +/- 21 to 178 +/- 20 (p less than 0.001); sotalol 153 +/- 19 to 176 +/- 20 (p less than 0.001); atenolol 152 +/- 25 to 153 +/- 23 (NS); pindolol 149 +/- 11 to 152 +/- 10 (NS); propranolol 152 +/- 26 to 155 +/- 26 (NS); timolol 144 +/- 23 to 144 +/- 21 (NS). PER: nadolol 172 +/- 14 to 190 +/- 20 (p less than 0.001); oxprenolol 164 +/- 16 to 188 +/- 15 (p less than 0.001); propranolol 166 +/- 22 to 173 +/- 18 (NS).(ABSTRACT TRUNCATED AT 250 WORDS)

The early electrophysiological patterns of regional subendocardial ischaemia were studied by using the paced endocardial evoked response and simultaneous endocardial monophasic action potential recordings in 16 experiments in open chested dogs. Ischaemia was produced by transient (1-3 min) coronary artery occlusion. Regional subendocardial isochaemia caused asynchronous activation due to differential conduction delay and shortened repolarization as evaluated by the duration of the paced evoked response from 175 +/- (SD) 18.7 ms to 167 +/- 16 ms (P less than 0.001). These changes occurred within 60 s of occlusion and reversed rapidly after release of the occlusion. In simultaneous endocardial monophasic action potentials there was a decrease in plateau amplitude and the duration of repolarization shortened from 180 +/- (SD) 21.2 ms to 167 +/- 20.4 ms (P less than 0.001). The delay in endocardial activation after 2 min ischaemia was 5.5 ms, which is considerably shorter than the conduction delay previously reported in the subepicardial layers. The calcium-channel blocking drug verapamil (infused at 0.4 mg/kg) altered the rate at which shortening of repolarization and asynchronous activation occurred during ischaemia in six experiments. These experiments suggest that intracavitary electrodes could provide earlier and more sensitive detection of regional subendocardial ischaemia and may permit the assessment of therapy on the early electrical changes in the intact heart.

SUMMARYRetrograde infusion of blood into a pulmonary vein raised the pressure by 0 5-1 kPa in the cannulated vein. There were no changes in heart rate, arterial blood pressure, left atrial pressure, right atrial pressure or the pressure in the other pulmonary veins. The rise in pulmonary venous pressure was associated with an increase in urinary sodium concentration and excretion. However, there was no change in urine volume. The natriuresis was abolished by cooling the vagi to 9 'C. It is argued that receptors up-stream in the pulmonary veins themselves may be involved in the increase in sodium excretion that follows a rise in left atrial pressure.