Effects of habitat destruction and resource supplementation in a predator-prey metapopulation model.

We developed a mean field, metapopulation model to study the consequences of habitat destruction on a predator-prey interaction. The model complements and extends earlier work published by Bascompte and Solé (1998, J. theor. Biol.195, 383-393) in that it also permits use of alternative prey (i.e., resource supplementation) by predators. The current model is stable whenever coexistence occurs, whereas the earlier model is not stable over the entire domain of coexistence. More importantly, the current model permits an assessment of the effect of a generalist predator on the trophic interaction. Habitat destruction negatively affects the equilibrium fraction of patches occupied by predators, but the effect is most pronounced for specialists. The effect of habitat destruction on prey coexisting with predators is dependent on the ratio of extinction risk due to predation and prey colonization rate. When this ratio is less than unity, equilibrial prey occupancy of patches declines as habitat destruction increases. When the ratio exceeds one, equilibrial prey occupancy increases even as habitat destruction increases; i.e., prey "escape" from predation is facilitated by habitat loss. Resource supplementation reduces the threshold colonization rate of predators necessary for their regional persistence, and the benefit derived from resource supplementation increases in a nonlinear fashion as habitat destruction increases. We also compared the analytical results to those from a stochastic, spatially explicit simulation model. The simulation model was a discrete time analog of our analytical model, with one exception. Colonization was restricted locally in the simulation, whereas colonization was a global process in the analytical model. After correcting for differences between nominal and effective colonization rates, most of the main conclusions of the two types of models were similar. Some important differences did emerge, however, and we discuss these in relation to the need to develop fully spatially explicit analytical models. Finally, we comment on the implications of our results for community structure and for the conservation of prey species interacting with generalist predators.

Duane retraction syndrome associated with Rubinstein-Taybi syndrome.

The authors present a case report of Duane retraction syndrome (DRS) associated with Rubinstein-Taybi syndrome (RTS). RTS is a multisystem condition characterized by psychomotor developmental delay, broad thumbs and great toes, short stature, and characteristic facies with a beaked nose. DRS is an ocular disorder characterized by retraction of the globe with narrowing of the palpebral fissure in attempted adduction, with abduction and/or adduction deficiency, and, frequently, upshoot or downshoot of the affected eye on adduction. The case report described represents the first reported case of DRS associated with RTS, an association not previously recognized. This association raises the possibility that the abnormal CNS development in RTS may occasionally involve the ocular motor nerves.

Strength-interval relation for ventricular functional refractoriness.

Successful initiation and termination of presumed reentrant ventricular tachycardia frequently depends on the ability to deliver closely coupled impulses to the region of the tachycardia origin. To evaluate systematically the relative influence of local latency and large-scale conduction delay in limiting the delivery of closely coupled impulses, the strength-interval relation of the effective refractory period (RP), and the local and remote functional RP in 35 patients at paced cycle length of 500 ms were measured. The pacing threshold was less than or equal to 0.25 mA in all patients. The drive-train (S1) and the extrastimulus (S2) were applied from the same site, the right ventricular (RV) apex, in 25 patients, and from separate sites (RV apex and RV outflow tract) in 10 patients. The effect of procainamide (plasma concentration 10.1 +/- 2.3 micrograms/ml) on the strength-interval relations in 10 patients was also assessed. Although effective RP decreased significantly with each successive increase in current strength (p less than 0.001), local functional RP decreased only up to current strength of 4 mA, and remote functional RP decreased only up to 2 mA. Procainamide shifted the effective RP and local and remote functional RP strength-interval curves uniformly to the right without altering their relation. These data indicate that large-scale conduction delay provides the principal limitation for using increasing current strengths of a single extrastimulus to initiate or terminate ventricular tachycardia.

Verapamil decreases MAC for halothane in dogs.

Verapamil hydrochloride is a calcium entry blocking drug that is being prescribed with increasing frequency for cardiovascular disorders in the perioperative setting. Verapamil's calcium channel blocking effect is not selective, because it also exerts activity on the sodium channel. Because of the well-described effects of sodium channel blockers on anesthetic requirements, the authors studied the MAC for halothane in dogs before and after a therapeutic dose of verapamil 0.5 mg . kg-1. There was a 25% reduction in halothane MAC from 0.97-0.72% (P less than 0.01) when a therapeutic plasma level of verapamil (64 ng . ml-1) was present. Anesthetic requirements for halothane are reduced by dl-verapamil possibly on the basis of its local anesthetic-like sodium channel blocking properties. Adjustments in anesthetic dosage may be necessary in patients receiving verapamil.

Indomethacin-responsive hypercalcemia in a patient with renal-cell adenocarcinoma.

PIP: A case is reported of a man who experienced hypercalcemia as a result of developing liver and renal-cell cancer. Repeated skeletal surveys and bone scans failed to reveal any bone metastases. The hypercalcemia was unresponsive to hydration and oral phosphate. However, it responded immediately to oral administration of indomethacin. The mechanism of this calcium-lowering effect is unknown. On the death of the patient, biopsies of the metastic liver and lung tissue were performed. The liver metastatis yielded 7 times the PGE (prostaglandin E)-like and 5 times the PGF-like material found in the normal adjacent liver. The lung metastatis yielded only 1/2 the PGE-like and PGF-like material obtained from normal adjacent lung. The results of this case study would indicate that some forms of hypercalcemia secondary to neoplastic disease are responsive to indomethacin and may be due to increased PG production by the tumor tissue.^ieng