Depressed renal and vascular nitric oxide synthase expression in cyclosporine-induced hypertension

With the longer life expectancy of the population, calcific aortic stenosis has become a common cardiac problem in the elderly. When patients with moderate to severe aortic stenosis become symptomatic, the prognosis is usually poor in absence of valve replacement and sudden death is a feared complication. It has been hypothesized that malignant ventricular arrhythmias could be responsible for the high incidence of sudden death in symptomatic patients with aortic stenosis. The purpose of this review is to analyze the prevalence, the electrophysiologic mechanisms, and the possible role of ventricular arrhythmias in the development of symptoms and in the outcome of adult subjects with aortic stenosis.     

Congestion control of packet-switched networks with three types of input buffer limits

Congestion in a store-and-forward data communications network manifests itself by a rapid degradation of network throughput and a fast increase in the average transit delay. A study of a congestion control mechanism in a packet-switched data network is presented. Buffer limits are placed on the input, transit and exit packets in each switching node. By a judicious choice of the buffer limits, it is shown that the network throughput can be maintained at a constant level, while the average transit delay remains within acceptable bounds for offered loads beyond the congestion point.     

Retinal emboli in patients with mitral valve prolapse

Small fibrin-platelet emboli caused by prolapsed mitral valves may cause retinal occlusive disease with a wide range of ophthalmic manifestations, including amaurosis fugax in young people, retinal or choroidal arteriolar occlusion, and retinal neovascularization (atypical Eales' disease). Six patients with retinal occusive disease underwent extensive noninvasive cardiac and systemic tests and were found to have prolapsed mitral valves. Patients with unexplained ocular emboli should be examined by a cardiologist for possible mitral valve prolapse.     

Anal endosonography in patients with anorectal symptoms after haemorrhoidectomy

Although allergic persons can react to foods containing trace quantities of unlabeled or unintended food allergens, there are few data available on the quantities of these allergens required to evoke allergic symptoms. We report a milk-allergic 3-year-old boy who experienced throat itching, facial angioedema, and vomiting within 20 min of ingesting 4 to 6 oz (ca. 113.4 to 170.1 g) of lemon sorbet. Subsequent analysis of two sorbet samples provided by the parents and a third sample purchased locally by the investigators revealed trace quantities of milk allergens, whey protein (8.8 micrograms/ml), or lactose (200 ppm). The quantity of whey protein ingested was estimated to be 120 to 180 micrograms (equivalent to 23 to 24 microliters of milk). All three sorbet samples had been manufactured in the same plant within a 4-month period; the equipment used to produce and package the sorbet was also used to produce and package ice cream. No milk allergen or whey protein was detected in 38 other marketplace sorbet samples submitted by the manufacturer for testing. We concluded that trace quantities of whey proteins (< 200 micrograms) can elicit systemic reactions in exquisitely milk-allergic individuals. Such individuals should avoid eating frozen desserts prepared using equipment also used for producing or packaging ice cream, unless manufacturers can demonstrate unequivocally that their cleaning practices are sufficient to prevent milk contamination. Adequate tests are not currently available to food manufacturers but are under development.     

"Moon-cars" are dangerous

We investigated the number and seriousness of moon-car accidents in our region (a moon-car is a toy-vehicle, see Fig. 1). The study was retrospective combined with a telephone-interview. Forty-seven patients were seen in the emergency room after a moon-car accident in the period 1/1 1990-31/12 95. There were 12 fractures, including five fractures of the tibial shaft and one supracondylar humeral fracture which was operated. There were 17 wounds, 14 of which were sutured. Seventeen patients had distorsions/contusions, three cases of head contusions (observed for concussion) and two with teeth damages. We found that the number of moon-car accidents is increasing (13 patients the last year), and that the accidents are not only minor. New rules in day care centres should be able to especially limit the number of more serious accidents.     

Effects of methylprednisolone on the physical properties of the human red cell

Prompted by evidence suggesting preserved red cell deformability in cardiac surgical patients pretreated with pharmacologic dosages of methylprednisolone, we performed in vitro experiments to examine the ability of similar levels of methylprednisolone and hydrocortisone to modify erythrocyte membrane changes produced by metabolic depletion or membrane-active compounds. Variables measured included cell morphology, blood biscosity, membrane deformability, osmotic fragility, red cell cholesterol, and glycolytic intermediates. In incubated samples, methylprednisolone partially prevented the transition of discs to echinocytes, the rise in whole blood viscosity, the decrease in membrane deformability, and the loss of red cell cholesterol which accompany ATP depletion, but it had no apparent effect on red cell glycolysis. The drug also inhibited esterification of cholesterol in cell-free serum. In unimcubated samples to which lysolecithin was added, methylprednisolone partially prevented and reversed morphologic and rheologic responses without affecting membrane cholesterol. Hydrocortisone demonstrated similar properties. Possible mechanisms for these actions are discussed. The concept is advanced that preserved blood fluidity may contribute to the beneficial responses to these drugs in certain clinical conditions.     

Pathogenesis of trimethyltin neuronal toxicity. Ultrastructural and cytochemical observations

The ultrastructural cytopathologic and cytochemical effects of trimethyltin (TMT) neurotoxicity were delineated in hippocampal and pyriform neurons of acutely intoxicated adult rats. TMT produced neuronal necrosis that preferentially involved hippocampal formation pyriform cortex. The first subcellular alterations were multifocal collection of dense-cored vesicles and tubules and membrane-delimited vacuoles in the cytoplasm of the perikaryon and proximal dendrite. Ultrastructural cytochemical examination revealed that the vesicles and tubules had acid phosphatase activity analagous to Golgi-associated endoplasmic reticulum (GERL). Shortly after the appearance of the GERL-like vesicles and tubules, autophagic vacuoles and polymorphic dense bodies accumulated in the neuronal cytoplasm. Some dense bodies appeared to arise from the dense-cored tubules. Neuronal necrosis was characterized by increased electron density of the cytoplasm and large, electron-dense intranuclear masses. Alterations of mitochondria and other organelles were not observed in the early stages of cell injury. No light- or electron-microscopic alterations were found in liver or kidney. Comparable subcellular alterations were observed in adult and neonatal rats chronically intoxicated with TMT. A series of other trialkyl and tricyclic tins and dimethyltin did not produce similar pathologic findings. The GERL-like accumulations are unique in neuronal cytopathology. These findings suggests that GERL and autophagy play an important role in the pathogenesis of TMT-induced neuronal injury.