Fragment length polymorphisms among independent isolates of Epstein-Barr virus from immunocompromised and normal hosts

DNA restriction fragment length polymorphisms of Epstein-Barr virus (EBV) DNA were used as a molecular epidemiological tool to study multiple isolates of virus from the same and different individuals. We studied 35 EBV isolates: 19 from seven immunocompromised children and 16 from seven college students with mononucleosis. Analysis of the fragment length polymorphisms in this collection of isolates permitted several conclusions. Sites of polymorphism were most often encountered in regions with repetitive DNA. Epidemiologically unrelated patients harbored viruses that could be readily distinguished; by contrast, two infants and their mothers harbored similar viruses. Isolates from different sites in the same patient were similar. Variations between different clinical isolates of EBV mimic those found between different laboratory strains of the virus. Fragment length polymorphisms thus provide a useful marker for studying transmission and pathogenesis of EBV infections.     

Body composition of patients with spinal cord injury

Body composition of 10 control subjects and 37 spinal cord injured (SCI) patients was measured by dilution of 3H2O and Na2 35SO4. SCI patients were classified into four groups by ascending level of lesion, low and high paraplegics and low and high quadriplegics. The studies show diminishing total body water, intracellular water, lean body mass and body cell mass and increasing fat mass with higher spinal lesions. No differences in body weight or extracellular water were observed so that the ratio of extracellular water/total body water was increased as the level of injury increased.     

Antioxidant enzyme activities and total nitrite/nitrate levels in the collar model. Effect of nicardipine.

There is a large body of literature describing the causative role of oxidative stress mediated by increased levels of reactive oxygen species in the pathogenesis of cardiovascular disease such as atherosclerosis, hypertension, and restenosis after angioplasty. The positioning of a soft silicone collar around the rabbit carotid artery elicits intimal thickening. The findings from recent studies demonstrated that both intimal thickening and atherosclerosis lead to synthesis of inducible nitric oxide synthase, resulting in abundant amounts of nitric oxide. We investigated the effects of collaring and nicardipine treatment on the activities of antioxidant enzymes, superoxide dismutase and catalase, and total nitrite/nitrate levels, stable products of nitric oxide. Placing the collar increased the total nitrite/ nitrate levels and decreased superoxide dismutase activity in collared arteries. Treatment with nicardipine (20 mg/kg/day, s.c.) prevented enhanced nitric oxide degradation without affecting superoxide dismutase and catalase activities. Our results suggest that enhanced nitric oxide production and superoxide anion are generated in response to the collaring, resulting in oxidative stress within the segment in this model.     

High alveolar surface tension increases clearance of technetium 99m diethylenetriamine-pentaacetic acid.

The effect of high alveolar surface tension on alveolar epithelial permeability was studied in anesthetized closed-chest mongrel dogs. Alveolar surface tension was elevated by displacement of pulmonary surfactant from the alveolar hypophase by the aerosolized detergent dioctyl sodium sulfosuccinate (OT). After measurement of baseline hemodynamics, arterial blood gases, and airway pressure, the dogs were separated into groups: Group I inhaled a 1% solution of OT (15 mg/kg) in a vehicle of equal parts saline and ethanol; group II inhaled the same volume of vehicle without OT. The pulmonary clearance of technetium 99m diethylenetriamine-pentaacetic acid (99mTc-DTPA) (half-time in minutes) was studied immediately after aerosol (OT and vehicle) delivery and compared with that of historical control values. No change was seen in arterial blood gases and airway pressure after vehicle inhalation, whereas OT caused a marked fall in arterial oxygen tension and increase in airway pressure. Vehicle inhalation effected only a slight increase in DTPA clearance, whereas OT significantly reduced half-time over control and group II. These data suggest that high alveolar surface tension increases alveolar epithelial permeability.     

Scientific and regulatory issues relevant to assessing risk for developmental neurotoxicity: an overview

The effects of chemical exposure on the developing nervous system have been documented in both humans and animals for a variety of agents. However, the comparability of these effects has not been carefully evaluated to determine the predictability of animal models to adverse effects in humans. A workshop sponsored by the U.S. Environmental Protection Agency (EPA) and the National Institute on Drug Abuse was held on April 11-13, 1989, to address the Qualitative and Quantitative Comparability of Human and Animal Developmental Neurotoxicity. Invited experts were asked to review the human and animal data on several agents that are known to cause developmental neurotoxicity in humans, including lead, methylmercury, selected abused agents, anticonvulsants, polychlorinated biphenyls (PCBs), ethanol and X-irradiation, and to make quantitative comparisons on a specific end point basis as well as on a functional category basis. In addition, they were asked to make quantitative comparisons when adequate dose-effect data were available. The data also were evaluated in the context of the proposed EPA developmental neurotoxicity testing battery to determine whether or not the battery would adequately detect the effects of each agent. Finally, four work groups were asked to reach consensus on issues relating to: 1) comparability of end points across species for developmental neurotoxicity; 2) testing methods in developmental neurotoxicity for use in human risk assessment; 3) weight-of-evidence and quantitative evaluation of data from developmental neurotoxicity studies; and 4) triggers for developmental neurotoxicity testing.     

Effects of epinephrine on retinal and choroidal blood flow through different routes of drug administration

Epinephrine (1, 3 and 10 micrograms/kg) was found to increase retinal and choroidal blood flow (22, 49 and 67%) when it was administered intravenously. The increase in retinal and choroidal blood flow coincided well with the increase in systemic blood pressure (44, 65 and 96%, respectively). When epinephrine (2%) was instilled to the eyes topically the retinal and choroidal blood flow decreased (15%) while systemic blood pressure remained unchanged. It is suggested that the decrease in retinal and choroidal blood flow by topical epinephrine could be the cause of epinephrine maculopathy reported previously. L-Timolol (0.25%, topically) did not affect retinal and choroidal blood flow significantly.     

Hereditary characteristics of enzyme deficiency and dermatoglyphics in congenital color blindness

The hereditary characteristics of enzyme deficiency and dermatoglyphics in congenital color blindness (CCB) were studied. We propose that there is a linkage between the two loci on the X-chromosome determining CCB and glucose-6-phosphate dehydrogenase (G6PD), based on our study of a high incidence of G6PD deficiency in 156 male cases with CCB. The CCB gene is closely linked with that of G6PD deficiency from our pedigree investigations. The rise in the frequency of eight or more whorls, the low value of atd angle and the presenting rate of real palmar patterns of the thenar, hypothenar and I, areas presented the hereditary traits of congenital color blindness.     

Uveal effusion syndrome

The history and clinical findings are presented of a patient who suffered from the uveal effusion syndrome over a 10-year period from 1956. The funduscopic appearance is illustrated both at the time of initial presentation and 36 years later. This condition typically affects healthy middle-aged men and causes recurrent, spontaneous, serous retinal and ciliochoroidal detachments, often resulting in significant visual impairment. Two separate hypotheses have been postulated to explain the pathogenesis of the uveal effusion syndrome, one relating to abnormally thickened sclera, the other to chronic bulbar hypotony. Both are discussed, as is the rationale behind the current management of this unusual condition.