Decreased erythrocyte Na+,K(+)-ATPase activity associated with cellular potassium loss in extremely low birth weight infants with nonoliguric hyperkalemia

To determine whether a shift of potassium ions from the intracellular space to the extracellular space accounts, in part, for the hyperkalemia seen in extremely low birth weight infants, we examined potassium concentration in serum and erythrocytes from extremely low birth weight infants with hyperkalemia (n = 12) or with normokalemia (n = 27). In addition, to determine whether the shift of potassium was associated with low sodium-potassium-adenosinetriphosphatase (Na+,K(+)-ATPase) activity, we studied the activity of ATPase in the last 16 infants enrolled in the study. Fluid intake and output were measured during the first 3 days of life. Infants were considered to have hyperkalemia if the serum potassium concentration was 6.8 mmol/L or greater. Blood was obtained daily for intracellular sodium and potassium levels by means of lysis of erythrocytes. The remaining erythrocyte membranes were frozen and analyzed for Na+,K(+)-ATPase activity. There were significantly lower intracellular potassium/serum potassium ratios in the infants with hyperkalemia for each day of the 3-day study (p < 0.001). In the hyperkalemic group, there was lower Na+,K(+)-ATPase activity than in the infants with normokalemia (p = 0.006). Low Na+,K(+)-ATPase activity was associated with lower intracellular potassium/serum potassium ratios (p = 0.006), higher serum potassium values (p = 0.02), and lower intracellular potassium concentration (p = 0.009). The urinary data demonstrated that there was no difference in glomerulotubular balance between the two groups. We conclude that nonoliguric hyperkalemia in extremely low birth weight infants may be due, in part, to a shift of potassium from the intracellular space to the extracellular space associated with a decrease in Na+,K(+)-ATPase activity.     

Cross-infection control in Malaysian dental practice

STUDY OBJECTIVE: The aim was to study the spectrum of clinical problems and outcomes in infants born at an urban academic hospital. In consequence, as part of the overall study, the incidence of congenital anomalies and the outcomes of affected infants were recorded. DESIGN: This was a prospective, hospital-based study, undertaken on liveborn infants born over a 3-year period, 1 May 1986 to 30 April 1989. SETTING: Kalafong Hospital, Pretoria. MAIN RESULTS: A total of 17,351 liveborn infants was examined and the total congenital anomalies incidence was 11.87 per 1,000 livebirths. The central nervous system was the system most frequently involved (2.30 per 1,000 livebirths), followed by the musculoskeletal system (2.13 per 1,000 livebirths). The commonest individual congenital anomaly was Down syndrome (1.33 per 1,000 livebirths), followed by neural tube defects (0.99 per 1,000 livebirths) and ventricular septal defects (0.69 per 1,000 livebirths). In 11% (2.25 per 1,000 livebirths) of neonatal deaths, infant loss was attributable to congenital anomalies. CONCLUSIONS: The incidence of congenital anomalies in black South African neonates, born in an urban setting, is as high as in other First- and Third-World countries, and the incidence of some individual congenital anomalies is higher. This study indicates the need for further research and the establishment of prenatal, genetics and paediatric facilities to manage these problems.     

Organization of glutamate receptors at the synapse

Glutamate receptors can be divided in several groups with distinct functional properties. An additional level of complexity has emerged from recent high resolution immunogold analyses which have provided evidence for a differential targeting of glutamate receptors to specific subsynaptic membrane domains. Notably, different types of glutamate receptor may differ in their distance to the release site and in their spatial relation to glutamate transporters. These data imply that the subsynaptic expression of a given glutamate receptor may bias its response to a released quantum of transmitter and suggest that receptor targeting may be implicated in the modulation of glutamatergic neurotransmission.     

Mesoscopic inhomogeneities in Pb0.85 (Li1/2 La1/2)0.15 (Zr1-y TiY)O3 solid solutions in the vicinity of FE-AFE phase stability boundary

Results of the study of mesoscopic inhomogeneities in the Pb _0.85 (Li_1/2 La_1/2) _0.15 (Zr_1-y Ti_y)0₃ solid solutions system are presented. It is demonstrated that these formations have some peculiarities in solid solutions for which FE and AFE phases coexist     

Effect of vitamin E and beta carotene on the incidence of primary nonfatal myocardial infarction and fatal coronary heart disease

BACKGROUND: Oxidized low-density lipoprotein is involved in the pathogenesis of atherosclerosis. In epidemiological studies antioxidants have been inversely related with coronary heart disease. Findings from controlled trials are inconclusive. METHODS: We studied the primary preventive effect of vitamin E (alpha tocopherol) and beta carotene supplementation on major coronary events in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study, a controlled trial undertaken primarily to examine the effects of these agents on cancer. A total of 27 271 Finnish male smokers aged 50 to 69 years with no history of myocardial infarction were randomly assigned to receive vitamin E (50 mg), beta carotene (20 mg), both agents, or placebo daily for 5 to 8 years (median, 6.1 years). The end point was the first major coronary event, either nonfatal myocardial infarction (surviving at least 28 days; n = 1204) or fatal coronary heart disease (n = 907). RESULTS: The incidence of primary major coronary events decreased 4% (95% confidence interval, -12% to 4%) among recipients of vitamin E and increased 1% (95% confidence interval, -7% to 10%) among recipients of beta carotene compared with the respective nonrecipients. Neither agent affected the incidence of nonfatal myocardial infarction. Supplementation with vitamin E decreased the incidence of fatal coronary heart disease by 8% (95% confidence interval, -19% to 5%), but beta carotene had no effect on this end point. CONCLUSIONS: Supplementation with a small dose of vitamin E has only marginal effect on the incidence of fatal coronary heart disease in male smokers with no history of myocardial infarction, but no influence on nonfatal myocardial infarction. Supplementation with beta carotene has no primary preventive effect on major coronary events.