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Biomedical subjects

R J Roberts

Publications and source records attributed to R J Roberts.

At least 235 records · Page 13Linked to original sources
PubMed1981

alpha-Tocopherol (vitamin E) content of lung, liver, and blood in the newborn rat and human infant: influence of hyperoxia.

Increases in liver and lung alpha-tocopherol (vitamin E) content occur concurrent with birth and the onset of suckling in the newborn rat and are prevented by denying pups access to dams. Liver alpha-tocopherol concentration peaks at 24 hours of age and then declines, whereas the lung concentration of alpha-tocopherol continues to increase in the early neonatal period. These tissue changes are not reflected by changes in the blood alpha-tocopherol concentration. Significant increases in lung alpha-tocopherol result from administering alpha-tocopherol (100 mg/kg body weight, sc) on days 0, 2, and 4 of age. Studies of lung alpha-tocopherol concentrations in infants with varying histories of alpha-tocopherol exposure confirm the findings in the rat, and suggest that increases in lung alpha-tocopherol concentration result from administration of alpha-tocopherol in the immediate newborn period. Studies of alpha-tocopherol values in alpha-tocopherol-treated and control newborn rats reveal no significant changes in lung tocopherol concentration resulting from exposure to hyperoxia.

Animals↗
PubMed1981

Aminoglycoside dosage in pediatric patients:considerations regarding pharmacokinetic-based dose adjustment in patients requiring high versus low dose therapy.

Pharmacokinetic-based adjustment of individual aminoglycoside dosage regimens is currently being utilized in the clinical setting in an attempt to avoid toxicity and/or enhance efficacy. In this report, comparison have been made between initial and adjusted aminoglycoside dosage employed in toddlers and older children with cystic fibrosis or leukemia (high daily dose) and neonates (low daily dose) with suspected or proven infection. The initial versus adjusted mean aminoglycoside dosage was 14.1 and 17.0 mg/kg/day, respectively, in toddlers and older children with cystic fibrosis, and 7.1 and 11.5 mg/kg/day, respectively, in toddlers and older children with leukemia. Neonates with suspected or proven infection had an initial mean total daily dose of 7.4 mg/kg/day and the adjusted mean daily dose was 5.4 mg/kg/day. The use of a single pharmacokinetic dosing model for all patients, irrespective of evidence of increased or decreased drug elimination, results in widely differing drug dosages. Important and serious questions must be considered regarding the balance between efficacy and toxicity resulting from the rigid manner by which dosage adjustment protocols are employed.

Adolescent↗
PubMed1981

The development of the newborn rat lung in hyperoxia: a dose-response study of lung growth, maturation, and changes in antioxidant enzyme activities.

To examine the dose-response relationships of oxygen-induced lung changes, newborn rats were exposed to various patterns of concentrations of hyperoxia (0.4, 0.8, and greater than 0.95 FiO2) for up to 12 days. Prominent findings included microscopic evidence of lung injury and retarded alveolar development (secondary septal development delayed by as much as 88%), lower whole lung DNA (50% of control), lung-to-body-weight ratios (by as much as 18%), and significantly less compliance in the lungs afer exposures of 6 or 12 day duration to all concentrations of hyperoxia. Significant increases in the activities of the lung protective enzymes superoxide dismutase (129 to 160% of control), catalase (112 to 274% of control), and glutathione peroxidase (118 to 256% of control) were noted when activity was expressed on a DNA basis after 12 day exposures to the various patterns of hyperoxia. Lung changes noted after a 7-day recovery period in air included interstitial thickening (117% of control), persistance of the microscopic injury, and retarded alveolar development seen immediately after initial 6-day hyperoxic exposures. At the conclusion of a second wk of recovery in air, the lungs of hyperoxic exposed animals resembled controls in most respects, but a significantly altered compliance was exhibited by the lungs of animals initially exposed to 6 days of 0.4 or greater than 0.95 FiO2. The dose dependency of oxygen-induced lung injury is complex. Straightforward, stepwise dose-response adequately describes the evolution of microscopic injury and slowing of alveolar development in hyperoxia, but the dose dependency is not as clearly identified in the oxygen-induced retardation of lung growth including DNA content and in changes in antioxidant enzyme activities. Changes in lung compliance clearly do not follow expected dose response relationships.

Animals↗
PubMed1980

Steps toward computer analysis of nucleotide sequences.

Advances in recombinant DNA technology have allowed the isolation of large numbers of biologically interesting fragments of DNA. Concomitant improvements in methods for nucleic acid sequencing have led many investigators to characterize their clones by sequencing them. This has resulted in the accumulation of such large amounts of sequence data that computer-assisted methods, with programs directed toward the manipulation of nucleic acid sequences, have become indispensable during the collection and analysis of that data.

Autoanalysis↗
PubMed1980

Oxygen-induced lung injury in the newborn piglet.

Oxygen-induced lung toxicity was studied in artificially fed newborn miniature piglets. Paired littermates of newborn piglets were exposed to either 96-98% oxygen or air for 2, 4, 7 or 10 days. Development of pulmonary edema, as monitored by both the lung wet weight to dry weight ratio and the lung wet weight to body weight ratio, was evident 4 days after the start of oxygen exposure. Examination of light and electron micrographs showed that pulmonary edema was located mainly in the perivascular and interstitial spaces. Endothelial and type I cells were normal in appearance throughout the oxygen exposure. After exposure to 10 days of oxygen, type II cells appeared to show a decrease in the size of lamellar bodies and an increase in the number and size of mitochondria. The activity of pulmonary antioxidant defenses, as measured by the activity of superoxide dismutase (SOD), glutathione peroxidase (GP) and glutathione reductase (GR), and the level of reduced glutathione (GSH), showed a progressive increase in activity with duration of oxygen exposure, culminating in a significantly higher SOD, GP and GSH level in 7-day oxygen-exposed piglets. It is concluded that the newborn piglet is less susceptible to oxygen-induced lung injury compared to adults of other species, and the increase in the lung complement of SOD, GR, GP and GSH may contribute to the apparent resistance to oxygen toxicity.

Animals↗
PubMed1980

Morphologic disturbance of lung maturation in fetuses of alloxan diabetic rabbits.

Maturation of lungs was studied morphologically in fetuses of does made diabetic with alloxan. The lungs of fetuses of does treated with alloxan 24 h after mating appeared to be less mature than control lungs, as shown by significant decrease in areal density of air space (p < 0.01) and by increases in areal density of alveolar epithelium and capillaries (p < 0.02). In alloxan fetuses, ultrastructural techniques revealed that type II cells had 10 times the control value for areal density of glycogen (p < 0.01) and 2.5 times that of rough endoplasmic reticulum (p < 0.05), but the proportion of type II cells and the number of lamellar bodies per type II cell profile were similar in both groups. Ultrastructural examination of capillaries demonstrated that their migration and the fusion of their basement membrane with that of alveolar epithelium did not occur as frequently in alloxan fetuses as in control fetuses. Biochemically, the lungs of alloxan fetuses contained significantly more glycogen and protein (p < 0.01) than control lungs, but the deoxyribonucleic acid was similar. The alloxan fetuses had a disturbance of lung structural maturation that was consistent with our previous findings of delayed functional maturation without accompanying change in disaturated phosphatidylcholine levels and ratio of lecithin to sphingomyelin.

Animals↗
PubMed1980

Carbon monoxide intoxication in children.

Carbon monoxide poisoning is currently a danger of ill-defined proportions in the pediatric population. A patient with possible residual neurologic effects from carbon monoxide as well as a retrospective study of pediatric patients with acute diagnosis of carbon monoxide poisoning has been presented. Although it has been impossible to conclude from these cases alone that carbon monoxide can produce residual neurological injury in children, evidence to support this concern can be found in the data presented and existing literature. First, the acute manifestations of carbon monoxide poisoning in the children are similar to those reported for adults who are known to suffer from residual neurological effects. Second, experimental studies in neonatal animals have produced effects which persist several weeks to months after the acute exposure to carbon monoxide. More information is needed regarding the long-term effects of carbon monoxide on the pediatric population. It may be totally inappropriate to establish "safe carbon monoxide levels" for children on the basis of experience from adult exposure.

Adolescent↗
PubMed1979

Computer programs for the assembly of DNA sequences.

A collection of user-interactive computer programs is described which aid in the assembly of DNA sequences. This is achieved by searching for the positions of overlapping common nucleotide sequences within the blocks of sequence obtained as primary data. Such overlapping segments are then melded into one continuous string of nucleotides. Strategies for determining the accuracy of the sequence being analyzed and reducing the error rate resulting from the manual manipulation of sequence data are discussed. Sequences mapping from 97.3 to 100% of the Ad2 virus genome were used to demonstrate the performance of these programs.

Adenoviridae↗