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Biomedical subjects

J H Knelson

Publications and source records attributed to J H Knelson.

15 recordsLinked to original sources
PubMed1978

Spirometric changes in normal children with upper respiratory infections.

Recent evidence that certain uncomplicated upper respiratory infections induce pulmonary function abnormalities in adults prompted a prospective study in children, in whom such infections occur more frequently. In a longitudinal study, 55 children 2.5 to 11 years of age were observed for a mean duration of 2 years. Spirometry and lung volume studies were obtained routinely every 3 months, during each upper respiratory infection, and 4 weeks after illnes, providing data for 617 "well" and 237 "illness" observations. After grouping of data by sex and age (less than 84 of greater than 84 months), each spirometric parameter was analyzed using linear regression with individual identification, height, and clinical status (normal versus upper respiratory illness) as independent variables. Adjusted mean values of forced vital capacity, 1-sec forced expiratory volume, peak expiratory flow, maximal mid-expiratory flow, and expiratory flow at 50 per cent of the forced vital capacity all decreased during upper respiratory illness. The data suggest that lower respiratory tract involvement without signs or symptoms of lower airway or alveolar disease occurs with upper respiratory illnesses of varied etiologic origin in childhood.

Body Height↗
PubMed1977

Cytogenetic effects of inhaled ozone in man.

Peripheral blood samples were collected from 30 normal male volunteers before and at intervals after inhaling 0.4 ppm ozone for 4 h. Data from 4 of the subjects were excluded from the analysis because of missing data points. The blood samples were cultured for 48 h, slides made and stained with a uniform Giemsa stain, and 100 metaphase spreads per subject per treatment scored for chromosome aberrations. Cells with suspected aberrations were photographed, destained, restained with a banding procedure and rephotographed to identify the specific chromosomes and regions involved. Pre-exposure, immediate post-exposure, 3 days post-exposure, 2 weeks post-exposure and 4 weeks post-exposure means for the percentage of cells with 46 chromosomes were 93.0, 93.6, 91.7, 94.5 and 94.2, respectively; in the same order, the mean number of cells with chromatid and/or chromosome breaks per order, the mean number of cells with chromatid and/or chromosome breaks per 100 cells was 0.96, 0.85, 1.00, 0.88 and 0.81 respectively, and for chromatid and/or chromosome gaps per 100 cells: 1.35, 0.96, 1.35, 0.81 and 0.77, respectively. The means for each of these parameters as well as the mean frequencies of complex aberrations are not statistically significantly different between blood sampling times. The distribution of aberrations by chromosome and light and dark bands is not significantly influenced by ozone exposure. These data indicate no apparent detectable human cytogenetic effect due to exposure to ozone under the conditions of this experiment.

Adult↗
PubMed1977

Whole and disaturated lung phosphatidylcholine in cortisol-treated, intrauterine growth-retarded and twin control lambs at different gestational ages.

Lambs 116--124 days gestation infused in utero for 75 h with cortisol showed, when compared to twin controls, more mature lung histology and pressure-volume relationships. 32P orthophosphate incorporation into whole lung phosphatidylcholine (PC) was increased in the four cortisol-treated lambs at 116--117 days but not at 121, 123, and 124 days gestation. 14C palmitate incorporation into PC or disaturated phosphatidylcholine (DSPC) was not enhanced at 116--117 days gestation. At 121 days in a cortisol-treated and at 128 days in a growth-retarded lamb fetus not treated with cortisol, a larger quantity of DSPC was present although the incorporation of 14C palmitate into DSPC per milligram DNA was the same. This indicated that the synthesis of DSPC had been initiated in the cortisol-treated and growth-retarded animals prior to the controls and at the time of sacrifice both were incorporating 14C palmitate at a similar rate suggesting similar rates of synthesis.

Animals↗
PubMed1974

Problem of estimating respiratory lead dose in children.

Children may be exposed to lead in their environment by a variety of mechanisms, but the final two common pathways involve ingestion and/or inhalation. The serious public health problem of overt lead intoxication from eating lead-based paint has tended to obscure low level toxicity which may be related to atmospheric lead pollution. No data exist which relate potential body burden or blood lead levels in children to ambient air lead levels. Extrapolation from respiratory lead uptake kinetics in adults is complicated by the differences in respiratory physiology, metabolism, and body compartment sizes existing between children and adults. These differences and models from pediatric pharmacology have been used to approach the problem of predicting respiratory lead dose in children from data based on adult uptake studies.

Adolescent↗
PubMed1972

Changes in the alveolar lining with onset of breathing.

Changes in the alveolar lining of newborns were investigated by sacrificing rabbits at birth and at intervals shortly after birth, and examining their lungs in the electron microscope. An orderly, reproducible sequence of changes in the Type II alveolar lining cells and alveolar space was demonstrated, and the observations correlated well with biochemical events. Type II cell inclusions, dense and numerous at birth, enlarged and became less dense ((1/2)-1 hour), appeared to empty their contents into the alveolar space and disappear (1(1/2) hours) and then reappeared with a mixture of sizes and densities in each cell (2 hours). Few lamellar figures were present in the alveolus at birth, the number reaching a maximum at 1(1/2) hours and then decreasing. The first evidence of a noncellular alveolar lining was at 1(1/2) hours, when lamellar figures and granular material adhered to small corners of the alveolar wall. At 2(1/2) hours, a thick dense layer covered much of the wall. At 6 hours, the layer was thinner and denser, and at 24 hours the thin osmiophilic surfactant lining was present.

Animals↗