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Biomedical subjects

L Bowman

Publications and source records attributed to L Bowman.

At least 73 records · Page 4Linked to original sources
PubMed1991

Reinforcement of incontinent stools in the treatment of encopresis.

In this paper, fecal incontinence and constipation were treated in two mentally retarded individuals using a novel intervention wherein incontinent stools were first rewarded in order to increase the frequency of bowel movements. This intervention was implemented only after more traditional pediatric and behavioral treatments were unsuccessful. The reinforcement of incontinent stools procedure resulted in an increase in both the frequency and the number of continent stools for both individuals. Hypotheses regarding the failure of previous treatments and the success of the current treatment are discussed as well as directions for future research.

Adolescent↗
PubMed1990

Plant DNA topoisomerase I is recognized and inhibited by human Scl-70 sera autoantibodies.

Type I topoisomerases (EC 5.99.1.2) are those enzymes capable of relaxing negatively supercoiled DNA without the need for ATP. The central role played by these enzymes in cell function suggests that the structure of type I topoisomerases may be highly conserved in eukaryotic cells. However, the extent of the conservation among eukaryotes is unknown. Human DNA topoisomerase I is an autoimmune antigen (Scl-70) of scleroderma patients. We have found that the autoimmune antibodies in human Scl-70 sera recognize protein from various plants, and these proteins display DNA relaxation function. In addition, Scl-70 antibodies were able to inhibit enzymatic activity of plant topoisomerase I. Therefore, the immunological cross-reactivity of the plant topoisomerase with human antibodies demonstrates that, despite divergence of eukaryotic organisms, these plant and animal enzymes retain structurally similar enzymatic features.

Autoantibodies↗
PubMed1990

Aberrant sleep patterns in children with the Rett syndrome.

Previous studies on the characteristics of disturbed sleep/wake patterns in children with the Rett syndrome have yielded inconsistent findings. In the current study, momentary time sampling procedures were used to measure the sleep/wake patterns of 20 girls with classical Rett syndrome. These patients had significantly more total sleep than age peers (M = 110.1; Zm = 2.58; p = .01), significantly less nighttime sleep (M = 80.8; Zm = -7.53; p less than .0001), and significantly more daytime sleep (M = 24.5; Zm = 8.71; p less than .0001). Night sleep was negatively correlated with age (r = -.59; p less than .01); day sleep was positively correlated with age (r = .54; p = .01). These girls also displayed night wakings on 20.9% of nights, delayed sleep onset on 67.8% of nights and early wakings on 24.5% of nights. These data clearly demonstrate that children with the Rett syndrome have markedly impaired sleep/wake patterns and suggests that the sleep dysfunction may worsen over time.

Adolescent↗
PubMed1990

Metabolic changes in alveolar type II cells after exposure to hydrogen peroxide.

Since oxygen metabolites may play an important role in pulmonary oxidant injury, the effects of hydrogen peroxide (H2O2) on energy metabolism in alveolar type II cells isolated from rats were studied. The major effect of H2O2 is a rapid and dramatic reduction in the steady-state level of cellular ATP; e.g., ATP levels are reduced by 77 +/- 3% after only 5 min of exposure to H2O2 (0.5 mM). Cellular oxygen consumption is affected in a similar manner, suggesting that ATP synthesis is impaired. Experiments with isolated lung mitochondria demonstrate that exposure to 0.5 mM H2O2 for 5 min inhibits the rate of mitochondrial ATP synthesis by 51 +/- 3%. The site of mitochondrial ATP synthesis inhibition by H2O2 appears to be the adenosinetriphosphatase-synthase enzyme complex which phosphorylates ADP to ATP. Mitochondrial electron transport is unaffected. The association of 3-O-methylglucose with type II cells and glycolytic metabolism, measured as lactate production, are reduced by 25-35% by H2O2. The data also show that the cells are capable of recovery following exposure to H2O2, at least at lower exposure levels. These results indicate that exposure of type II cells to H2O2 alters the energy state of the cells by decreasing ATP synthesis. In turn, other important cellular functions may be impaired.

3-O-Methylglucose↗
PubMed1989

Carbon tetrachloride inhibits synthesis of pulmonary surfactant disaturated phosphatidylcholines and ATP production in alveolar type II cells.

Other studies have shown that inhalation of carbon tetrachloride (CCl4) decreases the amount of pulmonary surfactant lining the alveolar surface. Therefore, we studied the effects of CCl4 on the synthesis of surfactant phosphatidylcholines (PCs) in rat alveolar type II cells in vitro. The rate of incorporation of choline, palmitate or glycerol into disaturated PC (DSPC) is decreased in a concentration-dependent manner. The CCl4 concentrations which cause maximal inhibition and 50% inhibition are similar for each substrate. The rate of incorporation of choline or glycerol into total PC is diminished to the same extent as their incorporation into DSPC. In addition, the rate of incorporation of glycerol into phosphatidylglycerol is decreased by the same extent as its incorporation into PC. All of these data suggest that there is a common site(s) at which CCl4 inhibits PC synthesis and that the inhibition occurs early in the biosynthetic pathway. However, individual enzymes involved in phospholipid synthesis do not seem to be affected by the solvent. Exposure of alveolar type II cells to CCl4 does cause a rapid and dramatic loss in cellular ATP, a cofactor required by some enzymes involved in PC synthesis. Studies with isolated lung mitochondria suggest that CCl4 inhibits the enzyme complex which catalyzes the synthesis of ATP from ADP. In addition, CCl4 causes a decrease in the amount of 3-O-methylglucose associated with type II cells, suggesting that glucose influx is impaired. This may also contribute to lower cellular ATP levels. The results of this study suggest that inhalation of CCl4 may impair surfactant phospholipid synthesis by decreasing ATP levels in alveolar type II cells.

Adenosine Triphosphate↗
PubMed1989

Aminoglycoside dosing in pediatric patients.

We assessed the performance of a predictive algorithm for dosing aminoglycoside antibiotics in 75 pediatric patients and Bayesian feedback in 36. The absolute errors for peak and trough concentrations were 1.83 and 0.80 micrograms/ml, respectively, which seem clinically acceptable for most patients. However, the algorithm had significant negative bias for both peaks and troughs. Implementation of Bayesian feedback eliminated bias in a second set of concentrations and significantly decreased its magnitude for both peaks (p = 0.028) and troughs (p = 0.005). This method may allow more accurate dosing of aminoglycoside antibiotics in pediatric patients, though it would most likely be improved by better definition of population parameters and their variability.

Algorithms↗
PubMed1989

Nitroglycerin delivery through a polyethylene-lined intravenous administration set.

Adsorption and delivery of nitroglycerin through a new polyethylene-lined (PEL) i.v. administration set was compared with adsorption and delivery through an identical set composed of polyvinyl chloride (PVC) rather than PEL tubing. The new delivery system consisted of PEL tubing, a transparent PVC chamber, and a silastic segment for insertion in a peristaltic pump. Nitroglycerin was prepared in concentrations of 50, 125, and 200 micrograms/mL in 0.9% sodium chloride injection and run through both administration sets at flow rates of 12 and 60 mL/hr. Samples were obtained at 0, 0.5, 1, 2,4, and 8 hours from each of three sites: bottle, junction before silastic segment, and distal end of tubing. Nitroglycerin content was assayed using a modified high-performance liquid chromatography technique. A slight but significant average loss of nitroglycerin (2.3 +/- 9.3%) was observed at the distal end with the PEL set, whereas the PVC set showed a significant average nitroglycerin loss of 39.7 +/- 12.7% at the distal end. These differences were independent of infusion rate, nitroglycerin concentration, or time of sampling. Flow rate, concentration, and time had no significant effect on nitroglycerin adsorption with the PEL set, but all three had a significant effect on nitroglycerin adsorption with the PVC set. An unexpected finding was the approximately 14% loss of nitroglycerin from the admixture bottle over time. This phenomenon, which has been observed by other investigators, needs further investigation to determine its cause. It appears that a partially PVC-based administration set should provide consistent delivery of i.v. nitroglycerin to the patient.

Chemistry, Pharmaceutical↗
PubMed1988

Association of chlorphentermine with phospholipids in rat alveolar lavage materials, alveolar macrophages and type II cells.

Administration of chlorphentermine to rats leads to an increase in the phospholipid content of pulmonary surfactant materials and alveolar macrophages. It is known that this drug binds to pure phospholipids and prevents their degradation by phospholipases. Therefore, experiments were carried out to determine if chlorphentermine binds to surfactant phospholipids in vitro and to measure the in vivo association of drug with phospholipids in alveolar lavage materials from rats injected with [14C]chlorphentermine. The presence of chlorphentermine in alveolar macrophages, type II cells and other small pneumocytes (a population of lung cells which does not include alveolar macrophages or type II cells) from treated animals was also assessed. Binding of the drug to surfactant phospholipids, as measured with the fluorescent probe, 1-anilino-8-naphthalene sulfonate, occurs in vitro and does not differ in various subfractions of alveolar lavage materials isolated by differential centrifugation. Following daily administration of chlorphentermine to rats for 3 days, the drug appears to be associated with surfactant phospholipids such that the molar ratio is 1:100 (chlorphentermine/phospholipid). Chlorphentermine is also associated with alveolar macrophages (molar ratio, 1:18) and type II cells (molar ratio, 1:33). Not much drug is associated with the population of other lung cells (molar ratio, 1:333). In alveolar macrophages, approx. 70% of the drug seems to be bound to phospholipid and/or sequestered in subcellular organelles. However, only 20% of the chlorphentermine is bound and/or sequestered in type II cells. The results of these experiments suggest that following chlorphentermine administration, the drug is associated with phospholipids in acellular pulmonary lavage materials, alveolar macrophages and type II cells. This drug-phospholipid interaction may impair phospholipid degradation and lead to a phospholipidosis in surfactant materials and alveolar macrophages.

Animals↗
PubMed1988

Preservation of left ventricular ejection fraction during percutaneous transluminal coronary angioplasty by distal transcatheter coronary perfusion of oxygenated Fluosol DA 20%.

The cardioprotective efficacy of coronary perfusion during angioplasty was evaluated. Forty-two patients underwent transcatheter infusion of oxygenated Fluosol DA, 20% emulsion (FDA-20), a perfluorocarbon oxygen transport fluid, into the distal coronary artery during balloon inflations. Left ventricular function was continuously monitored by two-dimensional echocardiography, and left ventricular ejection fraction was quantitatively analyzed from the video record by an area-length method with a validated computer algorithm. Each patient had multiple nonperfused and perfused balloon inflations lasting more than 45 seconds. Nineteen of the 42 patients also received control solutions of oxygenated Ringer's lactate and nonoxygenated FDA-20. The ejection fraction of nonperfused sequences fell from a baseline value of 57 +/- 15% to 36 +/- 14% at 45 seconds of inflation time (p less than 0.0005). Falls of similar magnitude were seen in the lactated Ringer's and nonoxygenated FDA-20 perfused balloon inflations. The ejection fraction fall was associated with a 54% rise in end-systolic volume (p less than 0.0005) and a 4% rise in end-diastolic volume (p = ns) compared to baseline. Inflations perfused with oxygenated FDA-20 showed a 45-second, left ventricular ejection fraction of 53 +/- 13% (p = ns compared to baseline), which was significantly greater (p less than 0.0001) than the 45-second ejection fraction of the nonperfused, or control solution perfused sequences. Results indicate that the profound fall in ejection fraction occurring during percutaneous transluminal coronary angioplasty can be ameliorated by distal coronary perfusion with an oxygenated perfluorocarbon emulsion.

Adult↗
PubMed1988

Degradation of pulmonary surfactant disaturated phosphatidylcholines by alveolar macrophages.

Experiments were performed to determine whether rat pulmonary surfactant disaturated phosphatidylcholines (DSPC) are degraded by alveolar macrophages in vitro. When [3H]choline-labeled surfactant materials are incubated with unlabeled alveolar macrophages, approximately 40% of the labeled DSPC is broken down in 6 h. There is just a slight decrease in the specific activity of DSPC, which suggests that most products of degradation are not reincorporated into DSPC, at least during the 6-h incubation period. There is a time- and temperature-dependent association of surfactant DSPC with alveolar macrophages, and some of the cell-associated materials are released from the cell fragments after sonication. Association of surfactant with the cells precedes degradation. The breakdown of surfactant DSPC by intact alveolar macrophages lags behind that produced by sonicated cell preparations with disrupted cell membranes. These data and other information suggest that the surfactant materials are internalized by the cells, before the breakdown. The products of degradation probably include free choline and fatty acids, most of which appear in the extracellular fluid. The breakdown processes do not seem to depend on the physical form of the surfactant or on the presence of surfactant apoproteins. Incubation of the cells alone also results in disappearance of intracellular DSPC, some of which may be surfactant phospholipid taken up by the cells in vivo. These results indicate that alveolar macrophages can degrade surfactant DSPC and suggest that these cells may be involved in catabolism of pulmonary surfactant materials.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1986

Alterations in rat alveolar surfactant phospholipids and proteins induced by administration of chlorphentermine.

Chlorphentermine is a cationic amphiphilic drug which produces a phospholipid storage disorder in rat lungs. Experiments were carried out to characterize changes in the composition of acellular alveolar lavage materials and to study possible mechanisms by which pulmonary surfactant phospholipidosis is produced by administration of the drug. Following ten daily injections of chlorphentermine (25 mg/kg body weight), there are 12.2- and 13.6-fold increases of pulmonary lavage total phospholipids and disaturated phosphatidylcholines (disaturated PC), respectively. In addition, there is a 2.8-fold increase in total protein and a 12.7-fold increase in the surfactant apoprotein group with molecular weights from 28,000 to 32,000. We measured incorporation of labeled palmitate, choline and glycerol into disaturated PC in type II cells and alveolar macrophages isolated from control and chlorphentermine-treated animals. The drug does not affect the incorporation of labeled substrates into disaturated PC in either cell type. However, in alveolar macrophages there is a decrease in the rate of intracellular degradation of recently synthesized disaturated PC in chlorphentermine-treated animals. The drug also inhibits the phospholipase-induced catabolism of rat surfactant disaturated PC which occurs during incubation of alveolar lavage fluid in vitro at 37 degrees C. When the lavage fluid is divided into subfractions by differential centrifugation, a larger percentage of the phospholipid is distributed in the less sedimentable subfractions in chlorphentermine-treated animals relative to controls, suggesting the accumulation of older surfactant materials. These results suggest that chlorphentermine-induced phospholipidosis of pulmonary surfactant materials is due to decreased rates of phospholipid degradation.

Animals↗
PubMed1985

Response to measles vaccine in Haitian infants 6 to 12 months old. Influence of maternal antibodies, malnutrition, and concurrent illnesses.

To study the factors affecting the serologic response to measles vaccination, we evaluated 595 Haitian infants from 6 through 12 months of age, and their mothers, at the beginning of an immunization program. Thirty-four per cent of the infants had preexisting serologic evidence of measles infections by 11 months of age. Among infants more than nine months of age, those who had had measles had a significantly lower nutritional status than those who had not (P less than 0.01). After vaccination, seroconversion rates increased from 45 per cent at 6 months to 100 per cent at 12 months. The lowest rate of vaccine failure compatible with acceptably low rates of natural infections could be achieved by vaccination after eight months of age. Infants born to mothers with low levels of antibody to measles (hemagglutination-inhibition antibody titers less than 1:40) were significantly more likely to have had natural measles (P less than 0.01) or to have seroconversion after vaccination (P less than 0.001) at 6 to 10 months of age than were infants born to mothers with higher of age than were infants born to mothers with higher titers. Malnutrition and acute infections did not affect seroconversion rates. These data support the World Health Organization recommendation to administer measles vaccine in under-developed countries as soon after nine months of age as possible, regardless of nutritional status or the presence of minor illnesses.

Age Factors↗
PubMed1985

Catabolism of rat surfactant disaturated phosphatidylcholines during incubation of alveolar lavage materials in vitro at 37 degrees C.

Incubation of rat alveolar lavage materials in vitro at 37 degrees C results in degradation of the endogenous surfactant disaturated phosphatidylcholines (disaturated PC). When exogenous dipalmitoylphosphatidylcholine (DPPC) vesicles are incubated with lavage materials, there is catabolism of the DPPC. The degradation process is temperature- and Ca2+-dependent and has a pH optimum of 6.5-7.0. The products formed during catabolism of [3H]palmitate- and [14C]choline-labeled disaturated PC are free palmitate and water-soluble choline products. No lysophosphatidylcholines are formed. Measurements of lactate dehydrogenase levels in lavage fluid, use of more gentle lavage techniques, use of Ca2+, Mg2+ and protein in the lavage medium, and measurements of bacterial contamination all suggest that enzymes are neither released into pulmonary lavage fluid via cellular damage nor are bacterial in origin. Degradation of surfactant disaturated PC does not occur during incubation of lavage materials from rabbits, mice or guinea pigs. These results suggest that phospholipases and/or lysophospholipases are present in rat alveolar lavage materials. Possible origins of these enzymes are discussed.

Animals↗
PubMed1985

Incorporation of [3H]palmitate and [14C]choline into disaturated phosphatidylcholines in rat alveolar macrophages.

We studied the synthesis of disaturated phosphatidylcholines in rat alveolar macrophages and, in some cases, compared it with that which occurs in isolated alveolar type II cells. Alveolar macrophages suspended in phosphate-buffered medium incorporate palmitate, choline and glycerol into disaturated phosphatidylcholines. The time-course for incorporation of palmitate into disaturated phosphatidylcholines is linear for 20-30 min and reaches a maximum in 2-3 h. Incorporation is dependent on extracellular palmitate with a Vmax (at 1 mM) of 1.53 nmol palmitate incorporated into disaturated phosphatidylcholines per 5 X 10(5) cells per 2 h and a K 1/2 of 0.19 mM palmitate. Exposure of the cells to zymosan particles increases incorporation of palmitate disaturated phosphatidylcholines by almost 2-fold, while cholinergic and beta-adrenergic agonists have no effect. On a per cell basis, alveolar macrophages incorporate only one-third to one-half as much palmitate into disaturated phosphatidylcholines as do type II cells isolated by centrifugal elutriation. The following results suggest there is extensive remodeling of disaturated phosphatidylcholines in alveolar macrophages: (1) palmitate- and choline-labeled disaturated phosphatidylcholines are catabolized by the cells; (2) the products of catabolism are palmitate and water-soluble choline products; (3) addition of unlabeled palmitate and choline to the medium enhances catabolism of the labeled phospholipid. Addition of oleate also enhances catabolism, suggesting that modification of phospholipids is not specific for the saturated variety. Some of the recently labeled disaturated phosphatidylcholines is released from alveolar macrophages into the extracellular space. Several possible functions of alveolar macrophage disaturated phosphatidylcholines are discussed.

Animals↗
PubMed1985

The response of rat alveolar macrophages to chronic inhalation of coal dust and/or diesel exhaust.

The use of diesel-powered equipment in underground mines has raised questions regarding possible synergistic effects of coal dust and diesel emissions. Therefore, the effects of chronic exposure of rats to coal dust and/or diesel exhaust on various properties of alveolar macrophages were investigated. Inhalation exposure of rats was 7 hr/day, 5 days/week for 2 years. Exposure groups were: filtered air controls, 2 mg/m3 coal dust, 2 mg/m3 diesel particulate, and 1 mg/m3 coal dust plus 1 mg/m3 diesel exhaust. Exposure to coal dust and/or diesel exhaust had little effect on oxygen consumption, membrane integrity, lysosomal enzyme activity, or protein content of alveolar macrophages. However, exposure to coal dust increased macrophage yield, enhanced chemiluminescence, and increased the activity of the cell membrane (i.e., increased cellular spreading and surface ruffling). In contrast, diesel emissions depressed chemiluminescence and decreased the ruffling of the cell membrane. Therefore, the data suggest that exposure to coal dust and/or diesel exhaust does not affect the viability of alveolar macrophages. However, coal dust may activate alveolar macrophages while diesel emissions may depress the phagocytic activity of these cells. The combination of exposures to coal dust and diesel exhaust results in a phagocytic activity which is an average of the effects of separate exposures.

Animals↗