Biomedical subjects
D O Gebhardt
Publications and source records attributed to D O Gebhardt.
The distribution of o,p'-DDD (mitotane) among serum lipoproteins in normo- and hypertriglyceridemia.
We found that the distribution of the lipophilic chemotherapeutic agent o,p'-DDD (mitotane) among serum (lipo)proteins was altered in hypertriglyceridemia, with relatively more o,p'-DDD accumulating in the chylomicron and very-low-density lipoprotein (VLDL) fraction. Intralipid, an artificial chylomicron emulsion, or isolated VLDL could extract o,p'-DDD from the other serum (lipo)proteins. There was an inverse relationship between the relative amount of o,p'-DDD found in the fraction exhibiting a density of less than 1.006 g/ml (chylomicrons plus VLDL) and the relative amount observed in the LDL or HDL fractions of serum. Our results indicate that hypertriglyceridemia may impede the entry of o,p'-DDD into the brain or the adrenals. For therapeutic monitoring of o,p'-DDD levels in severe hypertriglyceridemia, we recommend that the chylomicron and VLDL fraction first be removed from the serum by ultracentrifugation.
Quantitative determination of plasma lipoproteins.
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Heterogeneity of lipoprotein A-I.
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Distribution of lipophilic xenobiotics among plasma lipoproteins.
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Fluorescence polarization of amniotic fluid as an index of fetal lung maturity.
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A semi-automated and standardized method of determining the lamellar body content of amniotic fluid.
We have simplified and standardized the method of determining the lamellar bodies (LB) in amniotic fluid as a measure of fetal lung maturity. For this purpose we have first diluted the amniotic fluid and then concentrated its LB by low-speed centrifugation at the interface of a 10% Nycodenz solution. As a standard we use liposomes which consist of phospholipids enclosing a Nycodenz solution with a density similar to that of the LB. The phosphorus content of the LB and liposome standard is then determined by an automated fluorimetric method. There is an excellent correlation between the newly described procedure and the lecithin/sphingomyelin ratio. One technician can easily analyse 40 samples in a working day.
Pancreatic lipase and phospholipase A2 concentration in amniotic fluid and the prenatal diagnosis of cystic fibrosis.
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The fluorimetric determination of the lecithin/sphingomyelin ratio of amniotic fluid after HPLC.
We have investigated whether fluorimetric determination of the lecithin/sphingomyelin ratio is feasible after HPLC. We found that the saturated phospholipid, dipalmitoyl lecithin, which is secreted by the fetal lung, and which cannot be detected by ultraviolet spectrophotometry, can be determined fluorimetrically. For this purpose we have added the fluorescence-enhancing substance, 1,6-diphenyl-1,3,5-hexatriene to the effluent. With the aid of a continuous-flow system we showed that the method can be used for a rapid assay of the ratio of these phospholipids in amniotic fluid.
Use of octadecyl (C18) columns for the estimation of oestrogens in the urine of non-pregnant women.
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A problem concerning determination of the lecithin/sphingomyelin ratio of amniotic fluid.
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An explanation of the low lecithin/sphingomyelin ratio of amniotic fluid in early pregnancy.
We have attempted to determine why the lecithin/sphingomyelin (L/S) ratio of amniotic fluid is lower than 2 during an early stage of pregnancy. We found that, at 16 wk of gestation, long before the fetal lung secretes lecithin into the amniotic fluid, the L/S ratio was about 1. High-density lipoprotein isolated from the amniotic fluid also had such a low L/S ratio. The L/S ratios of the high-density lipoprotein from umbilical cord blood and maternal blood, however, were much higher, viz. 3.7 (+/- 0.25) and 6.4 (+/- 0.33), respectively. The increase coincided with a decrease in their fluorescence polarization. We suggest that the low L/S ratio of 16 wk amniotic fluid is caused by lipolysis of its lecithin, which is derived from fetal or maternal high-density lipoproteins.
The immunochemical determination of apolipoprotein A, total apolipoprotein A-I and 'free' apolipoprotein A-I in serum of patients on chronic haemodialysis.
We have determined by radial immunodiffusion the apolipoprotein A content of undelipidated serum samples from 30 patients on chronic haemodialysis and 28 controls using an antiserum against high density lipoprotein (anti-apolipoprotein A). We found that the patients had lower concentrations of apolipoprotein A than the controls. When an antiserum against apolipoprotein A-I was used and the samples were delipidated prior to radial immunodiffusion there was, however, no difference in the total amount of apolipoprotein A-I between the two groups. We were able to explain this difference by measuring the amount of 'free' apolipoprotein A-I after crossed immunoelectrophoresis of undelipidated samples, using the antiserum against apolipoprotein A-I. We found that the patients had a higher level of 'free' apolipoprotein A-I than the control group. Since apolipoprotein A-I inhibits hepatic triglyceride lipase, the increase in triglycerides observed in patients on haemodialysis may be caused by the greater concentration of 'free' apolipoprotein A-I in their serum.
What is the correct lecithin/sphingomyelin ratio for human high-density lipoprotein?
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The lipoprotein profile and phospholipase activity of subretinal fluid.
We have studied the lipoprotein profile of subretinal fluid by crossed immunoelectrophoresis using an antiserum against apolipoprotein A-I. If the detachment had occurred recently, we found that the subretinal fluid contained only the alpha 1-lipoprotein of serum. However, if the detachment was of longer duration an increasing amount of an electrophoretically slower-moving lipoprotein was also present in the subretinal fluid. We present evidence that subretinal fluid contains an enzyme, phospholipase A, which can form the slower-moving component from alpha 1-lipoprotein. Since the retina has a high phospholipid content, permanent damage may be caused to its structure by the action of this hydrolysing enzyme.
More about immunoassay of apolipoprotein A-1.
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Fluorometric procedure for determining "lamellar body" phospholipids in the particulate fraction of amniotic fluid after filtration.
A rapid (30-min) semiautomated continuous-flow procedure is described for use in assessing the phospholipids of the particulate ("lamellar body") fraction of human amniotic fluid. The method is based on measuring the difference in fluorescence of 1,6,-diphenyl-1,3,5-hexatriene added to amniotic fluid before and after micropore filtration. The filtration step removes "lamellar body" particles, which are considered to contain the fetal lung surfactant. The phospholipid values for the filtered particles are independent of background fluorescence, which increases when amniotic fluid is contaminated by bilirubin pigments or blood components. Over a wide range (3-150 mumols/L) the fluorescence increases linearly with the phospholipid concentration of the amniotic fluid. There is a good agreement between the value for particulate "lamellar body" phospholipid, the ratio of the "lamellar body" phospholipids to total amniotic fluid phospholipids, and the lecithin/sphingomyelin ratio.
Azathioprine teratogenicity: review of the literature and case report.
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