AST (Association of Surgical Technologists) member survey: summary of results.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Paulson.
Explore the source record for details and available documents.
A case of mesonephric rest hyperplasia, an incidental finding in the hysterectomy specimen of a 48-year-old woman, was initially misdiagnosed as a well-differentiated cervical adenocarcinoma. We highlight the histologic, histochemical, and immunohistochemical features of this potential diagnostic pitfall and review the relevant literature.
(R,S)-Bambuterol was isolated from plasma and urine by solid-phase extraction and analysed as its trimethylsilyl derivative by gas chromatography/chemical ionization mass spectrometry with ammonia as the reagent gas. Deuterium-labelled bambuterol was used as internal standard. An esterase inhibitor was added to plasma to prevent hydrolysis of bambuterol in the plasma sample. Bambuterol could be measured in plasma down to 1 nmol l-1 with a within-day variation of less than 5% (coefficient of variation). The lower limit of measurement in urine was judged to be 8 nmol l-1, a concentration at which the within-day variation was 5.4% (coefficient of variation).
The objective of this study was to examine the effect of an aqueous extract of smokeless tobacco (ST) on the development of the CD-1 mouse fetus. Three ST dosages were administered three times daily by gastric intubation during gestational days 1-17: 1 X ST equivalent to a dose of 4 mg nicotine/kg body weight, 3 X ST equivalent to 12 mg nicotine, and 5 X ST equivalent to 20 mg nicotine/kg body weight. Maternal plasma nicotine levels were determined 30 minutes after the second daily intubation at five different times during the gestational period. At these ST dosages, the weight gain of ST-treated dams was not significantly affected in comparison to treated controls, though the difference was significant (P less than .05) in comparison to untreated controls. The mean maternal plasma nicotine level for the low dosage (1 X) group was 99.0 ng/ml, which reasonably approximates human consumption levels. The 3 X ST and 5 X ST dosages produced higher nicotine plasma values, 398 ng/ml and 623 ng/ml, respectively, were considerably more toxic to the dams, and resulted in 18% and 31% maternal deaths. Fetal weights were reduced by 7.4% (P less than .001) in the highest ST dosage group (5 X), whereas at the 1 X and 3 X dosages fetal weight differences were not significantly different from treated controls. Resorptions increased in a dose-related manner (P less than .05), ranging from 4.7% in the 1 X, to 6.4% in the 3 X and 8.9% in the 5 X dosage compared to 3.2% in treated controls. External malformations were few and minor in extent. Internal malformations increased in a linear, dose-related manner (P less than .05). Placental weights were unaffected by ST. The results of skeletal examinations were inconclusive. Precocious ossification was seen in 60% and 70% of the parameters measured in the 1 X and 3 X dosage groups, respectively, in comparison to controls. In the 5 X ST group ossification levels were less than in controls for 30% of the parameters measured. Under these experimental conditions the lowest ST dosage (1 X) produced a negligible effect on the CD-1 mouse fetus and the dam. The highest ST dose (5 X) demonstrated embryotoxicity, growth retardation, few malformations, and maternal toxicity. The intermediate dose (3 X) showed a range of effects between the highest and lowest doses to both the fetus and the dam.
1. The pharmacokinetics of the two enantiomers of terbutaline, (+)T and (-)T, and the racemate (+/-)T, have been evaluated after single intravenous and oral dosage to six healthy volunteers. 2. The mean systemic clearance, CL, was 0.19 and 0.13 l h-1 kg-1 for (+)T and (-)T, respectively. This difference was statistically significant. The mean clearance of (+/-)T was 0.20 l h-1 kg-1. Volumes of distribution were similar (1.9 l kg-1) after the three intravenous administrations. The differences in CL were reflected in values of the elimination half-life and MRT. 3. The difference in CL of the isomers could be explained by a corresponding difference in their renal clearance, CLR. Competition for stereoselective active reabsorption in the tubule might explain why (+)T seemed to enhance the CLR of (-)T when the drug was given as the racemate. 4. Oral bioavailability, calculated from plasma data, of (+)T was 7.5% and that of (-)T was 14.8%. This difference was statistically significant and was mainly due to a difference in absorption of (+)T and (-)T, but also to a difference in their subsequent first-pass metabolism. The bioavailability of (+/-)T was similar to that of (-)T. 5. (-)T appears to govern the absorption properties of the racemate, while (+)T determines its elimination behaviour. Systemic metabolism of the two enantiomers was similar and, therefore, a greater first-pass metabolism of (+)T would reflect a higher capacity of the gut wall to metabolise this isomer.
Liquid chromatography-mass spectrometry (LC-MS) and coupled column chromatography can be used to overcome problems likely to occur in direct separation and determination of drug enantiomers in biological samples. This is exemplified here with the direct separation and determination of terbutaline in human plasma at the nmol/l level. A beta-cyclodextrin column with an aqueous mobile phase was used for chiral separation. For coupled column chromatography, the concentration of each enantiomer was calculated from the enantiomeric area ratio and the racemate concentration. A deuterium-labelled internal standard was used in the LC-MS experiments.
The objective of this study was to examine the effect of smokeless tobacco (ST) on the development of the CD-1 mouse fetus. ST was administered continuously via Alzet osmotic minipumps during the critical gestational days 7-14 and 6-13. Two ST dosages were administered, 3.2 mg/ml (Dosage I) and 6.4 mg/ml (Dosage II), which yielded plasma nicotine levels within the range comparable to those of an average ST user or smoker (36.0 ng/ml). Plasma nicotine levels were maintained in the range of 29.4 +/- 4.8 ng/ml to 44.3 +/- 16.0 ng/ml for the Dosage I group of dams, and in the range of 34.6 +/- 10.9 ng/ml of 75.5 +/- 19.9 ng/ml for the Dosage II group of dams. The main effect on the fetus was weight reduction, with Dosage I producing a tendency toward weight reduction (p = .08). Dosage II produced a significant 8.6% weight reduction from normal (p less than .0001) and an increase in fetal deaths (p less than .03). Dosage I produced an increase in the incidence of hemorrhages and supernumerary ribs, and a significant delay (p less than .05) in ossification of the supraoccipital bone, the sacrococcygeal vertebrae, and the bones of the forefoot and hindfoot. There were no significant differences between placental weights. Weights of dams were significantly reduced only at the higher ST exposure levels. We conclude that at plasma nicotine levels comparable to those of an average ST user, ST produces weight reduction, delayed ossification, and increase in hemorrhages and fetolethality in the CD-1 mouse fetus.
A moving belt interface was used to identify budesonide metabolites, obtained from rat and mouse liver incubations, by liquid chromatography/mass spectrometry (LC/MS). The metabolites were separated on a small-bore C18 column with an ethanol/water gradient as mobile phase at a flow rate of 0.2 ml min-1. A spray device was used for deposition of the aqueous solvent on to the belt. Chemical ionization mass spectra were obtained with methane as the reagent gas. Deuterium-labelled budesonide, which was used to facilitate metabolite identification by the isotope cluster technique, was found to be slightly separated from the unlabelled analogue on the LC column. Incubations were also performed under 18O2 to elucidate the mechanism of a new metabolic pathway (16 alpha, 17 alpha-acetal splitting) and to confirm the oxidative nature of reactions leading to hydroxylated metabolites. The moving belt LC/MS technique afforded higher sensitivity, and gave more abundant MH+ ions of the compounds studied, than previously found by direct probe mass spectrometry. Phthalate ester background, partly from the polymide belt, complicated the identification of minor metabolites.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The metabolism of budesonide, (22RS)-16 alpha, 17 alpha-butylidenedioxy-11 beta,21-dihydroxypregna-1,4-diene- 3,20-dione, was studied in the 9000g supernatant fraction of livers from rat, mouse, and man. The two budesonide C-22 epimers produced different metabolites. This was explained by substrate-selective oxidation of the nonsymmetric 16 alpha, 17 alpha-acetal substituent. Epimer 22R gave 16 alpha-hydroxyprednisolone, while epimer 22S produced a metabolite tentatively identified as 23-hydroxybudesonide. Otherwise, budesonide followed the general metabolic pathways reported for synthetic glucocorticoids. Thus, oxidative metabolism predominated, 6 beta-hydroxybudesonide and delta 6-budesonide being identified in all investigated species. Reductive metabolism, giving 4,5 beta-dihydrobudesonide and 3,4,5 beta-tetrahydrobudesonide, was most pronounced in the rat. Rates and routes of budesonide metabolism were most similar in mouse and human livers. This implies that the mouse is a more relevant species than the rat in studies of the pharmacology and toxicology of budesonide.
To identify risk factors predicting the involvement of boat operators in incidents resulting in at least one fatality, the authors obtained data from a mail survey of registered boat owners in the State of Ohio and from the Boating Accident Report (BAR) files for 1983-86 compiled by the Ohio Department of Natural Resources. Additionally, they reviewed Ohio death certificates for those years to identify cases missed by the BAR system. Forty percent of the fatal incidents would have been missed by a search of death certificates alone. During the period studied, 107 boating incidents resulted in 124 deaths. There were 0.9 fatal incidents per million boat-operator hours. Factors found to be associated with an increased risk of a fatal boating incident were the operator being younger than 30 years, having fewer than 20 hours of boat operating experience, and lacking formal boat safety training. Canoes, kayaks, rowboats, and inflatables were associated with a higher rate of fatal incidents per million hours of use than were motorboats. Young age and lack of experience were associated independently with increased risk, explaining some of the effects associated with types of boats and with lack of training. The findings suggest that supervised experience, safety training programs aimed at young operators, and interventions specific to certain types of boats are likely to reduce boating fatalities.