Search PubMed⌕ Search

Biomedical subjects

G Long

Publications and source records attributed to G Long.

At least 73 records · Page 4Linked to original sources
PubMed1979

Cutaneous and venous complications of pentazocine abuse.

A 55-year-old man with a two-year history of intramuscular pentazocine abuse had classical cutaneous findings as well as secondary venous thrombosis, which, to our knowledge, is previously undescribed. Histologic evaluation, including direct immunofluorescent microscopy, did not establish the mechanism of tissue destruction.

Humans↗
PubMed1976

Plasma protein binding and placental transfer of bupivacaine.

The maternal venous and umbilical venous plasma concentrations of bupivacaine were determined at delivery following epidural administration of the drug to 31 women in labor. In each case the umbilical venous plasma concentration of bupivacaine was lower than the maternal venous plasma concentration. There was no significant difference between the concentration of unbound bupivacaine in umbilical venous and maternal venous plasma at delivery. The difference in umbilical and maternal plasma concentrations of bupivacaine appears to be a consequence of greater bupivacaine binding to maternal than to fetal total plasma protein. The intersubject variation of the ratio of bupivacaine concentration in fetal plasma/bupivacaine concentration in maternal plasma was found to be related to individual variation in the extent of protein binding of bupivacaine in maternal and umbilical plasma and correlated positively with the variation of the ratio of total protein concentration in umbilical and maternal plasma.

Blood Proteins↗
PubMed1974

The effects of r- and K-selection on components of variance for two quantitative traits.

The genetic and environmental components of variance for two quantitative characters were measured in the descendants of Drosophila melanogaster populations which had been grown for several generations at densities of 100, 200, 300, and 400 eggs per vial. Populations subject to intermediate densities had a greater proportion of phenotypic variance available for selection than populations from either extreme. Selection on either character would be least effective under pure r-selection, a frequent attribute of selection programs.

Alleles↗
PubMed1971

Primary FFARACS.

Explore the source record for details and available documents.

Education, Medical↗
PubMedDate not supplied

Induction of urinary bladder hyperplasia in Sprague-Dawley rats orally administered tri-n-butyl phosphate.

The effects of tri-n-butyl phosphate (TBP) were investigated in the Sprague-Dawley rat over an 18-wk period. Groups of randomized female (average weight [AW] = 206 +/- 10 g) and male (AW = 294 +/- 13 g) rats were divided into low-dose, high-dose, and control groups (12 rats/sex X group). Tri-n-butyl phosphate was administered by gavage once a day for 5 days/wk over an 18-wk period. Low-dose animals received 0.20 g/kg X day throughout the experiment and high-dose animals received 0.30 g/kg X day for the first 6 wk. For the remaining 12 wk, the high-dose level was increased to 0.35 g/kg X day. Histopathological examination of tissues revealed that all test rats examined developed diffuse hyperplasia of the urinary bladder epithelium. Similar changes were not found in the control animals.

Administration, Oral↗
PubMedDate not supplied

Chloroform: exposure estimation, hazard characterization, and exposure-response analysis.

Chloroform has been assessed as a Priority Substance under the Canadian Environmental Protection Act. The general population in Canada is exposed to chloroform principally through inhalation of indoor air, particularly during showering, and through ingestion of tap water. Data on concentrations of chloroform in various media were sufficient to serve as the basis for development of deterministic and probabilistic estimates of exposure for the general population in Canada. On the basis of data acquired principally in studies in experimental animals, chloroform causes hepatic and renal tumors in mice and renal tumors in rats. The weight of evidence indicates that chloroform is likely carcinogenic only at concentrations that induce the obligatory precursor lesions of cytotoxicity and proliferative regenerative response. Since this cytotoxicity is primarily related to rates of formation of reactive, oxidative metabolites, dose response has been characterized in the context of rates of formation of reactive metabolites in the target tissue. Results presented here are from a "hybrid" physiologically based pharmacokinetic (PBPK) animal model that was revised to permit its extension to humans. The relevant measure of exposure response, namely, the mean rate of metabolism in humans associated with a 5% increase in tumor risk (TC05), was estimated on the basis of this PBPK model and compared with tissue dose measures resulting from 24-h multimedia exposure scenarios for Canadians based on midpoint and 95th percentiles for concentrations in outdoor air, indoor air, air in the shower compartment, air in the bathroom after showering, tap water, and food. Nonneoplastic effects observed most consistently at lowest concentrations or doses following repeated exposures of rats and mice to chloroform are cytotoxicity and regenerative proliferation. As for cancer, target organs are the liver and kidney. In addition, chloroform has induced nasal lesions in rats and mice exposed by both inhalation and ingestion at lowest concentrations or doses. The mean rate of metabolism associated with a 5% increase in fatty cysts estimated on the basis of the PBPK model was compared with tissue dose measures resulting from the scenarios already described, and lowest concentrations reported to induce cellular proliferation in the nasal cavities of rats and mice were compared directly with midpoint and 95th percentile estimates of concentrations of chloroform in indoor air in Canada. The degree of confidence in the underlying database and uncertainties in estimates of exposure and in characterization of hazard and dose response are delineated.

Air Pollutants↗
PubMedDate not supplied

An HPLC method for analysis of clonazepam in serum.

A sensitive, accurate, and precise method for the analysis of clonazepam in serum was developed. The drug and internal standard from serum extracts were methylated to obviate carbamazepine interference and then resolved on a 5 micron C18 HPLC column. The mobile phase could also be used for many other basic drugs.

Benzodiazepinones↗