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Biomedical subjects

A Viau

Publications and source records attributed to A Viau.

At least 19 recordsLinked to original sources

The Modified-Modified Schober Test for range of motion assessment of lumbar flexion in patients with low back pain: a study of criterion validity, intra- and inter-rater reliability and minimum metrically detectable change.

PURPOSE: The objective was to estimate the psychometric properties of the Modified-Modified Schober Test (MMST). DESIGN: This study compared range of motion measurements of lumbar flexion in low back pain (LBP) patients using the MMST with measurements calculated on X-rays as the gold standard, and compared the measurements taken by two independent examiners. METHOD: This study was conducted at the main hospital in the Outaouais area, Quebéc, Canada. Thirty-one subjects with LBP from private and public clinics participated in the study. After a warm-up session, measurements with the MMST were taken in neutral position and an X-ray technician took an exposure in the same position. RESULTS: Pearson's correlation test (r) between measurements made with the MMST and the gold standard, intra-class correlation coefficient (ICC), minimum metrically detectable change (MMDC) and confidence interval (CI) were used to analyze the data. The MMST demonstrated moderate validity (r=0.67; 95%CI 0.44-0.84), excellent reliability (intra: ICC=0.95; 95%CI 0.89-0.97; inter: ICC=0.91; 95%CI 0.83-0.96) and a MMDC of 1 cm. CONCLUSIONS: In our sample of LBP patients, the MMST showed moderate validity but excellent reliability and MMDC.

Adult↗

Pharmacokinetics of benzo[a]pyrene in the rat.

Groups of 4 male Wistar rats were dosed intravenously with 14C-labeled benzo[a]pyrene dissolved in an Emulphor/water vehicle at 3 different dose levels and killed at 1 of 15 specific time intervals from 5 min to 32 h after dosing. 14C-Radiolabel concentration-time data were obtained for blood, brain, adipose, heart, kidney, liver, lung, spleen, and testes. Benzo[a]pyrene concentration-time data were obtained for blood, adipose, kidney, liver, and lung. Appropriate mathematical models were fitted to these data and to the data for metabolites derived as the residuals from 14C-radiolabel minus benzo[a]pyrene difference, where applicable. Nonlinear kinetics were found for 14C-radiolabel in liver, while the data from lung for both 14C-radiolabel and for benzo[a]pyrene per se supported the binding of benzo[a]pyrene in that tissue.

Adipose Tissue↗

The subchronic toxicity of acridine in the rat.

The subchronic toxicity of acridine was investigated in rats following dietary exposure at 0, 1, 10, 100 and 500 ppm for 13 weeks. The growth rate and food consumption were not affected by treatment and no clinical signs of toxicity were observed. There was a slight but significant decrease in spleen weight, both in absolute terms and as a percent of body weight, in the 500 ppm males and a slight increase in absolute thymus weight in the females of the same dose group. Both hepatic ethoxyresorufin O-deethylase (EROD) and pentoxyresorufin O-dealkylase (PROD) activities were slightly, but significantly, elevated in females in the 500 ppm dose group. No haematological or other biochemical changes were observed. Females also displayed dose-related increases in inorganic phosphate and uric acid levels. Treatment-related histopathological changes were seen in the thyroid, liver and kidney and included hepatic anisokaryosis and vesiculation of nuclei and glomerular adhesions, reticulin sclerosis and nuclear pyknosis in the kidney. Residue data showed a dose-dependent accumulation of acridine in liver, kidney and adipose with the highest concentration being found in the fat of the 500 ppm dose group. Based on these data, the no observable adverse effect level of acridine was judged to be 100 ppm or 12 mg/kg bw/day.

Acridines↗

Tissue distribution and elimination of trichlorobenzenes in the rat.

The tissue distribution and excretion of three trichlorobenzene isomers (TCB) were investigated in the rat. Single doses of TCBs were administered orally to groups of 5 fasted rats at 10 mg/kg body weight. Serial sacrifices were carried out and the radioactivity contents were determined in tissues and blood. For all three TCB isomers, radioactivity appeared in the blood and tissues at 0.5 h, and peaked around 2-4 h after dosing. Fat, skin, and liver had high concentrations of the parent compound while kidney and muscle had high levels of metabolites. Elimination of TCB from tissues and blood can best be described by a two-compartmental open pharmacokinetic model. The terminal half-lives were 145, 93 and 68 h for 1,2,3-, 1,2,4 and 1,3,5-TCB isomer respectively. Ninety-five percent of the administered 1,2,3- and 89% of the 1,3,5-isomers were eliminated within 48 h in the urine and feces with the former being the major route.

Animals↗

Metabolites of 1,2,3,4-tetrachlorobenzene in monkey urine.

[14C(U)]-Labeled 1,2,3,4-tetrachlorobenzene was administered orally to squirrel monkeys. Urine was collected from these animals, pooled and analyzed for metabolites by thin-layer chromatography, high-performance liquid chromatography, and gas chromatography-mass spectroscopy. N-Acetyl-s-(2,3,4,5-tetrachlorophenyl) cysteine was shown to be the major metabolite and accounted for 85% of the radioactivity found in urine. A minor metabolite was identified as 2,3,4,5-tetrachlorophenol. This study demonstrates for the first time that an N-acetyl cysteine conjugate has been isolated and identified as metabolite of a chlorinated benzene. This pattern of chlorobenzene metabolism is significantly different from the one obtained with the rat and rabbit, where tetrachlorophenols constitute the major metabolites.

Acetylcysteine↗

Metabolism of 1,2,3,4-, 1,2,3,5-, and 1,2,4,5-tetrachlorobenzene in the rat.

Adult male rats were given orally single doses of 14C-labeled 1,2,3,4-, 1,2,3,5-, or 1,2,4,5-tetrachlorobenzene (TCB) at 10 mg/kg body weight, and were housed in individual metabolism cages to collect urine and feces for radioassay. For 1,2,3,4- and 1,2,3,5-TCB, approximately 46-51% of the doses were excreted in urine and feces within 48 h after administration. During the same period only 8% of the administered 1,2,4,5-tetrachlorobenzene was excreted. Analysis of urine indicted that the tetrachlorobenzenes were biotransformed to a number of polar compounds. The metabolites for each of the three TCBs in decreasing order of quantities were as follows: 1,2,3,4-TCB, to 2,3,4,5- and 2,3,4,6-tetrachlorophenol and a trace of tetrachlorothiophenol and 2,3,4-trichlorophenol; 1,2,3,5-TCB, to 2,3,4,6-tetrachlorophenol, isomeric hydroxythrichlorothiophenols, and a trichlorophenol; 1,2,4,5-TCB, to 2,3,5,6-tetrachlorophenol, tetrachloroquinol, and a trichlorophenol.

Animals↗

Tissue distribution and elimination of 2,8-dihydromirex in the rat.

The tissue distribution and elimination kinetics of 14C-labeled dihydromirex were investigated in the rat. Dihydromirex was distributed in all tissues examined after iv or oral administration; the highest concentrations were found in the fat, liver, and skin. The pattern of distribution was similar to that of photomirex and mirex. Elimination of dihydromirex from the blood after an iv dose was expressed by a four-compartment model, whereas fecal excretion was represented by a biphasic curve. Excretion of dihydromirex occurred predominantly in the feces; only minute amounts were found in the urine and bile. Dihydromirex constituted 90-100% of the total radioactivity in tissues and feces. No metabolite was detected.

Adipose Tissue↗

Experimental alterations in cyclic adenosine monophosphate concentrations in the cat basilar artery.

Levels of cyclic adenosine monophosphate (AMP) in the basilar artery and in circulating blood of cats were determined after the production of spasm by topical application of blood to the vessel and following treatment with agents known to alter cyclic AMP. Isoproterenol, known to stimulate adenyl cyclase, and aminophylline, a phosphodiesterase inhibitor, were studied alone and in combination. Cyclic AMP of the basilar artery fell from a mean control value of 43 to 26 pmoles per milligram of protein following the production of vasospasm. Intravenous administration of isoproterenol alone and in combination with aminophylline produced dilatation of the basilar artery, which was associated with a marked rise in the cyclic AMP concentration in the vessel. The finding that cerebral vasospasm is associated with a fall and vasodilation with a rise in cyclic AMP concentration supports the hypothesis of an active role for cyclic nucleotides in the regulation of cerebrovascular smooth muscle tone.

Aminophylline↗