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Biomedical subjects

Timothy A Moore

Publications and source records attributed to Timothy A Moore.

5 recordsLinked to original sources
PubMed2006

Classification of lower cervical spine injuries.

STUDY DESIGN: Blinded assessment by multiple observers of consecutive case series. OBJECTIVES: Measure the reliability of a new system of determining stability in subaxial cervical spine injuries. SUMMARY OF BACKGROUND DATA: Classification is fundamental to allow communication, determine prognosis, and direct treatment. Current systems have many limitations, including difficultly of use, lack of proven reliability and validity, and no assessment of stability. A new system to assess instability is proposed. METHODS: A literature review of the most commonly described classification systems is reported. The Cervical Spine Injury Severity Score was tested for reliability by 10 examiners who graded 35 consecutive cases of cervical trauma. Plain radiographs and CT were saved as read using Efilm Lite in random order. Each was scored and intraobserver and interobserver agreement was measured using intraclass correlation coefficients (ICC). RESULTS: Intraobserver agreement was excellent with ICC ranging from 0.97 to 0.99. Interobserver agreement was also excellent with mean 0.80 ranging from 0.75 to 0.98. CONCLUSION: A new cervical spine classification system of injury is paramount to treatment and outcomes. A new system may increase reliability and therefore allow more accurate determination of stability and dictate treatment.

Cervical Vertebrae↗
PubMedDate not supplied

Characterization of metabolites and disposition of tertiary amyl methyl ether in male F344 rats following inhalation exposure.

Tertiary amyl methyl ether (TAME) is a fuel additive used to reduce carbon monoxide in automobile emissions. Because of the potential for human exposure, this study was conducted to develop methods for the characterization and quantitation of metabolites in expired air and excreta of rats exposed to a mixture of [13C]- and [14C]TAME ([2,3,4-13C]- and [2-14C]2-methoxy-2-methylbutane). The distribution of TAME in rats was determined following inhalation exposure, and TAME-derived metabolites were characterized in expired air and urine. Male rats were exposed for 6 h via nose-only inhalation to 2500 ppm [14C/13C]TAME, and expired air, urine and feces were collected for up to 7 days. Over 95% of the total recovered radioactivity was excreted by 48 h after exposure. Recovered radioactivity was expired as organic volatiles (44%) and 14CO2 (3%) and excreted in urine (51%) and feces (1%). Both TAME and its metabolite tertiary amyl alcohol (TAA) accounted for > or =90% of the radiolabel in expired air 0-8 h following exposure termination. Three major urinary metabolites of TAME were identified: (1) a direct glucuronide conjugate of TAA; (2) a product of oxidation at the methylene carbon of TAA (2,3-dihydroxy-2-methylbutane); (3) a glucuronide conjugate of metabolite 2. Metabolite 1 accounted for most of the TAME-derived metabolites excreted 0-8 h following exposure termination. Further metabolic products of TAA (metabolites 2 and 3) accounted for most of the excreted TAME-derived metabolites at later time points.

Air Pollutants↗
PubMedDate not supplied

Blood pharmacokinetics of tertiary amyl methyl ether in male and female F344 rats and CD-1 mice after nose-only inhalation exposure.

Interest in understanding the biological behavior of aliphatic ethers has increased owing to their use as gasoline additives. The purpose of this study was to investigate the blood pharmacokinetics of the oxygenate tertiary amyl methyl ether (TAME), its major metabolite tertiary amyl alcohol (TAA) and acetone in rats and mice following inhalation exposure to TAME. Species differences in the area under the curve (AUC) for TAME were significant at each exposure concentration. For rats, the blood TAME AUC increased in proportion with an increase in exposure concentration. For mice, an increase in exposure concentration (100-500 ppm) resulted in a disproportional increase in the TAME AUC. Mice had greater (two- to threefold) blood concentrations of TAA compared with rats following exposure to 2500 or 500 ppm TAME. Mice had a disproportional increase in the TAA AUC with an increase in exposure concentration (100-500 ppm). This difference could result from saturation of a process (e.g. oxidation, glucuronide conjugation) that is involved in the further metabolism of TAA. For each species, gender and exposure concentration, acetone increased during exposure and returned to control values by 16 h following exposure. The source of acetone could be both as a metabolite of TAA or an effect on endogenous metabolism produced by exposure to TAME.

Acetone↗
PubMedDate not supplied

Species and gender differences in the metabolism and distribution of tertiary amyl methyl ether in male and female rats and mice after inhalation exposure or gavage administration.

Tertiary amyl methyl ether (TAME) is a gasoline fuel additive used to reduce emissions. Understanding the metabolism and distribution of TAME is needed to assess potential human health issues. The effect of dose level, duration of exposure and route of administration on the metabolism and distribution of TAME were investigated in male and female F344 rats and CD-1 mice following inhalation or gavage administration. By 48 h after exposure, >96% of the administered radioactivity was expired in air (16-71%) or eliminated in urine and feces (28-72%). Following inhalation exposure, mice had a two- to threefold greater relative uptake of [14C]TAME compared with rats. Metabolites were excreted in urine of rats and mice that are formed by glucuronide conjugation of tertiary amyl alcohol (TAA), oxidation of TAA to 2,3-dihydroxy-2-methylbutane and glucuronide conjugation of 2,3-dihydroxy-2-methylbutane. A saturation in the uptake and metabolism of TAME with increased exposure concentration was indicated by a decreased relative uptake of total [14C]TAME equivalents and an increase in the percentage expired as volatiles. A saturation of P-450 oxidation of TAA was indicated by a disproportional decrease of 2,3-dihydroxy-2-methylbutane and its glucuronide conjugate with increased exposure concentration.

Administration, Oral↗