Biomedical subjects
Publications and source records attributed to T Hood.
Five lead-resistant strains of Staphylococcus aureus were isolated. Plasmid-free lead-sensitive variants were obtained from the three plasmid-bearing strains. Lead-resistant strains tolerated an approximately 600 x higher Pb(NO3)2 concentration than lead-sensitive strains. Both types of strains initially bound lead, but only the resistant strains accumulated the metal as an intracellular lead-phosphate.
We examined binding to excitatory amino acid and inhibitory amino acid receptors in frozen hippocampal sections prepared from surgical specimens resected from 8 individuals with medically refractory temporal lobe epilepsy. The excitatory receptors studied included N-methyl-D-aspartate (NMDA), strychnine-insensitive glycine, phencyclidine, and quisqualate. The inhibitory receptors studied were gamma-aminobutyric acid type A (GABAA) and benzodiazepine. Excitatory and inhibitory amino acid receptor binding were differentially altered in the patients with temporal lobe epilepsy in comparison to 8 age-comparable autopsy control subjects, and changes in receptor binding were regionally selective in four areas. Binding to phencyclidine receptors associated with the NMDA channel was reduced by 35 to 70% in all regions in the hippocampi of the patients. In contrast, binding to the NMDA recognition site and its associated glycine modulatory site was elevated by 20 to 110% in the cornu ammonis (CA) 1 area and dentate gyrus of the hippocampus of the patients. Binding to these sites was unaffected in area CA4. Binding to the quisqualate-type excitatory amino acid receptor was unchanged in all regions except the stratum lacunosum moleculare CA1, where it was increased by 63%. GABAA and benzodiazepine receptor binding was reduced by 20 to 60% in CA1 and CA4, but unchanged in dentate gyrus. The data indicate that excitatory and inhibitory amino acid receptors are altered in the hippocampus of patients with temporal lobe epilepsy.
The purpose of this study was to determine the effect of exercise duration on lipoprotein responses. Twenty two normolipidemic male volunteers, ages 19-31 yrs (X +/- SEM = 23.1 +/- 2.94) participated in the study. Each was novice a runner (training less than 5 mi/wk). Subjects were assessed for baseline lipid measures of high density lipoprotein (HDL-C), low density lipoprotein (LDL-C), total cholesterol (TC) and triglycerides (TG). They were then evaluated for VO2max and ventilatory threshold (VT). Later they were matched for VO2max and randomly assigned to one of three groups which exercised for 15, 30 or 45 min respectively at a VO2 20% below VT. Subjects were evaluated again for HDL-C, LDL-C, TC and TG from blood samples taken pre-exercise and immediately post-exercise, as well as 1, 24 and 48 hrs post-exercise. A 3 X 4 split plot ANOVA found no difference for any lipid measure during the baseline period. A 3 X 5 split-plot ANOVA (covarying for pre-exercise measures) and post-hoc comparisons of pre- and post-exercise lipid levels indicated no significant differences occurred for either TC, TG or LDL-C measures (p less than 0.05). With respect to HDL-C, the 30 min group had significantly lower HDL-C at the 24 hr measure than did 45 min group (46.41 +/- 1.70 vs 53.34 +/- 1.73 mg.dl-1 respectively). No other differences were found. These findings indicate exercise duration will have an effect on acute responses of lipoprotein following exercise of low intensity.
Explore the source record for details and available documents.