PubMed Health⌕ Search

Biomedical subjects

D E Thomas

Publications and source records attributed to D E Thomas.

31 records · Page 2Linked to original sources

Plasma amino acids in patients with senile dementia and in subjects with Down's syndrome at an age vulnerable to Alzheimer changes.

Plasma concentration of tryptophan, tyrosine, leucine and thiamine were reduced in senile dementia of Alzheimer type. In Down's syndrome, where Alzheimer-type histology appears consistently at an early age, there was a definite type of abnormality, raised concentrations of isoleucine, leucine, phenylalanine and cystine. Because of the competition between amino acids for transfer into the brain, either or both of these types of change could lie in the aetiological chain underlying the development of Alzheimer pathology. Alternatively, these patterns could reflect the requirements of aberrant central/peripheral protein turnover.

Adult↗

Tryptophan and nutritional status of patients with senile dementia.

The nutritional status of 23 severely demented patients was compared with that of 23 similarly aged controls in the community. A 3-day weighed intake on all subjects showed lower mean intakes of energy, protein, ascorbic acid and nicotinic acid in the mean intakes of energy, protein, ascorbic acid and nicotinic acid in the patient group. This group had lower levels of plasma ascorbic acid and red cell folate and of urinary N-methylnicotinamide excretion relative to creatinine. Over a third of both controls and patients had evidence of thiamin deficiency, as judged by a raised percentage erythrocyte transketolase activity. An earlier finding in patients with senile dementia of reduced fasting plasma concentrations of tryptophan was confirmed for total and protein bound fractions. With the possible exception of ascorbic acid, the data could not be explained satisfactorily in terms of intake. It is suggested that the association between the phenomena of aging, senile dementia and nutritional status merits further investigation.

Aged↗

Comparison of single-dose and conventional trimethoprim-sulfadiazine therapy in experimental Staphylococcus intermedius cystitis in the female dog.

Cystitis was produced in 4 groups of 6 female dogs each, using salicylic acid, ethanol, and Staphylococcus intermedius. Group-I dogs served as nontreated controls. Starting 2 days after infection was induced, group-II dogs were treated with trimethoprim-sulfadiazine at a dosage of 15 mg/kg given orally 2 times a day for 21 days; groups-III and -IV dogs were treated with single oral dosages of the antibiotic at 60 mg/kg and 90 mg/kg, respectively. Group-I dogs (controls) remained infected for the 26-day duration of the study. The response to therapy seen in group-II dogs was better than the therapeutic responses in groups-III and -IV dogs (P less than 0.05). Results of the present study do not support the efficacy of single-dose therapy for this model of cystitis.

Administration, Oral↗

Effects of phenobarbital treatment on 3-methylindole toxicosis in ponies.

To study the role of cytochrome P-450-dependent mixed function oxidase reactions in equine 3-methylindole (3MI) toxicosis, ponies were given 20 mg of phenobarbital/kg of body weight at 72, 60, 48, 36, and 24 hours before 100 mg of oral 3MI/kg to induce cytochrome P-450 or no treatment (controls). Maximal 3MI plasma concentration was decreased and clearance was faster in phenobarbital-treated ponies. Plasma 3MI was still detectable 12 and 36 hours after dosing in phenobarbital-treated and control ponies, respectively. Phenobarbital treatment induced a distribution phase with transition from a 1-compartment to a 2-compartment extravascular model. Bronchiolitis occurred in all ponies 72 hours after 3MI, but was more severe in those treated with phenobarbital. Appearance of a distribution phase, increased total body clearance, and more severe bronchiolitis in phenobarbital-treated ponies indicated that mixed function oxidases are involved in metabolism and conversion of 3MI to a toxic metabolite.

Animals↗

Pharmacokinetics of small doses of 3-methylindole given to horses.

The pharmacokinetics of 3-methylindole (3MI) given orally in 2 doses (10 mg/kg and 20 mg/kg) to horses were determined. The pharmacokinetic plasma-concentration profiles for 3MI (10- and 20-mg/kg dosages) in horses were represented by a 2-compartment open model with first-order absorption, as determined by nonlinear least-squares regression analysis. Absorption of 3MI at both dosages was rapid. Comparisons of the peak plasma concentrations, the postdistribution half lives, total clearances, and areas under the curve of the plasma-concentration profiles between the 10- and the 20-mg/kg dosages may indicate the presence of nonlinear or dose-dependent kinetics for 3MI in horses.

Administration, Oral↗

How many beds should a hospital department serve?

Departmental cost functions are constructed for selected hospital departments, using total number of beds in the hospital served as a proxy output measure. Calculation of maxima or minima for the resulting cost functions reveals that, on average, different departments have extremes in their cost functions of different levels of output. A relative cost index is constructed, using parameters of the departmental cost functions, and departmental costs are compared across regions. The significance of departmental differences in optimum output is discussed with regard to sharing of services and modified system design.

Costs and Cost Analysis↗

Elevated in vivo expression of the costimulatory molecule B7-BB1 (CD80) on antigen presenting cells from a patient with SLE.

The CD28/CTLA4-B7-family plays an important role in T-cell costimulation and is crucial for IL-2 production and tolerance induction. The costimulatory molecule B7-BB1 (CD80) is expressed on activated antigen presenting cells, but its expression on peripheral blood mononuclear cells is very low. Here we report a patient with untreated SLE whose peripheral blood antigen presenting cells expressed increased amounts of B7-BB1.

Anti-Inflammatory Agents↗