Biomedical subjects

G deBoer

Publications and source records attributed to G deBoer.

4 recordsLinked to original sources

PubMed1984

Multiple primary squamous cell carcinomas in the upper digestive tract.

Multiple squamous cell carcinomas are common and patients carry a constant and excessive risk of developing a new cancer at any time (13-21 X the normal). Among 6,203 cases of primary squamous carcinoma of the upper digestive tract, 648 patients (10.4%) developed two or more independent tumors. Altogether, 761 additional malignancies were observed, with up to five cancers being seen in individual patients. There were 279 patients with a prior or synchronous cancer and 409 patients who developed 462 metachronous tumors. There was a substantial risk for developing a second primary cancer in the upper aerodigestive tract. Overall the observed to expected ratio was 2.48, specifically 2.32 for males and 2.89 for females.

Carcinoma, Squamous Cell↗

PubMed1984

Effects of feeding frequency on glucose concentration, glucose turnover, and insulin concentration in steers.

Patterns of diurnal variation of glucose production, utilization, and concentration and of variation of insulin concentration in blood plasma were studied. Four Holstein steers (200 kg) were in a switchback design. Each received 4.6 kg of 70% chopped alfalfa hay and 30% dry cracked corn daily, either as two equal meals at 12-h intervals or 12 equal meals at 2-h intervals. None of mean daily glucose production, utilization, and concentration nor mean insulin concentration was affected by feeding frequency. In response to feeding, insulin was released simultaneously with increased glucose production, suggesting that glucose production and insulin release are regulated by a common effector system. Feeding twice daily resulted in a sinusoidal pattern of glucose specific radioactivity. On the basis of changes of glucose concentration, glucose utilization closely followed production. Within-day variation of glucose production for steers fed twice daily was greater than indicated by variation of glucose concentration. Such variation of production will lead to errors in estimates of glucose production from short (less than 12 h) isotope infusion experiments with steers fed twice daily. Conversely, daily glucose production was not different for steers fed twice or 12 times daily; therefore, frequent feeding is both necessary and appropriate for investigations of glucose kinetics.

Animals↗

PubMed1984

Glucose kinetics, plasma metabolites, and endocrine responses during experimental ketosis in steers.

Phlorizin and 1,3-butanediol were used to determine effects of glucosuria and ketonemia on concentrations of metabolites in blood plasma and on kinetics of glucose metabolism. Four steers received four treatments (control; control plus dietary 1,3-butanediol; control plus phlorizin injections; and control plus phlorizin and 1,3-butanediol) in a Latin square design. Treatments lasted 14 days. All steers received a 30% grain, 70% forage ration in equal meals every 2 h. Metabolite concentrations in blood plasma and urine and glucose kinetics were measured on each of the last 3 days of each treatment period. Phlorizin caused glucosuria; decreased plasma glucose, glucose total entry rate, and glucose recycling; and increased plasma free fatty acids and glucose irreversible loss. Glucose pool size was increased by 1,3-butanediol. Phlorizin plus 1,3-butanediol caused glucosuria and ketonuria; decreased plasma glucose; and increased blood ketone bodies, plasma free fatty acids, glucose irreversible loss, and glucose pool size. Growth hormone, insulin, and glucagon were not affected by treatment. Physiological perturbations in these steers were characteristic of some of those in ketotic cows.

Acidosis↗

PubMed1984

Plasma and liver metabolites and glucose kinetics as affected by prolonged ketonemia-glucosuria and fasting in steers.

For 28 days, four steers received 1,3-butanediol, which causes ketonemia, and phlorizin, which causes glucosuria. Steers also were fasted for 9 days. Effects of treatments on concentrations of metabolites in blood and liver and on kinetics of glucose metabolism were determined. Treatments were: control, control with dietary butanediol plus injected phlorizin, and fasting. Fasting caused hypoinsulinemia and decreased liver glycogen by 60%. Butanediol plus phlorizin and fasting caused 18 and 19% decreases of plasma glucose and 2.5- and 6-fold increases of free fatty acid concentrations in blood plasma. Glucose irreversible loss averaged 371, 541, and 182 g/day during control, butanediol plus phlorizin treatment, and fasting. Butanediol plus phlorizin increased liver ketone body concentrations, caused glucosuria, ketonuria, and ketonemia, but did not affect insulin, glucagon, or growth hormone concentrations in plasma or triglyceride and glycogen contents in liver. Steers given butanediol plus phlorizin did not show all the usual signs of lactation ketosis, but the treatment still offers promise for studying causes and effects of ketosis.

Acidosis↗