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Biomedical subjects

C J Bailey

Publications and source records attributed to C J Bailey.

At least 181 records · Page 10Linked to original sources

Epidural morphine infusion. Continuous pain relief.

Epidural morphine infusion is an effective and relatively safe route for postoperative analgesia. Lanz , Theiss , Reiss , and Sommer performed research supporting the use of epidural morphine. Following lumbar epidural anesthesia for orthopedic operations, 174 patients underwent the following study. At the end of surgery under double-blind conditions, 57 patients in group 1 received 0.1 mg/kg of morphine in 15 ml of normal saline epidurally and normal saline 0.01 ml/kg intramuscularly. Patients in group 2 (57 patients) received intramuscular morphine 0.1 mg/kg and normal saline 15 ml epidurally. Patients in group 3 (60 patients) received normal saline 15 ml epidurally and normal saline 0.01 ml/kg intramuscularly. Postoperative pain was less frequent, of shorter duration, and less severe following epidural morphine (group 1). Sympathetic block was only partial; patients still noticed pressure due to a dressing or cast. There was no motor blockade and active mobilization occurred earlier. Following epidural morphine, alertness was heightened, patients were more cooperative, and respiratory depression and postoperative pneumonia were less than after systemic administration of narcotics.(ABSTRACT TRUNCATED AT 250 WORDS)

Catheterization↗

Dietary components and plasma insulin responses to fasting and refeeding in genetically obese hyperglycaemic (ob/ob) mice.

To investigate the role of dietary components in the hyperinsulinaemia of the obese hyperglycaemic (ob/ob) syndrome, plasma insulin responses to fasting and refeeding were examined in Aston ob/ob mice supplied with standard diet, non-digestible-carbohydrate test food, and isoenergetic test foods from which either carbohydrate, protein or fat was omitted. During fasting, plasma insulin concentrations fell more rapidly and to a greater extent than plasma glucose. Refeeding the standard diet raised insulin concentrations above normal, associated with a 25% compensatory increase in food intake over 24 h. Test foods supplied to previously fed or fasted mice produced glucose responses consistent with the available carbohydrate content. Carbohydrate-free food (protein and fat) provided a small insulinotropic stimulus; the effect of protein-free food (carbohydrate and fat) was greater; and the combination of carbohydrate with protein (fat-free food) evoked a marked insulin response. In contrast, insulin concentrations declined in mice given the non-digestible-carbohydrate food. Consumption of the standard diet was increased after 24 h feeding non-digestible-carbohydrate food, but was unaffected by a 30 h fast initiated 54 h previously. These results demonstrate that hyperinsulinaemia in ob/ob mice is not merely triggered by the ingestion of bulk, but depends on the type of nutrient ingested. Dietary carbohydrate appears to be the major stimulus to the hyperinsulinaemia, with an important augmentation in the presence of protein. Since direct glucose stimulation of insulin release is defective in ob/ob mice, the hyperinsulinaemia must be mediated by increased activity of the enteroinsular axis.

Animals↗

Thyroid hormones, gonadal and adrenocortical steroids and the function of the islets of Langerhans.

Thyroid hormones, gonadal and adrenocortical steroids, are glucoregulatory hormones. Thyroid hormones increase the provision of glucose to meet the enhanced energy demands which they impose. Glucose tolerance is decreased, associated with increased hepatic glucose production, although the glucose-raising effects of thyroid hormones are partially offset by an increased rate of glucose utilization especially in the postabsorptive state. The insulin secretory capacity of the pancreatic B cells is reduced by an excess of thyroid hormones, and the onset of diabetes may be hastened as pancreatic insulin reserves are depleted. Natural estrogens can improve glucose tolerance through a beta-cytotropic effect and enhanced insulin sensitivity. Progesterone may produce similar effects in the absence of estrogens, but progestins appear to antagonize the effects of estrogens. Testosterone exerts only marginal effects on glucose tolerance. Glucocorticoids decrease glucose tolerance by increased hepatic glucose production and impaired peripheral glucose utilization. Glucocorticoids reduce insulin sensitivity and responsiveness in peripheral tissues. However, the diabetogenic influence of glucocorticoid excess is partly compensated by a beta-cytotropic effect and a condition of diabetes develops when the functional reserve of the endocrine pancreas becomes limiting.

Adrenal Cortex Hormones↗

Plasma immunoreactive gastric inhibitory polypeptide in obese hyperglycaemic (ob/ob) mice.

Gastric inhibitory polypeptide (GIP), a recognized component of the enteroinsular axis, is raised in the plasma and intestine of obese hyperglycaemic (ob/ob) mice. To evaluate the control of plasma GIP and its role in the hyperinsulinaemia of the ob/ob syndrome, GIP and insulin were determined at different ages in fed mice, and at 10-12 weeks of age after fasting/refeeding and administration of GIP, different nutrients and insulin to mice fasted for 18 h. Plasma GIP and insulin were raised in adult (10- and 20-week-old) compared with younger (3- and 5-week-old) mice, although GIP was not increased in the presence of hyperinsulinaemia at 3 weeks of age. Fasting suppressed and refeeding promptly restored plasma GIP and insulin concentrations. Administration of GIP to mimic postprandial concentrations evoked a marked but transient insulin response which was protracted in the presence of rising hyperglycaemia. Orally administered fat, glucose and amino acids raised GIP concentrations with fat having a particularly strong effect. Glucose and amino acids also evoked prominent increases of insulin, but fat produced only a small rise in insulin in the absence of increasing glucose concentrations. Consistent with glucose-potentiation, a mixture of all three nutrients greatly augmented the insulin response without further increase of plasma GIP. Glucose-induced increase in endogenous insulin and doses of exogenous insulin up to 100 units/kg did not suppress basal, fat-stimulated or glucose-stimulated GIP release. The results indicate that raised GIP concentrations make an important contribution to the hyperinsulinaemia and related metabolic abnormalities of the ob/ob syndrome.

Amino Acids↗

Comparison of methods for classifying community residential settings for mentally retarded individuals.

Research on differential effects of residential environments has been hampered by the lack of a formal classification scheme for placement types. Two systematic approaches (dimensional and typological) were used to develop classification systems. Each approach was evaluated on criteria applicable to general classification schemes and residential environments for retarded persons. A third, nested system was derived that satisfied rules for development and evaluative criteria.

Adolescent↗

Effect of metformin on insulin receptor binding and glycaemic control in type II diabetes.

To investigate the effect of metformin on insulin receptor binding and diabetic control, eight obese type II diabetic patients were studied before treatment, after one and four weeks of taking metformin (500 mg thrice daily), and four weeks after withdrawal of the drug. After one and four weeks of treatment the number of erythrocyte insulin receptors had increased by 116% and 184% respectively. This was due almost entirely to an increase in the number of low affinity binding sites. The number of receptors was still raised four weeks after metformin had been withdrawn. Diabetic control as assessed by urinary glucose, glycosylated haemoglobin (HbA1), and glucose tolerance values was significantly improved during metformin treatment, while plasma insulin concentrations were not altered. These results indicate that metformin produces a rapid and protracted increase in low affinity insulin receptors in type II diabetes, associated with greater insulin sensitivity and improved diabetic control.

Aged↗

Purification and properties of tryptophan synthase from baker's yeast (Saccharomyces cerevisiae).

Tryptophan synthase was purified from baker's yeast. The purified enzyme exhibited one band on polyacrylamide-gel electrophoresis, had no detectable N-terminal amino acid and C-terminal alanine. The amino acid composition was close to that predicted by recent studies on the DNA sequence of the structural gene for the enzyme. Kinetic parameters for the following three activities were measured: indole-serine condensation, indolylglycerol phosphate lyase and the overall reaction of serine with 1-(indol-3-yl)glycerol 3-phosphate. The Km for indole was much lower than suggested by previous investigations, and the value of 11 microM was measured by a fluorimetric assay.

Amino Acids↗

Effect of metformin on hepatocyte insulin receptor binding in normal, streptozotocin diabetic and genetically obese diabetic (ob/ob) mice.

The effect of metformin on hepatocyte insulin receptor binding was examined in normal, streptozotocin diabetic and genetically obese diabetic (ob/ob) mice. In normal mice, chronic administration of metformin (60 mg X kg-1 X day-1 for 50 weeks) increased the number of low affinity receptors by 148%. During acute studies, metformin increased (30%) the number of low affinity receptors after 24 h. When metformin was withdrawn after treatment for 96 h, the number of low affinity receptors decreased, approaching control values by 48 h. In severely insulin resistant ob/ob mice, the concentrations of high and low affinity receptors were reduced by 60% and 27%, respectively. A high dose of metformin (240 mg X kg-1 X day-1 for 4 weeks) increased the concentration of high and low affinity receptors in ob/ob mice by 63% and 86%, respectively. However, the hypoglycaemic response to exogenous insulin was not altered. In streptozotocin-diabetic mice, the number of low affinity receptors was increased by 68% compared with normal mice. Metformin (60 mg X kg-1 X day-1 for 10 weeks) did not significantly alter the number of insulin receptors in streptozotocin-diabetic mice, but the hypoglycaemic response to exogenous insulin was improved by 94%. The results raise the possibility that metformin might affect post-receptor sites of insulin action independently of effects at the receptor level.

Animals↗

Glucose and insulin response to conditioned feeding in lean and genetically obese hyperglycemic (ob/ob) mice.

The study reported here investigated the role of neuroendocrine reflexes in the stimulation of insulin secretion associated with feeding in lean and genetically obese hyperglycemic (ob/ob) mice. Twenty-week-old mice were conditioned over four weeks to restricted feeding periods of consecutively seven, four and two hours a day. Basal plasma glucose concentrations before feeding were raised in conditioned lean mice but lowered in conditioned ob/ob mice, with normalization of glycemia in ob/ob mice by four weeks. Conditioned mice consumed more food during the feeding period than control mice prefasted for the same time. Although the quantity of food consumed was less than the normal 24-hour intake of age-matched mice fed ad libitum, body weights were well maintained, indicating adaptations of metabolic efficiency or energy expenditure or both. During the feeding period, conditioned mice displayed a markedly enhanced plasma insulin response accompanied by a smaller increase in plasma glucose despite the consumption of more food. An anticipatory rise in plasma insulin was not evident when food was withheld during the prescribed two-hour feeding period after four weeks of conditioning. The results demonstrate that basal glucose concentrations were normalized in ob/ob mice but raised in lean mice by the restricted conditioned feeding procedure. Basal insulin concentrations and body weights were not significantly altered, but conditioning to expect food augmented the insulin response initiated by feeding in both lean and ob/ob mice.

Animals↗

Use of a gamma- or hard beta-emitting radioisotope to assess milk intake in suckling mouse pups.

A radioisotopic method to assess milk intake during suckling in mice is described. The method is based on the transfer of a gamma- or hard beta-emitting radioisotope from the lactating mother to the litter. The radioactivity of individual pups is determined at intervals by whole-body counting. The transfer of 22Na, 32P as orthophosphate, 51Cr as chromate, and 125I as iodide was examined; 125I showed particularly suitable characteristics. The procedure proved to be simple, accurate and reproducible for the comparison of mild consumption between pups within a litter and between litters. The procedure was suitable for studies using a foster mother.

Animal Population Groups↗

Abnormalities of GIP in spontaneous syndromes of obesity and diabetes in mice.

The role of GIP in the pathogenesis of spontaneous syndromes of obesity-diabetes was examined in ob/ob mice of the Aston stock and db/db mice of the C57BL/KsJ background. Compared with lean controls, fed adult ob/ob and db/db mice, respectively, exhibited 1.8-fold and 2.1-fold increases in body weight, 1.8-fold and 2.8-fold elevations of plasma glucose, and 15.4-fold and 5.6-fold elevations of plasma insulin. As indicated by the relative magnitude of the hyperglycemia and hyperinsulinemia, db/db mice displayed a particularly severe form of diabetes. Plasma GIP concentrations of ob/ob and db/db mice were elevated 15.1-fold and 6.2-fold, respectively; the increments closely corresponded with the degrees of hyperinsulinemia. Small intestinal weight was increased 1.4-fold and 1.8-fold in ob/ob and db/db mice, respectively, but the intestinal GIP content expressed as microgram/g intestine or microgram/intestine was raised only in ob/ob mice (1.9-fold and 2.8-fold, respectively). Since glucose stimulation of insulin release is defective in both mutant strains, the results strongly implicate pathologically raised GIP concentrations in the hyperinsulinemia and related metabolic abnormalities of the obesity-diabetes syndromes. It is suggested that hypersecretion of GIP results in part from loss of normal feedback inhibition by endogenous insulin.

Animals↗

A circular-dichroism study of epidermolytic toxins A and B from Staphylococcus aureus.

The far-u.v. circular-dichroism spectra of the two epidermolytic toxins was analysed into fractional contributions of 0.09 helix and 0.46 beta-sheet to each toxin structure. Trifluoroethanol perturbation caused an initial increase in dichroic absorption at 205 nm and then a change characterized as a beta-sheet-to-alpha-helix transition. The intense near-u.v. spectra suggested that the toxins have unusually rigid, though different, aromatic-side-chain arrangements.

Bacterial Toxins↗

Hormonal control of glucose homeostasis during development and ageing in mice.

Age-related changes in the hormonal control of glucose homeostasis were examined in immature (5-wk-old), young adult (10-wk-old) and older adult (30 and 60-wk-old mice). In immature mice, basal plasma glucose and insulin concentrations were higher than young adult mice. Glucose tolerance was impaired in immature mice, although the plasma insulin response to glucose and other secretagogues (arginine and glucagon) was well developed, and the hypoglycaemic effect of exogenous insulin was not impaired. Glucagon and epinephrine evoked a greater acute hyperglycaemia in immature mice, suggesting that these hormones exert a stronger rapid glucose-raising effect in preadult life. Basal plasma glucose and insulin concentrations were lowest in young adult mice, and increased with advancing adult age. Glucose tolerance was best in young adult mice and deteriorated with age, while plasma insulin concentrations after administration of glucose, arginine and glucagon were lowest in young adult mice and increased with age. However, in response to these secretagogues, the percentage increase in plasma insulin above basal was reduced in older adult mice. This indicates a defect of stimulus-recognition-secretion-coupling in the B-cells of older adult mice. The raised plasma glucose concentrations of older adult mice could not be attributed to an increase in the acute hyperglycaemic action of glucagon or epinephrine. The hypoglycaemic response to exogenous insulin decreased with age, suggesting that tissue sensitivity to insulin was impaired. Treatment with growth hormone and cortisone for 5 days produced a greater antagonism of insulin in older mice than young adult or immature mice. Growth hormone impaired glucose tolerance at each age, but only produced a marked hyperinsulinaemia in older adult mice. In contrast, cortisone produced a marked hyperinsulinaemia at each age, but only impaired glucose tolerance in older adult mice.

Aging↗

Plasma glucose and insulin response to glucagon and arginine in Aston ob/ob mice: evidence for a selective defect in glucose-mediated insulin release.

Fed adult obese hyperglycaemic (ob/ob) mice fail to produce a positive plasma insulin response to an intraperitoneal (ip) glucose challenge. The present study demonstrates that both fed and fasted ob/ob mice produce a marked positive plasma insulin response to an ip challenge by glucagon or arginine throughout the phases of development and regression of the ob/ob syndrome. These observations provide evidence that failure of the B-cells to respond to glucose in fed adult ob/ob mice cannot be attributed to inadequate amounts of releasable insulin. In addition, the results show that the B-cells of fed adult ob/ob mice do not incur a generalized defect of stimulus-recognition-secretion-coupling.

Animals↗

Role of dietary factors in the hyperinsulinemia of genetically obese hyperglycemic (ob/ob) mice.

To investigate the role of different macronutrients in the hyperinsulinemia of genetically obese hyperglycemic (ob/ob) mice, we examined the insulin response of fasted adult ob/ob mice to the voluntary ingestion of foods with different protein, fat and carbohydrate compositions. During a 3-hour period after ingestion, there was a marked association between the extent of the insulin response and the rise in plasma glucose concentrations. The data suggest that dietary carbohydrate is the nutrient predominantly responsible for the severity of the hyperinsulinemia in adult ob/ob mice. The pronounced insulin-releasing effect of dietary carbohydrate in these mice cannot be attributed to a direct action of glucose on the pancreatic B cells. Thus, the results indicate an important role of the enteroinsular axis in the genesis of the marked insulin-releasing effect of dietary carbohydrate in adult ob/ob mice.

Animals↗