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Biomedical subjects

K Robertson

Publications and source records attributed to K Robertson.

84 records · Page 5Linked to original sources
PubMed1977

Enterochromaffin cells in the duodenal mucosa of children with coeliac disease.

A cell counting technique was used to count enterochromaffin (EC) cells in the duodenal mucosa of 10 children with coeliac disease and 10 controls, and significantly greater numbers of EC cells were found in children with coeliac disease. In four children with a clinical history suggestive of coeliac disease, but with minor histopathological changes in the duodenum, gluten challenge resulted in increased numbers of EC cells. Abnormalities of 5-hydroxytryptamine metabolism in coeliac disease may result from hyperplasia of EC cells in the small intestine.

Celiac Disease↗
PubMedDate not supplied

Basal and glucagon-stimulated plasma C-peptide concentrations in healthy dogs, dogs with diabetes mellitus, and dogs with hyperadrenocorticism.

Serum glucose and plasma C-peptide response to i.v. glucagon administration was evaluated in 24 healthy dogs, 12 dogs with untreated diabetes mellitus, 30 dogs with insulin-treated diabetes mellitus, and 8 dogs with naturally acquired hyperadrenocorticism. Serum insulin response also was evaluated in all dogs, except 20 insulin-treated diabetic dogs. Blood samples for serum glucose, serum insulin, and plasma C-peptide determinations were collected immediately before and 5, 10, 20, 30, and (for healthy dogs) 60 minutes after i.v. administration of 1 mg glucagon per dog. In healthy dogs, the patterns of glucagon-stimulated changes in plasma C-peptide and serum insulin concentrations were identical, with single peaks in plasma C-peptide and serum insulin concentrations observed approximately 15 minutes after i.v. glucagon administration. Mean plasma C-peptide and serum insulin concentrations in untreated diabetic dogs, and mean plasma C-peptide concentration in insulin-treated diabetic dogs did not increase significantly after i.v. glucagon administration. The validity of serum insulin concentration results was questionable in 10 insulin-treated diabetic dogs, possibly because of anti-insulin antibody interference with the insulin radioimmunoassay. Plasma C-peptide and serum insulin concentrations were significantly increased (P < .001) at all blood sampling times after glucagon administration in dogs with hyperadrenocorticism, compared with healthy dogs, and untreated and insulin-treated diabetic dogs. Five-minute C-peptide increment, C-peptide peak response, total C-peptide secretion, and, for untreated diabetic dogs, insulin peak response and total insulin secretion were significantly lower (P < .00l) in diabetic dogs, compared with healthy dogs, whereas these same parameters were significantly increased (P < .01) in dogs with hyperadrenocorticism, compared with healthy dogs, and untreated and insulin-treated diabetic dogs. Although not statistically significant, there was a trend for higher plasma C-peptide concentrations in untreated diabetic dogs compared with insulin-treated diabetic dogs during the glucagon stimulation test. Baseline C-peptide concentrations also were significantly higher (P < .05) in diabetic dogs treated with insulin for less than 6 months, compared with diabetic dogs treated for longer than 1 year. Finally, 7 of 42 diabetic dogs had baseline plasma C-peptide concentrations greater than 2 SD (ie, > 0.29 pmol/mL) above the normal mean plasma C-peptide concentration; values that were significantly higher, compared with the results in healthy dogs (P < .001) and with the other 35 diabetic dogs (P < .001). In summary, measurement of plasma C-peptide concentration during glucagon stimulation testing allowed differentiation among healthy dogs, dogs with impaired beta-cell function (ie, diabetes mellitus), and dogs with increased beta-cell responsiveness to glucagon (ie, insulin resistance). Plasma C-peptide concentrations during glucagon stimulation testing were variable in diabetic dogs and may represent dogs with type-1 and type-2 diabetes or, more likely, differences in severity of beta-cell loss in dogs with type-1 diabetes.

Adrenocortical Hyperfunction↗
PubMedDate not supplied

Evidence for glucuronide (small molecule) sorting by human hepatic endoplasmic reticulum.

The entry of substrates into, and the export of glururonides from, the lumen of hepatic endoplasmic reticulum (ER) in vitro (sealed microsomes) has been measured using radioactivity-labelled materials and a rapid filtration assay. Analysis of liver microsomes from a jaundiced patient showed the accumulation of bilirubin glucuronides within the lumen of the ER. Further analysis of these hepatic microsomes revealed that newly synthesized 1-naphthol glucuronide could exit from the microsomes whereas bilirubin glucuronide was accumulated within the microsomes. These results suggest the existence of mechanisms for the sorting of small molecules, destined for export through bile canalicular or basolateral plasma membranes, by ER. Furthermore, these sorting processes may be regulated by specific transporters within the ER.

Bilirubin↗
PubMedDate not supplied

Relapse in the skull after myeloablative therapy for high-risk neuroblastoma.

Patterns of relapse were determined for 20 high-risk neuroblastoma patients treated with chemotherapy, surgery, primary and metastatic site radiation (21 Gray), myeloablative chemotherapy, peripheral blood stem cell rescue, and 13-cis-retinoic acid. The median follow-up duration after transplant is 21 months (range, 8-34 months). The event-free survival and overall survival at 2 years were 45 and 75%, respectively. There were 2 primary site recurrences. Metastatic sites that became MIBG-scan negative on induction chemotherapy were not irradiated. Four patients relapsed in irradiated metastatic sites, 3 in the skull, 1 in the liver. Failure also occurred at 2 skull sites treated with chemotherapy only, and at 5 new sites: 1 skull, 2 distant lymph nodes, and 2 bones other than skull. Eight of 20 patients had skull metastasis at presentation; 6 were irradiated and 3 were controlled. Skull metastasis warrants more aggressive evaluation and treatment.

Antineoplastic Combined Chemotherapy Protocols↗