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Biomedical subjects

K N Ching

Publications and source records attributed to K N Ching.

30 records · Page 2Linked to original sources
PubMed1987

Modulatory effects of corticotropin-releasing factor on the delayed corticosteroid feedback in humans: implications of feedback sites.

We recently demonstrated the presence of a delayed phase of glucocorticoid feedback on nonstress-induced ACTH secretion in normal volunteers. In this study, we investigate the effects of corticotropin-releasing factor (CRF) on that delayed feedback pathway with an attempt to determine the sites on which glucocorticoid exerts its delayed feedback effects. Thirty normal subjects were subjected to study and each subject received a single midnight dosage of 30 mg/kg BW metyrapone before each test. The whole experiment was divided into two studies. In study I, we found that ovine CRF (oCRF) 1 microgram/kg BW alone as an IV bolus injection caused an increase in the plasma ACTH level, which persisted for at least 120 minutes. Continuous infusion of cortisol 25 mg/h alone for two hours produced a significant decrease in the plasma ACTH level; this fall of ACTH began 30 minutes after the onset of cortisol administration. When IV bolus injection of oCRF 1 microgram/kg BW and the continuous infusion of cortisol 25 mg/h for two hours were both given, the plasma ACTH level increased firstly and then decreased 60 minutes after the onset of cortisol administration, progressing thereafter to the end of the study. Study II showed in those who received the IV bolus injection of human CRF (hCRF) 100 micrograms and the continuous infusion of cortisol 25 mg/h for two hours, the plasma ACTH level increased firstly and began to decline 45 minutes after the onset of cortisol administration, progressing thereafter to the end of the test.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1986

Evidence for a delayed, integral, and proportional phase of glucocorticoid feedback on ACTH secretion in normal human volunteers.

To investigate the mechanisms responsible for glucocorticoid feedback on nonstress-induced ACTH secretion in normal subjects, 24 volunteer subjects (14 males and 10 females, 21 to 43 years) were divided into six groups in a randomized fashion and studied. Each subject received a single midnight dose of 30 mg/kg per body weight of metyrapone and then cortisol was administered according to different protocols in the next morning to provide extreme variations of the input signal. It was found that no obvious inhibition in plasma ACTH levels was shown during the first 15 min despite the fact that cortisol was given at rather larger doses and short time intervals. However, a significant suppression in plasma ACTH levels began to manifest approximately 30 min after cortisol administration in each study group and it became apparent that the degree of inhibition of ACTH level at 75 min correlated with the plasma cortisol concentrations at the same moment (r = 0.97, P less than 0.01) as well as with the dosage of cortisol during this time, whatever administered (r = 0.99, P less than 0.01). In summary, our data provided evidence for a delayed, proportional, and integral phase of glucocorticoid feedback on nonstress-induced ACTH secretion in normal human volunteers.

Adrenocorticotropic Hormone↗
PubMed1986

Carcinoid tumor of the pancreas causing the diarrheogenic syndrome: report of a case combined with multiple endocrine neoplasia, type I.

A case of carcinoid tumor of the pancreas with the watery diarrhea, hypokalemia, and hypochlorhydria syndrome in association with hyperparathyroidism and the amenorrhea-galactorrhea syndrome is presented. Resection of the three grossly enlarged, hyperplastic parathyroid glands restored eucalcemia in this patient. A subsequent excision of the 370 gm pancreatic carcinoid tumor resulted in a cure of the watery diarrhea and a return of the gastric acid secretion to normal. Immunocytochemical studies of the pancreatic tumor demonstrated a positive stain only for serotonin, and negative results for vasoactive intestinal polypeptide, pancreatic polypeptide, glucagon, insulin, cholecystokinin, gastrin, and calcitonin were obtained. These studies suggest that in this patient, serotonin was a causative agent of the watery diarrhea syndrome.

Adenoma, Islet Cell↗