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Biomedical subjects

R S Pruthi

Publications and source records attributed to R S Pruthi.

22 records · Page 2Linked to original sources

Pediatric genitourinary tumors.

Each year significant advances are made in the clinical evaluation and treatment of genitourinary tumors in children as well as in the understanding of the molecular biology of tumorigenesis and genetics. In addition, the long-term outcome and complications of current treatments are now becoming available for review. The purpose of this article is to review recent literature on pediatric genitourinary Wilms' tumor, rhabdomyosarcoma, and testicular carcinoma in situ.

Adolescent↗

Secretin receptors in a new preparation of plasma membranes from intrahepatic biliary epithelium.

Secretin is thought to cause choleresis by acting on a receptor expressed by bile duct epithelial cells. In this study, the receptor was characterized using a new preparation of intrahepatic bile duct plasma membranes. Hyperplastic biliary trees were obtained from 3-week bile duct-ligated rats. The biliary trees were homogenized, filtered, and subjected to an aqueous two-phase partition technique to yield highly purified plasma membranes (confirmed by a 14-fold enrichment in gamma-glutamyl transpeptidase activity and a 10-fold enrichment in 125I-secretin binding). 125I-secretin bound saturably with high affinity and in a dose-dependent fashion (Kd = 1.3 +/- 0.1 nM, Bmax = 273 +/- 23 fmole/mg) to purified plasma membranes. The binding characteristics of secretin were most consistent with a single site receptor model. Competitive binding studies indicated that the secretin-related peptides glucagon, peptide histidine isoleucine, gastric inhibitory peptide, and growth hormone releasing factor did not inhibit binding. Vasoactive intestinal peptide (1 microM) reduced maximal binding by 19 +/- 1%. The GTP analogs guanylylimidodiphosphate and guanosine 5'-O-[3-thiotriphosphate] (1 microM) inhibited binding by 16 +/- 2 and 13 +/- 1%, respectively. In conclusion, secretin binds to a specific, high-affinity receptor in intrahepatic bile duct epithelium that is coupled to a G-protein-linked signal transduction system.

Animals↗

The effect of octreotide on hepatic regeneration in rats.

The effect of the long-acting somatostatin analog octreotide on liver regeneration was studied in rats in vitro and in vivo. The effect of continuous subcutaneous octreotide infusion on regenerative liver weight and relative DNA synthesis was examined in rats that had undergone 70% hepatectomy. Administration of octreotide resulted in a 33% reduction of regenerating liver weight at 72 hours and a 67% reduction of regenerative hepatocellular hyperplasia at 24 hours. This effect was reversed within 12 hours after withdrawal of the drug. The mechanism for the inhibitory effect of octreotide appears to be indirect, because experiments in hepatocyte cultures did not demonstrate a direct inhibitory effect on serum-free or epidermal growth factor-induced regenerative hepatocyte proliferation. Because insulin levels were suppressed by octreotide in the in vivo experiments, suppression of hepatotrophs may be the mechanism by which octreotide inhibits liver regeneration.

Animals↗

Intracerebroventricular neuropeptide Y stimulates bile secretion via a vagal mechanism.

UNLABELLED: The effect of intracerebroventricular injection of neuropeptide Y on biliary secretion was studied in conscious dogs, prepared with gastric and duodenal fistulas and cerebroventricular guides. Bile secretion was increased in a dose-dependent fashion by intracerebroventricular neuropeptide Y. The peak increase was seen after 500 pM/kg of neuropeptide Y which resulted in a 30 x 2% increase in bile flow over the period 30-150 minutes after injection. ( CONTROL: 23 x 2 (1 x 2) ml/2 hours; neuropeptide Y 500 pM/kg: 30 x 5 (1 x 1) ml/2 hours). Biliary lipid composition was not altered significantly but bicarbonate output was increased at all doses tested. Intravenous infusion of neuropeptide Y (1000 pM) for 1 hour had no significant effect. Intracerebroventricular neuropeptide Y (1000 pM/250-300 mg body weight) also increased bile flow in urethane-anaesthetised rats. This effect was abolished by cervical vagotomy. The demonstration of a central stimulation of alkaline bile flow suggests that bile secretion may be subject to central modulation.

Animals↗