Background: Laparoscopic adrenalectomy for Conn's syndrome, Cushing's disease, cortisol-producing adenomas, and nonfunctioning adenomas has been well established. This study was intended to evaluate the clinical outcomes of patients undergoing laparoscopic adrenalectomy for pheochromocytoma, and to assess the efficacy and safety of a minimally invasive approach.
Methods: Data were collected prospectively on all patients undergoing laparoscopic adrenalectomy for pheochromocytoma over a 5-year period.
The NPXY motif that was identified in the low density lipoprotein receptor serves as an internalization signal, and subsequent studies have indicated that the NPXY sequence is also an important recognition element for internalization of both insulin and transferrin receptors. The insulin-like growth factor (IGF-I) receptor contains an NPXY sequence (residues 947-950) in the immediate submembranous domain, and we sought to determine whether these residues play a role in facilitating ligand-mediated internalization of the IGF-I receptor. To study this, we have constructed stable cell lines expressing NPXY deletion mutant receptors (CHONPXY) or wild-type receptors (CHOWT).
View Article and Find Full Text PDFTo study the function of exon 21 of the insulin receptor, a mutant human insulin receptor lacking this domain was constructed. The mutant HIR delta E21 cDNA was transfected into Rat-1 fibroblasts and stable cell lines were selected. The HIR delta E21 receptors were expressed on the cell surface, and they bound insulin with the same affinity as did the wild-type-expressing cell line, hIRcB.
View Article and Find Full Text PDFThe contribution of the insulin receptor beta-subunit acidic domain, amino acids 1262-1291, to receptor function was analyzed. A mutant insulin receptor complementary DNA lacking this domain was created. Rat-1 fibroblasts were stably transfected with plasmids containing the mutant insulin receptor complementary DNA and clonal cell lines derived (hIR1262).
View Article and Find Full Text PDFAcetaminophen overdose is generally treated with oral N-acetylcysteine. While N-acetylcysteine is protective, an additional effective mode of treatment is desirable in large overdoses. A growing body of evidence suggests that cimetidine significantly reduces the hepatotoxicity of an acetaminophen overdose and that its hepatoprotective action may be additive to that of N-acetylcysteine.
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