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Background: HERG potassium channel blockade is the major cause for drug-induced long QT syndrome, which sometimes cause cardiac disrhythmias and sudden death. There is a strong interest in the pharmaceutical industry to develop high quality medium to high-throughput assays for detecting compounds with potential cardiac liability at the earliest stages of drug development. Cultivation of cells at lower temperature has been used to improve the folding and membrane localization of trafficking defective hERG mutant proteins. The objective of this study was to investigate the effect of lower temperature maintenance on wild type hERG expression and assay performance. Results: Wild type hERG was stably expressed in CHO-K1 cells, with the majority of channel protein being located in the cytoplasm, but relatively little on the cell surface. Expression at both locations was increased several-fold by cultivation at lower growth temperatures. Intracellular hERG protein levels were highest at 27C and this correlated with maximal 3H-dofetilide binding activity. In contrast, the expression of functionally active cell surface-associated hERG measured by patch clamp electrophysiology was optimal at 30C. The majority of the cytoplasmic hERG protein was associated with the membranes of cytoplasmic vesicles, which markedly increased in quantity and size at lower temperatures or in the presence of the Ca2 + -ATPase inhibitor, thapsigargin. Incubation with the endocytic trafficking blocker, nocodazole, led to an increase in hERG activity at 37C, but not at 30C. Conclusion: Our results are consistent with the concept that maintenance of cells at reduced temperature can be used to boost the functional expression of difficult-to-express membrane proteins and improve the quality of assays for medium to high-throughput compound screening. In addition, these results shed some light on the trafficking of hERG protein under these growth conditions Drug. system of the American Hospitsl Formulary Service. See reference 5. Who had undergone enucleation for retinoblastoma in one eye with salvage of the other eye and who had maintained tumor quiescence for a period of 12 months or longer in that eye. Our purpose was to determine how these patients fared following intraocular surgery of the salvaged eye. Patients and Methods. We performed a retrospective review of all germline retinoblastoma cases from January 1, 1985, until December 31, 2000, to identify all patients who had undergone unilateral enucleation with salvage of the other eye. Cases were drawn from the records of the University of Tennessee, Memphis, Department of Ophthalmology, Memphis; the records of the Ophthalmic Oncology Service at St Jude Children's Research Hospital, Memphis; and the private records of Retina Associates of Florida, Tampa. Cases were enrolled only if the salvaged eye achieved a 12-month period of tumor quiescence and then subsequently underwent intraocular surgery for nontumor-control reasons. Tumor quiescence was defined as lack of documented tumor growth, lack of vitreous or subretinal seeding, lack of anterior chamber seeding, and lack of metastases. Eligible intraocular surgery included cataract extraction, barrier laser for retinal break, scleral buckle procedure, pars plana vitrectomy, and Nd: YAG laser capsulotomy. Original treatment of the retinoblastoma was recorded, as was the ReeseEllsworth classification. The 3 primary outcomes were tumor activity, visual acuity, and development of complications. Tumor activity was classified as quiescent, recurrent, and.

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Not clear whether insulin exerts a specific effect to regulate synthesis and secretion of leptin or merely promotes adipocyte differentiation. In contrast, studies on insulin treatment of isolated human adipose cells have generally not shown acute stimulation of leptin secretion 12, 30 ; . Studies in isolated rat adipose cells are equivocal: two studies reported effects at both the mRNA and protein levels while a third study showed no increase in leptin mRNA in response to incubation with insulin 4, 8, 10 ; . Our results document stimulation of both production and secretion of leptin in tissue fragments. Moreover, these effects are easier to quantify in tissue fragments because isolated adipose cells contain much less leptin, thus making it difficult to see an effect. Furthermore, after 2 h in culture, isolated adipose cells no longer respond to insulin with increased leptin secretion, indicating they can easily lose the ability to produce leptin. We observed that insulin increased leptin secretion in vitro. Why then have no increases in circulating leptin been detected in in vivo insulin clamp studies 12, 13, 3133 ; ? Possible simple explanations include a species difference between rats and humans or the possibility that some adipose cells do not respond like those in epididymal fat tissue. It could be that a delay occurs between secretion by fat cells and appearance in the blood. Another possibility is that insulin affects the clearance of leptin even though leptin appears to be cleared by passive filtration 34 ; . However, the most likely explana and modicon.

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