In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Context: Targeting the energy storing white adipose tissue (WAT) by pharmacological and dietary means in order to promote its conversion to energy expending "brite" cell type holds promise as an anti-obesity approach. Present study was designed to investigate/revisit the effect of capsaicin on adipogenic differentiation with special reference to induction of "brite" phenotype during differentiation of 3T3-L1 preadipocytes.', 'Multiple techniques such as Ca2+ influx assay, Oil Red-O staining, nutrigenomic analysis in preadipocytes and matured adipocytes have been employed to understand the effect of capsaicin at different doses. In addition to in-vitro experiments, in-vivo studies were carried out in high-fat diet (HFD) fed rats treated with resiniferatoxin (RTX) (a TRPV1 agonist) and in mice administered capsaicin.', 'TRPV1 channels are expressed in preadipocytes but not in adipocytes. In preadipocytes, both capsaicin and RTX stimulate Ca2+ influx in dose-dependent manner. This stimulation may be prevented by capsazepine, a TRPV1 antagonist. At lower doses, capsaicin inhibits lipid accumulation and stimulates TRPV1 gene expression, while at higher doses it enhances accumulation of lipids and suppresses expression of its receptor. In doses of 0.1-100 M, capsaicin promotes expression of major pro-adipogenic factor PPAR and some of its downstream targets. In concentrations of 1 M, capsaicin up-regulates anti-adipogenic genes. Low-dose capsaicin treatment of 3T3-L1 preadipocytes differentiating into adipocytes results in increased expression of brown fat cell marker genes. In white adipose of mice, capsaicin administration leads to increase in browning-specific genes. Global TRPV1 ablation (i.p. by RTX administration) leads to increase in locomotor activity with no change in body weight.\Question: Does capsaicin induce '' brite '' phenotype in differentiating 3T3-L1 preadipocytes?
Our findings suggest the dual modulatory role of capsaicin in adipogenesis. Capsaicin inhibits adipogenesis in 3T3-L1 via TRPV1 activation and induces brown-like phenotype whereas higher doses.

Context: To introduce an elastomeric continuous infusion pump for pain control after outpatient orbital implant surgery.', 'Retrospective, noncomparative consecutive case series of all patients undergoing enucleation, evisceration, or secondary orbital implantation using the On-Q pain system between August 2004 and January 2006. Postoperative pain score, need for narcotics, and adverse events were recorded. The On-Q catheter is inserted intraoperatively through the lateral lower eyelid into the muscle cone under direct visualization, prior to the orbital implant placement. The On-Q system continually infuses anesthesia (bupivacaine) to the retrobulbar site for 5 days.', 'Among 20 patients, mean postoperative period pain score, with On-Q in place, was 1.3 (scale of 0 to 10). Nine patients (45%) did not need any adjunctive oral narcotics. Two patients experienced postoperative nausea. One catheter connector leaked, thereby decreasing delivery of retrobulbar anesthetic resulting a pain level of 6, the highest level in the study. There were no postoperative infections. No systemic toxic effects from bupivacaine were observed clinically.\Question: Do on-Q pump for pain control after orbital implant surgery?
The On-Q pain pump is widely available, low cost, and requires minimal patient manipulation for the use in orbital implant surgery. The device was safe and appeared to minimize postoperative pain in the authors' case series.

Context: Thyroid-stimulating hormone (TSH) levels within populations do not follow Gaussian distribution, and normal limits are derived after mathematical normalization. The clinical relevance of these limits is unknown. The objective of this study was to compare upper and lower TSH limits by four data normalization methods with non-normalized data and assess their clinical relevance.', 'Results of blood samples taken by community physicians and stored in a computerized database were analysed after removing samples from patients with evidence of thyroid illness. TSH values were normalized by the Hoffmann and Tukey methods and each method with natural log transformation. Non-normalized data for TSH in the uppermost and lowermost percentile were also calculated. Clinical relevance was determined by alterations in thyroid hormone levels at, below and above the limits for each method.', 'The maximal reduction from non-normalized data for the upper normal limit (UNL) was by the Hoffman method 43% = 31 mIU/l). The maximal increase for the lower normal limit (LNL) was also by the Hoffman method (708% = 081 mIU/l). There was very limited difference in average FT3 and FT4 between patients with TSH within, below or above the normal range for all methods.\Question: Do normal limits for serum thyrotropin vary greatly depending on method?
Different normalization methods alter the normal limits greatly. However, in individuals without thyroid illness, thyroid hormone values are stable over a wide range of TSH levels including beyond the UNL for all methods. Indeed, there may be no true universal upper TSH cut-off level and clinical decision-making cannot rely on these calculated limits.