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.

Q: Context: Radiation induces an important apoptosis response in irradiated organs. The objective of this study was to investigate the radioprotective effect of tetramethylpyrazine (TMP) on irradiated lymphocytes and discover the possible mechanism of protection.', 'Lymphocytes were pretreated for 12 h with TMP (25-200 molL(-1)) and then exposed to 4 Gy radiation. Cell apoptosis and the signaling pathway were analyzed.', 'Irradiation increased cell death, DNA fragmentation, activated caspase activation and cytochrome c translocation, downregulated B-cell lymphoma 2 (Bcl-2) and up-regulated Bcl-2-associated X protein (Bax). Pretreated with TMP significantly reversed this tendency. Several anti-apoptotic characteristics of TMP, including the ability to increase cell viability, inhibit caspase-9 activation, and upregulate Bcl-2 and down-regulate Bax in 4Gy-irradiated lymphocytes were determined. Signal pathway analysis showed TMP could translate nuclear factor-B (NF-B) from cytosol into the nucleus.\Question: Does tetramethylpyrazine protect lymphocytes from radiation-induced apoptosis through nuclear factor-B?

A: The results suggest that TMP had a radioprotective effect through the NF-B pathway to inhibit apoptosis, and it may be an effective candidate for treating radiation diseases associated with cell apoptosis.
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Q: Context: To examine peripheral nerve stimulation (PNS) thresholds for normal human subjects in magnetic resonance imaging (MRI) gradient coils, and determine if observed thresholds could be predicted based on gross physiologic measurements.', 'PNS thresholds for 21 healthy normal subjects were measured using a whole-body gradient coil. Subjects were exposed to a trapezoidal echo-planar imaging (EPI) gradient waveform and the total change in gradient strength (DeltaG) required to cause PNS as a function of the duration of the gradient switching time (tau) were measured. Correlation coefficients and corresponding P values were calculated for the PNS threshold measurements against simple physiologic measurements taken of the subjects, including weight, height, girth, and average body fat percentage, in order to determine if there were any easily observable dependencies.', 'No convincing correlations between threshold parameters and gross physiologic measurements were observed.\Question: Do simple anatomical measurements correlate significantly to individual peripheral nerve stimulation thresholds as measured in MRI gradient coils?

A: These results suggest it is unlikely that a simple physiologic measurement of subject anatomy can be used to guide the operation of MRI scanners in a subject-specific manner in order to increase gradient system performance while avoiding PNS.
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Q: 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?

A:
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.
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