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.

Example Input: Context: In this study, we compared the diagnostic performance of the standard SPECT with motion-frozen (MF) myocardial perfusion SPECT (MPS) in obese patients.', 'A total of 90 consecutive obese patients (body mass index, 30.1-46.8, average, 34.3 +/- 3.6; age, 63 +/- 12 y; 30% women) underwent standard supine rest (201)Tl/stress (99m)Tc dual-isotope gated MPS and cardiac catheterization within 3 mo. MF images were obtained by nonlinear warping of cardiac phases to the end-diastolic position. Total perfusion deficit (TPD) was obtained for summed (S-TPD) and motion-frozen (MF-TPD) datasets with sex-specific standard and MF normal limits.', 'The area under the receiver-operating-characteristic (ROC) curve for detection of coronary artery disease (CAD) by MF-TPD was significantly larger than that for S-TPD (0.93 +/- 0.25 vs. 0.88 +/- 0.32, P < 0.05). MF-TPD had higher specificity (77% vs. 55%, P < 0.05) and accuracy (89% vs. 80%, P < 0.05) than did S-TPD.\Question: Does motion-frozen myocardial perfusion SPECT improve detection of coronary artery disease in obese patients?
Example Output: MF processing of MPS improves CAD detection in obese patients.

Example Input: Context: Urothelial carcinoma associated 1 (UCA1) functions as an oncogene, which promotes cancer cell proliferation, invasion, and metastasis, and is responsible for drug resistance. This study aimed to determine the expression level of UCA1 in ovarian cancer and to further investigate its clinical significance.', 'The expression levels of UCA1 in ovarian cancer and normal ovaries were determined by quantitative real-time PCR. The relationship between UCA1 expression and clinical features and the prognostic value of UCA1 for overall survival were examined.', 'UCA1 expression in ovarian cancer tissues was significantly upregulated compared with normal ovarian tissues. High UCA1 expression was related to lymph node metastasis, FIGO stage, and response to chemotherapy. Kaplan-Meier analysis demonstrated that high UCA1 expression was associated with poorer overall survival in patients with ovarian cancer. Cox proportional hazards analysis showed that high UCA1 expression was an independent prognostic marker of poor outcome. This effect remained significant in the further stratification analysis.\Question: Does uCA1 overexpression predict clinical outcome of patients with ovarian cancer receiving adjuvant chemotherapy?
Example Output: Our findings provided the first evidence that UCA1 may serve as an indicator of response to chemotherapy and prognosis of ovarian cancer. UCA1 may play an important role in the progression of ovarian cancer.

Example Input: Context: Dexmedetomidine (DEX) has been implicated in modulating the inflammatory response in central nervous system (CNS). However, the mechanism is still poorly understood. In this study, we evaluate the effects of DEX on lipopolysaccharide (LPS)-induced microglia activation and elucidate its possible signaling pathway involved in its anti-inflammatory effects.', 'BV2 and primary microglia were pretreated with various concentrations of DEX (001, 01, 1, and 10 M) and/or PD98059 for 1 hour, then microglia were incubated with LPS (1 g/ml) for 24 hours. Nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression were measured by Griess reagent and real-time polymerase chain reaction. Furthermore, two intracellular signaling cascades including extracellular signal-regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK) were investigated by western blot analysis.', 'Dexmedetomidine significantly attenuated LPS-induced NO production and iNOS expression in both BV2 cells and primary microglial cells. Lipopolysaccharide activated both ERK1/2 and JNK signal pathways; however, DEX exerted a specific inhibitory effect on ERK1/2 rather than JNK. Intriguingly, treatment of primary microglia and BV2 cells with DEX in combination with ERK1/2 inhibitor (PD98059) enhanced attenuation of LPS-induced NO production and iNOS expression.\Question: Does dexmedetomidine inhibit inducible nitric oxide synthase in lipopolysaccharide-stimulated microglia by suppression of extracellular signal-regulated kinase?
Example Output:
Dexmedetomidine attenuates NO and iNOS accumulation by inhibiting extracellular signal-regulated kinase (ERK) activation in both BV2 cells and primary microglial cells.