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: To ascertain the prevalence of psychiatric symptoms and substance use disorders among adolescents with a lifetime history of foster care placement, using data from a nationally representative sample of U.S. adolescents.', 'We studied adolescents aged 12-17 years in the public use file of the 2000 National Household on Drug Abuse (n = 19,430, including 464 adolescents with history of foster care placement). Psychiatric symptoms and substance use disorders were ascertained through direct interviewing of adolescents. Logistic regression analyses were used to estimate the odds of past-year psychiatric symptoms and substance use disorders among adolescents involved with foster care, as compared to those without a lifetime history of foster care placement (comparison group).', 'Adolescents involved with foster care had more past-year psychiatric symptoms, and especially more conduct symptoms, and past-year substance use disorders than those never placed in foster care. Adolescents involved with foster care were about four times more likely to have attempted suicide in the preceding 12 months (adjusted odds ratio [AOR] 3.95; 95% confidence interval [CI] 2.78, 5.61), and about five times more likely to receive a drug dependence diagnosis in the same period (AOR 4.81; 95% CI 3.22, 7.18).\Question: Do psychiatric symptoms and substance use disorders in a nationally representative sample of American adolescents involved with foster care?
Example Output: Adolescents involved with foster care have a higher prevalence of psychiatric symptoms and drug use disorders than those never placed in foster care. Additionally, the results of this study suggest that they may be at elevated risk for suicide attempts.

Example Input: Context: Infection of human immunodeficiency virus (HIV) has been associated with several chronic diseases, including pulmonary artery hypertension and atherosclerosis. However, the underlying mechanisms of these vascular complications are largely unknown. The objective of this study was to test a novel hypothesis that HIV Nef, an accessory HIV protein, may directly affect endothelial functions and gene expression in pulmonary arteries.', 'Fresh porcine pulmonary artery rings and human pulmonary artery endothelial cells (HPAECs) were treated with HIV Nef for 24 h. With a myograph device, vasomotor function was determined with thromboxane A2 analog, U46619, for contraction, bradykinin, and sodium nitroprusside for relaxation. The expression of endothelial nitric oxide synthase (eNOS) was determined with real-time PCR and immunohistochemistry. Nitric oxide (NO) production was determined by Calorimetric Nitric Oxide Assay kit. Superoxide anion levels were detected with lucigenin-enhanced chemiluminescence assay and dihydroethidium (DHE) staining.', 'The endothelium-dependent vasorelaxation in response to bradykinin was significantly reduced in HIV Nef-treated porcine pulmonary artery rings in a concentration-dependent manner. In response to bradykinin (10(-8) mol/L), HIV Nef (10 ng/mL) significantly reduced vasorelaxation by 32% compared with untreated controls (P < 0.05). In addition, HIV Nef significantly decreased eNOS expression in the vessels and HPAECs. HIV Nef at 10 ng/mL significantly decreased NO production in HPAECs by 21% compared with controls (P < 0.05). Furthermore, HIV Nef significantly increased superoxide anion production in porcine pulmonary arteries and HPAECs compared with controls (P < 0.05). Consequently, Mn (III) tetrakis porphyrin, a superoxide dismutase mimic, effectively blocked HIV Nef-induced vasomotor dysfunction and superoxide anion production. The specificity of HIV Nef action was confirmed by anti-Nef antibody blocking and Nef heat inactivation.\Question: Does hIV Nef protein cause endothelial dysfunction in porcine pulmonary arteries and human pulmonary artery endothelial cells?
Example Output: HIV Nef protein significantly decreases endothelium-dependent vasorelaxation in porcine pulmonary arteries. It also reduces eNOS expression and induces oxidative stress in both porcine pulmonary arteries and HPAECs. This study demonstrates a new mechanism of HIV Nef, which causes endothelial dysfunction and may contribute to the human pulmonary artery disease in HIV-infected patients.

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 (0·01, 0·1, 1, and 10 μM) and/or PD98059 for 1 hour, then microglia were incubated with LPS (1 μg/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.