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: It has been shown that maternal mental health is associated with poorer skills development in the offspring. However, the evidence evaluating the association between social anxiety disorder (SAD) and cognitive or language development, is scarce.', 'To evaluate the association between maternal SAD and performance in cognitive and language tests in 30-month old children.', 'This was a cohort study involving young women evaluated since pregnancy.', 'We evaluated 520 mother-child dyads who received prenatal medical assistance through the National Public Health System in a southern Brazilian city, from October 2009 to March 2011.', 'We used the Mini Neuropsychiatric Interview Plus (MINI Plus) to assess SAD among young mothers. Cognitive and language performance in their offspring was analyzed using the Bayley Scales of Infant and Toddler Development - 3rd Edition.', 'We found an association between maternal SAD and performance in cognitive and language tests. Children of mothers with SAD had in average 4.5 less points in the Bayley scale, when compared to those with mothers without SAD: in the cognitive (β=-4.53 [95% CI -7.8; -1.1] p=0.008) and language subscales (β=-4.54 [95% CI -9.0; -0.5] p=0.047).\Question: Is cognitive and language performance in children associated with maternal social anxiety disorder : A study of young mothers in southern Brazil?

A: Our findings suggest that children with mothers suffering from SAD have poorer cognitive abilities and language skills.
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Q: Context: We examined the effects of cilostazol on mitogen-activated protein kinase (MAPK) activity and its relationship with cilostazol-mediated protection against apoptosis in lipopolysaccharide (LPS)-treated endothelial cells.', 'Human umbilical vein endothelial cells (HUVECs) were exposed to LPS and cilostazol with and without specific inhibitors of MAPKs; changes in MAPK activity in association with cell viability and apoptotic signaling were investigated.', 'Cilostazol protected HUVECs against LPS-induced apoptosis by suppressing the mitochondrial permeability transition, cytosolic release of cytochrome c, and subsequent activation of caspases, stimulating extracellullar signal-regulated kinase (ERK1/2) and p38 MAPK signaling, and increasing phosphorylated cAMP-responsive element-binding protein (CREB) and Bcl-2 expression, while suppressing Bax expression. These cilostazol-mediated cellular events were effectively blocked by MAPK/ERK kinase (MEK1/2) and p38 MAPK inhibitors.\Question: Does cilostazol protect endothelial cells against lipopolysaccharide-induced apoptosis through ERK1/2- and P38 MAPK-dependent pathways?

A: Cilostazol protects HUVECs against LPS-induced apoptosis by suppressing mitochondria-dependent apoptotic signaling. Activation of ERK1/2 and p38 MAPKs, and subsequent stimulation of CREB phosphorylation and Bcl-2 expression, may be responsible for the cellular signaling mechanism of cilostazol-mediated protection.
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Q: Context: Efavirenz frequently causes central nervous system (CNS) symptoms. We evaluated genetic associations with efavirenz discontinuation for CNS symptoms within 12 months of treatment initiation.', 'Patients had initiated efavirenz-containing regimens at an HIV primary care clinic in the Southeastern United States and had at least 12 months of follow-up data. Polymorphisms in CYP2B6 and CYP2A6 defined efavirenz metabolizer categories. Genome-wide genotyping enabled adjustment for population stratification.', 'Among 563 evaluable patients, 99 (17.5%) discontinued efavirenz within 12 months, 29 (5.1%) for CNS symptoms. The hazard ratio (HR) for efavirenz discontinuation for CNS symptoms in slow versus extensive metabolizers was 4.9 [95% confidence interval (CI): 1.9-12.4; P=0.001]. This HR in Whites was 6.5 (95% CI: 2.3-18.8; P=0.001) and 2.6 in Blacks (95% CI: 0.5-14.1; P=0.27). Considering only slow metabolizers, the HR in Whites versus Blacks was 3.1 (95% CI: 0.9-11.0; P=0.081). The positive predictive value of slow metabolizer genotypes for efavirenz discontinuation was 27% in Whites and 11% in Blacks.\Question: Does pharmacogenetics of efavirenz discontinuation for reported central nervous system symptoms appear to differ by race?

A:
Slow metabolizer genotypes were associated significantly with efavirenz discontinuation for reported CNS symptoms. This association was considerably stronger in Whites than in Blacks.
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