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: 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?

A: 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.
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Q: Context: Our previous work demonstrated altered messenger RNA expression of integrin -5 and -8, using an in silico analysis of publically available data from patients with biliary atresia (BA); however, we were unable to demonstrate statistically significant differences in protein expression because of sample size. In the present study, we repeated the analysis of liver fibrosis and protein expression of the integrins in a larger cohort of patients with BA and compared them with patients undergoing liver biopsy for other diagnoses, with the hypothesis that 1 of the integrins would be differentially expressed.', 'Liver specimens were obtained at 2 collaborating institutions. Samples from infants with BA (n = 23) were compared with samples from those who underwent liver biopsy for neonatal hepatitis (n = 9). All of the specimens were analyzed by 2 pathologists (C.R. and R.A.), who were blinded to the diagnoses. Standard Ishak scoring was performed to evaluate fibrosis and inflammation, and immunohistochemical (IHC) positivity was graded from 0 to 4. Comparisons between the IHC positivity and Ishak scoring for the BA and control groups were performed using the Student t test with P < 0.01 considered significant because of the multiple comparisons. Interobserver variability was assessed by intraclass correlation (ICC).', 'Pooled analysis from specimens from patients with BA showed significantly more fibrosis than controls based on Ishak scores (3.21 1.82 vs 1.17 1.00, P < 0.005). IHC evaluation showed increased integrin 8 protein expression when compared with controls (2.67 0.81 vs 1.72 0.62, P < 0.005); however, there were no significant differences in integrin 5 (1.93 0.84 vs 1.50 0.90, P = 0.23) or integrin 6 (0.85 1.20 vs 0.94 0.85, P = 0.82) expression. These data were confirmed on individual analysis. Interobserver agreement was fair for integrin 5 (ICC 0.52), good for integrin 6 (ICC 0.72), and excellent for integrin 8 (ICC 0.79) and fibrosis (ICC 0.89).\Question: Is integrin -8 , but not -5 or -6 , protein expression increased in livers of children with biliary atresia?

A: Our data show that integrin 8, but not integrin 5 or integrin 6, protein expression is increased in liver specimens of patients with BA. These data support the mounting evidence that transforming growth factor- (TGF-) activation is responsible for the fibrosis found in BA. Anti-integrin 8 or more global integrin blocking strategies may be therapeutic options in BA, but further work is clearly needed.
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Q: Context: The bioavailability of natural food folates is lower than that of synthetic folic acid, but no agreement exists as to the extent of the difference.', 'In a 4-wk dietary intervention study, we determined the aggregate bioavailability of food folates from fruit, vegetables, and liver relative to that of folic acid.', 'Seventy-two healthy adults were randomly divided into 4 treatment groups. Group A (n = 29) received a high-folate diet with 369 mug food folate/d and a placebo capsule; groups B, C, and D (n = 14 or 15) received a low-folate diet with 73 microg food folate/d and folic acid capsules. These capsules contained 92 microg folic acid/d for group B, 191 microg for group C, and 289 microg for group D. In addition, all 72 subjects daily ingested a capsule with 58 microg [(13)C(11)]-labeled folic acid. We measured the percentage of [(13)C(11)]-labeled folate in plasma folate at the end of the intervention and ascertained the changes in serum folate concentrations over the 4 wk of the intervention.', 'Bioavailability of food folate relative to that of folic acid was 78% (95% CI: 48%, 108%) according to [(13)C(11)]-labeled folate and 85% (52%, 118%) according to changes in serum folate concentrations.\Question: Is bioavailability of food folates 80 % of that of folic acid?

A:
The aggregate bioavailability of folates from fruit, vegetables, and liver is approximately 80% of that of folic acid. The consumption of a diet rich in food folate can improve the folate status of a population more efficiently than is generally assumed.
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