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.

Input: Consider Input: Context: For patients with cystic fibrosis (CF) Pseudomonas aeruginosa infection is a major contributor to progressive lung disease. While colonizing strains are thought to be primarily environmental, which environments are important in lung colonization is unclear.', 'We took 11,674 samples from a broad range of sites over 3-8 visits to homes with (7) and without (8) CF patients.', 'Twenty-eight percent of sampled drains yielded P. aeruginosa at least once, and a general mixed linear model estimated that 6.3% of samples from drains yield P. aeruginosa. This is more than eight times the estimated recovery from any other type of household environment.\Question: Is pseudomonas aeruginosa in CF and non-CF homes found predominantly in drains?

Output: These findings implicate drains as important potential sources of P. aeruginosa infection. They suggest that maximizing P. aeruginosa control efforts for drains would reduce exposure with minimal extra burden to CF patients and families.


Input: Consider Input: Context: Although N-terminal pro-B-type natriuretic peptide (NT-proBNP) has a strong relationship with incident cardiovascular disease (CVD), few studies have examined whether NT-proBNP adds to risk prediction algorithms, particularly in women.', 'This study sought to evaluate the relationship between NT-proBNP and incident CVD in women.', "Using a prospective case-cohort within the WHI (Women's Health Initiative) observational study, we selected 1,821 incident cases of CVD (746 myocardial infarctions, 754 ischemic strokes, 160 hemorrhagic strokes, and 161 other cardiovascular [CV] deaths) and a randomly selected reference cohort of 1,992 women without CVD at baseline.", 'Median levels of NT-proBNP were higher at study entry among incident cases (120.3 ng/l [interquartile range (IQR): 68.1 to 219.5 ng/l]) than among control subjects (100.4 ng/l [IQR: 59.7 to 172.6 ng/l]; p\xa0< 0.0001). Women in the highest quartile of NT-proBNP (≥140.8 ng/l) were at 53% increased risk of CVD versus those in the lowest quartile after adjusting for traditional risk factors (1.53 [95% confidence interval (CI): 1.21 to 1.94]; p for trend\xa0<0.0001). Similar associations were observed after adjustment for Reynolds Risk Score covariables (1.53 [95% CI: 1.20 to 1.95]; p for trend\xa0<0.0001); the association remained in separate analyses of CV death (2.66 [95% CI: 1.48 to 4.81]; p for trend\xa0<0.0001), myocardial infarction (1.39\xa0[95% CI: 1.02 to 1.88]; p for trend\xa0= 0.008), and stroke (1.60 [95% CI: 1.22 to 2.11]; p for trend\xa0<0.0001). When added to traditional risk covariables, NT-proBNP improved the c-statistic (0.765 to 0.774; p\xa0= 0.0003), categorical net reclassification (0.08; p\xa0< 0.0001), and integrated discrimination (0.0105; p\xa0<\xa00.0001). Similar results were observed when NT-proBNP was added to the Reynolds Risk Score.\Question: Do b-type natriuretic peptides improve cardiovascular disease risk prediction in a cohort of women?

Output: In this multiethnic cohort of women with numerous CV events, NT-proBNP modestly improved measures of CVD risk prediction.


Input: Consider Input: Context: Observational and clinical studies suggest different responses upon sex hormone replacement therapy in ischaemic heart disease. Few studies, however, have examined the impact of oestrogen receptor-dependent mechanisms on the extent of injury after myocardial infarction (MI). Therefore, we set out to evaluate the effect of oestrogen (E2) replacement on infarct size and remodelling, and the respective role of the oestrogen receptors (ER)alpha and -beta in this process, using ERalpha- and ERbeta-deficient mice.', 'Wild type (WT) (ERalpha(+/+) and ERbeta(+/+)), ERalpha-deficient (ERalpha(-/-)) and ERbeta-deficient (ERbeta(-/-)) mice were ovariectomized and subsequently supplemented with E2 or placebo using subcutaneous 60-day release pellets. MI was induced by left coronary artery ligation. Two weeks following MI, haemodynamic function was assessed and infarct size was determined.', 'There was no significant difference in infarct size between E2- or placebo-treated WT (ERalpha(+/+) and ERbeta(+/+)) mice. Surprisingly, E2 treatment did result in smaller infarct sizes in ERalpha(-/-) mice, but increased the infarct size in ERbeta(-/-) mice. Increase of the left ventricular mass post-MI was significantly larger in the E2-treated ERalpha(-/-) animals compared with placebo-treated animals. E2 treatment also significantly increased post-MI mortality in ERalpha(+/+), ERbeta(+/+) and ERalpha(-/-) animals, but not in ERbeta(-/-) mice.\Question: Does oestrogen modulate cardiac ischaemic remodelling through oestrogen receptor-specific mechanisms?


Output: Although E2 modulates the infarct size in ERalpha(-/-), it also appears to be responsible for the higher mortality following MI. ERbeta appears to be the receptor involved in the modulating effects of E2 in the infarcted heart.