Given a passage, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Input: Consider Input: The main objective of this study was to analyse the outcomes after total knee arthroplasty (TKA) of a group of patients with at least one self-reported allergy and a group of patients without reported allergies. We hypothesized there is a significant negative influence on clinical outcome scores after TKA in patients with self-reported allergies.', "Four-hundred and seventy-five patients who had undergone TKA were analysed preoperatively and 1year after surgery. The WOMAC, KSS and SF-36 scores were obtained. The patients' Yesavage depression questionnaire score was also recorded. The scores of the 330 (69.5%) patients without self-reported allergies were compared to the scores of the 145 (30.5%) patients with at least one self-reported allergy in the medical record.", 'Preoperative scores were similar in both groups. The WOMAC post-operative scores (23.6 vs 20.4; p=0.037) and the KSS-Knee score (91.1 vs 87.6; p=0.027) were worse in the group of patients with self-reported allergies than in the group without allergies. The scores from the Yesavage depression questionnaire and in the SF-36 were similar in both groups.

Output: Do patient-reported allergies cause inferior outcomes after total knee arthroplasty?

Input: Consider Input: Hostility may be associated with greater systemic inflammation. However, contradictory evidence exists. Certain individuals or dimensions of hostility may be more susceptible to these effects. Main and interactive effects of hostility with sex and/or age were evaluated on markers of inflammation, independently of traditional risk factors for coronary artery disease.', '199 healthy men (81) and women (118), aged 20-64 years (M=41 11 years) were recruited. Hostility was assessed using the Cook-Medley Hostility Inventory (CMHo) and ecological momentary assessments (EMA) of quarrelsome behavior and angry affect in daily living. Blood samples were drawn to measure inflammatory activity (Il-6, TNF-, hsCRP, Il-8, Il-10, Il-18, MCP-1) and lipid oxidation (Myeloperoxidase; MPO). Correlations and hierarchical regression analyses were performed controlling for pertinent behavioral, psychological, medical, and socio-demographic factors.', 'Significant univariate associations emerged between CMHo and Il-6, TNF-, MCP-1 (p<.05). Hierarchical regressions showed interactions of hostility with sex (Il-6, TNF-; p<.05) and age (hsCRP, Il-6, TNF-; p<.05). For example, in simple slope analyses, hostility was positively related to TNF- in women (b=0.009, p=0.006) but not men. Greater hostility was also related to greater Il-6 levels among younger women (b=. 027, p=0.000).

Output: Is the relation between hostility and concurrent levels of inflammation sex , age , and measure dependent?

Input: Consider Input: Cigarette smoke disrupts the protective barrier established by the airway epithelium through direct damage to the epithelial cells, leading to cell death. Since the morphology of the airway epithelium of smokers does not typically demonstrate necrosis, the most likely mechanism for epithelial cell death in response to cigarette smoke is apoptosis. We hypothesized that cigarette smoke directly up-regulates expression of apoptotic genes, which could play a role in airway epithelial apoptosis.', 'Microarray analysis of airway epithelium obtained by bronchoscopy on matched cohorts of 13 phenotypically normal smokers and 9 non-smokers was used to identify specific genes modulated by smoking that were associated with apoptosis. Among the up-regulated apoptotic genes was pirin (3.1-fold, p < 0.002), an iron-binding nuclear protein and transcription cofactor. In vitro studies using human bronchial cells exposed to cigarette smoke extract (CSE) and an adenovirus vector encoding the pirin cDNA (AdPirin) were performed to test the direct effect of cigarette smoke on pirin expression and the effect of pirin expression on apoptosis.', 'Quantitative TaqMan RT-PCR confirmed a 2-fold increase in pirin expression in the airway epithelium of smokers compared to non-smokers (p < 0.02). CSE applied to primary human bronchial epithelial cell cultures demonstrated that pirin mRNA levels increase in a time-and concentration-dependent manner (p < 0.03, all conditions compared to controls). Overexpression of pirin, using the vector AdPirin, in human bronchial epithelial cells was associated with an increase in the number of apoptotic cells assessed by both TUNEL assay (5-fold, p < 0.01) and ELISA for cytoplasmic nucleosomes (19.3-fold, p < 0.01) compared to control adenovirus vector.
Output: Is upregulation of pirin expression by chronic cigarette smoking associated with bronchial epithelial cell apoptosis?