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.

Q: To compare the efficacy and safety of prophylactic modalities for heterotopic ossification prevention after elbow and acetabular surgeries.', 'The retrospective chart review was conducted at the Aga Khan University Hospital and comprised record of patients who underwent open reduction and internal fixation for elbow and acetabular fractures between 2010 and 2013. Data was classified into three groups: Group A patients had received single dose of radiotherapy; Group B patients had received indomethacin, and Group C patients had not received any prophylaxis. Outcome variables included time-to-fracture healing, heterotopic ossification, non-union and wound infection.', 'Of the 104patients 70(67.3%) had elbow fractures and 34(32.7%) had acetabular fractures. Out of the 70patients with elbow fractures, 28(27%) were in Group A, 24(23%) in Group B, and 18(17%) in Group C. In Group A, 4(22%) patients had wound infection compared to 1(5.5%) patient in Group C (p=0.131). One (4%) patient in Group B and 1(5.5%) in Group C developed heterotopic ossification (p=0.486). Non-union occurred in 1(4%) patient in Group B and 1(5.5%) in Group C. Out of the 34 patients with acetabular fractures, 11(32.3%) were in Group A, 10(29.4%) in Group B, and 13(38.2%) in Group C. In Group A, 2(18.2%) patients developed wound infection. Only 1(7.6%) patient in Group C developed heterotopic ossification.

A: Do prophylaxis against heterotopic ossification after elbow and acetabular fractures - Do we really need it?
****
Q: Hypoxemia is a common complication of chronic obstructive pulmonary disease and a major factor in patients' prognosis and quality of life. The response to exercise has been evaluated by various means but no standardization has been accepted.", 'To suggest a simple outpatient technique for evaluating the response of arterial oxygen saturation to exercise for use as a marker of disease severity.', 'Ninety-six patients with various degrees of COPD were divided into three groups: mild (forced expiratory volume in 1 sec > 65%), moderate (FEV1 between 50 and 65%), and severe (FEV1 < 50%). Using continuous oximeter recording we measured oxygen saturation during 15 steps of climbing, and quantified oxygen desaturation by measuring the "desaturation area," defined as the area under the curve of oxygen saturation from the beginning of exercise through the lowest desaturation point and until after recovery to the baseline level of oxygen percent saturation. Desaturation was correlated to spirometry, lung gas volumes, blood gas analysis, and 6 min walking distance.', 'A good correlation was found between severity of COPD and baseline SaO2, lowest SaO2, recovery time, and desaturation area. A negative correlation was found between desaturation area and FEV1 (r = -0.65), FEV1/forced vital capacity (r = -0.58), residual volume to total lung capacity (r = 0.52), and diffusing lung capacity for carbon monoxide (r = -0.52). In stepwise multiple regression analysis only FEV1 correlated significantly to desaturation area. A good correlation was noted between 6 min walking distance and desaturation area with the 15 steps technique (r = 0.56).

A: Do quantitative 15 steps exercise oximetry as a marker of disease severity in patients with chronic obstructive pulmonary disease?
****
Q: Loss-of-function mutations in the progranulin gene (PGRN) were identified in frontotemporal lobar degeneration (FTLD) with ubiquitin-immunoreactive neuronal inclusions (FTLD-U). We assessed whether PGRN also contributes to genetic risk for Alzheimer disease (AD) in an extended Belgian AD patient group (n = 779, onset age 74.7 +/- 8.7 years).', 'A mutation analysis of the PGRN coding region was performed. The effect of missense mutations was assessed using in silico predictions and protein modeling. Risk effects of common genetic variants were estimated by logistic regression analysis and gene-based haplotype association analysis.', 'We observed seven missense mutations in eight patients (1.3%). Convincing pathogenic evidence was obtained for two missense mutations, p.Cys139Arg and p.Pro451Leu, affecting PGRN protein folding and leading to loss of PGRN by degradation of the misfolded protein. In addition, we showed that PGRN haplotypes were associated with increased risk for AD.

A:
Does genetic variability in progranulin contribute to risk for clinically diagnosed Alzheimer disease?
****