Given a passage with a context and an answer, 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.
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Question: Context: 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.
Answer: Our data support a role for PGRN in patients with clinically diagnosed Alzheimer disease (AD). Further, we hypothesize that at least some PGRN missense mutations might lead to loss of functional protein. Whether the underlying pathology in our cases proves to be AD, frontotemporal lobar degeneration, or a combination of the two must await further investigations.

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

Question: Context: Brassica napus (AACC) is self-compatible, although its ancestor species Brassica rapa (AA) and Brassica oleracea (CC) are self-incompatible. Most B.napus accessions have dominant self-compatibility (SC) resulting from an insertion of 3.6 kb in the promoter region of BnSCR-1 on the A genome, while recessive SC in B.napus has rarely been observed. Expression and cloning of SRK and SCR genes and genetic analysis were carried out to dissect bases of recessive SC in B.napus.', 'Eleven accessions were screened to identify stable recessive SC and had the S genotype BnS-7 on the A genome and BnS-6 on the C genome similarly to BrS-29 and BoS-15, respectively. In eight SC accessions, BnSCR-7 and BnSCR-6 were nearly undetectable and harbored no structural mutations in the promoters, while SRK genes were expressed at normal levels and contained intact CDS, with the exception of BnSRK-7 in line C32. SRK and SCR genes were expressed normally but their CDSs had no mutations in three SC accessions. In self-incompatible S-1300 and 11 F1 hybrids, SRK genes and BnSCR-1300 transcripts were present at high levels, while expression of the BnSCR-7 and BnSCR-6 were absent. Plants of S genotype S1300S1300 were completely SI, while SI phenotypes of SBnS-7SBnS-7 and S1300SBnS-7 plants were segregated in BC1 and F2 populations.
Answer: The recessive SC in eight accessions is caused by the loss of function of BnSCR-7 and BnSCR-6 in pollen. Translational repression contributes to the recessive SC in three accessions, whose SRK and SCR genes were expressed normally and had identical CDSs to BrS-29 or BoS-15. SI in 11 F1 hybrids relies on the expression of BnSCR-1300 rather than SRK genes. Other factor(s) independent of the S locus are involved in recessive SC. Therefore, diverse causes underlie recessive SC in B. napus, yielding insight into these complex mechanisms.

Answer: Do gene expression and genetic analysis reveal diverse causes of recessive self-compatibility in Brassica napus L?

Question: Context: Obesity is associated with increased morbidity and mortality in critically injured blunt trauma patients.', 'Case-control study of all critically injured blunt trauma patients between January 2002 and December 2002.', 'Academic level I trauma center at a county referral hospital.', 'Two hundred forty-two consecutive patients admitted to the intensive care unit following blunt trauma. Patients were divided into 2 groups by body mass index. The obese group was defined as having a body mass index of 30 kg/m2 or higher, and the nonobese group was defined as having a body mass index lower than 30 kg/m2.', 'Univariate and multivariate analyses were performed to identify risk factors for mortality. Complications and length of stay were also evaluated.', 'Of the 242 patients, 63 (26%) were obese, and 179 (74%) were nonobese. The obese and nonobese groups were similar with regard to age (mean +/- SD, 49 +/- 18 years vs 45 +/- 22 years), male sex (63% vs 72%), Glasgow Coma Scale score (mean +/- SD, 11 +/- 5 vs 11 +/- 5), and injury severity score (mean +/- SD, 21 +/- 13 vs 20 +/- 14). The obese group had a higher body mass index (mean +/- SD, 35 +/- 7 vs 24 +/- 3; P<.001). Mechanisms of injury and injury patterns were similar between groups. The obese group had a higher incidence of multiple organ failure (13% vs 3%; P =.02) and mortality (32% vs 16%; P=.008). Obesity was an independent predictor of mortality with an adjusted odds ratio of 5.7 (95% confidence interval, 1.9-19.6; P=.003).
Answer: Critically injured obese trauma patients have similar demographics and injury patterns as nonobese patients. Obesity is an independent predictor of mortality following severe blunt trauma.

Answer:
Is obesity an independent risk factor of mortality in severely injured blunt trauma patients?