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: Individuals with Williams syndrome, a neurogenetic condition caused by deletion of a set of genes at chromosomal location 7q11.23, exhibit a remarkable suite of traits including hypersociality with high, nonselective friendliness and low social anxiety, expressive language relatively well-developed but under-developed social-communication skills overall, and reduced visual-spatial abilities. Deletions and duplications of the Williams-syndrome region have also been associated with autism, and with schizophrenia, two disorders centrally involving social cognition. Several lines of evidence have linked the gene GTF2I (General Transcription Factor IIi) with the social phenotypes of Williams syndrome, but a role for this gene in sociality within healthy populations has yet to be investigated.', 'We genotyped a large set of healthy individuals for two single-nucleotide polymorphisms in the GTF2I gene that have recently been significantly associated with autism, and thus apparently exhibit functional effects on autism-related social phenotypes. GTF2I genotypes for these SNPs showed highly significant association with low social anxiety combined with reduced social-communication abilities, which represents a metric of the Williams-syndrome cognitive profile as described from previous studies.

A: Are cognitive-behavioral phenotypes of Williams syndrome associated with genetic variation in the GTF2I gene , in a healthy population?
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Q: Pathologic change in Alzheimer disease (AD) begins some years before symptoms. MRS has the potential to detect metabolic abnormalities reflecting this early pathologic change. Presenilin 1 (PS1) and amyloid precursor protein (APP) mutation carriers have a nearly 100% risk of developing AD and may be studied prior to symptom onset.', 'Short echo time proton MR spectra were acquired from a midline posterior cingulate voxel in presymptomatic carriers of PS1 or APP mutations ("presymptomatic mutation carriers" [PMCs]; n = 7) and age- and sex-matched control subjects (n = 6). Ratios of N-acetyl aspartate (NAA), myo-inositol (MI), and choline-containing compounds (Cho) to creatine (Cr) were measured and NAA/MI calculated. Regression analyses and t tests were performed after log transformation.', 'PMC and control subjects were matched for age and sex. PMC subjects were 1.7 to 21.6 years (mean 9.8 years) before expected symptom onset, predicted from family-specific mean age at onset. Age did not significantly affect metabolite ratios. Geometric mean ratios in control subjects were as follows: NAA/Cr = 1.75, MI/Cr = 0.59, and NAA/MI = 2.95. NAA/Cr and NAA/MI were significantly reduced in PMC relative to controls (NAA/Cr mean decrease 10% [95% CI 2 to 18%]; NAA/MI mean decrease 25% [95% CI 3 to 44%]). MI/Cr was increased in PMC, but the differences did not achieve significance (19% increase [95% CI 1% decrease to 41% increase]; p = 0.07)). In PMCs, reduction in NAA/MI (p = 0.001) and MI/Cr (p = 0.002) were related to proximity of expected age at onset.

A: Does mRS show abnormalities before symptoms in familial Alzheimer disease?
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Q: Protocols call for the start of hormonal therapy with levothyroxine after the declaration of brain death. As the hormonal perturbations occur during the process of brain death, the role of the early initiation of levothyroxine therapy (LT) to salvage organs is not well defined. The aim of this study was to evaluate the impact of early LT (before the declaration of brain death) on the number of solid organs procured per donor.', 'We performed an 8-year retrospective analysis of all trauma patients who progressed to brain death. Patients who consented for organ donation, received LT, and donated solid organs were included. Patients were dichotomized into two groups: early LT group, patients who received LT before the declaration of brain death, and late LT group, those who received LT after brain death. The two groups were compared for differences in demographics, clinical characteristics, need for vasopressor, and number of solid organ donation.', 'A total of 100 solid organ donors were identified of which, 41% (n=77) donors who received LT therapy were included. LT before the declaration of brain death was initiated in 37 patients compared with 40 patients who had it started after the declaration of brain death. There was no difference in demographics between the two groups except that patients in the early LT group were more likely to be hypotensive on presentation (54% vs. 25%, p = 0.001). Early LT therapy was associated with an increase in solid organ procurement rate (odds ratio, 1.9; 95% confidence interval, 1.4-2.7; p = 0.01). Sixty-seven patients donated a total of 291 solid organs.

A:
Does levothyroxine therapy before brain death declaration increase the number of solid organ donations?
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