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.

[EX 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.
[EX A]: Are cognitive-behavioral phenotypes of Williams syndrome associated with genetic variation in the GTF2I gene , in a healthy population?

[EX Q]: Our previous in-vivo and in-vitro studies demonstrated that inflammation accelerated the progression of atherosclerosis via the dysregulation of the low-density lipoprotein receptor (LDLr) pathway. The current study aimed to investigate the effects and their underlying mechanisms of inflammation on lipid accumulation in the radial arteries of endstage renal disease (ESRD) patients with arteriovenostomy.', '30 ESRD patients with arteriovenostomy were included. The patients were divided into two groups based on their plasma levels of C-reactive protein: a control (n = 16) and an inflamed group (n = 14). The expression of tumor necrosis factor-alpha (TNF-alpha) and monocyte chemotactic protein-1 of the radial arteries were increased in the inflamed group. Foam cell formation and lipid droplet accumulation were examined by hematoxylin and eosin (H & E) and Oil Red O staining. Intracellular cholesterol trafficking-related proteins were examined by immunohistochemistry and immunofluorescent staining.', 'There was significant lipid accumulation in the radial arteries of the inflamed group compared with the control. Further analysis demonstrated that this accumulation was correlated with the increased protein expression of LDLr, sterol regulatory element-binding protein-2 (SREBP-2), and SREBP cleavageactivating protein (SCAP). Confocal microscopy showed that inflammation enhanced the translocation of SCAP escorting SREBP-2 from the endoplasmic reticulum to the Golgi, thereby activating LDLr gene transcription. Interestingly, upregulated LDLr expression was positively associated with the increased protein expression of mammalian target of rapamycin (mTOR), which had enhanced coexpression with SREBP-2. This finding suggests that the activation of mTOR may be involved in LDLr pathway disruption through the upregulation of SREBP-2 expression.
[EX A]: Does activation of mTOR contribute to foam cell formation in the radial arteries of patients with end-stage renal disease?

[EX Q]: Genetic factors are reported to affect fracture incidence. Many groups have explored the correlation of fracture risk with ESR1 IVS1-397T>C. The observed associations, however, are largely inconsistent. This meta-analysis of data from early-released studies was performed in an effort to determine the role of IVS1-397T>C in fracture.', 'Relevant studies were searched through Pubmed, Embase, ScienceDirect, and Wiley Online Library databases. 16 studies meeting all selection criteria were finally identified. We calculated ORs with 95% CIs to assess risk of fracture. Subgroup analyses were performed by subtype, ethnicity and gender.', 'Data on 2916 cases and 19170 controls were analyzed in the meta-analysis. Overall, we found moderately decreased risk in association with IVS1-397 CC genotype (OR = 0.82, 95% CI = 0.73-0.92; OR = 0.84, 95% CI = 0.76-0.94). The decrease persisted in both hip fracture (OR = 0.82, 95% CI = 0.71-0.94; OR = 0.83, 95% CI = 0.73-0.94) and vertebral fracture (OR = 0.67, 95% CI = 0.50-0.91; OR = 0.78, 95% CI = 0.64-0.97; OR = 0.82, 95% CI = 0.68-0.98) when data were stratified by subtype. We also found a significant trend of decreasing risk in relation to the CC genotype in Caucasian, male and female. All fixed-effects meta-analysis results were homogeneous.
[EX A]:
Does estrogen receptor ( ESR1 ) IVS1-397T > C polymorphism lower risk of fracture?