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.

[EX Q]: Context: To conduct clinical and genetic studies in a European family with autosomal dominant Stargardt-like macular dystrophy (adSTGD-like MD) and to investigate the functional consequences of a novel ELOVL4 mutation.', 'Ophthalmic examination and mutation screening by direct sequencing of the ELOVL4 gene was performed in two affected individuals. Wild-type and mutant ELOVL4 genes were expressed as enhanced green fluorescent protein (EGFP) fusion proteins in transient transfection in NIH-3T3 and HEK293 cells. To determine the subcellular localization of ELOVL4, an endoplasmic-reticulum (ER)-specific marker for pDsRed2-ER was cotransfected with ELOVL4 constructs. Transfected cells were viewed by confocal microscopy. Western blot analysis was performed to assess protein expression using an anti-GFP antibody.', 'Affected patients exhibited macular atrophy with surrounding flecks characteristic of adSTGD-like MD. A novel ELOVL4 p.Tyr270X mutation was detected in affected individuals. In cell-transfection studies, wild-type ELOVL4 localized preferentially to the ER. In contrast, the mutant protein appeared to be mislocalized within transfected cells.
Answer: In a European family with adSTGD-like MD, a novel ELOVL4 mutation was found to underlie the disorder. Transfection studies indicated that, unlike wild-type ELOVL4, the mutant protein does not localize to the ER but rather appears to be sequestered elsewhere in an aggregated pattern in the cytoplasm. Further analysis of the function of normal and mutant ELOVL4 will provide insight into the mechanism of macular degeneration.
[EX A]: Does a novel mutation in the ELOVL4 gene cause autosomal dominant Stargardt-like macular dystrophy?

[EX Q]: Context: Diabetic cardiomyopathy (DCM) is associated with suppressed autophagy and augmented apoptosis in the heart although the interplay between the two remains elusive. The ability of mammalian sterile 20-like kinase 1 to regulate both autophagy and apoptosis prompted us to investigate it as a possible candidate in the progression of DCM.', 'Wild-type, Mst1 (also known as Stk4) transgenic and Mst1-knockout mice were challenged with streptozotocin to induce experimental diabetes. In addition, cultured neonatal mouse cardiomyocytes were subjected to simulated diabetes to probe mechanisms.', 'Mst1 knockout alleviated while Mst1 overexpression aggravated cardiac dysfunction in diabetes. Diabetic Mst1 transgenic mice exhibited decreased LC3 expression and enhanced protein aggregation. In contrast, typical autophagosomes were observed in diabetic Mst1-knockout mice with increased LC3 expression and reduced protein aggregation. Mst1 downregulation promoted autophagic flux as demonstrated by increased LC3-II and decreased p62 expression in the presence of bafilomycin A1. Furthermore, Mst1 overexpression increased, while Mst1 knockout decreased, cardiomyocyte apoptosis both in vivo and in vitro. Co-immunoprecipitation assays showed that Mst1 overexpression promoted Beclin1 binding to B cell lymphoma 2 (Bcl-2) and induced dissociation of Bcl-2 from Bax in diabetic mice. Conversely, Mst1 knockout disrupted the Beclin1-Bcl-2 complex and enhanced the interaction between Bcl-2 and Bax.
Answer: Mst1 knockout restores autophagy and protects against apoptosis in cardiomyocytes, en route to the rescue against DCM.
[EX A]: Does mST1 coordinately regulate autophagy and apoptosis in diabetic cardiomyopathy in mice?

[EX Q]: Context: Eradication of Helicobacter pylori is not routinely recommended for the symptomatic relief and the prevention of gastric cancer in patients with functional dyspepsia. The present study investigated a useful indicator of H. pylori eradication in such patients by determining the optimal cutoff value of a 13C-urea breath test (UBT).', 'One hundred dyspeptic patients participated in the study. Dyspepsia was scored, and a 13C-UBT administered. A level of delta 13C-UBT of>4 per thousand was diagnosed as H. pylori-positive. After the stomach was endoscopically sprayed with phenol red, biopsy specimens were taken from the antrum, body and cardia of the stomach for the assessment of H. pylori density, and activity (neutrophil infiltration) and degree (lymphocyte infiltration) of gastritis.', 'Correlation between delta 13C-UBT and dyspepsia score was not found. Delta 13C-UBT significantly correlated with H. pylori density score in the total stomach (r = 0.53, P < 0.0001), neutrophil (r = 0.34, P = 0.0005) and lymphocyte score (r = 0.69, P < 0.0001). Twenty-six of the 100 subjects had a neutrophil score of >or=4, lymphocyte score of >or=4, and H. pylori score of >or=4. Their 95% confidence interval of mean was 58.2 per thousand, which reflects moderate to marked acute and chronic gastritis, and dense H. pylori colonization.
Answer: The 13C-UBT is a reliable semiquantitative test to assess H. pylori density and the activity and degree of gastritis. It is proposed that H. pylori eradication therapy might be beneficial for patients with functional dyspepsia with a delta 13C-UBT of >58.2 per thousand.
[EX A]:
Is delta ( 13 ) C-urea breath test value a useful indicator for Helicobacter pylori eradication in patients with functional dyspepsia?