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.

Example Input: Context: Despite advances in the diagnosis and management of idiopathic noncirrhotic portal hypertension, its pathogenesis remains elusive. Insight may be gained from study of early-onset familial idiopathic noncirrhotic portal hypertension, in which Mendelian mutations may account for disease. We performed exome sequencing of eight subjects from six kindreds with onset of portal hypertension of indeterminate etiology during infancy or childhood. Three subjects from two consanguineous families shared the identical rare homozygous p.N46S mutation in DGUOK, a deoxyguanosine kinase required for mitochondrial DNA replication; haplotype sharing demonstrated that the mutation in the two families was inherited from a remote common ancestor. All three affected subjects had stable portal hypertension with noncirrhotic liver disease for 6-16 years of follow-up. This mutation impairs adenosine triphosphate binding and reduces catalytic activity. Loss-of-function mutations in DGUOK have previously been implicated in cirrhosis and liver failure but not in isolated portal hypertension. Interestingly, treatment of patients with human immunodeficiency viral infection with the nucleoside analogue didanosine is known to cause portal hypertension in a subset of patients and lowers deoxyguanosine kinase levels in vitro; the current findings implicate these effects on deoxyguanosine kinase in the causal mechanism.
Answer: Our findings provide new insight into the mechanisms mediating inherited and acquired noncirrhotic portal hypertension, expand the phenotypic spectrum of DGUOK deficiency, and provide a new genetic test for a specific cause of idiopathic noncirrhotic portal hypertension. (Hepatology 2016;63:1977-1986).
Example Output: Does recurrent recessive mutation in deoxyguanosine kinase cause idiopathic noncirrhotic portal hypertension?

Example Input: Context: Formyl peptide receptor 1 (FPR1) as a regulator of innate inflammatory response has been implicated in tumor progression of gliomas. The purpose of the present study was to evaluate the prognostic significance and the ligand-receptor interaction of FPR1 in gastric cancer (GC).', 'FPR1 was immunohistochemically-analyzed in tissue sections originating from 116 GC patients. Reverse transcription-polymerase chain reaction (RT-PCR) was used for the assessment of interaction between FPR1 and the FPR1 ligand annexin A1 (AnxA1) in GC cells.', 'High FPR1 expression was significantly associated with stage IV disease, submucosal invasion, serosal invasion, and clinical outcome of GC. Multivariate analysis showed that high FPR1 expression was an independent risk factor of poor overall survival in GC patients. FPR1 expression increased significantly when AnxA1 overexpression was present in GC cells. A positive feedback regulation of FPR1 was involved in the AnxA1-FPR1 signal transduction.
Answer: FPR1 expression may be used as a novel indicator to predict outcome in GC patients after gastrectomy.
Example Output: Is formyl Peptide receptor 1 expression associated with tumor progression and survival in gastric cancer?

Example Input: Context: Most patients are admitted to the hospital through the emergency department (ED), and ED waiting times partly reflect the availability of inpatient beds. We test whether the balance between daily hospital admissions and discharges affects next-day ED length of stay.', 'We conducted a cross-sectional study of hospitals in metropolitan Toronto, served by a single emergency medical services provider in a publicly funded system. During a 3-year period, we evaluated the daily ratio of admissions to discharges at each hospital and the next-day median ED length of stay in the same hospital by using linear regression.', 'Across hospitals, the daily mean (SD) 50th percentile ED length of stay averaged 218 (51) minutes. As the inpatient admission-discharge ratio increased or decreased, next-day ED length of stay changed accordingly. Compared with ratios of 1.0, those less than 0.6 were associated with an 11-minute (95% confidence interval [CI] 5 to 16 minutes) shorter next-day median ED length of stay; at admission-discharge ratios of 1.3 to 1.4, ED length of stay was significantly prolonged by 5 minutes (95% CI 3 to 6 minutes). Admission-discharge ratios on weekends and among medical inpatients had a stronger influence on next-day ED length of stay; effects were also greater among higher-acuity and admitted ED patients.
Answer: Disequilibrium between the number of admitted and discharged inpatients significantly affects next-day ED length of stay. Better matching of daily hospital discharges and admissions could reduce ED waiting times and may be more amenable to intervention than reducing admissions alone. The admission-discharge ratio may also provide a simple way of tracking and enhancing hospital system performance.
Example Output:
Does disequilibrium between admitted and discharged hospitalized patients affect emergency department length of stay?