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 Input:
Context: Parenteral control of gastric acid hypersecretion in conditions such as Zollinger-Ellison syndrome (ZES) or idiopathic gastric acid hypersecretion is necessary perioperatively or when oral medications cannot be taken for other reasons (e.g., during chemotherapy, acute upper gastrointestinal bleeding, or in intensive care unit settings).', 'We evaluated the efficacy and safety of 15-minute infusions of the proton pump inhibitor pantoprazole (80-120 mg every 8-12 hours) in controlling acid output for up to 7 days. Effective control was defined as acid output >10 milliequivalents per hour (mEq/h) (<5 mEq/h in patients with prior acid-reducing surgery) for 24 hours.', 'The 21 patients enrolled had a mean age of 51.9 years (range, 29-75) and a mean disease duration of 8.1 years (range, <0.5-21); 13 were male, 7 had multiple endocrine neoplasia syndrome type I, 4 had undergone acid-reducing surgery, 2 had received chemotherapy, and 13 had undergone gastrinoma resections without cure. Basal acid output (mean +/- SD) was 40.2 +/- 27.9 mEq/h (range, 11.2-117.9). In all patients, acid output was controlled within the first hour (mean onset of effective control, 41 minutes) after an initial 80-mg intravenous pantoprazole dose. Pantoprazole, 80 mg every 12 hours, was effective in 17 of 21 patients (81%) for up to 7 days. Four patients required upward dose titration, 2 required 120 mg pantoprazole every 12 hours, and 2 required 80 mg every 8 hours. At study end, acid output remained controlled for 6 hours beyond the next expected dose in 71% of patients (n = 15); mean acid output increased to 4.0 mEq/h (range, 0-9.7). No serious or unexpected adverse events were observed.
Answer: Intravenous pantoprazole, 160-240 mg/day administered in divided doses by 15-minute infusion, rapidly and effectively controlled acid output within 1 hour and maintained control for up to 7 days in all ZES patients.

Ex Output:
Does intravenous pantoprazole rapidly control gastric acid hypersecretion in patients with Zollinger-Ellison syndrome?

Ex Input:
Context: Studies that investigate the subjective benefit from a bone conduction implant (BCI) sound processor in patients with single-sided sensorineural deafness (SSD) have been limited to examining short- and mid-term benefit. In the current study, we performed a survey among 44 SSD BCI users with a median follow-up time of 50 months.', 'Forty-four experienced SSD BCI users participated in the survey, which consisted of the Abbreviated Profile of Hearing Aid Benefit, the Single-Sided Deafness Questionnaire, the Short Hearing Handicap Inventory for Adults, and a self-made user questionnaire. For patients with tinnitus, the Tinnitus Questionnaire was also completed. The results of the survey were correlated with contralateral hearing loss, age at implantation, duration of the hearing loss at the time of implantation, duration of BCI use, and the presence and burden of tinnitus.', 'In total, 86% of the patients still used their sound processor. The Abbreviated Profile of Hearing Aid Benefit and the Short Hearing Handicap Inventory for Adults show a statistically significant overall improvement with the BCI. The Single-Sided Deafness Questionnaire and the user questionnaire showed that almost 40% of the patients reported daily use of the sound processor. However, the survey of daily use reveals benefit only in certain circumstances. Speech understanding in noisy situations is rated rather low, and 58% of all patients reported that their BCI benefit was less than expected.
Answer: The majority of the patients reported an overall improvement from using their BCI. However, the number of users decreases during a longer follow-up time and patients get less enthusiastic about the device after an extended period of use, especially in noisy situations. However, diminished satisfaction because of time-related reductions in processor function could not be ruled out.

Ex Output:
Do long-term subjective benefit with a bone conduction implant sound processor in 44 patients with single-sided deafness?

Ex Input:
Context: Experimental studies in acute pancreatitis (AP) suggest a strong association of acinar cell injury with cathepsin B-dependent intracellular activation of trypsin. However, the molecular events subsequent to trypsin activation and their role, if any, in cell death is not clear. In this study, we have explored intra-acinar events downstream of trypsin activation that lead to acinar cell death.', 'Acinar cells prepared from the pancreas of rats or mice (wild-type, trypsinogen 7, or cathepsin B-deleted) were stimulated with supramaximal cerulein, and the cytosolic activity of cathepsin B and trypsin was evaluated. Permeabilized acini were used to understand the differential role of cytosolic trypsin vs cytosolic cathepsin B in activation of apoptosis. Cell death was evaluated by measuring specific markers for apoptosis and necrosis.', 'Both invitro and invivo studies have suggested that during AP cathepsin B leaks into the cytosol from co-localized organelles, through a mechanism dependent on active trypsin. Cytosolic cathepsin B but not trypsin activates the intrinsic pathway of apoptosis through cleavage of bid and activation of bax. Finally, excessive release of cathepsin B into the cytosol can lead to cell death through necrosis.
Answer: This report defines the role of trypsin in AP and shows that cytosolic cathepsin B but not trypsin activates cell death pathways. This report also suggests that trypsin is a requisite for AP only because it causes release of cathepsin B into the cytosol.

Ex Output:
Does release of Cathepsin B in Cytosol cause Cell Death in Acute Pancreatitis?