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.

Input: Consider Input: Context: Increased oxidative stress and myocyte apoptosis co-exist in the remote non-infarcted myocardium (RM) following a large myocardial infarction. We proposed that these phenomena are causally related.', 'On day 3 after induction of myocardial infarction, Sprague-Dawley rats were randomized to receive probucol and pyrrolidine dithiocarbamate (MI-T), or vehicle only (MI) for 7 weeks. Control rats (C) received vehicle. At 7 weeks, lipidperoxidation within the RM was assessed by measuring thiobarbituric acid reactive substances, which were significantly increased in MI vs. C, while MI-T was not different from C. There was a significant increase in cardiac myocytes positive for in situ TdT-UTP nick-end labeling within the RM in MI vs. C, which was inhibited in MI-T. Furthermore, internucleosomal DNA fragmentation was clearly demonstrated on agarose gels from RM in the MI group, while it was much less apparent on gels from RM in the C and MI-T groups. Western blot analysis showed a significant increase in p53, Bax and caspase-3 protein expression within the RM of MI vs. C, all of which were inhibited in the MI-T group. Furthermore, there was evidence for an increase in caspase-3 activity within the RM from MI vs. C, which was normalized in the MI-T group.
Answer: Long-term treatment with the antioxidants probucol and pyrrolidine dithiocarbamate attenuates oxidative stress, myocyte apoptosis, caspase-3 like activity and the expression of p53, bax and caspase-3 within RM in rats after a large myocardial infarction.

Output: Do antioxidants attenuate myocyte apoptosis in the remote non-infarcted myocardium following large myocardial infarction?


Input: Consider Input: Context: Gastric lipase is an important enzyme for dietary triglyceride digestion in normal subjects. Its regulation is unknown, as is the relation between the quantity and activity of the enzyme.', 'In a dose-response study we investigated the effect of low doses of pentagastrin (less than 1000 ng/kg/h) on the output of gastric lipase measured by a kinetic assay and an enzyme-linked immunosorbent assay (ELISA).', 'In five healthy volunteers stepwise intravenous pentagastrin infusions of 0, 50, 100, 500, and 1000 ng/kg/h resulted in a stepwise increase in the lipase output, as measured with ELISA. However, the lipolytic activity, measured with a kinetic assay, decreased as the pH of the gastric contents decreased.
Answer: We conclude that secretion of the gastric lipase is stimulated by pentagastrin, but the simultaneous secretion of acid counteracts the lipolytic activity of the enzyme when food is not present.

Output: Do low doses of pentagastrin stimulate gastric lipase secretion in man?


Input: Consider Input: Context: Smoking parents are the main source of passive smoke exposure in childhood. Only few studies have assessed the effect of maternal or paternal cigarette smoke exposure in childhood on the development and severity of COPD.', 'We recruited n = 251 COPD-patients, n = 113 were clinically stable (no exacerbations for up to 24 years backdated from the day of interview), and - according to their history - n = 138 had more than one exacerbation during this time period. All COPD-patients were interviewed by a physician using a structured questionnaire on main health outcomes, social status, smoking history of their parents and themselves. Furthermore, pulmonary function was measured, and concomitant lung diseases were excluded.', 'Both COPD groups were comparable in age, gender, smoking history at the beginning of the disease, and cigarette pack-years smoked. Patients whose mothers smoked during childhood had poorer lung function values: FEV (1) 45.2 % vs. 54 % (p = 0.037). Non-smoking patients with a history of maternal smoking had a 7-times higher exacerbation rate compared to patients without passive smoke exposure (p = 0.073). Paternal cigarette smoke exposure had no effect.
Answer: Maternal cigarette smoke exposure in childhood aggravates the COPD disease and predisposes the patient for a higher disease severity.


Output: Does [ Parental smoking and passive smoke exposure in childhood promote the COPD exacerbation rate ]?