instruction:
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.
question:
Accumulated evidence suggests that oxidative stress is involved in amyloid beta (Abeta)-induced cognitive dysfunction. Silibinin (silybin), a flavonoid derived from the herb milk thistle (Silybum marianum), has been shown to have antioxidative properties; however, it remains unclear whether silibinin improves Abeta-induced neurotoxicity. In the present study, we examined the effect of silibinin on the memory impairment and accumulation of oxidative stress induced by Abeta(25-35) in mice.', 'Aggregated Abeta(25-35) (3 nmol) was intracerebroventricularly administered to mice. Treatment with silibinin (2, 20 and 200 mg.kg(-1), once a day, p.o.) was started immediately after the injection of Abeta(25-35). Locomotor activity was evaluated 6 days after the Abeta(25-35) treatment, and cognitive function was evaluated in a Y-maze and novel object recognition tests 6-11 days after the Abeta(25-35) treatment. The levels of lipid peroxidation (malondialdehyde) and antioxidant (glutathione) in the hippocampus were measured 7 days after the Abeta(25-35) injection.', 'Silibinin prevented the memory impairment induced by Abeta(25-35) in the Y-maze and novel object recognition tests. Repeated treatment with silibinin attenuated the Abeta(25-35)-induced accumulation of malondialdehyde and depletion of glutathione in the hippocampus.
answer:
Does silibinin prevent amyloid beta peptide-induced memory impairment and oxidative stress in mice?

question:
It is well established that African Americans (AA) experience greater pain associated with a variety of clinical conditions, and greater pain sensitivity to experimental pain tasks relative to non-Hispanic Whites (W). Notably, African Americans do not show the same relationships involving endogenous pain regulatory mechanisms and pain sensitivity documented in Caucasians, including positive associations between blood pressure, norepinephrine, cortisol and greater pain tolerance.', 'The purpose of this study was to examine the relationship between plasma oxytocin (OT) and pain sensitivity and to explore the relation of OT to other factors known to influence pain perception.', 'OT concentration and sensitivity to ischemic, cold pressor, and thermal pain tasks were assessed in African American (n=25) and non-Hispanic White (n=23) pre-menopausal women.', 'African American women demonstrated significantly lower pain tolerance across tasks compared with Whites (F(1,46)=6.31, p=0.0156) and also exhibited lower plasma OT levels (AA: 3.90, W: 7.05 pg/mL; p=0.0014). Greater OT levels were correlated with greater tolerance to ischemic pain (r=0.36, p=0.013) and accounted for a marginally significant portion of the ethnic difference in ischemic pain tolerance (B=+0.29, p=0.06). Greater OT was also correlated with greater tolerance of cold pressor pain (r=0.31, p=0.03); however, this association was no longer seen after the variance due to ethnicity was accounted for.
answer:
Is ethnicity associated with alterations in oxytocin relationships to pain sensitivity in women?

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