TASK DEFINITION: In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.
PROBLEM: Context: Living a purposeful life is associated with better mental and physical health, including longevity. Accumulating evidence shows that these associations might be explained by the association between life purpose and regulation of physiological systems involved in the stress response. The aim of this study was to investigate the prospective associations between life purpose and allostatic load over a 10-year period.', 'Analyses were conducted using data from the Midlife in the United States (MIDUS) survey. Assessment of life purpose, psychological covariates and demographics were obtained at baseline, while biomarkers of allostatic load were assessed at the 10-year follow-up.', 'We found that greater life purpose predicted lower levels of allostatic load at follow-up, even when controlling for other aspects of psychological well-being potentially associated with allostatic load. Further, life purpose was also a strong predictor of individual differences in self-health locus of control-i.e., beliefs about how much influence individuals can exert on their own health-which, in turn, partially mediated the association between purpose and allostatic load. Although life purpose was also negatively linked to other-health locus of control-i.e., the extent to which individuals believe their health is controlled by others/chance-this association did not mediate the impact of life purpose on allostatic load.\Question: Does purpose in life predict allostatic load ten years later?

SOLUTION: The current study provides the first empirical evidence for the long-term physiological correlates of life purpose and supports the hypothesis that self-health locus of control acts as one proximal psychological mechanism through which life purpose may be linked to positive biological outcomes.

PROBLEM: Context: To investigate whether the association between APOE-epsilon4 and memory decline is modified by baseline cognition and age in a population-based elderly sample.', 'The study sample consisted of 1,243 subjects, 62 to 85 years old, with a Mini-Mental State Examination (MMSE) score between 21 and 30 and known APOE phenotypes. Memory performance was measured with an abbreviated Auditory Verbal Learning Test (AVLT) at baseline and repeated after 3 years (n = 854). Memory decline was defined as a decrease of at least 1 SD from the mean change score on immediate recall (IR), delayed recall (DR), and retention, based on the AVLT.', 'Multivariate logistic regression analyses showed that APOE-epsilon4 is associated with memory decline in cognitively impaired subjects (MMSE score, 21 to 26) (OR for decline on IR adjusted for age, sex, education, and baseline recall score, 3.8; 95% CI, 1.4 to 10.0; adjusted OR for decline on DR, 2.9; 95% CI, 1.2 to 7.0; adjusted OR for decline on retention, 3.3; 95% CI, 1.1 to 10. 1), but not in cognitively normal subjects (MMSE score, 27 to 30) (adjusted OR for decline on IR, 1.1; 95% CI, 0.6 to 2.0; adjusted OR for decline on DR, 1.0; 95% CI, 0.6 to 1.8; adjusted OR for decline on retention, 1.5; 95% CI, 0.7 to 3.0). In particular, cognitively impaired epsilon4 carriers older than 75 years were at high risk of memory decline (adjusted OR for decline on IR, 4.5; 95% CI, 1.4 to 13.8; adjusted OR for decline on DR, 3.6; 95% CI, 1.2 to 10.8; adjusted OR for decline on retention, 6.6; 95% CI, 1.5 to 29.7).\Question: Is aPOE-epsilon4 associated with memory decline in cognitively impaired elderly?

SOLUTION: APOE-epsilon4 was associated with memory decline in subjects with cognitive impairment, but not in normally functioning subjects. Contrary to AD studies, our study suggests that the risk of APOE-epsilon4 on memory decline does not decrease at higher ages.

PROBLEM: Context: Isorhamnetin (Isor), a 3-O-methylated metabolite of quercetin, has shown antioxidant and anti-proliferative effects in previous studies. In this study, we investigated the anti-inflammatory effect of Isor on LPS-induced acute lung injury (ALI). Accordingly, we evaluated the effect of Isor on cytokine production elevated by LPS (1\xa0μg/ml) in vitro. An in vivo ALI murine model was also established via lipopolysaccharide inhalation (LPS, 20\xa0mg/kg), and the cytokine levels and inflammatory cell count in bronchoalveolar lavage fluid (BALF) were evaluated. The observed lung injury was assessed using histopathologic sections via H&E straining. Furthermore, to investigate whether the anti-inflammatory effect of Isor is associated with NF-κB and MAPKs pathway activation, the phosphorylated levels of ERK, JNK, IκBa and NF-κB(p65) were determined.', 'Isor significantly inhibited LPS-induced TNF-α, IL-1β and IL-6 secretion both in vitro and in vivo. Neutrophil infiltration and edema in an ALI model were substantially alleviated. The histopathological changes induced by LPS were lessened by Isor. Additionally, Isor notably suppressed the phosphorylation of ERK, JNK, IκBa and NF-κB(p65) activated by LPS in vivo.\Question: Does isorhamnetin protect mice from lipopolysaccharide-induced acute lung injury via the inhibition of inflammatory responses?

SOLUTION:
Isor showed efficient protective effects on an LPS-induced ALI model. MAPKs and NF-κB pathways are critical for Isor to perform its protective effects.