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:
To fully understand the cytotoxicity of after-degradation QDs, we synthesized CdS QDs and investigated its toxicity mechanism.', 'Biomimetic method was proposed to synthesize cadmium sulfide (CdS) QDs. Thereafter MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay was conducted to evaluate their cytotoxicity. To investigate the toxicity mechanism, we subsequently conducted intracellular reactive oxygen species (ROS) measurement with DCFH-DA, glutathione (GSH) measurement with DTNB, and cellular cadmium assay using atomic absorption spectrometer. Microsized CdS were simultaneously tested as a comparison.', "MTT assay results indicated that CdS QDs are more toxic than microsized CdS especially at concentrations below 40 microg/ml. While microsized CdS did not trigger ROS elevation, CdS QDs increase ROS by 20-30% over control levels. However, they both deplete cellular GSH significantly at the medium concentration of 20 microg/ml. In the presence of NAC, cells are partially protected from CdS QDs, but not from microsized particles. Additionally, nearly 20% of cadmium was released from CdS nanoparticles within 24h, which also accounts for QDs' toxicity.
answer:
Do intracellular oxidative stress and cadmium ions release induce cytotoxicity of unmodified cadmium sulfide quantum dots?


question:
Both diet quality (DQ) and physical activity (PA) have been shown to play a role in the prevention of functional capacity (FC) decline. Because older adults (OA) with T2D are at a higher risk of FC decline compared to their non-diabetic counterparts, our aim was to determine if DQ alone, or combined with PA is associated with FC decline in OA with T2D over a 3-year follow-up in a secondary analysis of the NuAge cohort.', "In 159 OA with T2D (mean age=75 years), FC change was calculated as the difference in FC scores at T1 and T4 measured by the SMAF (Système de Mesure de l'Autonomie Fonctionnelle). Baseline DQ was calculated from three non-consecutive 24-h dietary recalls collected at T1 using the validated Canadian Healthy Eating Index (C-HEI). PA change was calculated from Physical Activity Scale for the Elderly (PASE) as T4-T1. Associations were evaluated between FC decline and four combinations of variables: C-HEI score < or ≥70 with PASE change < or > median and analyzed by GLM while controlling for covariates.", 'Neither DQ alone nor DQ combined with PA change were associated with FC decline over follow-up.
answer:
Is decline in functional capacity unaffected by diet quality alone or in combination with physical activity among generally healthy older adults with T2D from the NuAge cohort?


question:
Prenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives. LPS-exposure resulted in the production of cytokines and oxidative damage. On the contrary, astaxanthin is a carotenoid compound, showed neuroprotective properties via its antioxidant capacity. This study examines the effect of astaxanthin on the prenatal maternal LPS-induced postnatal behavioral deficit in mice.', 'We found that prenatal LPS-exposed mice showed extensive immobile phase in the tail suspension test, higher frequent head dipping in the hole-board test and greater hypolocomotion in the open field test. All these values were statistically significant (p\xa0<\xa00.05). In addition, a marked elevation of the level of lipid peroxidation, advanced protein oxidation product, nitric oxide, while a pronounced depletion of antioxidant enzymes (superoxide dismutase, catalase and glutathione) were observed in the adult offspring mice that were prenatally exposed to LPS. To the contrary, 6-weeks long treatment with astaxanthin significantly improved all behavioral deficits (p\xa0<\xa00.05) and diminished prenatal LPS-induced oxidative stress markers in the brain and liver.
answer:

Does astaxanthin ameliorate prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring?