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.

[EX Q]: Context: Serum ferritin concentration >100\xa0ng/mL was associated with a higher risk of death in hemodialysis patients in Japan, whereas such an association was less clear in hemodialysis patients in Western countries. Since Japanese dialysis patients are generally less inflamed than those in Western countries, inflammation may modify the association between serum ferritin and the adverse outcomes.', 'We performed an observational cohort study using data from 2606 Japanese hemodialysis patients who participated in the Dialysis Outcomes and Practice Patterns Study (DOPPS) III (2005-2008) or DOPPS IV (2009-2012). The predictor was serum ferritin category (<50, 50-99.9, 100-199.9, and ≥200\xa0ng/mL), and the primary and secondary outcomes were all-cause mortality and cardiovascular hospitalization, respectively. C-reactive protein (CRP, cut-off by 0.3\xa0mg/dL) and serum albumin (cut-off by 3.8\xa0g/dL) were stratification factors related to systemic inflammation.', 'After adjustment for relevant confounding factors, a U-shaped association was observed between serum ferritin and all-cause mortality in the group with low CRP levels, whereas such relationship was not significant in the high CRP counterparts. In contrast, we found a linear association between serum ferritin and cardiovascular hospitalization in the low CRP and high CRP groups commonly. Similar results were obtained when the total cohort was stratified by serum albumin.\Question: Do both low and high serum ferritin levels predict mortality risk in hemodialysis patients without inflammation?
[EX A]: Serum ferritin showed different patterns of association with all-cause mortality in hemodialysis patients with versus without inflammation, whereas its association with cardiovascular hospitalization was similar regardless of inflammatory conditions.

[EX Q]: Context: Burns cause thermal injury to local tissue and trigger systemic acute inflammatory processes, which may lead to multiple distant organ dysfunction. We investigated the protective effect of dietary whey supplementation on distant organs in a rat model.', 'Forty-eight rats were divided into six groups of eight: groups 1 and 2 were the controls, fed a standard diet and a whey-supplemented diet, respectively; groups 3 and 4 were fed a standard diet and subjected to burn injury; and groups 5 and 6 were fed a whey-supplemented diet and subjected to burn injury. We measured the oxidative stress variables, as well as glutathione in the liver and kidney, and histologically examined skin samples obtained 4 h (groups 3 and 5) and 72 h (groups 4 and 6) after burn injury.', 'Glutathione (GSH) levels remained the same in the liver but were slightly elevated in the kidneys after burn injury in the rats fed a standard diet. Whey supplementation caused a significant increase in hepatic GSH levels 4 h after burn injury. Moreover, there was a significant rebound effect in the liver and kidney GSH levels after 72 h and whey supplementation potentiated this effect. Hepatic and renal lipid peroxide levels were also increased 4 h after burn injury in the rats fed a standard diet. Whey supplementation significantly suppressed the burn-induced increase in hepatic and renal lipid peroxide levels. Histological examination revealed that although whey supplementation resulted in decreased subepidermal inflammation, the indicators of wound healing and collagen deposition were not improved.\Question: Does whey feeding suppress the measurement of oxidative stress in experimental burn injury?
[EX A]: Whey pretreatment suppressed hepatic and renal oxidative stress measurements after experimental burn injury.

[EX Q]: Context: Our objective was to determine whether paclitaxel-induced apoptosis in human lung cancer cells is Fas dependent.', 'Human lung cancer cell lines were evaluated for morphologic evidence of apoptosis, DNA fragmentation (TUNEL positivity), and caspase-3 activation after paclitaxel treatment. Human lung adenocarcinoma, squamous cell carcinoma, undifferentiated lung carcinoma, and bronchoalveolar carcinoma cell lines were each cultured in 10 micromol/L paclitaxel.', 'After 24 hours of culture in paclitaxel, a 22% to 69% increase in the number of apoptotic cells was evident by means of methylene blue-azure A-eosin staining with characteristic blebbing and nuclear condensation. TUNEL assay also confirmed an increase of 19.9% to 73.0% of cells with nuclear fragmentation. Caspase-3 activity, assayed by Z-DEVD cleavage, increased from 20% to 215% (P <.05). ZB4, an antagonistic anti-Fas antibody, did not block paclitaxel induction of caspase-3 activity (155.8 vs 165.8 U, not significant). Apoptotic morphologic changes were inhibited in cells cultured in the presence of paclitaxel and Ac-DEVD-CHO, a caspase-3 inhibitor.\Question: Is paclitaxel-induced apoptosis in non-small cell lung cancer cell lines associated with increased caspase-3 activity?
[EX A]:
Paclitaxel induces apoptosis in lung cancer cell lines, as assessed by a consistent increase in caspase-3 activity, DNA laddering, and characteristic morphologic changes. Paclitaxel-induced apoptosis in human lung cancer cells is associated with caspase-3 activation but is not Fas dependent.