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.

Ex Input:
Context: To study the effect of Cleistocalyx nervosum extract (CE) on diethylnitrosamine (DEN) and phenobarbital (PB) induced oxidative stress in early stages of rat hepatocarcinogenesis.', 'Male Wistar rats were divided into 4 groups, with Group 1 as a negative control and Group 2 was a positive control receiving DEN injections once a week and PB in drinking water for 6 weeks. Two weeks before DEN initiation and PB treatment, Groups 3 and 4, were fed with 500 and 1000 mg/kg of CEs, respectively, for 8 weeks.', 'A number of GST-P-positive foci, preneoplastic lesions, in the liver were markedly increased in carcinogen administered rats, but was comparatively decreased in rats treated with 1000 mg/kg of CE. The CE reduced malondialdehyde in serum and in the livers of rats treated with DEN and PB. Moreover, CE significantly increased the activities of glutathione peroxidase and catalase in rat liver.
Answer: CE appeared to exert its chemopreventive effects by modulating antioxidant status during DEN and PB induced early stages of hepatocarcinogenesis in rats.

Ex Output:
Does cleistocalyx nervosum extract ameliorate chemical-induced oxidative stress in early stages of rat hepatocarcinogenesis?


Ex Input:
Context: The pulmonary endothelium plays an important role in the metabolism of the amino acid arginine, the exclusive precursor molecule for nitric oxide (NO). Despite decreased circulating arginine levels, endothelial NO production is elevated during endotoxemia. However, the regulation of pulmonary artery endothelial arginine transport has not been studied. We hypothesized that endotoxin stimulates carrier-mediated arginine transport by the pulmonary endothelium.', 'The relative contributions of the various transport systems to total arginine transport by porcine pulmonary artery endothelial cells (PAECs) was determined by assaying the uptake of 3H-L-arginine in the presence or absence of Na+. PAECs were then incubated with various concentrations of Escherichia coli endotoxin, and y(+)-mediated arginine transport was measured at different time points thereafter. Kinetic studies were performed over a range of arginine concentrations to determine changes in transport affinity and maximum rate of metabolism. To address the role of RNA and protein synthesis in the increased transport, uptake was measured after exposure of cells to the transcriptional inhibitor actinomycin D and the protein synthesis inhibitor cycloheximide.', 'Most (75%) of arginine transport by PAECs was mediated by the high-affinity Na(+)-independent transport system y+. Endotoxin stimulated y(+)-mediated arginine transport by PAECs twofold to fivefold, a response that was time and dose dependent. The accelerated transport was detectable within 2 hours and maximal at 12 hours. Kinetic studies revealed that the accelerated arginine transport was the result of a 68% increase in the maximal transport velocity (1519 +/- 65 pmol/mg protein/30 sec in endotoxin-treated cells vs 903 +/- 96 in control cells; p < 0.01) without a change in transport affinity. The endotoxin-mediated increase in arginine uptake was abrogated by actinomycin D and cycloheximide.
Answer: Endotoxin stimulates Na(+)-independent arginine transport by PAECs through a process that requires de novo RNA and protein synthesis, possibly of the transporter itself. This response may be designed to support arginine-dependent biosynthetic pathways in the lung during septic states.

Ex Output:
Does endotoxin stimulate arginine transport in pulmonary artery endothelial cells?


Ex Input:
Context: To examine whether the elevated preoperative plasma D-dimer levels show correlation with chemoresistance and poor prognosis in serous ovarian cancer patients.', 'Preoperative plasma D-dimer levels were measured in 125 patients with primary serous ovarian cancer (SOC).The correlations of plasma D-dimer levels with clinicopathological features, chemotherapeutic response, and survival outcome were further analyzed. Kaplan-Meier estimates were used to compute the survival functions and were compared using log-rank tests. Cox proportional-hazard regression analysis was used to evaluate the effects of D-dimer on progression-free survival (PFS) and overall survival (OS), controlling for potential confounding factors.', 'The median follow-up period was 49 (range 5-85) months. Elevated plasma D-dimer levels were positively associated with advanced FIGO stage (P = 0.010), residual tumor size (P = 0.017), the presence of malignant ascites (P = 0.028), increased serum CA125 level (P = 0.014), and neo-adjuvant chemotherapy (P = 0.008). The patients with elevated plasma D-dimer levels had significantly higher chemoresistance rates (56.41 %) compared to the normal plasma D-dimer levels (20.93 %). Additionally, it was found by the univariate analysis that elevated plasma D-dimer levels were closely related with a low 5-year PFS rate (28.21 vs 52.33 %, P = 0.002) and a poor 5-year OS (30.77 vs 63.95 %, P < 0.001). However, after adjustment for other factors, high plasma D-dimer levels were only closely correlated with a poor 5-year OS (HR 1.901, 95 % CI 1.021-3.540; P = 0.043).
Answer: Elevated preoperative plasma D-dimer levels were associated with chemoresistance and poor disease outcome in serous ovarian cancer patients. Further validation of this easily available parameter as a promising prognostic biomarker for patients with SOC in prospective studies should be encouraged.

Ex Output:

Is elevated preoperative plasma D-dimer level a useful predictor of chemoresistance and poor disease outcome for serous ovarian cancer patients?