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 Q]: Context: The aim of this study was to investigate the relationship between intraoperative vasopressin infusion and postoperative cardiac enzymes.', 'A prospective, double-blind, randomized, controlled study.', 'A single tertiary cardiac center.', 'One hundred consecutive patients undergoing cardiac surgery with or without cardiopulmonary bypass.', 'The study was approved by the Institutional Review Board, and patients provided informed consent to participate. Patients were randomized by computer into 2 equal groups: Vasopressin or control. The blinded study included vasopressin administered at a dose of 1.8 U/h or 1.8 mL/h of normal saline, along with catecholamines. The drug was administered continually during surgery while patients needed catecholamines. The intervention was discontinued upon admission to the intensive care unit when information regarding the true character of the drug was reported to the doctor in charge of patients in the intensive care unit by one of the investigators. Primary outcomes were CK-MB and troponin T levels measured at 0, 6, and 12 hours postoperatively.', 'Of the 100 patients, 8 were excluded; the remaining 92 were randomized to either the vasopressin (n = 47) or control (n = 45) group. There were no significant differences in demographic data between the groups. Postoperatively at 0, 6, and 12 hours, there were no differences in CK-MB (U/l) (37.5 ± 57.9 v 32.0 ± 21.5, 29.4 ± 41.1 v 24.4 ± 23.1, and 21.4 ± 21.3 v. 21.8 ± 32.4, respectively) and troponin T (752.4 ± 638.2 v 762.7 ± 557.1, 753.8 ± 507.3 v 777.6 ± 515.0, and 774.6 ± 572.6 v 698.7 ± 540.2, respectively) values.
Answer: Vasopressin infusion has been used to treat catecholamine-unresponsive shock. In this study, intraoperative vasopressin was used safely as a possible first-line drug for treating hypotension; however, it did not increase the levels of cardiac enzymes after cardiac surgery.
[EX A]: Does vasopressin raise cardiac enzymes following cardiac surgery : a randomized double-blind clinical trial?

[EX Q]: Context: Cancer cells frequently exhibit resistance to the cytotoxic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Pretreatment of TRAIL-resistant cells with cisplatin sensitizes them to this ligand. Cisplatin also has been shown to enhance adenoviral transgene expression.', 'This study aims to evaluate the ability of cisplatin to enhance the expression and the cytotoxic effect of the tumor-specific adenoviral vector Ad/gTRAIL, which expresses a green fluorescent protein-TRAIL fusion protein.', 'Cultured cancer cells and normal human cells were infected with Ad/gTRAIL with or without cisplatin pretreatment. Adenoviral transgene expression was determined by using flow cytometry to measure green fluorescent protein fluorescence. Cytotoxicity was measured by using thiazolyl blue tetrazolium bromide assays and an apoptosis enzyme-linked immunosorbent assay kit.', 'Green fluorescent protein-TRAIL fusion protein expression was significantly enhanced by cisplatin pretreatment in cancer cells. Cisplatin treatment before Ad/gTRAIL infection resulted in a 2- to 12-fold increase in green fluorescent protein fluorescence intensity across cancer lines. Although Ad/gTRAIL induced mild cytotoxicity in all cancer lines (inhibitory concentration of 50% values of >500 pfu/cell), pretreatment with cisplatin resulted in a dose-dependent enhancement of Ad/gTRAIL-mediated cytotoxicity, as indicated by the drastic reduction of inhibitory concentration of 50% values to 4 to 42 pfu/cell in all cell lines. There was no cytotoxicity noted in normal cells treated with both cisplatin and Ad/gTRAIL.
Answer: Cisplatin pretreatment enhances Ad/gTRAIL cytotoxicity in malignant cells while not affecting normal cells. The mechanisms underlying this effect might include both enhancement of the susceptibility of cisplatin-treated cells to TRAIL and cisplatin-mediated enhancement of TRAIL expression in Ad/gTRAIL infected cells. These findings provide a rationale for development of Ad/gTRAIL-based therapy for thoracic malignancies.
[EX A]: Does cisplatin enhance apoptosis induced by a tumor-selective adenovirus expressing tumor necrosis factor-related apoptosis-inducing ligand?

[EX Q]: Context: To determine interrelationships between the expression of long intergenic (noncoding) RNA-p21 (lincRNA-p21), NF-κB activity, and responses to methotrexate (MTX) in rheumatoid arthritis (RA) by analyzing patient blood samples and cell culture models.', 'Expression levels of long noncoding RNA and messenger RNA (mRNA) were determined by quantitative reverse transcription-polymerase chain reaction. Western blotting and flow cytometry were used to quantify levels of intracellular proteins. Intracellular NF-κB activity was determined using an NF-κB luciferase reporter plasmid.', 'Patients with RA expressed reduced basal levels of lincRNA-p21 and increased basal levels of phosphorylated p65 (RelA), a marker of NF-κB activation. Patients with RA who were not treated with MTX expressed lower levels of lincRNA-p21 and higher levels of phosphorylated p65 compared with RA patients treated with low-dose MTX. In cell culture using primary cells and transformed cell lines, MTX induced lincRNA-p21 through a DNA-dependent protein kinase catalytic subunit (DNA PKcs)-dependent mechanism. Deficiencies in the levels of PRKDC mRNA in patients with RA were also corrected by MTX in vivo. Furthermore, MTX reduced NF-κB activity in tumor necrosis factor α-treated cells through a DNA PKcs-dependent mechanism via induction of lincRNA-p21. Finally, we observed that depressed levels of TP53 and lincRNA-p21 increased NF-κB activity in cell lines. Decreased levels of lincRNA-p21 did not alter NFKB1 or RELA transcripts; rather, lincRNA-p21 physically bound to RELA mRNA.
Answer: Our findings support a model whereby depressed levels of lincRNA-p21 in RA contribute to increased NF-κB activity. MTX decreases basal levels of NF-κB activity by increasing lincRNA-p21 levels through a DNA PKcs-dependent mechanism.
[EX A]:
Does methotrexate inhibit NF-κB activity via long intergenic ( noncoding ) RNA-p21 induction?