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: 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: Dyschloremia is common in critically ill patients, although its impact has not been well studied. We investigated the epidemiology of dyschloremia and its associations with the incidence of acute kidney injury and other intensive care unit outcomes.', 'This is a single-center, retrospective cohort study at Mayo Clinic Hospital-Rochester. All adult patients admitted to intensive care units from January 1st, 2006, through December 30th, 2012 were included. Patients with known acute kidney injury and chronic kidney disease stage 5 before intensive care unit admission were excluded. We evaluated the association of dyschloremia with ICU outcomes, after adjustments for the effect of age, gender, Charlson comorbidity index and severity of illness score.', 'A total of 6,025 patients were enrolled in the final analysis following the implementation of eligibility criteria. From the cohort, 1,970 patients (33%) developed acute kidney injury. Of the total patients enrolled, 4,174 had a baseline serum chloride. In this group, 1,530 (37%) had hypochloremia, and 257 (6%) were hyperchloremic. The incidence of acute kidney injury was higher in hypochloremic and hyperchloremic patients compared to those with a normal serum chloride level (43% vs.30% and 34% vs. 30%, respectively; P < .001). Baseline serum chloride was lower in the acute kidney injury group vs. the non-acute kidney injury group [100 mmol/L (96-104) vs. 102 mmol/L (98-105), P < .0001]. In a multivariable logistic regression model, baseline serum chloride of ≤94 mmol/L found to be independently associated with the risk of acute kidney injury (OR 1.7, 95% CI 1.1-2.6; P = .01).
Answer: Dyschloremia is common in critically ill patients, and severe hypochloremia is independently associated with an increased risk of development of acute kidney injury.
[EX A]: Does dyschloremia be a Risk Factor for the Development of Acute Kidney Injury in Critically Ill Patients?

[EX Q]: Context: Reports on hormone receptor expression of pancreatic cancer (PaCa) cells and treatment responses to antihormonal therapy are conflicting. We examined estrogen receptor (ER) expression in PaCa cells and investigated its function in estrogen-mediated cell proliferation.', 'Protein levels of ERalpha and ERbeta in 8 human PaCa lines were detected by Western blot analysis. Cell proliferation was measured by sulforhodamine B analysis. ER modulators included diethylstilbestrol (DES), estradiol (E2), 4-hydroxytamoxifen (Tam), genistein (Gen), and Coumestrol (Coum).', "ERalpha levels were detected in all eight, and ERbeta in seven cell lines. ERbeta/ERalpha ratio ranged from 0.4 to 111 (median: 6.4, >5 in seven lines). Median maximal growth stimulation (in %, observed at 20 to 200 nM) was 19 (DES), 39 (E2), 20 (Tam), 22 (Gen), and -9 (Coum); median maximal inhibition (at 40 to 60 microM) was 59 (DES), 36 (E2), 25 (Tam), 43 (Gen), and 50 (Coum). The extent of E2 and Gen stimulatory effects correlated with the ERbeta/ERalpha ratio (Kendall's tau: 0.714, P = 0.024), but not ERalpha or ERbeta levels alone. Only Coum-induced inhibition correlated with the ERbeta/ERalpha ratio (P = 0.006) and with ERalpha expression (r = 0.753, P = 0.03). Gemcitabine-induced PaCa cytotoxicity (at IC(40)) was significantly reduced by E2, Gen, and Coum.
Answer: PaCa proliferation in vitro is highly estrogen sensitive, and in contrast to other reports, ERs are frequently expressed. In 7/8 cell lines, ERbeta expression outweighs ERalpha expression. The impact of the ERbeta/ERalpha ratio on estrogen-mediated growth stimulation and reduced cytotoxicity at physiological concentrations may have clinical implications on PaCa therapy.
[EX A]:
Does estrogen receptor beta/alpha ratio predict response of pancreatic cancer cells to estrogens and phytoestrogens?

