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.

Input: Consider Input: To observe the effects of Sanhuangyinchi decoction (SHYCD) pretreatment on acute hepatic failure (AHF) induced by D-galactosamine and lipopolysaccharide (LPS) in rats and explore the possible mechanisms involving antioxidant stress and cell apoptosis-related protein expression.', 'Forty-eight SD rats were randomized equally into control group, AHF model group, high-, medium- and low-dose SHYCD groups, and Bicyclol group. Five days after administration of the corresponding drugs, the rats were challenged with peritoneal D-galactosamine (700 mg/kg) plus LPS (10 ug/kg) injections to induce AHF acute hepatic failure except for those in the control group. At 48 h after the injections, blood samples were collected from the rats to detect the levels of ALT, AST, TBIL, PT, INR and FIB, and pathological changes and superoxide dismutase (SOD) and malondialdehyde (MDA) contents in the liver were examined; immunohistochemistry and western blotting were used to detect caspase-3 protein expression in the liver.', 'The levels of ALT, AST, TBIL, TP and INR in the 3 SHYCD groups and Bicyclol group significantly decreased (P<0.05) while FIB significantly increased in comparison with those in the model group. SHYCD obviously ameliorated the pathological changes, enhanced SOD activity (P<0.05), and decreased MDA levels (P<0.05) and caspase-3 expression (P<0.05) in the liver tissue. SHYCD at the medium dose produced similar effects to Bicyclol (P>0.05) and showed better effects at the high dose than Bicyclol (P<0.05).

Output: Does [ Sanhuangyinchi decoction pretreatment ameliorate acute hepatic failure in rats by suppressing antioxidant stress and caspase-3 expression ]?


Input: Consider Input: Clinical predictors associated with acute paraquat (PQ) poisoning have not been systematically studied.', 'To identify independent predictors of death in patients with acute PQ poisoning.', 'This is a retrospective study executed in the emergency department of a university hospital. One hundred three consecutive patients poisoned with PQ between January 1999 and December 2004 were enrolled. Urine PQ concentration, electrolyte and renal function, detailed history, and Acute Physiology and Chronic Health Evaluation II were extracted from medical records. The outcome measure was 30-day mortality. Multivariate analysis was done by Cox-proportional hazard regression model. Receiver operating characteristics area under the curve was calculated for selected predictors.', 'The crude 30-day mortality was 67.9% (70 of 103). Independent predictors of death were acute renal failure (hazard ratio, 3.53; 95% confidence interval, 1.97-6.32), hypokalemia (2.07, 1.21-3.51), hypothermia (2.91, 1.67-5.07), suicide (2.11, 1.04-4.29), and self-reported ingested dose (2.06, 1.38-3.06). The receiver operating characteristics area under the curve of serum potassium concentrations, maximal urine PQ concentrations, and Acute Physiology and Chronic Health Evaluation II scores were 0.75 (95% confidence interval, 0.60-0.81), 0.71 (0.66-0.84), and 0.80 (0.71-0.88), respectively. Under the cutoff value of 3.6 mEq/L, hypokalemia had a sensitivity of 75% and specificity of 54% in predicting mortality.

Output: Are hypokalemia and hypothermia associated with 30-day mortality in patients with acute paraquat poisoning?


Input: Consider Input: Aurora kinase A (AurkA) is over-expressed in melanoma and its inhibition has been observed to limit tumor growth, suggesting a potential role in melanoma treatment.', 'A human melanoma cell line with the B-RAF (V600E) mutation (A375mel) was exposed to B-RAF inhibitor (GSK2118436), MEK inhibitor (GSK1120212) and AurkA inhibitor (MLN8054) as single agents or in various combinations (BRAF plus AurkA inhibitor, MEK plus AurkA inhibitor or triple combination BRAF plus MEK plus AurkA inhibitor). Cell proliferation was assessed using xCELLigence technology. Total protein extracts were examined for p53 and c-Myc protein expression by Western blot analysis. Drug anti-tumor effects were further assessed using a 3D-human melanoma skin reconstruction model, in which tissues were incubated with serum-free medium containing control, B-RAF plus MEK inhibitor, MEK plus AurkA inhibitor or the triple combination.', 'AurkA inhibitor plus B-RAF inhibitor, AurkA inhibitor plus MEK inhibitor or triple combination had a markedly greater anti-proliferative effect on A375 (BRAFV600E) melanoma cells than single agents. In the 3D human skin model, the triple combination had a greater anti-tumor effect at the epidermal/dermal junction than control or either double combination. However, S-100 and Ki-67 positively stained spindle-shaped cells were detected in the dermal stratum, suggesting the presence of alive and proliferating melanoma cells.


Output: Do aurkA inhibitors enhance the effects of B-RAF and MEK inhibitors in melanoma treatment?


