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.

Input: Consider Input: Context: Prostaglandin D2 (PGD2) and cysteinyl leukotrienes (cysLTs) are lipid mediators derived from mast cells, which activate TH2 cells. The combination of PGD2 and cysLTs (notably cysteinyl leukotriene E4 [LTE4]) enhances TH2 cytokine production. However, the synergistic interaction of cysLTs with PGD2 in promoting TH2 cell activation is still poorly understood. The receptors for these mediators are drug targets in the treatment of allergic diseases, and hence understanding their interaction is likely to have clinical implications.', 'We aimed to comprehensively define the roles of PGD2, LTE4, and their combination in activating human TH2 cells and how such activation might allow the TH2 cells to engage downstream effectors, such as neutrophils, which contribute to the pathology of allergic responses.', 'The effects of PGD2, LTE4, and their combination on human TH2 cell gene expression were defined by using a microarray, and changes in specific inflammatory pathways were confirmed by means of PCR array, quantitative RT-PCR, ELISA, Luminex, flow cytometry, and functional assays, including analysis of downstream neutrophil activation. Blockade of PGD2 and LTE4 was tested by using TM30089, an antagonist of chemoattractant receptor-homologous molecule expressed on TH2 cells, and montelukast, an antagonist of cysteinyl leukotriene receptor 1.', 'PGD2 and LTE4 altered the transcription of a wide range of genes and induced diverse functional responses in TH2 cells, including cell adhesion, migration, and survival and cytokine production. The combination of these lipids synergistically or additively enhanced TH2 responses and, strikingly, induced marked production of diverse nonclassical TH2 inflammatory mediators, including IL-22, IL-8, and GM-CSF, at concentrations sufficient to affect neutrophil activation.
Answer: PGD2 and LTE4 activate TH2 cells through different pathways but act synergistically to promote multiple downstream effector functions, including neutrophil migration and survival. Combined inhibition of both PGD2 and LTE4 pathways might provide an effective therapeutic strategy for allergic responses, particularly those involving interaction between TH2 cells and neutrophils, such as in patients with severe asthma.

Output: Do prostaglandin D2 and leukotriene E4 synergize to stimulate diverse TH2 functions and TH2 cell/neutrophil crosstalk?


Input: Consider Input: Context: Recently, the Arg389Gly beta1-adrenoceptor (beta1AR) gene polymorphism has been detected. The Arg variant exhibited increased responsiveness to agonist-induced stimulation in vitro. Functional studies in isolated human atrial muscle strips and in-vivo studies revealed contradictory results regarding the functional relevance of this polymorphism. We sought to characterize the functional consequences of the Arg389Gly beta1-AR polymorphism in 30 consecutive healthy male volunteers in vivo.', 'beta1-AR genotype was determined by PCR and restriction analysis, which was confirmed by DNA sequencing. We compared heart rate, blood pressure, and contractile response of the various genotype carriers with a modified dobutamine stress echocardiography protocol.', 'Subjects homozygous for the Arg389 beta1AR showed a significantly higher increase in fractional shortening upon cumulative doses of dobutamine as compared to subjects carrying one or two copies of the Gly389 allele. A statistically significant difference was observed at a dobutamine dose of 10 microg/kg/min (46.5 +/- 1.3 vs. 41.8 +/- 1.0 %; P = 0.023) and was maximal at 40 microg/kg/min (61.9 +/- 1.4 vs. 52.8 +/- 1.6; P = 0.001). As a result, the systolic blood pressure response to dobutamine was significantly enhanced in individuals homozygous for the Arg389 allele, whereas the effect on heart rate did not differ between the two groups. Normalization for changing afterload conditions by calculating the pressure-dimension ratio revealed similar effects, indicating that the beta1AR-mediated effects are mainly a result of increased myocardial inotropy.
Answer: These data indicate that the Arg389Gly beta1AR polymorphism is functionally relevant in vivo and determines contractile responsiveness to catecholamines in humans.

Output: Does the Arg389Gly beta1-adrenoceptor gene polymorphism determine contractile response to catecholamines?


Input: Consider Input: Context: We investigated whether aprepitant, a neurokinin-1 antagonist, could decrease chemotherapy-induced nausea and vomiting (CINV) following cisplatin, when a conventional anti-emetic regimen had failed.', 'This was a prospective study (April 2011-April 2012) of patients with lung cancer, treated with cisplatin at the Beijing Cancer Hospital, and initially receiving granisetron, dexamethasone, and metoclopramide as anti-emetics. If patients experienced vomiting of grade ≥2 and required rescue anti-emetic medications during the first cycle, oral aprepitant was added in subsequent cycles (day 1: 125 mg; days 2-3: 80 mg once daily). Acute (day 1) and delayed (days 2-5) nausea and vomiting, use of rescue medications, and occurrence of adverse reactions were monitored after the start of chemotherapy.', 'Twenty-five of 132 patients (18.9 %) were administered aprepitant for secondary prophylaxis against emesis during the second cycle of chemotherapy. The incidences of acute and delayed nausea were 52 and 100 % in the first cycle, but 8 and 72 % in the second cycle. The incidences of acute and delayed vomiting were 20 and 100 % in the first cycle, but 0 and 36 % in the second cycle. No patients required rescue medications or intravenous rehydration during the second cycle. Aprepitant was not associated with additional adverse events.
Answer: In patients with lung cancer receiving cisplatin-based chemotherapy, the addition of aprepitant to a 5-HT3 antagonist, dexamethasone, and metoclopramide improves protection against CINV when the conventional anti-emetic regimen fails.


Output: Does addition of aprepitant improve protection against cisplatin-induced emesis when a conventional anti-emetic regimen fails?