In this task, you are given a passage which has a question and the context. You have to generate an answer to the question based on the information present in the context.

Input: Consider Input: Context: Allergic rhinitis (AR) is a complex chronic inflammatory disease of the nasal mucosa, caused by an interaction between genetic and environmental factors. As evidence suggests that some genetic variants may increase susceptibility to both AR and asthma, the objective of this study was to identify asthma susceptibility variants associated with AR in the Chinese population.', 'A cohort of 402 individuals with physician-diagnosed AR and 416 healthy controls were recruited from the Han Chinese population in Beijing. DNA was extracted from the peripheral blood and a total of 12 single-nucleotide polymorphisms (SNPs) shown to be associated with asthma in Japanese subjects were selected for genotyping using the SequenomMassARRAY technology platform.', 'Analysis of frequency differences of allele between the AR patients and control subjects showed that the C allele of rs204993 in the pre-B-cell leukemia homeobox 2 (PBX2) gene from the 6p21.3 locus was significantly associated with AR (p = 0.0006, pcorrected = 0.0340). Genotype analysis further confirmed the difference in distribution of this variant between AR patients and controls in the both the dominant (pT/C+C/C vs T/T = 7.37×10(-5) ) and co-dominant (pT/C vs T/T = 1.98 × 10(-4) , pC/C vs T/T = 0.004) models.\Question: Does variant of PBX2 gene in the 6p21.3 asthma susceptibility locus is associate with allergic rhinitis in Chinese subjects?

Output: These results suggest that the PBX2 gene in the 6p21.3 asthma susceptibility locus may be associated with increased risk for both AR and asthma in Chinese subjects.


Input: Consider Input: Context: Endotoxin, when delivered shortly before or during mechanical ventilation, increases susceptibility to ventilation-associated lung injury. However, it is unclear whether increased susceptibility to ventilator-associated lung injury is still present after clinical recovery from a transient endotoxin challenge.', 'Anesthetized rats were submitted to a 4-h period of mechanical ventilation with low (8 ml/kg) or high (24, 27, or 30 ml/kg) tidal volumes (VTs) 24 h after transient illness had been provoked by a single nonlethal intravenous injection of Escherichia coli endotoxin. Control animals were injected with phosphate-buffered saline and underwent the same protocol.', 'At 24 h, endotoxin-treated nonventilated animals showed no symptoms of clinical illness, and oxygenation was comparable with that of controls, but lung neutrophil counts were increased. Compared with controls, mechanical ventilation with high VT induced a stronger pulmonary inflammatory response and more severe lung injury in endotoxin-treated animals, as indicated by impaired oxygenation, increased lung wet-to-dry weight ratio, and increased levels of protein, neutrophils, and cytokines in lung lavage fluid. In addition, the highest VT resulted in increased mortality in endotoxin-treated animals. Low VT after endotoxin treatment did not cause functional pulmonary impairment but induced an inflammatory response.\Question: Does increased susceptibility to ventilator-associated lung injury persist after clinical recovery from experimental endotoxemia?

Output: In this animal model, a 24-h delay after a single systemic injection of endotoxin resulted in clinical recovery and preserved pulmonary function but did not prevent increased susceptibility to ventilator-associated lung injury provoked by high VT. Residual pulmonary inflammation and neutrophilic infiltration at initiation of mechanical ventilation probably contribute to these findings.


Input: Consider Input: Context: To determine the effect of ketamine on the apoptosis of human uroepithelial cells (SVHUC-1) and the pathogenesis of ketamine-associated cystitis.', 'SV-HUC-1 cells were cultured under various concentrations of ketamine and differenttime. Flow cytometry was used to analyze the rate of cell apoptosis. The protein levels of Bax, Bcl-2, pro-caspase-3, and cleaved caspase-3 were detected by Western blot.', 'Compared with the control group, the apoptotic rate of ketamine cultured SV-HUC-1 cells increased. The expression of Bax increased, Bcl-2 expression decreased, and Bax/Bcl-2 in the ketamine cultured SV-HUC-1 cells was significantly higher. The protein level of pro-caspase-3 was significantly lower, and that of cleaved caspase-3 was significantly higher than that in the control group (P<0.05), positively correlated with the dose of ketamine and time of culture (P<0.05).\Question: Does [ Ketamine induce apoptosis of human uroepithelial SV-HUC-1 cells ]?


Output: Ketamine can induce the apoptosis of SV-HUC-1 cells in a dose and time dependent manner.