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.

Example Input: Context: A malaria management protocol was developed and implemented at a tertiary care children's hospital in September 1999. We retrospectively evaluated children admitted with malaria 10-years preimplementation and 7-years postimplementation to determine the impact the protocol had on management and time delay to appropriate antimalarial therapy.", 'This before and after study compared all admissions with the discharge diagnosis of malaria in the study period. Retrospective chart review was used to determine the time from emergency department (ED) registration to administration of antimalarial treatment. Other outcomes measured included mortality, length of hospital stay, and intensive care unit admission.', 'Fifty-eight admissions were identified during the defined period, most of which were due to Plasmodium falciparum[r] malaria. Thirty-one (53.4%) cases were before implementation of the protocol. Children were more likely to receive appropriate investigations to assess for possible severe malaria before transfer from the ED to the ward after protocol implementation (18% vs. 63%, P = 0.005). Analysis of index cases of malaria, excluding patients diagnosed after the diagnosis of a sibling, showed there was a significant reduction in time to medication administration (8 vs. 5.5 hours, P = 0.036).\Question: Does protocol for management of imported pediatric malaria decrease time to medication administration?
Example Output: After broad-based implementation of a malaria treatment protocol in a pediatric hospital, children received more thorough investigations, were more likely to receive therapy before leaving the ED and had a shorter delay before receiving appropriate antimalarial therapy.

Example Input: Context: Phospholipid transfer protein (PLTP) transfers phospholipids between lipoproteins and plays an important role in HDL metabolism. PLTP exists as a high-activity and a low-activity form in the circulation. In vitro studies have shown that apolipoprotein (apo) E is involved in maintaining PLTP in the active form, while the low-activity form is associated with apo AI. We have therefore investigated whether plasma apo AI, B and E concentrations are important determinants of plasma PLTP activity in type 2 diabetes, a condition associated with increased plasma PLTP activity.', 'Plasma PLTP activity was assayed by measuring the transfer of radiolabelled phosphatidylcholine from liposomes to HDL; apo AI and B by rate nephelometry and apo E by a 2-point turbidimetric assay.', 'Type 2 diabetic patients (n = 230) had higher PLTP activity than controls (n = 97) (2374 +/- 628 nmol/mL/h versus 1862 +/- 585 respectively, p < 0.01). They also had increased fasting triglyceride and low HDL. Plasma apo B (p < 0.01) and apo E (p < 0.05) were increased, whereas apo AI was reduced (p < 0.01). Univariate analysis showed that plasma PLTP activity correlated mainly with apolipoproteins AI and E. Stepwise regression analysis showed that apo E was the main determinant of plasma PLTP activity, accounting for 23% of its variability in the diabetic subjects and 8% in the controls respectively.\Question: Is plasma apolipoprotein E concentration an important determinant of phospholipid transfer protein activity in type 2 diabetes mellitus?
Example Output: The associations between plasma apo AI and E concentrations and PLTP activity suggest that these apolipoproteins are important regulators of PLTP activity in vivo. The increase in PLTP activity in type 2 diabetes is partly related to the changes in these apolipoproteins.

Example Input: Context: Irinotecan is used in the first-line treatment of metastatic colorectal cancer. The UGT1A1-metabolizing enzyme, expressed in liver and colon, is primarily involved in the inactivation of its active metabolite 7-ethyl-10-hydroxycamptothecin (SN-38). Herein, we explored the role of DNA methylation in the silencing of UGT1A1 gene expression in colon cancer and its influence on cellular SN-38 detoxification.', 'UGT1A1 mRNA was repressed in most primary tumors (41 of 50; 82%) and in three colon cancer cell lines (HCT-116, HCT-15, and COLO-320DM). Bisulfite sequencing of the UGT1A1 gene revealed the aberrant methylation of specific CpG islands in UGT1A1-negative cells. Conversely, hypomethylation was observed in HT-29, HT-115, and LOVO cells that overexpress UGT1A1. Direct methylation of the UGT1A1 promoter resulted in the complete repression of transcriptional activity. Treatment with demethylating and histone deacetylase inhibitor agents had the capacity to reverse aberrant hypermethylation and to restore UGT1A1 expression in hypermethylated UGT1A1-negative cells but not in hypomethylated cells. Loss of UGT1A1 methylation was further associated with an increase in UGT1A1 protein content and with an enhanced inactivation of SN-38 by 300% in HCT-116 cells.\Question: Is irinotecan inactivation modulated by epigenetic silencing of UGT1A1 in colon cancer?
Example Output:
We conclude that DNA methylation represses UGT1A1 expression in colon cancer and that this process may contribute to the level of tumoral inactivation of the anticancer agent SN-38 and potentially influence clinical response.