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.
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Question: Context: Non-viral gene transfer efficiency is low as compared to viral vector systems. Here we describe the discovery of new drugs that are capable of enhancing non-viral gene transfer into mammalian cells using a novel two-stage screening procedure.', 'First, potential candidates are preselected from a molecular library at various concentrations by a semi-automated yeast transfection screen (YTS). The maximal transfection efficiency of every positive drug is subsequently determined in independent experiments at the optimal concentration and compared to the inhibitory effect of the drug on cell growth (IC50). In a subsequent mammalian cell transfection screen (MTS), the maximal transfection efficiency and the IC50 are determined for all preselected drugs using a human cell line and a luciferase reporter gene construct.', 'Employing our novel system we have been able to identify a new class of transfection enhancers, the tricyclic antidepressants (i.e. doxepin, maprotiline, desipramine and amoxapine). All positive drugs enhanced gene transfer in both yeast and human cell lines, but lower concentrations were sufficient for mammalian cells. With a triple combination of doxepin, amoxapine and chloroquine we obtained a transfection efficiency that exceeded that of chloroquine, one of the best-known transfection enhancers of mammalian cells, by nearly one order of magnitude.\Question: Does novel two-stage screening procedure lead to the identification of a new class of transfection enhancers?

Answer: Non-viral gene transfer efficiency can be increased significantly using new transfection enhancers that are identified by a novel, semi-automated two-stage screening system employing yeast cells in the first and specific human target cells in the second round.


Question: 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?

Answer: 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.


Question: Context: Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are secreted from enteroendocrine L cells in response to nutrient ingestion. As glutamine is an important metabolic fuel for the gut, the aim of this study was to investigate the effect of glutamine on the GLP-1-secreting cell line, GLUTag.', 'GLP-1 release was measured following incubation of GLUTag cells under a range of conditions. Single cells were studied by electrophysiology, calcium imaging and cytosolic ATP measurement using recombinant luciferase.', 'Glutamine was a more potent GLP-1 secretagogue than glucose or other amino acids, increasing GLP-1 release 7.1+/-0.7-fold ( n=19) at 10 mmol/l, with an estimated median effective concentration of between 0.1 and 1 mmol/l. Glutamine (10 mmol/l) induced a sodium-dependent inward current of 3.2+/-1.2 pA per cell ( n=9), which triggered membrane depolarisation and an increase in intracellular calcium. Asparagine and alanine produced electrophysiological and calcium changes that were at least as large as those caused by glutamine, but they were less effective GLP-1 secretagogues, suggesting that glutamine also potentiates secretion downstream of the calcium signal. This was confirmed by measuring secretion in the presence of 30 mmol/l KCl + diazoxide, or in alpha-haemolysin-permeabilised cells. Glutamine increased cytosolic ATP, but was less effective than glucose.\Question: Does glutamine potently stimulate glucagon-like peptide-1 secretion from GLUTag cells?

Answer:
Glutamine acts as a trigger and potentiator of GLP-1 release, consistent with its role as the major metabolic fuel for the gut. The results suggest that nutritional agents like glutamine might have beneficial effects in diabetes and obesity.