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.

[EX Q]: Context: Although meperidine is an effective treatment of postanesthetic shivering, its mechanism of action remains unknown. Investigation of other drugs might help clarify the mechanisms by which shivering can be controlled. Accordingly, we investigated the efficacy of clonidine, an alpha 2-adrenergic agonist, and ketanserin, a 5-hydroxytryptamine antagonist, in treating postanesthetic shivering.', 'First, 54 patients shivering after general anesthesia were allocated randomly to receive an intravenous bolus of saline, 150 micrograms clonidine, or 10 mg ketanserin. A second study explored the dose-dependence of clonidine. Forty shivering patients were given saline or clonidine, 37.5, 75, or 150 micrograms.', 'The duration of shivering was significantly shorter in those given clonidine (2.1 +/- 0.9 min) than in the other two groups and shorter in the ketanserin group (4.3 +/- 0.9 min) than in the saline group (12.0 +/- 1.6 min). Clonidine and ketanserin significantly decreased systolic arterial blood pressure when compared to saline. Core rewarming was significantly slower in the clonidine group. In the second study, 37.5 micrograms clonidine was no more effective than saline. Two minutes after treatment, 150 micrograms obliterated shivering in all patients. Five minutes after treatment, all patients given 75 micrograms had stopped shivering. Systolic arterial pressure and heart rate decreased significantly in patients given 75 and 150 micrograms clonidine.\Question: Are clonidine and ketanserin both effective treatment for postanesthetic shivering?
[EX A]: Clonidine (150 micrograms) and ketanserin (10 mg) both are effective treatment for postanesthetic shivering. The effect of clonidine on shivering is dose-dependent: whereas 37.5 micrograms had no effect, 75 micrograms clonidine stopped shivering within 5 min.

[EX Q]: Context: This study was conducted to determine if there was an increase in the urinary excretion of fluoride, after the use of fluoride mouth rinses in children.', 'The sample consisted of 58 children aged 5-8 years, randomly selected, residents in non-fluoridated water areas. Urine samples were collected prior to mouthwash and also 2 hours after use. The control sample, which received no treatment, consisted of 16 children of equivalent age and from the same community. Urinary excretion of fluoride was analysed by determining the pH, creatinine, F- ion and fluoride (mg)/creatinine (g) (F/Cr) ratio in urine. Results In the studied sample, the mean F/Cr ratio before fluoride mouth rinse was 0.26 mg/g and it rose to 1.58 mg/g 2 hours after mouth rinse. This difference of 1.33 mg/g was statistically highly significant (p<.001). In the control group no significant changes occurred. The average 2 hours afterward F/Cr ratios were 0.29 and 0.27 respectively (p=0.426).\Question: Does renal excretion of fluoride after fluoride mouth rinse in children?
[EX A]: After the use of a fluoride mouthwash, in children, there is a statistically significant increase of fluoride ion in urine, which can be attributed to the application of this product.

[EX Q]: Context: Alzheimer's disease (AD) is characterized by cerebral deposition of -amyloid peptide (A). A is produced by sequential cleavage of the Amyloid Precursor Protein (APP) by - and -secretases. Many studies have demonstrated that the internalization of APP from the cell surface can regulate A production, although the exact organelle in which A is produced remains contentious. A number of recent studies suggest that intracellular trafficking also plays a role in regulating A production, but these pathways are relatively under-studied. The goal of this study was to elucidate the intracellular trafficking of APP, and to examine the site of intracellular APP processing.", 'We have tagged APP on its C-terminal cytoplasmic tail with photoactivatable Green Fluorescent Protein (paGFP). By photoactivating APP-paGFP in the Golgi, using the Golgi marker Galactosyltranferase fused to Cyan Fluorescent Protein (GalT-CFP) as a target, we are able to follow a population of nascent APP molecules from the Golgi to downstream compartments identified with compartment markers tagged with red fluorescent protein (mRFP or mCherry); including rab5 (early endosomes) rab9 (late endosomes) and LAMP1 (lysosomes). Because -cleavage of APP releases the cytoplasmic tail of APP including the photoactivated GFP, resulting in loss of fluorescence, we are able to visualize the cleavage of APP in these compartments. Using APP-paGFP, we show that APP is rapidly trafficked from the Golgi apparatus to the lysosome; where it is rapidly cleared. Chloroquine and the highly selective -secretase inhibitor, L685, 458, cause the accumulation of APP in lysosomes implying that APP is being cleaved by secretases in the lysosome. The Swedish mutation dramatically increases the rate of lysosomal APP processing, which is also inhibited by chloroquine and L685, 458. By knocking down adaptor protein 3 (AP-3; a heterotetrameric protein complex required for trafficking many proteins to the lysosome) using siRNA, we are able to reduce this lysosomal transport. Blocking lysosomal transport of APP reduces A production by more than a third.\Question: Is the Amyloid Precursor Protein rapidly transported from the Golgi apparatus to the lysosome and where it is processed into beta-amyloid?
[EX A]:
These data suggests that AP-3 mediates rapid delivery of APP to lysosomes, and that the lysosome is a likely site of A production.