instruction:
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.
question:
Context: Evidence suggests that advance directives may improve end-of-life care among seriously ill patients, but improving completion rates remains a challenge.', 'This study tested the influence of increasing the number of options for completing an advance directive among seriously ill patients.', 'Outpatients (N = 316) receiving hemodialysis across 15 dialysis centers in the Philadelphia region between July 2014 and July 2015 were randomized to receive either the option to complete a brief advance directive form or expanded options including a brief, expanded, or comprehensive form. Patients in both groups could decline to complete an advance directive or take their selected version home. The primary outcome was a returned, completed advance directive. Secondary outcomes included whether patients wanted to complete an advance directive, decision satisfaction, quality of life at 3 months, and patient factors associated with advance directive completion.', 'Although offering more advance directive options was not significantly associated with increased rates of completion (13.1% in the standard group v. 12.2% in the expanded group, P = 0.80), it did significantly increase the proportion of patients who wanted to complete an advance directive and took one home (71.9% in standard v. 85.3% in expanded, P = 0.004). There was no difference in satisfaction (P = 0.65) or change in quality of life between groups (P = 0.63). A higher baseline quality of life was independently associated with advance directive completion (P = 0.006).\Question: Does a Randomized Trial of Expanding Choice set to Motivate Advance Directive Completion?
answer:
These results suggest that although an expanded choice set may initially nudge patients toward completing advance directives without restricting choice, increasing actual completion requires additional interventions that overcome downstream barriers.

question:
Context: Extended-release niacin effectively lowers plasma TG levels and raises plasma high-density lipoprotein (HDL) cholesterol levels, but the mechanisms responsible for these effects are unclear.', 'We examined the effects of extended-release niacin (2 g/d) and extended-release niacin (2 g/d) plus lovastatin (40 mg/d), relative to placebo, on the kinetics of apolipoprotein (apo) A-I and apoA-II in HDL, apoB-100 in TG-rich lipoproteins (TRL), intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL), and apoB-48 in TRL in 5 men with combined hyperlipidemia. Niacin significantly increased HDL cholesterol and apoA-I concentrations, associated with a significant increase in apoA-I production rate (PR) and no change in fractional catabolic rate (FCR). Plasma TRL apoB-100 levels were significantly lowered by niacin, accompanied by a trend toward an increase in FCR and no change in PR. Niacin treatment significantly increased TRL apoB-48 FCR but had no effect on apoB-48 PR. No effects of niacin on concentrations or kinetic parameters of IDL and LDL apoB-100 and HDL apoA-II were noted. The addition of lovastatin to niacin promoted a lowering in LDL apoB-100 attributable to increased LDL apoB-100 FCR.\Question: Does extended-release niacin alter the metabolism of plasma apolipoprotein ( Apo ) A-I and ApoB-containing lipoproteins?
answer:
Niacin treatment was associated with significant increases in HDL apoA-I concentrations and production, as well as enhanced clearance of TRL apoB-100 and apoB-48.

question:
Context: Amphetamine (AMPH)-like stimulants represent an intensively studied class of psychoactive drugs. Despite the well-known and potent arousal-enhancing effects of these drugs, the neurobiological substrates of AMPH-induced arousal have rarely been examined explicitly. Activity of the locus coeruleus-noradrenergic system is causally and positively related to behavioral and electroencephalographic (EEG) indices of arousal. For example, activation of locus coeruleus neurons or stimulation of medial basal forebrain noradrenergic beta-receptors elicits activation of forebrain EEG in the anesthetized rat. Further, stimulation of noradrenergic beta-receptors within the medial basal forebrain elicits a substantial increase in alert, active waking. These and other observations suggest that at least some of the arousal-enhancing actions of AMPH-like stimulants derive from AMPH-induced increases in noradrenergic neurotransmission at beta-receptors. The current study examines the extent to which AMPH-induced activation of cortical EEG is dependent on actions of central beta-receptors.', 'The effects of intracerebroventricular (ICV; 2 microl) pretreatment with either vehicle (artificial extracellular fluid) or the beta-antagonist, timolol (25, 50 or 100 microg), on the cortical EEG activating effects of intravenous AMPH (0.15 mg/kg) were examined in the halothane-anesthetized rat. EEG was recorded on polygraph and video recording tape and later analyzed using power spectral analyses (PSA). AMPH-induced alteration in cortical EEG activity was measured using PSA in vehicle- and timolol-pretreated animals.', 'Neither vehicle nor timolol ICV infusions altered cortical EEG activity patterns. In vehicle-pretreated animals, AMPH elicited a robust activation of cortical EEG, characterized by the substantial decrease in large-amplitude, slow-wave activity. Timolol pretreatment dose-dependently prevented AMPH-induced cortical EEG activation. This effect of timolol was statistically significant at the 50 microg and 100 microg dose.\Question: Is amphetamine-induced activation of forebrain EEG prevented by noradrenergic beta-receptor blockade in the halothane-anesthetized rat?
answer:
These observations indicate that, under these experimental conditions, AMPH-induced activation of the forebrain is dependent on actions of noradrenergic beta-receptors. Combined with previous observations, these observations support the hypothesis that AMPH-induced increases in arousal involve noradrenergic neurotransmission at beta-receptors.