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: . We aimed to evaluate the effectiveness of a multifaceted intervention, targeting staff-patient communication, in improving emergency department patient satisfaction.', 'We undertook a pre- and post-intervention study in a university-affiliated emergency department, over a 12-month period. The intervention included communication workshops, a patient education film, and a patient liaison nurse. At the patient level, the patient liaison nurse ensured optimal staff-patient community communication and played a role in staff communication education. The intervention was evaluated using patient surveys (containing general and communication-specific satisfaction items scored out of 100), complaint rates, and patient liaison nurse activity data.', "A total of 321 and 545 patients returned questionnaires in the pre- and post-intervention periods, respectively. Significant improvements were observed in patients' perceptions of being 'informed about delays' [score difference, 5.3; 95% confidence interval (CI), 0.6-10.0], that 'staff cared about them as a person' (difference, 4.4; 95% CI, 0.7-8.1), the overall emergency department facility assessment (difference, 3.9; 95% CI, 0.4-7.5) and overall emergency department care (difference, 3.8; 95% CI, 0.3-7.3). Non-significant improvements were seen in all other satisfaction items. In the post-intervention period, there was a 22.5% (95% CI, 14.6-32.8) decrease in the number of complaints received and a decrease in the complaint rate of 0.7 (95% CI, -0.3 to 1.6) complaints per 1000 patients. The patient liaison nurse activities included orientation of the patient including (i) explanation of tests, procedures, and delays; (ii) communication with a range of hospital staff; and (iii) general comfort measures including analgesia quality control.\Question: Does a multifaceted intervention improve patient satisfaction and perceptions of emergency department care?

Output: Significant improvements in a variety of patient satisfaction measures were achieved with an intervention comprising staff communication workshops, a patient education film, and a patient liaison nurse.

Input: Consider Input: Context: The basis of the treatment of painful diabetic neuropathy is the use of drugs that block the transmission of pain (antineuritics) and a good metabolic control of underlying disease.', 'To describe the outcomes of 17 type-2 diabetics with painful neuropathy, treated between 1988 and 2005 with symptomatic therapy plus intensified insulin.', 'Review of medical records of 17 type-2 diabetic patients, aged 63+/-11 years and a duration of diabetes of 15+/-8 years. All patients received intensified insulin therapy with 0.35 units/kg of NPH insulin (2/3 before breakfast and 1/3 evening meal), plus capillary glucose measurements and regular insulin (with sliding-scale centered in approximately 0.1 units/kg) before the 3 main meals. All patients were also treated with gabapentin, nortriptyline or clomipramine. Pain was assessed using a visual analog score of 10 points.', 'After 1 year, glycosilated hemoglobin decreased from 10.0+/-1.4% to 7.7+/-1.2% (p approximately =0.003). Pain decreased from 10 to 5.1+/-3.3 at one month, 2.3+/-3.2 at six months, and 3.1+/-3.6 at 1 year (p <0.01). There was a direct statistical correlation between the reduction of HbA1C and pain decline (r =0.736; p =0.037). Pain scores were lower than those reported elsewhere for Pregabalin (n =76; p =0.05), Lamotrigine (n =27; p <0.0005), Topiramate (n =208; p <0.005), and Gabapentin (n =84; p <0.025). The lack of difference to Sodium Valproate (n =21; p =0.07) had borderline significance.\Question: Is [ Intensified insulin therapy plus antineuritic medication more effective than antineuritics alone in painful diabetic neuropathy ]?

Output: The addition of intensified insulin therapy to the symptomatic treatment of painful neuropathy in type-2 diabetics, significantly enhanced the reduction of pain. The lowering of glycosilated hemoglobin was a significant predictor of success in pain reduction.

Input: Consider Input: Context: Circulatory shock results in hypoxia/reoxygenation processes that lead to the release of reactive oxygen species, endothelial injury, and multiple organ failure. Previous data suggest that beta2-adrenergic agonists prevent endothelial dysfunction. The study aimed at determining whether the beta2-adrenergic agonist formoterol protects endothelial cells against hypoxia/reoxygenation injury in vitro.', 'Prospective controlled trial.', 'University hospital research laboratory.', 'Cultured human umbilical vein endothelial cells (HUVECs).', "Confluent HUVECs were sealed in a flow-through chamber mounted on an inverted microscope and perfused with a constant flow of Krebs medium. After 1 hr of equilibration, HUVECs underwent 2 hrs of hypoxia and 1 hr of reoxygenation. Cell death at the end of reoxygenation and reactive oxygen species formation were assessed with fluorescent probes propidium iodide and 2',7'-dichlorodihydrofluorescein diacetate, respectively. The effects of the beta2-adrenergic agonist formoterol, the beta2-adrenergic antagonist ICI 118,551 and the nitric oxide synthase inhibitor L-NNA were investigated. Statistical analysis was performed with analysis of variance followed by post hoc Fisher's test.", 'Hypoxia/reoxygenation increased cell death (hypoxia/reoxygenation 29 +/- 4% vs. control 1 +/- 5%, p < .05) and endothelial reactive oxygen species production (hypoxia/reoxygenation 126 +/- 4% vs. control 108 +/- 4%, p < .05). Formoterol reduced cell death in a concentration-dependent manner (EC95 = 10 mol/L) and reduced endothelial reactive oxygen species production (hypoxia/reoxygenation + formoterol EC95 109 +/- 4% vs. hypoxia/reoxygenation 126 +/- 4%, p < .05). When added to formoterol EC95, ICI 118,551 and L-NNA abolished the formoterol-induced cell protection and reduced reactive oxygen species production.\Question: Does beta2-adrenergic agonist protect human endothelial cells from hypoxia/reoxygenation injury in vitro?
Output: These results indicate that formoterol reduces endothelial cell death and reactive oxygen species production in this in vitro hypoxia/reoxygenation model. These effects are beta2-adrenergic specific and are partially mediated by nitric oxide synthase.