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: Multiple intercostal recordings were supposed to get a more comprehensive view of the depolarization vector of the outflow tract ventricular arrhythmia (OT-VA), which may help to identify the OT-VA more accurately. This study was undertaken to develop a more accurate electrocardiogram (ECG) criterion for differentiating between left and right OT-VA origins.', 'We studied OT-VA with a left bundle branch block pattern and inferior axis QRS morphology in 47 patients with successful catheter ablation in the right ventricular OT (RVOT; n = 37) or aortic coronary cusp (ACC; n = 10). Superior and inferior precordial leads were taken together with the routine 12-lead ECG. The ECG during the OT-VA and during sinus beats were analyzed. Transition ratio, transition zone (TZ) index, R/S amplitude ratio, and R-wave duration ratio were measured in the regular, superior, and inferior precordial leads.', 'The combined TZ index, TZ index inferior was significantly smaller, while the V2 inferior transition ratio was significantly larger for ACC origins than RVOT origins (P < 0.05). The area under the curve for the combined TZ index by a receiver operating characteristic analysis was 0.974, which was significantly larger than other parameters. A cutoff value 0.25 predicted an ACC origin with 94% sensitivity and 100% specificity. This advantage of the parameter over others also held true for a subanalysis of OT-VAs with a lead V3 precordial transition or TZ index = 0.\Question: Does multiple Intercostal Space Electrocardiogram allow Accurate Localization of Outflow Tract Ventricular Arrhythmia Origin?
Example Output: The combined TZ index outperformed other ECG criteria to differentiate left from right OT-VA origins.

Example Input: Context: Chronic pancreatitis (CP) and pancreatic cancer (PCa) are characterized by intrapancreatic neuropathic alterations, including increased neural density and hypertrophy, pancreatic neuritis and neural invasion (NI) by cancer cells in PCa. The aim of this study was to identify the influence of these neuropathic changes on the quality of pancreatic innervation, intrapancreatic glia, and visceral pain.', 'Pancreatic nerve fiber qualities were characterized by immunohistochemical visualization of various markers, including those for sympathetic (tyrosine hydroxylase, TH) and cholinergic innervation (choline acetyltransferase, ChAT), as well as the glial transcription factor, Sox10, and the neuroepithelial progenitor cell marker, Nestin, in normal pancreas (NP, n=16), CP (n=20), and PCa (n=20) patients. The neural immunoreactivity scores of these markers were correlated with the severity of intrapancreatic neuropathic changes and with abdominal pain sensation of patients.', 'Pancreatic sympathetic innervation was significantly reduced in CP and PCa, whereas parasympathetic innervation did not show major changes. Nestin neuro-immunoreactivity was stronger, and Sox10-immunoreactivity was weaker in CP and PCa than in NP. Pancreatic sympathetic and cholinergic innervation was noticeably decreased in patients with severe pancreatic neuritis, NI by cancer cells, or abdominal pain. Moreover, the neural immunoreactivity for Sox10 and Nestin also varied with intrapancreatic neuropathic alterations and abdominal pain.\Question: Does pancreatic neuropathy result in '' neural remodeling '' and altered pancreatic innervation in chronic pancreatitis and pancreatic cancer?
Example Output: The quality of intrapancreatic nerve fibers and the activation state of intrapancreatic glia in CP and PCa are strikingly different from those in normal pancreas. This novel phenomenon of "neural remodeling" shows how pancreatic neuropathic pain and "visceral neuropathy" are associated with altered pancreatic innervation in CP and PCa.

Example Input: Context: Our aim was to investigate mechanisms of inflammation-induced endothelial dysfunction in humans.', 'Endothelial function in twenty-one healthy human volunteers was measured using forearm venous plethysmography before and 8 h after administration of typhoid vaccination to generate an inflammatory response. Basal and stimulated endothelial nitric oxide (NO) bioavailability was assessed by measurement of the responses to intra-arterial N(G)-monomethyl-l-arginine (l-NMMA) and bradykinin, respectively. The effects of supplementation with l-arginine or ascorbic acid were assessed to probe the effects of substrate deficiency and oxidative stress, respectively. Systemic effects were determined by measuring cytokine response, total anti-oxidant status (TAOS) and urinary protein excretion.', 'Vaccination induced a cytokine response, a fall in total anti-oxidant status and increased urinary albumin excretion (UAE). There was a reduction in the response to bradykinin (BK, P<0.005) and l-NMMA (P<0.0001) with no effect on the response to glyceryl trinitrate (GTN) and norepinephrine (NE). Following vaccination blood flow response to BK (but not GTN) was partially returned to pre-vaccine levels by infusion of ascorbic acid (P=0.01). Supplementation with l-arginine had no effect.\Question: Does inflammation-induced endothelial dysfunction involve reduced nitric oxide bioavailability and increased oxidant stress?
Example Output:
Inflammation causes widespread endothelial dysfunction, reduces vascular NO bioavailability and increases oxidative stress. These actions are partially reversible with local anti-oxidants. These findings suggest a role for reactive oxygen species in inflammation-induced endothelial dysfunction.