Neo4Qgis: Connection the QGIS Software and a Geographical Oriented Database to Graphs

El propósito de este estudio se centra en análisis, diseño e implementación de una herramienta para la gestión de información geográfica en bases de datos orientadas a grafos desde un cliente SIG, la metodología de desarrollo se basó en OpenUP, se realizó la identificación de los requerimientos funcionales y no funcionales que satisficieran las necesidades de información geográfica en bases de datos orientadas a grafos desde el cliente SIG, así mismo se definió y estableció la arquitectura que permitió satisfacer los requerimientos funcionales y no funcionales y se realizó la implementación de la herramienta que permitió la conexión y gestión de información geográfica por medio de un plugin en el software QGIS con la base de datos de Neo4j. Finalmente la evaluación del plugin se desarrolló teniendo en cuenta la norma ISO-9126, donde los resultados fueron satisfactorios en un 90 por ciento.This study is focused on analysis, design and implementation of a tool for managing geographic information in graphs oriented databases from a GIS client. The software development methodology was based on OpenUP, it was made the identification of functional and nonfunctional requirements that met the needs of geographic information in graphs oriented databases from the GIS client, also it was defined and established the architecture that allowed meet the functional and nonfunctional requirements and it was made the implementation of the tool which allowed to perform the connection with Neo4j database and the management of geographic information through a plugin in QGIS software. Finally, the plugin evaluation was developed taking into account the ISO-9126 standard, where the results were satisfactory by 90 percent

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)