Utilización de compost agotado de champiñón como capa de coberturas en nuevos ciclos de producción Using spent mushroom substrate as casing layers in new growing cycles

El objetivo de este trabajo fue evaluar el comportamiento agronómico de seis mezclas de cobertura, elaboradas a partir de sustrato postcultivo del champiñón Agaricus bisporus, en nuevos ciclos de cultivo. Los resultados obtenidos mostraron la viabilidad de la reintroducción del sustrato en nuevos ciclos de cultivo, ya sea como material de base único, si se somete a un proceso de lavado para eliminar sales solubles, o bien mezclado con otros materiales de baja conductividad, como es el caso de la turba rubia o la fibra de coco. Se destacan los altos valores de eficiencia biológica registrados, que llegaron hasta los 100 kg kg-1 de compost, similares a los proporcionados por los testigos, y los altos valores relativos observados (con respecto a los testigos) en el contenido en materia seca de los carpóforos cosechados con algunas de las nuevas coberturas elaboradas. Esta reutilización del compost constituye una alternativa interesante, con vistas a reemplazar a las tierras y a los sustratos orgánicos utilizados habitualmente como cobertura, con la doble ventaja de disminuir los costos de elaboración y el impacto ambiental.<br>The objective of this work was to evaluate the agronomic behaviour of six mixtures of casing, prepared from spent mushroom substrate (SMS), in new production cycles of Agaricus bisporus. The results obtained showed the feasibility of reuse of the SMS in new cultivation cycles when used alone by submitting it to a washing process to remove soluble salts, or mixed with other materials of low conductivity, such as Sphagnum peat or coconut fiber pith. The high values of biological efficiency recorded up to 100 kg kg-1 compost, similar to that of the controls, and the same high values observed in the dry matter content of the mushrooms harvested with some of the new casing layers prepared must be highlighted. The suggested use for SMS is an important alternative to consider, in order to replace soils and other organic substrates typically used as casing, with the added advantages of lowering the production costs and decreasing the environmental impact

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.)