Tensile Testing to Quantitate the Anisotropy and Strain Hardening of Mozzarella Cheese

We explored anisotropy of mozzarella cheese: its presence is debated in the literature. Tensile testing proved a good method because the location and mode of failure were clear. Mozzarella cheese cut direct from the block showed no significant anisotropy, though confocal microscopy showed good structure alignment at a microscale. Deliberately elongated mozzarella cheese showed strong anisotropy with tensile strength in the elongation or fibre direction ∼3.5× that perpendicular to the fibres. Temperature of elongation had a marked impact on anisotropy with maximum anisotropy after elongation at 70 °C. We suggest the disagreement on anisotropy in the literature is related to the method of packing the mozzarella cheese into a block after the stretching stage of manufacture. Tensile stress/strain curves in the fibre direction showed marked strain hardening with modulus just before fracture ∼2.1× that of the initial sample, but no strain hardening was found perpendicular to the fibre direction

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.)