Seismic Design Of Tunnels In Fault Zones

The tunnels due to their restrictions as a infrastructure work often overpass very disturbed tectonic zones. In those zones due to overthrust geological processes the rockquality are extremely poor in one side, and changes abruptly on the other side. These changes impose differential deformation on soil and tunnel linings. Especially for near faults tunnelswhere the directivity pulse and fling step phenomena plays an important role in the characterization of the seismic motion. This article gives the theoretical explanation and design consideration concerning the above mention problems. A numerical simulation whichis indented to study the behavior of the tunnel during this type of seismic events is presented.This example is taken from the design of a tunnel that shall be constructed in Albania

A Synthesis of Architectural Form for Three Different Structural Systems

Architectural form is often used but less frequently defined. Architectural form is an inclusive term that refers primarily to a building’s external outline or shape, and to a lesser degree references its internal organization and unifying principles. Shape encompasses various visual and relational properties; namely size, color and texture, position, orientation and visual inertia. Form is therefore generally and primarily understood as the shape or three dimensional massing, but also encompasses additional architectural aspects including structural configuration and form, in so far as they may organize and unify an architectural design

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.)