The Jama legal narrative part I: The JAMA Model and narrative interpretation patterns

For the purposes of starting to tackle, within artificial intelligence (AI), the narrative aspects of legal narratives in a criminal evidence perspective, traditional AI models of narrative understanding can arguably supplement extant models of legal narratives from the scholarly literature of law, jury studies, or the semiotics of law. Not only: the literary (or cinematic) models prominent in a given culture impinge, with their poetic conventions, on the way members of the culture make sense of the world. This shows glaringly in the sample narrative from the Continent-the Jama murder, the inquiry, and the public outcry-we analyse in this paper. Apparently in the same racist crime category as the case of Stephen Lawrence's murder (in Greenwich on 22 April 1993) with the ensuing still current controversy in the UK, the Jama case (some 20 years ago) stood apart because of a very unusual element: the eyewitnesses identifying the suspects were a group of football referees and linesmen eating together at a restaurant, and seeing the sleeping man as he was set ablaze in a public park nearby. Professional background as witnesses-cum-factfinders in a mass sport, and public perceptions of their required characteristics, couldn't but feature prominently in the public perception of the case, even more so as the suspects were released by the magistrate conducting the inquiry. There are sides to this case that involve different expected effects in an inquisitorial criminal procedure system from the Continent, where an investigating magistrate leads the inquiry and prepares the prosecution case, as opposed to trial by jury under the Anglo-American adversarial system. In the JAMA prototype, we tried to approach the given case from the coign of vantage of narrative models from AI

Gabor frames in finite dimensions

Gabor frames have been extensively studied in time-frequency analysis over the last 30 years. They are commonly used in science and engineering to synthesize signals from, or to decompose signals into, building blocks which are localized in time and frequency. This chapter contains a basic and self-contained introduction to Gabor frames on finite-dimensional complex vector spaces. In this setting, we give elementary proofs of the central results on Gabor frames in the greatest possible generality; that is, we consider Gabor frames corresponding to lattices in arbitrary finite Abelian groups. In the second half of this chapter, we review recent results on the geometry of Gabor systems in finite dimensions: the linear independence of subsets of its members, their mutual coherence, and the restricted isometry property for such systems. We apply these results to the recovery of sparse signals, and discuss open questions on the geometry of finite-dimensional Gabor systems

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.)