Equivariant configuration spaces

The compression theorem is used to prove results for equivariant configuration spaces that are analogous to the well-known non-equivariant results of May, Milgram and Segal

James bundles

We study cubical sets without degeneracies, which we call {square}-sets. These sets arise naturally in a number of settings and they have a beautiful intrinsic geometry; in particular a {square}-set C has an infinite family of associated {square}-sets Ji(C), for i = 1, 2, ..., which we call James complexes. There are mock bundle projections pi: |Ji(C)| -> |C| (which we call James bundles) defining classes in unstable cohomotopy which generalise the classical James–Hopf invariants of {Omega}(S2). The algebra of these classes mimics the algebra of the cohomotopy of {Omega}(S2) and the reduction to cohomology defines a sequence of natural characteristic classes for a {square}-set. An associated map to BO leads to a generalised cohomology theory with geometric interpretation similar to that for Mahowald orientation

A geometric approach to homology theory

The purpose of these notes is to give a geometrical treatment of generalized homology and cohomology theories

A framework for conceptualizing, representing, and analyzing distributed interaction.

The relationship between interaction and learning is a central concern of the learning sciences, and analysis of interaction has emerged as a major theme within the current literature on computersupported collaborative learning. The nature of technology-mediated interaction poses analytic challenges. Interaction may be distributed across actors, space, and time, and vary from synchronous, quasi-synchronous, and asynchronous, even within one data set. Often multiple media are involved and the data comes in a variety of formats. As a consequence, there are multiple analytic artifacts to inspect and the interaction may not be apparent upon inspection, being distributed across these artifacts. To address these problems as they were encountered in several studies in our own laboratory, we developed a framework for conceptualizing and representing distributed interaction. The framework assumes an analytic concern with uncovering or characterizing the organization of interaction in sequential records of events. The framework includes a media independent characterization of the most fundamental unit of interaction, which we call uptake. Uptake is present when a participant takes aspects of prior events as having relevance for ongoing activity. Uptake can be refined into interactional relationships of argumentation, information sharing, transactivity, and so forth. for specific analytic objectives. Faced with the myriad of ways in which uptake can manifest in practice, we represent data using graphs of relationships between events that capture the potential ways in which one act can be contingent upon another. These contingency graphs serve as abstract transcripts that document in one representation interaction that is distributed across multiple media. This paper summarizes the requirements that motivate the framework, and discusses the theoretical foundations on which it is based. It then presents the framework and its application in detail, with examples from our work to illustrate how we have used it to support both ideographic and nomothetic research, using qualitative and quantitative methods. The paper concludes with a discussion of the framework’s potential role in supporting dialogue between various analytic concerns and methods represented in CSCL

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.)