A Diachronic, Scale-Flexible, Relational, Perspectival Operation: In Defense of (Always-Reforming) Medium Specificity

At least since Friedrich Kittler declared fiber-optic cable the “end of media,” there has been an idea in cinema and media studies that as all media become digital, the concept of medium specificity makes less and less sense. Meanwhile, many wonder if our field is coherent, as media scholars turn their attention to such objects as dust, cities, and whales. I argue that digital convergence makes medium specificity more rather than less vital, though in a reformed formulation. While our far-flung objects cannot cohere our discipline, a use of medium specificity as a diachronic, scale-flexible, relational, perspectival operation can

Aca-Media Podcast Episode 70: Jordan Sjol on Medium Specificity

If you’re feeling sluggish from the holiday season, press play on this rich conversation between Jonathan Nichols-Pethick and Jordan Sjol to get your brain sparked and ready for a new year of smart conversations about media. The two DePauw colleagues talk about Sjol’s JCMS article, “A Diachronic, Scale-Flexible, Relational, Perspectival Operation: In Defense of (Always-Reforming) Medium Specificity” (don’t worry, they break it down word-by-word), as well as the recent feature film that Sjol co-wrote, How to Blow Up a Pipeline. Then Chris and Michael chat about how to name a department and how not to title a podcast

Nothing Re-Fused: Performing the Neo-Institution

In this paper, we outline the shape of a new institutional structure born of neo-liberal precariousness that we call the neo-institution. The neo-institution is immune to refusal, while at the same time an expert in extracting labor, time, knowledge, and attention. Because there is no way out of the aporia that is the neo-institution—no practical way to re-shape or refuse it—we propose to partly subtract ourselves from it by instigating another way to assemble. We advance the theoretical practice of stitching as a form of assembling that does not erase traces of labor and fight and that eludes any totalizing tendency. Understood as a way of assembling and writing, stitching is a practice of repairing, repurposing, and holding together. Finally, while fatigue, exhaustion, burnout, and depression are the inescapable result of neo-liberal precariousness, we praise the entropic ability of the body to refuse to be treated like refuse

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.)