2 research outputs found

    Fascism in Sci-Fi: Mobilizing Passions in Robert A. Heinlein\u27s Starship Troopers

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    This thesis responds to criticism of Robert A. Heinlein’s Starship Troopers (1959) as a “fascist” novel by further investigating the claim through a close reading of the novel that applies political theory scholarship on fascism. Chapters I and II introduce the novel along with its general reception and controversy. These chapters consider the accusations of “fascism” given to the novel while at the same time understanding that a clear, exact definition of “fascism” has long been grappled with by scholars since the rise of the regimes in Nazi Germany and Fascist Italy. Chapters III and IV apply political theory to examine Starship Troopers’s characters, language, and plot to find if the novel’s narrative expresses the “mobilizing passions” of fascism identified by Robert Paxton in The Anatomy of Fascism (2004). In addition to Paxton, the political theory analysis will also be aided by Roger Griffin’s The Nature of Fascism (1991) and Umberto Eco’s 1995 essay “Ur-Fascism.” The focus will be on “checking off” each mobilizing passion listed by Paxton, but consideration will also be given to how Starship Troopers buys into the “national rebirth” myth in Griffin’s definition of palingenetic populist ultranationalism as well as how it expresses certain fascist features observed by Eco. Chapters III and IV ultimately find that Starship Troopers’s narrative expresses all of the mobilizing passions listed. Chapter VI concludes the analysis by denouncing fascism and Starship Troopers’s vision of a false-utopia, pointing to the inherent ineffectuality and destructiveness of fascism. The concluding chapter closes with final remarks reflecting on applying current scholarship on fascism to the reading of a novel

    Effects of Anacetrapib in Patients with Atherosclerotic Vascular Disease

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    BACKGROUND: Patients with atherosclerotic vascular disease remain at high risk for cardiovascular events despite effective statin-based treatment of low-density lipoprotein (LDL) cholesterol levels. The inhibition of cholesteryl ester transfer protein (CETP) by anacetrapib reduces LDL cholesterol levels and increases high-density lipoprotein (HDL) cholesterol levels. However, trials of other CETP inhibitors have shown neutral or adverse effects on cardiovascular outcomes. METHODS: We conducted a randomized, double-blind, placebo-controlled trial involving 30,449 adults with atherosclerotic vascular disease who were receiving intensive atorvastatin therapy and who had a mean LDL cholesterol level of 61 mg per deciliter (1.58 mmol per liter), a mean non-HDL cholesterol level of 92 mg per deciliter (2.38 mmol per liter), and a mean HDL cholesterol level of 40 mg per deciliter (1.03 mmol per liter). The patients were assigned to receive either 100 mg of anacetrapib once daily (15,225 patients) or matching placebo (15,224 patients). The primary outcome was the first major coronary event, a composite of coronary death, myocardial infarction, or coronary revascularization. RESULTS: During the median follow-up period of 4.1 years, the primary outcome occurred in significantly fewer patients in the anacetrapib group than in the placebo group (1640 of 15,225 patients [10.8%] vs. 1803 of 15,224 patients [11.8%]; rate ratio, 0.91; 95% confidence interval, 0.85 to 0.97; P=0.004). The relative difference in risk was similar across multiple prespecified subgroups. At the trial midpoint, the mean level of HDL cholesterol was higher by 43 mg per deciliter (1.12 mmol per liter) in the anacetrapib group than in the placebo group (a relative difference of 104%), and the mean level of non-HDL cholesterol was lower by 17 mg per deciliter (0.44 mmol per liter), a relative difference of -18%. There were no significant between-group differences in the risk of death, cancer, or other serious adverse events. CONCLUSIONS: Among patients with atherosclerotic vascular disease who were receiving intensive statin therapy, the use of anacetrapib resulted in a lower incidence of major coronary events than the use of placebo. (Funded by Merck and others; Current Controlled Trials number, ISRCTN48678192 ; ClinicalTrials.gov number, NCT01252953 ; and EudraCT number, 2010-023467-18 .)
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