177 research outputs found

    Nature versus freedom : Hannah Arendt's theory of the political sphere from the polis to the modern world

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    My thesis bears on Hannah Arendt's theory of the political sphere. My objective is critically to assess Arendt's development of the theory from its introduction in her treatment of the self-understanding of the ancient Greek polis to its deployment in the modern context. With The Human Condition as the central text in my analysis, I consider the key philosophical-theoretical commitments surrounding the theory of the political sphere, notably Arendt's opposition of freedom to nature. I argue that problems arising in connection with Arendt's theory of the political sphere can be traced to the freedom-nature dichotomy

    On the minisymposium problem

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    The generalized Oberwolfach problem asks for a factorization of the complete graph KvK_v into prescribed 22-factors and at most a 11-factor. When all 22-factors are pairwise isomorphic and vv is odd, we have the classic Oberwolfach problem, which was originally stated as a seating problem: given vv attendees at a conference with tt circular tables such that the iith table seats aia_i people and ∑i=1tai=v{\sum_{i=1}^t a_i = v}, find a seating arrangement over the v−12\frac{v-1}{2} days of the conference, so that every person sits next to each other person exactly once. In this paper we introduce the related {\em minisymposium problem}, which requires a solution to the generalized Oberwolfach problem on vv vertices that contains a subsystem on mm vertices. That is, the decomposition restricted to the required mm vertices is a solution to the generalized Oberwolfach problem on mm vertices. In the seating context above, the larger conference contains a minisymposium of mm participants, and we also require that pairs of these mm participants be seated next to each other for ⌊m−12⌋\left\lfloor\frac{m-1}{2}\right\rfloor of the days. When the cycles are as long as possible, i.e.\ vv, mm and v−mv-m, a flexible method of Hilton and Johnson provides a solution. We use this result to provide further solutions when v≡m≡2(mod4)v \equiv m \equiv 2 \pmod 4 and all cycle lengths are even. In addition, we provide extensive results in the case where all cycle lengths are equal to kk, solving all cases when m∣vm\mid v, except possibly when kk is odd and vv is even.Comment: 25 page

    HDL-Associated Estradiol Stimulates Endothelial NO Synthase and Vasodilation in an SR-BI–Dependent Manner

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    Cardiovascular diseases remain the leading cause of death in the United States. Two factors associated with a decreased risk of developing cardiovascular disease are elevated HDL levels and sex — specifically, a decreased risk is found in premenopausal women. HDL and estrogen stimulate eNOS and the production of nitric oxide, which has numerous protective effects in the vascular system including vasodilation, antiadhesion, and anti-inflammatory effects. We tested the hypothesis that HDL binds to its receptor, scavenger receptor class B type I (SR-BI), and delivers estrogen to eNOS, thereby stimulating the enzyme. HDL isolated from women stimulated eNOS, whereas HDL isolated from men had minimal activity. Studies with ovariectomized and ovariectomized/estrogen replacement mouse models demonstrated that HDL-associated estradiol stimulation of eNOS is SR-BI dependent. Furthermore, female HDL, but not male HDL, promoted the relaxation of muscle strips isolated from C57BL/6 mice but not SR-BI null mice. Finally, HDL isolated from premenopausal women or postmenopausal women receiving estradiol replacement therapy stimulated eNOS, whereas HDL isolated from postmenopausal women did not stimulate eNOS. We conclude that HDL-associated estrodial is capable of the stimulating eNOS. These studies establish a new paradigm for examining the cardiovascular effects of HDL and estrogen

    The political economy of natural disaster damage

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    Economic damage from natural hazards can sometimes be prevented and always mitigated. However, private individuals tend to underinvest in such measures due to problems of collective action, information asymmetry and myopic behavior. Governments, which can in principle correct these market failures, themselves face incentives to underinvest in costly disaster prevention policies and damage mitigation regulations. Yet, disaster damage varies greatly across countries. We argue that rational actors will invest more in trying to prevent and mitigate damage the larger a country's propensity to experience frequent and strong natural hazards. Accordingly, economic loss from an actually occurring disaster will be smaller the larger a country's disaster propensity – holding everything else equal, such as hazard magnitude, the country's total wealth and per capita income. At the same time, damage is not entirely preventable and smaller losses tend to be random. Disaster propensity will therefore have a larger marginal effect on larger predicted damages than on smaller ones. We employ quantile regression analysis in a global sample to test these predictions, focusing on the three disaster types causing the vast majority of damage worldwide: earthquakes, floods and tropical cyclones

    New targets for therapy in breast cancer: Small molecule tyrosine kinase inhibitors

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    Over the past several years many advances have been made in our understanding of critical pathways involved in carcinogenesis and tumor growth. These advances have led to the investigation of small molecule inhibitors of the ErbB family of receptor tyrosine kinases across a broad spectrum of malignancies. In this article we summarize the rationale for targeting members of the ErbB family in breast cancer, and review the preclinical and clinical data for the agents that are furthest in development. In addition, we highlight directions for future research, such as exploration of the potential crosstalk between the ErbB and hormone receptor signal transduction pathways, identification of predictive markers for tumor sensitivity, and development of rational combination regimens that include the tyrosine kinase inhibitors
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