On the Term "Dunamis" in Aristotle's Definition of Rhetoric
The term dunamis, by which Aristotle defines rhetoric in the first chapter of The Art of Rhetoric, is a “power” term, as its various meanings in Aristotle’s corpus—from vernacular ones like “political influence” to strictly philosophical ones like “potentiality”—attest.1 In the Rhetoric, however, dunamis is usually translated as “ability” or “faculty,” a designation that, compared to other terms that describe persuasion in ancient Greek poetics and rhetoric (such as “bia” [“force”] or “eros” [“seduction”]), marks rhetoric as a neutral human capacity rather than the use of language entangled in the vagaries of violence and desire.2 John Kirby calls Aristotle’s definition “one of the boldest moves in the history of the philosophy of language: to redefine rhetoric, not as the use of peitho but as the study of peitho” (1990, 227). The presumption of rhetoric’s ethical neutrality implied by dunamis has indeed become commonplace in interpretations of Aristotle’s treatise itself and of rhetoric as a social phenomenon. As George Kennedy puts it in his authoritative translation of the Rhetoric, “Aristotle was the first person to recognize clearly that rhetoric as an art of communication was morally neutral, that it could be used either for good or ill” (1991, ix). In this article, I would like to probe another, perhaps not so reassuring, implication of dunamis as a term for rhetoric—that as “an ability to see all available means of persuasion,” it does not need to become (or emulate) practical oratory. In what follows, I suggest that Aristotle’s terminology, however neutral it may appear, constitutes an intellectually and politically motivated act of naming that severs rhetorical knowledge from historically specific rhetorical practices and thereby erects a protective barrier between practical rationality and discourses of democracy.
Rereading Aristotle's Rhetoric.
In this collection edited by Alan G. Gross and Arthur E. Walzer, scholars in communication, rhetoric and composition, and philosophy seek to reread Aristotle s "Rhetoric" from a purely rhetorical perspective. So important do these contributors find the "Rhetoric," in fact, that a core tenet in this book is that all subsequent rhetorical theory is but a series of responses to issues raised by the central work. The essays reflect on questions basic to rhetoric as a humanistic discipline. Some explore the ways in which the "Rhetoric "explicates the nature of the art of rhetoric, noting that on this issue, the tensions within the "Rhetoric "often provide a direct passageway into our own conflicts.Contributors are Jeanne Fahnestock, Thomas B. Farrell, Robert N. Gaines, Eugene Garver, Lawrence D. Green, Alan G. Gross, Carolyn R. Miller, Jeffrey Walker, Arthur E. Walzer, and Barbara Warnick. The editors comprehensive bibliographic essay describes resources that would be of particular help to the Greekless reader and classifies and summarizes nearly one-hundred books and articles written on the "Rhetoric.""
The Development of
. IRF4 is a critical transcriptional regulator of B cell development and function. A recent genome wide SNP association study identified IRF4 as a major susceptibility gene in CLL. Although the SNPs located in the 3’UTR of IRF4 gene were linked to a downregulation of IRF4 in CLL patients, whether low level of IRF4 is critical for CLL development remains unclear. In rodent, CLL cells are derived from B1 cells whose population is dramatically expanded in immunoglobulin heavy chain Vh11 knock-in mice. We bred Vh11 knock-in allele into IRF4 deficient mice (IRF4 -/- Vh11). Here, we report that IRF4 -/- Vh11 mice develop spontaneous early onset CLL with 100% penetrance. Further analysis shows that IRF4 -/- Vh11 CLL cells proliferate predominantly in spleen and express high levels of Mcl-1. IRF4 -/- Vh11 CLL cells are resistant to apoptosis but reconstitution of IRF4 expression in the IRF4 -/- Vh11 CLL cells inhibits their survival. Thus, our study demonstrates for the first time a causal relationship between low levels of IRF4 and the development of CLL. Moreover, our findings establish IRF4 -/- Vh11 mice as a novel mouse model of CLL that not only is valuable for dissecting molecular pathogenesis of CLL but could also be used for therapeutic purposes.