Conformal Field Theories, Graphs and Quantum Algebras

This article reviews some recent progress in our understanding of the structure of Rational Conformal Field Theories, based on ideas that originate for a large part in the work of A. Ocneanu. The consistency conditions that generalize modular invariance for a given RCFT in the presence of various types of boundary conditions --open, twisted-- are encoded in a system of integer multiplicities that form matrix representations of fusion-like algebras. These multiplicities are also the combinatorial data that enable one to construct an abstract ``quantum'' algebra, whose $6j$- and $3j$-symbols contain essential information on the Operator Product Algebra of the RCFT and are part of a cell system, subject to pentagonal identities. It looks quite plausible that the classification of a wide class of RCFT amounts to a classification of ``Weak $C^*$- Hopf algebras''.Comment: 23 pages, 12 figures, LateX. To appear in MATHPHYS ODYSSEY 2001 --Integrable Models and Beyond, ed. M. Kashiwara and T. Miwa, Progress in Math., Birkhauser. References and comments adde

Lectures on conformal field theory and Kac-Moody algebras

This is an introduction to the basic ideas and to a few further selected topics in conformal quantum field theory and in the theory of Kac-Moody algebras.Comment: 59 pages, LaTeX2e, extended version of lectures given at the Graduate Course on Conformal Field Theory and Integrable Models (Budapest, August 1996), to appear in Springer Lecture Notes in Physic

Differential cell susceptibilities to kras(G12D) in the setting of obstructive chronic pancreatitis

BACKGROUND & AIMS: Activating mutation of the KRAS gene is common in some cancers, such as pancreatic cancer, but rare in other cancers. Chronic pancreatitis is a predisposing condition for pancreatic ductal adenocarcinoma (PDAC), but how it synergizes with KRAS mutation is not known. METHODS: We used a mouse model to express an activating mutation of Kras in conjunction with obstruction of the main pancreatic duct to recapitulate a common etiology of human chronic pancreatitis. Because the cell of origin of PDAC is not clear, Kras mutation was introduced into either duct cells or acinar cells. RESULTS: Although Kras(G12D) expression in both cell types was protective against damage-associated cell death, chronic pancreatitis induced p53, p21, and growth arrest only in acinar-derived cells. Mutant duct cells did not elevate p53 or p21 expression and exhibited increased proliferation driving the appearance of PDAC over time. CONCLUSIONS: One mechanism by which tissues may be susceptible or resistant to KRAS(G12D)-initiated tumorigenesis is whether they undergo a p53-mediated damage response. In summary, we have uncovered a mechanism by which inflammation and intrinsic cellular programming synergize for the development of PDAC

The PHENIX Experiment at RHIC

The physics emphases of the PHENIX collaboration and the design and current status of the PHENIX detector are discussed. The plan of the collaboration for making the most effective use of the available luminosity in the first years of RHIC operation is also presented.Comment: 5 pages, 1 figure. Further details of the PHENIX physics program available at http://www.rhic.bnl.gov/phenix

On possibilities and limitations of using self-anchoring scales in web surveys

Self-anchoring rating scales, Nonresponse, Web surveys, Context effects, End anchors,