On the Deformation Quantization Description of Matrix Compactifications

Matrix theory compactifications on tori have associated Yang-Mills theories on the dual tori with sixteen supercharges. A noncommutative description of these Yang-Mills theories based in deformation quantization theory is provided. We show that this framework allows a natural generalization of the `Moyal B-deformation' of the Yang-Mills theories to non-constant background B-fields on curved spaces. This generalization is described through Fedosov's geometry of deformation quantization.Comment: 25 pages, harvmac file, no figures, corrected typos, added references, one comment added in sec.

D-branes on Group Manifolds and Deformation Quantization

Recently M. Kontsevich found a combinatorial formula defining a star-product of deformation quantization for any Poisson manifold. Kontsevich's formula has been reinterpreted physically as quantum correlation functions of a topological sigma model for open strings as well as in the context of D-branes in flat backgrounds with a Neveu-Schwarz B-field. Here the corresponding Kontsevich's formula for the dual of a Lie algebra is derived in terms of the formalism of D-branes on group manifolds. In particular we show that that formula is encoded at the two-point correlation functions of the Wess-Zumino-Witten effective theory with Dirichlet boundary conditions. The B-field entering in the formalism plays an important role in this derivation.Comment: 20 pages, harvmac file, no figures, corrected typo

Cardiopoietic cell therapy for advanced ischemic heart failure: results at 39 weeks of the prospective, randomized, double blind, sham-controlled CHART-1 clinical trial

Cardiopoietic cells, produced through cardiogenic conditioning of patients' mesenchymal stem cells, have shown preliminary efficacy. The Congestive Heart Failure Cardiopoietic Regenerative Therapy (CHART-1) trial aimed to validate cardiopoiesis-based biotherapy in a larger heart failure cohort

the evolving concept of tumor microenvironments

The role of the microenvironment in cancer development is being increasingly appreciated. This paper will review data that highlight an emerging distinction between two different entities: the microenvironment that altered/preneoplastic/neoplastic cells find in the tissue where they reside, and the peculiar microenvironment inside the focal lesion (tumor) that these cells contribute to create. While alteration in the tissue environment can contribute to the selective clonal expansion of altered cells to form focal proliferative lesions, the atypical, non-integrated growth pattern that defines such focal lesions leads to the appearance of what is correctly referred to as the tumor microenvironment. The latter represents a new and unique biological milieu, characterized by hypoxia, acidosis and other biochemical and metabolic alterations, including genetic instability, that can set the stage for tumor progression to occur. Thus, the two microenvironments act in sequence and play complementary roles in the development of overt neoplasia. This distinction has important implications for the understanding of disease pathogenesis and for the management of preneoplastic/neoplastic lesions at various stages of cancer development