Transapical approach for mitral valve repair during insertion of a left ventricular assist device.

Background: Severe mitral regurgitation (MR) is common in patients who are undergoing insertion of a left ventricular assist device (LVAD). This study analyzes the outcomes of a transapical approach for edge-to-edge repair of the mitral valve during insertion of a left ventricular assist device in 19 patients with MR.

Methods: This retrospective study includes 19 patients who were implanted between March 21, 2011, and August 31, 2011, at the University of Chicago.

HS1 functions as an essential actin-regulatory adaptor protein at the immune synapse.

HS1, the leukocyte-specific homolog of cortactin, regulates F-actin in vitro and is phosphorylated in response to TCR ligation, but its role in lymphocyte activation has not been addressed. We demonstrate that HS1-deficient T cells fail to accumulate F-actin at the immune synapse (IS) and, upon TCR ligation, form actin-rich structures that are disordered and unstable. Early TCR activation events are intact in these cells, but Ca2+ influx and IL-2 gene transcription are defective.

Dynamin 2 regulates T cell activation by controlling actin polymerization at the immunological synapse.

Actin reorganization at the immunological synapse is required for the amplification and generation of a functional immune response. Using small interfering RNA, we show here that dynamin 2 (Dyn2), a large GTPase involved in receptor-mediated internalization, did not alter antibody-mediated T cell receptor internalization but considerably affected T cell receptor-stimulated T cell activation by regulating multiple biochemical signaling pathways and the accumulation of F-actin at the immunological synapse. Moreover, Dyn2 interacted directly with the Rho family guanine nucleotide exchange factor Vav1, and this interaction was required for T cell activation.