Robust adaptive feedback canceller based on modified pseudo affine projection algorithm.

This paper presents an adaptive feedback cancellation (AFC) algorithm with robust and stable performance. The proposed algorithm is based on the pseudo affine projection (PAP) algorithm which approximates the affine projection (AP) with a complexity comparable to the NLMS. Direct application of the PAP to AFC, however, often exhibits instability because of the delayed estimate of the linear prediction (LP) coefficients. This problem is solved in the proposed algorithm by utilizing an inverse gain filter (IGF) before the update of adaptive filter and by estimating the LP coefficients from the input signal without delay. Simulation results confirmed robustness and stability of the proposed algorithm.

Characterization of the inflammatory and fibrotic response in a mouse model of cardiac pressure overload.

Myocardial fibrosis is an integral component of most cardiac pathologic conditions and contributes to the development of both systolic and diastolic dysfunction. Because of the availability of genetically manipulated animals, mouse models are essential for understanding the mechanisms involved in the pathogenesis of cardiac fibrosis. Accordingly, we characterized the inflammatory and fibrotic response in a mouse model of cardiac pressure overload due to transverse aortic constriction (TAC). Following TAC, mouse hearts exhibited induction of chemokines and proinflammatory cytokines, associated with macrophage, but not neutrophil, infiltration. Induction of inflammatory cytokines was followed by a late upregulation of transforming growth factor (TGF)-beta isoforms, activation of the Smad2/3 and Smad1/5 pathways, induction of matricellular proteins, and deposition of collagen. Inflammatory activity decreased after 28 days of TAC; at this timepoint established fibrosis was noted, accompanied by ventricular dilation and systolic dysfunction. Late induction of inhibitory mediators, such as TGF-beta, may play an essential role in the transition from inflammation to fibrosis by suppressing inflammatory gene synthesis while inducing matrix deposition. Our findings identify molecular mediators and pathways with a potential role in cardiac fibrosis laying the foundations for studies exploring the pathogenesis of fibrotic cardiac remodeling using genetically targeted mice.