Adaptive data echo cancellation using cost function adaptation

For a digital echo canceller it is desirable to reduce the adaptation time, during which the transmission of useful data is not possible. LMS is a non-optimal algorithm in this case as the signals involved are statistically non-Gaussian. Walach and Widrow (IEEE Trans. Inform. Theory 30 (2) (March 1984) 275-283) investigated the use of a power of 4, while other research established algorithms with arbitrary integer (Pei and Tseng, IEEE J. Selected Areas Commun. 12(9)(December 1994) 1540-1547) or non-quadratic power (Shah and Cowan, IEE.Proc.-Vis. Image Signal Process. 142 (3) (June 1995) 187-191). This paper suggests that continuous and automatic, adaptation of the error exponent gives a more satisfactory result. The family of cost function adaptation (CFA) stochastic gradient algorithm proposed allows an increase in convergence rate and, an improvement of residual error. As special case the staircase CFA algorithm is first presented, then the smooth CFA is developed. Details of implementations are also discussed. Results of simulation are provided to show the properties of the proposed family of algorithms. (C) 2000 Elsevier Science B.V. All rights reserved.

S-nitrosation of mitochondrial complex I depends on its structural conformation

Nitric oxide is known to cause persistent inhibition of mitochondrial respiration as a result of S-nitrosation of NADH: ubiquinone oxidoreductase (complex I) (Clementi, E., Brown, G. C., Feelisch, M., and Moncada, S. (1998) Proc. Natl. Acad. Sci. U. S. A. 95, 7631-7636). Little is known about whether such nitrosation occurs in physiological conditions and, if so, what are the possible cellular mechanisms. We have now found that the conformational state (active/deactive transition (Vinogradov, A. D. (1998) Biochim. Biophys. Acta 1364, 169-185)) of mitochondrial complex I is an important factor for the interaction of the enzyme with nitrosothiols and peroxynitrite. Only the deactivated, idle form of complex I was susceptible to inhibition by nitrosothiols and peroxynitrite. In contrast, the active form of the enzyme was insensitive to such treatment. Neither form of complex I was inhibited by nitric oxide itself. Our data suggest that the process of active/deactive transition plays an important role in the regulation of complex I activity and cellular respiration by nitric oxide. The implications of this finding for hypoxic or pathophysiological conditions in vivo are discussed.