skip to main content
OSTI.GOV title logo U.S. Department of Energy
Office of Scientific and Technical Information

Title: Effective Preconditioning Through Ordering Interleaved WithIncomplete Factorization

Abstract

No abstract prepared.

Authors:
; ;
Publication Date:
Research Org.:
COLLABORATION - Penn StateU.
OSTI Identifier:
926467
Report Number(s):
LBNL-58671
R&D Project: KS1210; BnR: KJ0101010; TRN: US200808%%11
DOE Contract Number:
DE-AC02-05CH11231
Resource Type:
Journal Article
Resource Relation:
Journal Name: SIAM Journal on Matrix Analysis andApplications; Journal Volume: 27; Journal Issue: 4; Related Information: Journal Publication Date: March 17,2006
Country of Publication:
United States
Language:
English
Subject:
99; FACTORIZATION; MATRICES; CALCULATION METHODS

Citation Formats

Raghavan, Padma, Lee, Ingyu, and Ng, Esmond G. Effective Preconditioning Through Ordering Interleaved WithIncomplete Factorization. United States: N. p., 2006. Web.
Raghavan, Padma, Lee, Ingyu, & Ng, Esmond G. Effective Preconditioning Through Ordering Interleaved WithIncomplete Factorization. United States.
Raghavan, Padma, Lee, Ingyu, and Ng, Esmond G. Fri . "Effective Preconditioning Through Ordering Interleaved WithIncomplete Factorization". United States. doi:.
@article{osti_926467,
title = {Effective Preconditioning Through Ordering Interleaved WithIncomplete Factorization},
author = {Raghavan, Padma and Lee, Ingyu and Ng, Esmond G.},
abstractNote = {No abstract prepared.},
doi = {},
journal = {SIAM Journal on Matrix Analysis andApplications},
number = 4,
volume = 27,
place = {United States},
year = {Fri Mar 17 00:00:00 EST 2006},
month = {Fri Mar 17 00:00:00 EST 2006}
}
  • Numerical experiments are presented whereby the effect of reorderings on the convergence of preconditioned Krylov subspace methods for the solution of nonsymmetric linear systems is shown. The preconditioners used in this study are different variants of incomplete factorizations. It is shown that certain reorderings for direct methods, such as reverse Cuthill-McKee, can be very beneficial. The benefit can be seen in the reduction of the number of iterations and also in measuring the deviation of the preconditioned operator from the identity.
  • Abstract not provided.
  • Salvianolic acid A (SalA) is a phenolic carboxylic acid derivative extracted from Salvia miltiorrhiza. It has many biological and pharmaceutical activities. The purpose of this study was to investigate the effect of SalA on concanavalin A (ConA)-induced acute hepatic injury in Kunming mice and to explore the role of SIRT1 in such an effect. The results showed that in vivo pretreatment with SalA significantly reduced ConA-induced elevation in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities and decreased levels of the hepatotoxic cytokines such as interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α). Moreover, the SalA pretreatment ameliorated the increasesmore » in NF-κB and in cleaved caspase-3 caused by ConA exposure. Whereas, the pretreatment completely reversed expression of the B-cell lymphoma-extra large (Bcl-xL). More importantly, the SalA pretreatment significantly increased the expression of SIRT1, a NAD{sup +}-dependent deacetylase, which was known to attenuate acute hypoxia damage and metabolic liver diseases. In our study, the increase in SIRT1 was closely associated with down-regulation of the p66 isoform (p66shc) of growth factor adapter Shc at both protein and mRNA levels. In HepG2 cell culture, SalA pretreatment increased SIRT1 expression in a time and dose-dependent manner and such an increase was abrogated by siRNA knockdown of SIRT1. Additionally, inhibition of SIRT1 significantly reversed the decreased expression of p66shc, and attenuated SalA-induced p66shc down-regulation. Collectively, the present study indicated that SalA may be a potent activator of SIRT and that SalA can alleviate ConA-induced hepatitis through SIRT1-mediated repression of the p66shc pathway. - Highlights: • We report for the first time that SalA protects against ConA-induced hepatitis. • We find that SalA is a potential activator of SIRT1. • SalA's protection against hepatitis involves SIRT1-mediated repression of p66shc.« less