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Computing the eigenvalues and orthogonal eigenvectors of an n n symmetric tridiagonal matrix is an important task that arises while solving any symmetric eigenproblem. All practical software requires O(n 3) time to compute all the eigenvectors and ensure their orthogonality when eigenvalues are close. In the rst part of this thesis we review earlier work(More)
Many drugs have been approved for relapsing forms of multiple sclerosis but are only partly effective, are injected, and are expensive. We aimed to investigate use of of oral simvastatin (80 mg) in 30 individuals with relapsing-remitting multiple sclerosis. The mean number of gadolinium-enhancing lesions at months 4, 5, and 6 of treatment was compared with(More)
Statins are inhibitors of HMG-CoA reductase that have been recently recognized as anti-inflammatory and neuroprotective drugs. Herein, we investigated anti-excitotoxic and anti-seizure effects of statins by using kainic acid (KA)-rat seizure model, an animal model for temporal lobe epilepsy and excitotoxic neurodegeneration. We observed that pre-treatment(More)
Inducible nitric oxide synthase (iNOS) is one of three NOS isoforms generating nitric oxide (NO) by the conversion of l-arginine to l-citrulline. iNOS has been found to be a major contributor to initiation/exacerbation of the central nervous system (CNS) inflammatory/degenerative conditions through the production of excessive NO which generates reactive(More)
X-adrenoleukodystrophy (X-ALD) is a complex disease where inactivation of ABCD1 gene results in clinically diverse phenotypes, the fatal disorder of cerebral ALD (cALD) or a milder disorder of adrenomyeloneuropathy (AMN). Loss of ABCD1 function results in defective beta oxidation of very long chain fatty acids (VLCFA) resulting in excessive accumulation of(More)
This study was designed to understand the role of inflammatory mediators involved in the neurobiology of childhood adrenoleukodystrophy (cALD) by comparing the differential expression of the inflammatory mediators with metabolite very long chain fatty acids that accumulate in this disease. Histopathological examinations indicated extensive demyelination and(More)
Globoid cell leukodystrophy (Krabbe disease) is an inherited neurological disorder caused by the pathogenomic accumulation of psychosine (galactosylsphingosine), a substrate for the deficient enzyme galactocerebroside beta-galactosidase. This study underscores the mechanism of action of psychosine in the regulation of oligodendrocyte cell death via the(More)
AMP-activated-protein-kinase (AMPK) is a key sensor and regulator of cellular and whole-body energy metabolism and plays a key role in regulation of lipid metabolism. Since lipid metabolism has been implicated in neuronal amyloid-beta (Abeta) homeostasis and onset of Alzheimer's disease, we investigated the involvement of AMPK in neuronal lipid metabolism(More)
Hyperphosphorylation and polymerization of microtubule-associated protein tau into paired helical filaments (PHFs) is one of the hallmarks of Alzheimer's disease (AD). Here we report that neuronal tau hyperphosphorylation under AD conditions is regulated by S-nitrosoglutathione (GSNO), an endogenous nitric oxide carrier molecule. In cultured rat cortical(More)
Glial cells secrete proinflammatory mediators in the brain in response to exogenous stimuli such as infection and injury. Previously, we documented that systemic maternal lipopolysaccharide (LPS)-exposure at embryonic gestation day 18 causes oligodendrocyte (OL)-injury/hypomyelination in the developing brain which can be attenuated by N-acetyl cysteine(More)