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malonic acid/atrophy

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ČlanciKlinička ispitivanjaPatenti
11 rezultatima
Adult rats received chronic dialytic delivery devices that exposed the striatum to a 100 mM, 400 mM, or 4 M solution of the reversible succinate dehydrogenase inhibitor malonic acid (MA). Three weeks of exposure to 100 or 400 mM MA produced no significant reduction in striatal cytochrome oxidase

When the Laughing Stops: Subacute Combined Spinal Cord Degeneration Caused by Laughing Gas Use.

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: Here we describe a case of subacute combined spinal cord degeneration caused by nitrous oxide (N2O, laughing gas) use. Because of its euphoric effects, the use of N2O has become increasingly popular in recent years. Unfortunately, the use of N2O leads to inactivation of vitamin B12. Vitamin B12
Proteomic strategies are herein proved to be a complementary approach to the well established amino acid composition analysis for the characterization of the aging and deterioration phenomena occurring to proteinaceous materials in works-of-art. Amino acid analyses on several samples demonstrated

Organic acids produced by self-sustaining coacervates in presence of p-nitroaniline and p-phenylene-diamine.

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Oleic and malonic acids were found in control samples while p-nitroaniline addition induced production of tricarballylic acid in eight and twelve days exposed samples. Fumaric and citric acids were found in sporadic instances. Addition of p-phenylene diamine to the mixture showed a degeneration

Neurodegenerative disorders: clues from glutamate and energy metabolism.

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It is well established that glutamate receptors play a major role in mediating acute ischemic neuronal degeneration in the CNS. Cerebral ischemia and head or spinal cord trauma are associated with excessive release and extracellular accumulation of glutamate, which leads to persistent activation of
It is thought that impairment of energy metabolism that results in deterioration of membrane function, leading to loss of the Mg2+ block on NMDA receptors, and allowing persistent activation of these receptors by glutamate, might be a cause of neuronal death in neurodegenerative disorders. Studies

3-Nitropropionic acid's lethal triplet: cooperative pathways of neurodegeneration.

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3-Nitropropionic acid (3-NP) is a mitochondrial toxin which interferes with ATP synthesis. Accidental ingestion of 3-NP by humans as well as other mammals results in neuronal degeneration within the basal ganglia and movement dysfunction characterized by dystonia, chorea, and hypokinesia. The

A Chemically Orthogonal Hole Transport Layer for Efficient Colloidal Quantum Dot Solar Cells.

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Colloidal quantum dots (CQDs) are of interest in light of their solution-processing and bandgap tuning. Advances in the performance of CQD optoelectronic devices require fine control over the properties of each layer in the device materials stack. This is particularly challenging in the present best

Novel magnetic resonance imaging findings in a patient with short chain acyl CoA dehydrogenase deficiency.

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Reports on magnetic resonance imaging findings in patients with short chain acyl -Coenzyme A dehydrogenase (SCAD) deficiency, an autosomal recessive disorder caused by mutations in the acyl-Coenzyme A dehydrogenase (ACADS), are limited. Many asymptomatic carriers of ACAD variants have also been

Carboxyfullerenes as neuroprotective agents.

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Two regioisomers with C3 or D3 symmetry of water-soluble carboxylic acid C60 derivatives, containing three malonic acid groups per molecule, were synthesized and found to be equipotent free radical scavengers in solution as assessed by EPR analysis. Both compounds also inhibited the excitotoxic

Fullerene-based antioxidants and neurodegenerative disorders.

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Water-soluble derivatives of buckminsterfullerene (C(60)) derivatives are a unique class of compounds with potent antioxidant properties. Studies on one class of these compounds, the malonic acid C(60) derivatives (carboxyfullerenes), indicated that they are capable of eliminating both superoxide
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