cystine/edema

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N-acetyl-l-cystine (NAC) protects against H9N2 swine influenza virus-induced acute lung injury.

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The antioxidant N-acetyl-l-cysteine (NAC) had been shown to inhibit replication of seasonal human influenza A viruses. Here, the effects of NAC on H9N2 swine influenza virus-induced acute lung injury (ALI) were investigated in mice. BALB/c mice were inoculated intranasally with 10(7) 50% tissue

A rapid procedure for the isolation of the Lys-49 myotoxin II from Bothrops moojeni (caissaca) venom: biochemical characterization, crystallization, myotoxic and edematogenic activity.

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Bothtrops moojeni snake venom was fractionated on a CM-Sepharose column which was previously equilibrated with 0.05 M ammonium bicarbonate buffer at pH 8.0 and subsequently eluted with an ammonium bicarbonate concentration gradient from 0.05 to 0.5 M at constant pH (8.0) and temperature (25 degrees

Inhibition of BECN1 Suppresses Lipid Peroxidation by Increasing System Xc- Activity in Early Brain Injury after Subarachnoid Hemorrhage.

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Lipid peroxidation plays a crucial role in early brain injury (EBI) after subarachnoid hemorrhage (SAH), and cystine/glutamate antiporter system X_c^- has been proved to be associated with glutathione (GSH) synthesis, which protects cells against oxidative damage. Antioxidant

Conversion of the electrohydraulic electrode to an electromechanical stone impactor: basic studies and a case report.

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A 3.3F electrohydraulic electrode (Wolf 2137.23) has been confined within a spring with a metal end cap, irrigated with water and covered with a 0.003-inch metal sheath (outside diameter 5F). The electrohydraulic lithotripsy discharge (Wolf Generator 2137.50) at E1 causes the metal cap to extend 3

Nephrotic syndrome occurring during tiopronin treatment for cystinuria.

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Cystinuria is an autosomal recessive disorder characterized with abnormal tubular reabsorption of cystine and dibasic amino acids leading to cystine urolithiasis. The classical form is caused by mutations in the SLC3A1 gene (OMIM 220100). The cornerstone of the treatment is high hydration and

Ocular changes in nephropathic cystinosis: The course of the gold-dust.

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OBJECTIVE Cystinosis is an autosomal recessive inherited lysosomal storage disease with an incidence of 1:100.000 up to 1:200.000 caused by a gene mutation of a lysosomal transport protein resulting in deposition of cystine in lysosomes in all cells and tissues. In the cornea, crystalline, gold-dust

[The olfactory neurotoxicity of cisplatin and effects of two drugs].

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32 guinea pigs were used as animal models for the study of cisplatin induced olfactory neurotoxicity and the effects of sodium thiosulfate (STS) and cystine on the toxicity by light and electron microscopy. The results revealed that the olfactory epithelium, olfactory nerve and the olfactory bulb

Canine urolithiasis: diagnosis and treatment.

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Over 97% of all uroliths in males less than a year of age and in females are phosphate, excluding males with portosystemic shunts and male Dalmatians . Uroliths in male Dalmatians usually are composed of urate. Uroliths associated with Staphylococcus aureus urinary tract infection are phosphate.

A case of intracranial hypertension and papilledema associated with nephropathic cystinosis and ocular involvement.

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An 11 year old boy with nephropathic cystinosis developed moderate to severe bilateral optic disc edema two months after he received a deceased donor renal allograft. The bilateral optic disc edema was found to be a result of intracranial hypertension diagnosed by lumbar puncture. No etiology was

In vivo imaging of system xc- as a novel approach to monitor multiple sclerosis.

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OBJECTIVE Glutamate excitotoxicity contributes to oligodendroglial and axonal damage in multiple sclerosis pathology. Extracellular glutamate concentration in the brain is controlled by cystine/glutamate antiporter (system xc-), a membrane antiporter that imports cystine and releases glutamate.

Salutary effects of a novel oxidative stress modulator on adenine-induced chronic progressive tubulointerstitial nephropathy.

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BACKGROUND Oxidative stress and inflammation promote the development and progression of chronic kidney disease. Oxidative stress is associated with depletion of tissue glutathione (GSH), the most abundant endogenous intracellular antioxidant, but degradation of oral GSH by digestive enzymes limits

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