Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.3.1 (NADPH oxidase)
 11,281 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic granulomatous disease (CGD) is an inherited disease of the phagocyte NADPH oxidase system that causes defective production of toxic oxygen metabolites, leading to impaired bacterial and fungal killing, and recurrent life threatening infections; mostly by catalase producing organisms. Nocardiosis in CGD is well described, however actinomycosis is rare. We describe a patient of CGD with actinomycosis and nocardiosis coinfection. A 43-year-old male with history of recurrent discharging sinuses presented with fever, dyspnea and cough. He had multiple discharging sinuses over neck and anterior chest wall. There was only partial response to intravenous penicillin. Needle aspirate from chest wall showed co-infection with actinomyces and nocardia. His nitroblue tetrazolium (NBT) reduction test was negative. He was treated with penicillin, amikacin and trimethoprim-sulfamethoxazole and had good clinical and radiological response.
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PMID:Actinomycosis and nocardiosis co-infection in chronic granulomatous disease. 2302 49

Patients with chronic heart failure (CHF) have dyspnea and exercise intolerance, which are caused in part by diaphragm abnormalities. Oxidants impair diaphragm contractile function, and CHF increases diaphragm oxidants. However, the specific source of oxidants and its relevance to diaphragm abnormalities in CHF is unclear. The p47(phox)-dependent Nox2 isoform of NAD(P)H oxidase is a putative source of diaphragm oxidants. Thus, we conducted our study with the goal of determining the effects of CHF on the diaphragm levels of Nox2 complex subunits and test the hypothesis that p47(phox) knockout prevents diaphragm contractile dysfunction elicited by CHF. CHF caused a two- to sixfold increase (P < 0.05) in diaphragm mRNA and protein levels of several Nox2 subunits, with p47(phox) being upregulated and hyperphosphorylated. CHF increased diaphragm extracellular oxidant emission in wild-type but not p47(phox) knockout mice. Diaphragm isometric force, shortening velocity, and peak power were decreased by 20-50% in CHF wild-type mice (P < 0.05), whereas p47(phox) knockout mice were protected from impairments in diaphragm contractile function elicited by CHF. Our experiments show that p47(phox) is upregulated and involved in the increased oxidants and contractile dysfunction in CHF diaphragm. These findings suggest that a p47(phox)-dependent NAD(P)H oxidase mediates the increase in diaphragm oxidants and contractile dysfunction in CHF.
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PMID:NAD(P)H oxidase subunit p47phox is elevated, and p47phox knockout prevents diaphragm contractile dysfunction in heart failure. 2620 74