Two cases of primary cutaneous nocardiosis caused by intralesional injection.

Nocardiosis is a rare localized or systemic suppurative disease caused by the actinomycete Nocardia species. The respiratory tract is the most common site of infection, but primary cutaneous nocardiosis can also be induced by direct inoculation. Nocardiosis is usually reported in immunocompromised patients, such as those with human immunodeficiency virus (HIV) infection, chronic obstructive pulmonary disease, autoimmune diseases, cancer, or in those who have had organ transplantation or corticosteroid administration. However, it can also affect individuals with no serious underlying condition. We reported two cases of primary cutaneous nocardiosis in immunocompetent patients after intralesional injection of steroid.

Extremely low frequency magnetic field induces oxidative stress in mouse cerebellum.

We have investigated whether extremely low frequency magnetic field (ELF-MF) induces lipid peroxidation and reactive oxygen species in mouse cerebellum. After exposure to 60 Hz ELF-MF at 2.3 mT intensity for 3 hours, there was a significant increase in malondialdehyde level and hydroxyl radical. ELF-MF significantly induced concomitant increase in superoxide dismutase without alteration in glutathione peroxidase activity. While glutathione contents were not altered, ascorbic acid levels were significantly decreased by ELF-MF exposure. These results indicate that ELF-MF may induce oxidative stress in mouse cerebellum. However, the mechanism remains further to be characterized.

Clozapine attenuates mitochondrial burdens and abnormal behaviors elicited by phencyclidine in mice via inhibition of p47 phox; Possible involvements of phosphoinositide 3-kinase/Akt signaling.

BACKGROUND: Oxidative stress and mitochondrial dysfunction have been implicated in the pathophysiology of schizophrenia. AIMS: We investigated whether antipsychotic clozapine modulates nicotinamide adenine dinucleotide phosphate oxidase and mitochondrial burdens induced by phencyclidine in mice. METHODS: We examined the effect of clozapine on nicotinamide adenine dinucleotide phosphate oxidase activation, mitochondrial burdens (i.e. oxidative stress and mitochondrial dysfunction), and activities of enzymatic antioxidant in the prefrontal cortex, and subsequent abnormal behaviors induced by repeated treatment with phencyclidine. p47 phox Knockout mice and LY294002, a phosphoinositide 3-kinase inhibitor, were employed to elucidate the pharmacological mechanism of clozapine. RESULTS: Phencyclidine treatment resulted in an early increase nicotinamide adenine dinucleotide phosphate oxidase activity, membrane translocation of p47 phox, interaction between p-Akt and p47 phox, and mitochondrial burdens in wild-type mice. Although these increases returned to near control level four days post-phencyclidine, mitochondrial superoxide dismutase and glutathione peroxidase activities were decreased at that time. Clozapine, LY294002, or p47 phox knockout significantly ameliorated social withdrawal and recognition memory deficits produced by phencyclidine. Importantly, LY294002 did not significantly alter the effects of clozapine against abnormal behaviors and the interaction between p-Akt and p47 phox induced by phencyclidine. Furthermore, neither LY294002 nor clozapine exhibited any additive effects to the protection afforded by p47 phox knockout against phencyclidine insult. CONCLUSION: Our results suggest that p47 phox gene mediates phencyclidine-induced mitochondrial burdens and abnormal behaviors, and that the interactive modulation between p47 phox and phosphoinositide 3-kinase/Akt is important for the understanding on the pharmacological mechanism of clozapine.