Positive regulation of NADPH oxidase 5 by proinflammatory-related mechanisms in human aortic smooth muscle cells.

NADPH oxidase Nox5 subtype expression is significantly increased in vascular smooth muscle cells (SMCs) underlying fibro-lipid atherosclerotic lesions. The mechanisms that up-regulate Nox5 are not understood. Consequently, we characterized the promoter of the human Nox5 gene and investigated the role of various proinflammatory transcription factors in the regulation of Nox5 in human aortic SMCs.

Forequarter amputation (upper limb and shoulder girdle) in a synovial sarcoma case--case report.

We are often confronted with severe cases - patients with very aggressive tumours that suppose a complex and in the same time radical approach--in our medical practice. The correct approach and management of such cases ensure both the surgical success and the patient survival. In this paper, we present the case of a young woman, who has been admitted in our clinic with a giant, irradiated tumour involving left axilla, shoulder and scapula.

AP-1-dependent transcriptional regulation of NADPH oxidase in human aortic smooth muscle cells: role of p22phox subunit.

Objective: NADPH oxidase (NADPHox) is the major source of reactive oxygen species in vascular diseases; the mechanisms of enzyme activation are not completely elucidated. AP-1 controls the expression of many genes linked to vascular smooth muscle cells (SMCs) dysfunction. In this study we searched for the role of AP-1 in the regulation of NADPHox expression and function in human aortic SMCs exposed to proinflammatory conditions.