[Application of nerve trunk stimulation therapy in functional rehabilitation of the lower limbs in the patients with cerebral apoplexy at convalescence stage].

Objective: To explore the value of nerve trunk stimulation in the rehabilitation of lower limb function in the patients with cerebral apoplexy at convalescence stage.

Methods: According the random number table, the patients with the lower limb dysfunction of cerebral apoplexy at convalescence stage were divided into a control group and a treatment group, 42 cases in each group. The drug therapy and the routine rehabilitation training were provided in the two groups.

Pyrrolidine dithiocarbamate ameliorates endothelial dysfunction in thoracic aorta of diabetic rats by preserving vascular DDAH activity.

Objective: Endothelial dysfunction plays a pivotal role in the development of diabetic cardiovascular complications. Accumulation of endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA) and inhibition of dimethylarginine dimethylaminohydrolase (DDAH) activity have been involved in diabetic endothelial dysfunction. This study was to investigate the effect of pyrrolidine dithiocarbamate (PDTC) on impairment of endothelium-dependent vasodilatation in diabetic rats and its potential mechanism.

Preservation of vascular DDAH activity contributes to the protection of captopril against endothelial dysfunction in hyperlipidemic rabbits.

Endothelial dysfunction plays a pivotal role in the pathogenesis of atherosclerosis. Endogenous inhibitor of nitric oxide synthase (NOS) asymmetric dimethylarginine (ADMA) has been recognized as an independent risk factor of endothelial dysfunction and the biomarker of atherosclerosis. This study was to investigate whether endogenous ADMA and its metabolic enzyme dimethylarginine dimethylaminohydrolase (DDAH) were involved in mechanisms of captopril protection against endothelial dysfunction in high fat diet feeding rabbits.

Improvement of endothelial dysfunction in atherosclerotic rabbit aortas by ex vivo gene transferring of dimethylarginine dimethylaminohydrolase-2.

Background: Elevated endogenous asymmetric dimethylarginine (ADMA) is an independent risk factor for atherosclerosis, and dimethylarginine dimethylaminohydrolase (DDAH) is the key enzyme responsible for the metabolism of ADMA. This study was to determine whether reduced vascular DDAH activity was implicated in endothelial dysfunction of atherosclerosis and whether ex vivo gene transferring of DDAH2 could upregulate vascular DDAH activity and improve endothelial dysfunction associated with atherosclerosis.

Methods: Recombinant adenovirus encoding human DDAH2 gene driven by a cytomegalovirus (CMV) promoter was constructed and used to infect thoracic aortic rings from hyperlipidemic rabbits.

Ex vivo gene transferring of human dimethylarginine dimethylaminohydrolase-2 improved endothelial dysfunction in diabetic rat aortas and high glucose-treated endothelial cells.

Objectives: Elevated level of asymmetric dimethylarginine (ADMA) is an independent risk factor for endothelial dysfunction. Dimethylarginine dimethylaminohydrolase (DDAH) is the key enzyme responsible for the degradation of endogenous ADMA. The purposes of this study were to determine whether suppressed DDAH2 expression would implicate in endothelial dysfunction associated with diabetes mellitus and further to investigate whether adenovirus-mediated DDAH2 gene overexpression could improve the hyperglycemia-induced endothelial dysfunction.

Dimethylarginine dimethylaminohydrolase-2 overexpression improves impaired nitric oxide synthesis of endothelial cells induced by glycated protein.

Nitric oxide (NO) synthesis is modulated by dimethylarginine dimethylaminohydrolase (DDAH) via metabolizing asymmetric dimethylarginine (ADMA), an endogenous NO synthase (NOS) inhibitor. This study investigated whether glycosylated bovine serum albumin (GBSA) could impair NO synthesis by inhibition of DDAH expression and activity, and whether DDAH2 overexpression could reverse the impaired NO synthesis induced by GBSA in endothelial cells. Overexpression of DDAH2 gene was established by liposome-mediated gene transfection in ECV304 endothelial cell line.