Etiology included indwelling catheters or pacemaker wires in 35 patients; mediastinal fibrosis in 31, idiopathic thrombosis in 2, hypercoagulable disorder in 1, and postsurgical thrombosis in 1. In 42 patients, OSR was done through a median sternotomy: repair was with spiral saphenous vein in 22, expanded polytetrafluoroethylene (ePTFE) in 13, femoral vein grafts in 6, and human allograft in 1. Fifteen OSRs followed failed PF-04929113 price EVR interventions. EVR was attempted in 32 patients and was successful in 28 (88%): 19 had stenting, 14 had percutaneous transluminal balloon angioplasty (PTA), 2 had thrombolytic therapy with PTA, and 3 had

stenting. All four technical failures subsequently underwent OSR. There were no early deaths in either group. Periprocedural morbidity was 19% after OSR and 4% in the EVR group. Six early surgical graft failures were GSK3326595 purchase successfully treated with surgical revision; one restenosis after EVR was restented. During a mean follow-up of 4.1 years (range, 0.1-17.5 years) after OSR, 11 patients underwent 18 secondary interventions. Mean follow-up after EVIL was 2.2 years (range, 0.2-6.4 years), and nine patients underwent

21 secondary EVR interventions. Primary, assisted primary, and secondary patency rates of surgical bypass grafts were, respectively, 45%, 68%, and 75% at 3 and 5 years. Primary, assisted primary and secondary patency rates after EVR were 44%, 96%, and 96% at 3 years. Assisted primary patency was significantly higher in vein grafts than in ePTFE grafts (P =.05). Assisted primary and secondary patency was significantly higher in patients undergoing stenting compared with PTA (P =.02). At last follow-up, 93% of patients in both OSR and EVR groups had significant relief from symptoms.

Conclusions: OSR of benign SVC syndrome is effective, with durable long-term relief from symptoms. EVR is less invasive but equally effective in the mid-term,

albeit at the cost of multiple secondary interventions, and is an appropriate primary treatment for benign SVC syndrome. OSR remains an excellent choice for patients who are not suitable for EVR or in whom the EVR fails.”
“3-Nitropropionic acid (3-NP), an inhibitor of the mitochondrial enzyme succinate dehydrogenase, induces neuronal degeneration in the striatum. It SDHB is known that dopamine (DA) enhances this toxic effect. In this work, we study how the increase of DA influences the toxic effect of 3-NP on DAergic terminals, GABAergic neurons, astroglia and microglia in the striatum. We increased the content of DA through the inhibition of its uptake by nomifensine or the inhibition of its catabolism by deprenyl. We found that although nomifensine and deprenyl enhanced the DA overflow produced by 3-NP perfusion, they protected against the damage induced by 3-NP in the DAergic terminals and the GABAergic neurons in the striatum.