(C) 2013 Elsevier B.V. All rights reserved.”
“Background: The impairment

of the ubiquitin-proteasome system HDAC inhibitor (UPS) is a cellular mechanism underlying the neurodegenerative process in Parkinson’s disease (PD). A mouse model induced by the selective proteasome inhibitor lactacystin targeting on substantia nigra has been demonstrated to be valuable in investigating etiopathogenesis and neuroprotection for PD. Objective: In the present study, we used adeno-associated virus type 2 vector (AAV2) encoding glial cell line-derived neurotrophic factor (GDNF) injected into the striatum of this animal model to test the effectiveness and possible mechanisms of GDNF gene therapy. Results: Our results showed that AAV2-mediated GDNF gene therapy significantly attenuated lactacystin-induced loss of nigral dopamine (DA) neurons and striatal DA levels. Furthermore, we found that GDNF protein is mostly expressed in astrocytes in the subventricular zone (SVZ) and dentate gyrus (DG). AAV2-mediated GDNF therapy can induce neurogenesis in the SVZ and DG, and increase the number of nigral newborn

DA neurons. Conclusion: These data indicate that AAV2-mediated find more GDNF gene therapy can protect the nigral DA neurons from the UPS impairment-induced degeneration, which may partly result from the nigral DA neuron regeneration in the brain, and such experimental results may have implications for the treatment of PD. Copyright (c) 2012 S. Karger AG, Basel”
“Objectives: It is still unclear whether residual defects seen after carotid endarterectomy (CEA) have clinical consequences. We investigated prevalence of residual defects in the carotid artery and their possible impact on clinical and Duplex ultrasound (DUS) follow-up.

Materials and methods: Sixty-five patients who had undergone CEA were prospectively examined

with 1-3 month postoperative computed tomographic angiography (CTA)., clinical and DUS follow-up. Defects in common (CCA), external (ECA) and internal carotid artery Quisinostat price (ICA) were scored as clamp marks, intimal step or flap, mural thrombus, kink, microdehiscence suture or residual stenosis.

Results: Fifty-eight patients (89.2%) had residual defects in CCA, ECA or ICA (143 defects). Intimal steps (n = 39) and residual stenosis (n = 17) were most noted defects. Only residual defects in ECA were significantly associated with significant higher PSV values both at short-term and long-term follow-up (1990 vs. 1400 mm s(-1) at 1 year and 2000 vs. 1230 mm s(-1) at 2 years, P-values 0.031 and 0.016).

Conclusion: Carotid artery residual defects on CTA after CEA are very common, simple fingerprints of the operative procedure, have no clear consequence. When CTA is performed clinically after CEA, knowledge of high Prevalence and type of defects detected on CTA may be of importance for radiologists and clinicians. (C) 2011 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved.