the other hand, there is evidence that i-LTP may exert a detrimental effect in the peri-infarct area, facilitating excitotoxic processes via the sustained, long-term enhancement of glutamate mediated neurotransmission. In the present work we will review the molecular and synaptic mechanisms underlying ischemia-induced synaptic plastic changes taking into account their potential adaptive and/or detrimental effects on the neuronal network in which they occur. Thereafter, we will consider the implications of brain plastic phenomena in the post-stroke recovery phase as well as during the rehabilitative and therapeutic intervention in human subjects. (C) 2008 Elsevier Ltd. All
“Type B dissections complicated by pain, malperfusion, or aneurysm expansion selleck products mandate surgical intervention. Success of this therapy is predicated on exclusion and thrombosis of the false lumen of the aneurysm. We report a case where cessation of flow was achieved using covered stent grafts in conjunction with coil embolization of the false lumen. The introduction of coils into the false lumen is a novel approach and may provide a helpful adjunct in endovascular treatment of complicated type B aortic dissections.”
“Neuroprotection for ischemic stroke refers to strategies, applied singly or in combination, that antagonize the injurious biochemical and molecular events that eventuate OTX015 ic50 in irreversible ischemic injury. There has been a recent explosion of interest in this field, with over 1000 experimental papers and over 400 clinical articles appearing within the past 6 years. These studies, in turn, are the outgrowth of three decades of investigative work to define the multiple mechanisms and mediators of ischemic brain injury, which constitute potential targets of neuroprotection. Rigorously conducted
experimental studies in animal models of brain ischemia provide incontrovertible proof-of-principle that high-grade protection of the Carteolol HCl ischemic brain is an achievable goal. Nonetheless, many agents have been brought to clinical trial without a sufficiently compelling evidence-based pre-clinical foundation. At this writing, around 160 clinical trials of neuroprotection for ischemic stroke have been initiated. Of the approximately 120 completed trials, two-thirds were smaller early-phase safety-feasibility studies. The remaining one-third were typically larger (>200 subjects) phase II or III trials, but, disappointingly, only fewer than one-half of these administered neuroprotective therapy within the 4-6 h therapeutic window within which efficacious neuroprotection is considered to be achievable. This fact alone helps to account for the abundance of “”failed”" trials.