The second patient, a 77-year-old woman who presented with a 5.5-cm aneurysm at the origin of a previously bypassed aberrant artery on the distal aortic arch, was treated using bilateral carotid-subclavian bypasses through neck incisions and a thoracic endoluminal graft exclusion of the arch aneurysm that covered both subclavian arteries.”
“Terminal Schwann cells (tSCs) are non-myelinating glia that wrap the nerve terminal at
the neuromuscular junction. They are required for the maintenance of the neuromuscular synapse and are likely to play essential roles in the restoration of synaptic connections after nerve injury. tSCs acquire a reactive 4SC-202 cost phenotype after nerve damage characterized by the extension of cellular processes that may facilitate reinnervation. The molecular signaling events underpinning the tSC reactive state remain elusive, in particular, little is known about transcription factors involved in the transcriptional reprogramming during tSC activation. Prior research implicated nine
members of the zinc-finger transcription factor family in Schwann cell (SC) development and myelination, and levels of one such protein were reported increased in other non-myelinating SCs after denervation. We hypothesize that zinc-finger transcription factors could play a role during tSC activation. Because of their relative paucity, tSCs are difficult to study molecularly. Here, we used the rat cervical sympathetic trunk (CST), an autonomic PI3K inhibitor nerve in which non-myelinating SCs are the predominant cell type, to isolate zinc-finger protein (ZFP) cDNAs
by reverse transcriptase-polymerase chain reaction. We isolated 29 unique ZFP sequences of which zinc proliferation 1 (Zipro1) was the most abundant. We found that after CST transection, levels for Zipro1 mRNA doubled and that Zipro1 protein expression increased in non-myelinating CST SCs. We also determined that Zipro1 is expressed in tSCs and its levels increased following skeletal muscle denervation. Thus, Zipro1 is a good candidate for a transcription factor involved in activation of non-myelinating SCs in general, and tSCs in particular. (C) 2008 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Intrathoracic carotid bifurcation is rare with only five other cases reported. This anatomic variant NU7026 chemical structure with posteromedial origin of the internal carotid artery (ICA) appears to be part of the Klippel-Feil syndrome, a rare congenital defect characterized by fusion of the cervical vertebrae. Caution is advised when planning thoracic and cervical vascular procedures. Angiography carries higher risk of unintentional ICA catheterization due to the short common carotid artery length. The intrathoracic location of the carotid bifurcation makes endarterectomy difficult and patients may do better with carotid artery stenting. Ultrasound can be confusing in these patients and MRA may be preferable.