No signs
of clotting or other technical incidents were recorded. (J Thorac Cardiovasc Surg 2011;141:1145-9)”
“The development of ectopic neural discharge at a site of peripheral nerve injury is thought to contribute to the initiation of sensory disturbances and pain. We have previously shown that this discharge can be initiated or increased by the neuropeptide calcitonin gene-related peptide (CGRP). We have now studied a potential therapeutic approach to reducing the discharge by evaluating the effect of a systemically administered monoclonal antibody to CGRP on injury-induced activity in the lingual nerve. In 16 anaesthetised adult ferrets the left lingual nerve was sectioned. One day after the injury, Selleck Paclitaxel the animals received a subcutaneous injection of either a monoclonal antibody to CGRP or a vehicle control. Three days after the injury, under a second anaesthetic, single-unit electrophysiological recordings were made from central to the injury site (469 and 391 units
were analysed in antibody and vehicle groups, respectively), and the proportion of units that were spontaneously active was determined. In the vehicle-treated animals 6.4 +/- this website 2.7 [SEM]% of the units were spontaneously active, with conduction velocities of 8.8-40.8 m/s and discharge frequencies of 0.03-2.7 Hz. In the monoclonal antibody-treated animals 5.7 +/- 2.0% of the units were spontaneously active, with conduction velocities of 13.9-38.8
m/s and discharge frequencies of 0.07-1.8 Hz. There was no significant difference between these two groups (for spontaneous activity and conduction velocity: p > 0.05, Student’s t-test; for discharge frequency: p > 0.05. Mann-Whitney test), suggesting that the spontaneous activity initiated by a nerve injury cannot be modulated by administration of a monoclonal antibody JQ-EZ-05 ic50 to CGRP. (C) 2011 Elsevier Ireland Ltd. All rights reserved.”
“Objectives: We evaluated results of an echocardiographically based strategy combining mitral annuloplasty with other procedures to treat chronic ischemic mitral regurgitation.
Methods: From March 2006 to February 2009, 147 patients underwent mitral valve surgery for chronic ischemic mitral regurgitation. Mean effective regurgitant orifice was 36 +/- 11 mm(2), and ejection fraction was 35% +/- 9%. On the basis of echocardiographic findings, in 10 cases a prosthesis was inserted and mitral annuloplasty was performed in 137 cases, isolated in 83, associated with chordal cutting in 12 cases (in 5 anterior leaflet was augmented with pericardial patch), and with exclusion of anteroseptal (n = 35) or inferior (n = 7) scars in 42.
Results: Thirty-day mortality was 4.8%; 3-year survival was 86% +/- 3%.