Impact of Anchor Location on Mitral Neochordae Forces: An In Vitro Study.

PURPOSE: This study examined changes in force distribution between the neochordae corresponding to different ventricular anchor locations. DESCRIPTION: Seven porcine mitral valves were mounted in a left heart simulator. Neochordae (expanded polytetrafluoroethylene) originated from either a simulated left ventricular apex, papillary muscle base, or papillary muscle tip location. The neochordae were attached at three sites along the P2 leaflet segment: P2Lateral; P2Center, and P2Medial. Mitral regurgitation was induced by cutting posterior leaflet P2 marginal chordae. The forces on each neochord required to restore normal mitral valve coaptation were quantified for different ventricular anchoring origins and leaflet insertion sites. EVALUATION: The results showed that under both normotensive and hypertensive conditions, the force exerted was much higher at P2Center than either P2Lateral or P2Medial, independent of ventricular anchor location. Also, forces on both P2Lateral and P2Medial were not statistically different. CONCLUSIONS: Artificial neochordae treatment for all anchoring locations was effective in correcting induced mitral regurgitation. The P2 central neochordae had a significantly higher force than both lateral neochords under all conditions.

Enhancing plasticity in central networks improves motor and sensory recovery after nerve damage.

Nerve damage can cause chronic, debilitating problems including loss of motor control and paresthesia, and generates maladaptive neuroplasticity as central networks attempt to compensate for the loss of peripheral connectivity. However, it remains unclear if this is a critical feature responsible for the expression of symptoms. Here, we use brief bursts of closed-loop vagus nerve stimulation (CL-VNS) delivered during rehabilitation to reverse the aberrant central plasticity resulting from forelimb nerve transection. CL-VNS therapy drives extensive synaptic reorganization in central networks paralleled by improved sensorimotor recovery without any observable changes in the nerve or muscle. Depleting cortical acetylcholine blocks the plasticity-enhancing effects of CL-VNS and consequently eliminates recovery, indicating a critical role for brain circuits in recovery. These findings demonstrate that manipulations to enhance central plasticity can improve sensorimotor recovery and define CL-VNS as a readily translatable therapy to restore function after nerve damage.

Twisting the arm: structural constraints in bicyclic expanded-ring N-heterocyclic carbenes.

A series of diaryl, mono-aryl/alkyl and dialkyl mono- and bicyclic expanded-ring N-heterocyclic carbenes (ER-NHCs) have been prepared and their complexation to Au(i) investigated through the structural analysis of fifteen Au(NHC)X and/or [Au(NHC)2]X complexes. The substituted diaryl 7-NHCs are the most sterically encumbered with large buried volume (%VB) values of 40-50% with the less flexible six-membered analogues having %VB values at least 5% smaller. Although the bicyclic systems containing fused 6- and 7-membered rings (6,7-NHCs) are constrained with relatively acute NCN bond angles, they have the largest %VB values of the dialkyl derivatives reported here, a feature related to the fixed conformation of the heterocyclic rings and the compressional effect of a pre-set methyl substituent.

Indirect evidence for a NiIII-oxyl oxidant in the reaction of a NiII complex with peracid.

The reaction of a NiII complex and meta-chloroperoxybenzoic acid (m-CPBA) resulted in the formation of a long-lived NiIII-chlorobenzoate complex that is a capable hydrocarbon oxidant. Analysis of the post-reaction decay products showed the formation of oxidised derivatives of the supporting ligand (a benzoxazine), and heterolytic O-O bond scission in m-CPBA. This evidence indicates formation of a more potent transient NiIII-oxyl species, which was further supported by DFT calculations.