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Brachial plexus root avulsions cause debilitating upper limb paralysis. Short-term neuroprotective treatments have reported preservation of motor neurons and function in model animals while reports of long-term benefits of such treatments are scarce, especially the morphological sequelae. This morphological study investigated the long-term suppression of c-Jun- and neuronal nitric oxide synthase (nNOS) (neuroprotective treatments for one month) on the motor neuron survival, ultrastructural features of lower motor neurons, and forelimb function at six months after brachial plexus roots avulsion. Neuroprotective treatments reduced oxidative stress and preserved ventral horn motor neurons at the end of the 28-day treatment period relative to vehicle treated ones. Motor neuron sparing was associated with suppression of c-Jun, nNOS, and pro-apoptotic proteins Bim and caspases at this time point. Following 6 months of survival, neutral red staining revealed a significant loss of most of the motor neurons and ventral horn atrophy in the avulsed C6, 7, and 8 cervical segments among the vehicle-treated rats ( n = 4). However, rats that received neuroprotective treatments c-Jun JNK inhibitor, SP600125 ( n = 4) and a selective inhibitor of nNOS, 7-nitroindazole ( n = 4), retained over half of their motor neurons in the ipsilateral avulsed side compared. Myelinated axons in the avulsed ventral horns of vehicle-treated rats were smaller but numerous compared to the intact contralateral ventral horns or neuroprotective-treated groups. In the neuroprotective treatment groups, there was the preservation of myelin thickness around large-caliber axons. Ultrastructural evaluation also confirmed the preservation of organelles including mitochondria and synapses in the two groups that received neuroprotective treatments compared with vehicle controls. Also, forelimb functional evaluation demonstrated that neuroprotective treatments improved functional abilities in the rats. In conclusion, neuroprotective treatments aimed at suppressing degenerative c-Jun and nNOS attenuated apoptosis, provided long-term preservation of motor neurons, their organelles, ventral horn size, and forelimb function.

Dexmedetomidine, selective α2-adrenergic agonist dexmedetomidine, has been widely used clinically for sedation and anesthesia. The role of dexmedetomidine has been an interesting topic of neonatological and anesthetic research since a series of advantages of dexmedetomidine, such as enhancing recovery from surgery, reducing opioid prescription, decreasing sympathetic tone, inhibiting inflammatory reactions, and protecting organs, were reported. Particularly, an increasing number of animal studies have demonstrated that dexmedetomidine ameliorates the neurological outcomes associated with various brain and spinal cord injuries. In addition, a growing number of clinical trials have reported the efficacy of dexmedetomidine for decreasing the rates of postoperative neurological dysfunction, such as delirium and stroke, which strongly highlights the possibility of dexmedetomidine functioning as a neuroprotective agent for future clinical use. Mechanism studies have linked dexmedetomidine's neuroprotective properties with its modulation of neuroinflammation, apoptosis, oxidative stress, and synaptic plasticity via the α2-adrenergic receptor, dependently or independently. By reviewing recent advances and preclinical and clinical evidence on the neuroprotective effects of dexmedetomidine, we hope to provide a complete understanding of the above mechanism and provide insights into the potential efficacy of this agent in clinical use for patients.

Background and Objective: Immediate post-operative structural changes in implanted synthetic meshes are believed to contribute to graft related complications. Our aim was to observe in vivo dimensional changes at the pore level., Method: Two different polyvinylidine fluoride (PVDF) meshes, CICAT and ENDOLAP (Dynamesh, FEG Textiltechnik) were implanted in 18 female Sprague Dawley (n=9/group). The meshes (30×25mm(2)) were overlaid on a full thickness incision (2×1cm(2)) and sutured on the abdominal wall. All animals underwent microCT imaging (res. 35µm/px) at day 1 and 15 postsurgery. A customized procedure was developed to semi-automatically detect the pore centers from the microCT dataset. Horizontal (transverse) and vertical (cranio-caudal) inter-pore distances were then recorded. The overall mesh dimensions were also noted from 3D models generated from in vivo microCT datasets. Inter-pore distances and the overall dimensions from microCT images of the meshes set in agarose gel phantom were used as controls. Mann-Whitney U test was done to check for significant differences., Results: Number of measurable vertical and horizontal inter-pore distances was 56.5(10.5) and 54.5(14.5) [median (IQR)] per animal. At day 1, we observed a 4.3% (CICAT) and 4.6% (ENDOLAP) increase in vertical inter-pore distance when compared to controls (p<0.001, p=0.003, respectively). Measurements fell back to phantom values by day 15 (3.7% and 4.9% decrease compared to day 1, p<0.001 for both). The horizontal inter-pore distances for ENDOLAP increased by 1.4% (p=0.003) during the two weeks period. The overall mesh dimensions did not change significantly day 1 and day 15. The in vivo measurement of the overall mesh dimensions demonstrated a 15.9% reduction in mesh area as compared to that in phantom controls., Conclusion: We report for the first time, in vivo changes in pore dimensions of a textile implant. This study clearly demonstrates the dynamic nature of a textile implant during the tissue integration process. For studied PVDF meshes, the process of tissue integration leads to limited but significant reduction over time as observed at the pore level. Remarkably the extent of this reduction does not account for the change in overall mesh dimensions., (Copyright © 2015 Elsevier Ltd. All rights reserved.)