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Axonal count is the base for efficient nerve transfer; despite its capital importance, few studies have been published on human material, most research approaches being performed on experimental animal models of nerve injury. Thus, standard analysis methods are still lacking. Quantitative data obtained have to be reproducible and comparable with published data by other research groups. To share results with the scientific community, the standardization of quantitative analysis is a fundamental step. For this purpose, the experiences of the Italian, Austrian, German, Greek, and Iberian-Latin American groups have been compared with each other and with the existing literature to reach a consensus in the fiber count and draw up a protocol that can make future studies from different centers comparable. The search for a standardization of the methodology was aimed to reduce all the factors that are associated with an increase in the variability of the results. All the preferential methods to be used have been suggested. On the other hand, alternative methods and different methods have been identified to achieve the same goal, which in our experience are completely comparable; therefore, they can be used indifferently by the different centers according to their experience and availability., Competing Interests: Declaration of Competing Interest The authors report no conflicts of interest to disclose., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Purpose: The main aim of this study was to research new treatments following peripheral nerve injury involving melatonin (Mel), acetyl-l-carnitine (ALCAR), and leptin (Lep) using updated unbiased methods at the stereological and electron microscopic levels., Materials and Methods: Wistar albino rats were randomly divided into nine equal groups; control (Cont), obese control (OG), obese group exposed to sciatic nerve resection (Gap) (OGG), obese group injected intraperitoneally (i.p.) with Mel (OMG), obese group injected with Mel i.p. with gap (OMGG), obese group injected with Lep i.p. (OLG), obese group injected with Lep i.p. with gap (OLGG), obese group injected with ALCAR i.p. (OAG), and obese group injected with ALCAR i.p. with gap (OAGG). Electromyography (EMG) procedures were performed. Following routine histological procedures, stereological analysis was performed for each group., Results: In terms of the number of myelinated axons, high significant increase in OGG was observed compared to OG and Cont (p < 0.01). In addition, a highly significant increase in axon surface area and myelin thickness of OGG compared to OG and Cont (p < 0.01) was noted. A significant decrease in myelin thickness/axon diameter ratio of OGG was found in comparison with the other groups. In terms of latency, there was a highly significant decrease in OGG compared to Cont and OG (p < 0.01). Myelinated axon numbers in OAGG, OMGG and OLGG increased highly significantly compared to other groups (p < 0.01). Latency in OMGG, a highly significant increase, was determined in OMG compared to Cont (p < 0.01). In addition, latency values in OGG were highly significantly greater than in OAC and OAGG (p < 0.01)., Conclusion: In particular, administration of Lep, Mel and ALCAR as neuroprotective agents may make a positive contribution to regeneration and myelination in obese rats., (Copyright © 2017 European Association for Cranio-Maxillo-Facial Surgery. Published by Elsevier Ltd. All rights reserved.)

Background: Neuregulin1 (Nrg1) and its receptors ErbB are crucial for heart development and for adult heart structural maintenance and function and Nrg1 has been proposed for heart failure treatment. Infarct size is the major determinant of heart failure and the mechanism of action and the role of each ErbB receptor remain obscure, especially in the post-ischemic myocardium. We hypothesized that Nrg1 and ErbB are affected at transcriptional level early after ischemia/reperfusion (I/R) injury, and that the protective postconditioning procedure (PostC, brief cycles of ischemia/reperfusion carried out after a sustained ischemia) can influence this pathway., Methods and Results: The Langendorff's heart was used as an ex-vivo model to mimic an I/R injury in the whole rat heart; after 30min of ischemia and 2h of reperfusion, with or without PostC, Nrg1 and ErbB expression were analysed by quantitative real-time PCR and Western blot. While no changes occur for ErbB2, ErbB4 and Nrg1, an increase of ErbB3 expression occurs after I/R injury, with and without PostC. However, I/R reduces ErbB3 protein, whereas PostC preserves it. An in vitro analysis with H9c2 cells exposed to redox-stress indicated that the transient over-expression of ErbB3 alone is able to increase cell survival (MTT assay), limiting mitochondrial dysfunction (JC-1 probe) and apoptotic signals (Bax/Bcl-2 ratio)., Conclusions: This study suggests ErbB3 as a protective factor against death pathways activated by redox stress and supports an involvement of this receptor in the pro-survival responses., (Copyright © 2017 Elsevier B.V. All rights reserved.)