Nerve repair is usually accomplished by direct suture when the two stumps can be approximated without tension. In the presence of a nerve defect, the placement of an autologous nerve graft is the current gold standard for nerve restoration. However, over the last 20 years, an increasing number of research articles reported on the use of non-nervous tubes (tubulization) for repairing nerve defects. The clinical employment of tubes (both biological and synthetic) as an alternative to autogenous nerve grafts is mainly justified by the limited availability of donor tissue for nerve autografts and the related morbidity. In addition, tubulization was proposed as an alternative to direct nerve sutures in order to create optimal conditions for nerve regeneration over the short empty space intentionally left between two nerve stumps. This paper outlines recent important advances in this field. Different tubulization techniques proposed so far are described, focusing in particular on studies that reported on the employment of tubes with patients. Our personal clinical experience on tubulization repair of sensory nerve lesions (digital nerves), using both biological and synthetic tubes, is presented, and the clinical results are compared. In our case series, both types of tubes led to good clinical results. Finally, we speculate about the prospects in the clinical application of tubulization for peripheral nerve repair.

Cachexia is a wasting syndrome associated with cancer, AIDS, multiple sclerosis, and several other disease states. It is characterized by weight loss, fatigue, loss of appetite, and skeletal muscle atrophy and is associated with poor patient prognosis, making it an important treatment target. Ghrelin is a peptide hormone that stimulates growth hormone (GH) release and positive energy balance through binding to the receptor GHSR-1a. Only acylated ghrelin (AG), but not the unacylated form (UnAG), can bind GHSR-1a; however, UnAG and AG share several GHSR-1a-independent biological activities. Here we investigated whether UnAG and AG could protect against skeletal muscle atrophy in a GHSR-1a-independent manner. We found that both AG and UnAG inhibited dexamethasone-induced skeletal muscle atrophy and atrogene expression through PI3Kβ-, mTORC2-, and p38-mediated pathways in myotubes. Upregulation of circulating UnAG in mice impaired skeletal muscle atrophy induced by either fasting or denervation without stimulating muscle hypertrophy and GHSR-1a-mediated activation of the GH/IGF-1 axis. In Ghsr-deficient mice, both AG and UnAG induced phosphorylation of Akt in skeletal muscle and impaired fasting-induced atrophy. These results demonstrate that AG and UnAG act on a common, unidentified receptor to block skeletal muscle atrophy in a GH-independent manner.

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