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Special Issue "Injury and Repair in the Nervous System"

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: closed (31 December 2017)

Special Issue Editor

Guest Editor
Prof. Dr. Tetsuro Tamaki

Muscle Physiology & Cell Biology Unit, Department of Human Structure and Function, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 2591193, Japan
Website | E-Mail
Interests: nerve-muscle physiology and cell biology; regenerative medicine (nerve-muscle-vascular system); stem cell biology

Special Issue Information

Dear Colleagues,

Severe injury to the nervous system is mostly irreparable to the living body, leading to permanent loss of related motor and sensory functions. Regeneration and/or repair of the nervous system is a process, which undergoes regrowth or renewal of damaged nervous tissue, whereas the process differs between the peripheral nervous system (PNS) and central nervous system (CNS). However, both processes should be including the regeneration of axons, synapses, neurons and glial/Schwann cells, and perineurium/endoneurium, as well as vascular system, which play a role for oxygen/nutrition supply and exclusion of wastes.

Prof. Dr. Tetsuro Tamaki
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • spinal cord injury
  • peripheral nerve injury
  • neuroregeneration
  • neurotrophic and neurotropic factors
  • nerve regeneration
  • neural tissue engineering
  • nerve guidance conduit
  • neural stem cells
  • autograft
  • allograft
  • axonal growth
  • myelin formation
  • Schwann cells
  • glial cells
  • neuron

Published Papers (5 papers)

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Research

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Open AccessArticle
Voluntary Exercise Positively Affects the Recovery of Long-Nerve Gap Injury Following Tube-Bridging with Human Skeletal Muscle-Derived Stem Cell Transplantation
J. Clin. Med. 2018, 7(4), 67; https://doi.org/10.3390/jcm7040067
Received: 5 March 2018 / Revised: 22 March 2018 / Accepted: 26 March 2018 / Published: 2 April 2018
Cited by 3 | PDF Full-text (4492 KB) | HTML Full-text | XML Full-text
Abstract
The therapeutic effects of voluntary exercise on the recovery of long-gap nerve injury following the bridging of an acellular conduit filled with human skeletal muscle-derived stem cells (Sk-SCs) have been described. Human Sk-SCs were sorted as CD34+/45 (Sk-34) cells, then [...] Read more.
The therapeutic effects of voluntary exercise on the recovery of long-gap nerve injury following the bridging of an acellular conduit filled with human skeletal muscle-derived stem cells (Sk-SCs) have been described. Human Sk-SCs were sorted as CD34+/45 (Sk-34) cells, then cultured/expanded under optimal conditions for 2 weeks. Surgery to generate a long-gap sciatic nerve injury was performed in athymic nude mice, after which the mice were divided into exercise (E) and non-exercise (NE) groups. The mice were housed in standard individual cages, and voluntary exercise wheels were introduced to the cages of the E group one week after surgery. After 8 weeks, the human Sk-34 cells were actively engrafted, and showed differentiation into Schwann cells and perineurial cells, in both groups. The recovery in the number of axons and myelin in the conduit and downstream tibial nerve branches, and the lower hindlimb muscle mass and their tension output, was consistently higher by 15–25% in the E group. Moreover, a significantly higher innervation ratio of muscle spindles, reduced pathological muscle fiber area, and acceleration of blood vessel formation in the conduit were each observed in the E group. These results showed that the combined therapy of tube-bridging, Sk-34 cell transplantation, and voluntary exercise is a potentially practical approach for recovery following long-gap nerve injury. Full article
(This article belongs to the Special Issue Injury and Repair in the Nervous System)
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Open AccessArticle
Amiloride Promotes Oligodendrocyte Survival and Remyelination after Spinal Cord Injury in Rats
J. Clin. Med. 2018, 7(3), 46; https://doi.org/10.3390/jcm7030046
Received: 29 December 2017 / Revised: 22 February 2018 / Accepted: 2 March 2018 / Published: 5 March 2018
Cited by 4 | PDF Full-text (6030 KB) | HTML Full-text | XML Full-text
Abstract
After spinal cord injury (SCI), secondary injury results in an expanding area of glial cell apoptosis. Oligodendrocyte precursor cells (OPCs) actively proliferate after SCI, but many of these cells undergo apoptosis. One of the factors that exacerbates secondary injury is endoplasmic reticulum (ER) [...] Read more.
After spinal cord injury (SCI), secondary injury results in an expanding area of glial cell apoptosis. Oligodendrocyte precursor cells (OPCs) actively proliferate after SCI, but many of these cells undergo apoptosis. One of the factors that exacerbates secondary injury is endoplasmic reticulum (ER) stress. In this study, we tested the effects of amiloride treatment on the fate of OPCs during secondary injury in rats. Amiloride is an FDA-approved diuretic for treating hypertension, which in rats enhances ER stress response and suppresses the apoptosis of glial cells after SCI. A severe contusive SCI was induced in Sprague-Dawley rats using an infinite horizon (IH)-impactor (200 kdyne). Beginning 24 h after SCI, 10 mg/kg of amiloride or phosphate buffered saline (PBS) was intraperitoneally administered daily for a period of 14 days. At 7, 14, 28, and 56 days after SCI, animals were subsequently euthanized in order to analyze the injured spinal cord. We labeled proliferating OPCs and demonstrated that amiloride treatment led to greater numbers of OPCs and oligodendrocytes in the injured spinal cord. Increased myelin basic protein (MBP) expression levels were observed, suggesting that increased numbers of mature oligodendrocytes led to improved remyelination, significantly improving motor function recovery. Full article
(This article belongs to the Special Issue Injury and Repair in the Nervous System)
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Review

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Open AccessReview
Traumatic Brain Injury: At the Crossroads of Neuropathology and Common Metabolic Endocrinopathies
J. Clin. Med. 2018, 7(3), 59; https://doi.org/10.3390/jcm7030059
Received: 11 February 2018 / Revised: 10 March 2018 / Accepted: 12 March 2018 / Published: 14 March 2018
Cited by 1 | PDF Full-text (876 KB) | HTML Full-text | XML Full-text
Abstract
Building on the seminal work by Geoffrey Harris in the 1970s, the neuroendocrinology field, having undergone spectacular growth, has endeavored to understand the mechanisms of hormonal connectivity between the brain and the rest of the body. Given the fundamental role of the brain [...] Read more.
Building on the seminal work by Geoffrey Harris in the 1970s, the neuroendocrinology field, having undergone spectacular growth, has endeavored to understand the mechanisms of hormonal connectivity between the brain and the rest of the body. Given the fundamental role of the brain in the orchestration of endocrine processes through interactions among neurohormones, it is thus not surprising that the structural and/or functional alterations following traumatic brain injury (TBI) can lead to endocrine changes affecting the whole organism. Taking into account that systemic hormones also act on the brain, modifying its structure and biochemistry, and can acutely and chronically affect several neurophysiological endpoints, the question is to what extent preexisting endocrine dysfunction may set the stage for an adverse outcome after TBI. In this review, we provide an overview of some aspects of three common metabolic endocrinopathies, e.g., diabetes mellitus, obesity, and thyroid dysfunction, and how these could be triggered by TBI. In addition, we discuss how the complex endocrine networks are woven into the responses to sudden changes after TBI, as well as some of the potential mechanisms that, separately or synergistically, can influence outcomes after TBI. Full article
(This article belongs to the Special Issue Injury and Repair in the Nervous System)
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Open AccessReview
Alternative Erythropoietin Receptors in the Nervous System
J. Clin. Med. 2018, 7(2), 24; https://doi.org/10.3390/jcm7020024
Received: 2 January 2018 / Revised: 24 January 2018 / Accepted: 26 January 2018 / Published: 2 February 2018
Cited by 5 | PDF Full-text (1854 KB) | HTML Full-text | XML Full-text
Abstract
In addition to its regulatory function in the formation of red blood cells (erythropoiesis) in vertebrates, Erythropoietin (Epo) contributes to beneficial functions in a variety of non-hematopoietic tissues including the nervous system. Epo protects cells from apoptosis, reduces inflammatory responses and supports re-establishment [...] Read more.
In addition to its regulatory function in the formation of red blood cells (erythropoiesis) in vertebrates, Erythropoietin (Epo) contributes to beneficial functions in a variety of non-hematopoietic tissues including the nervous system. Epo protects cells from apoptosis, reduces inflammatory responses and supports re-establishment of compromised functions by stimulating proliferation, migration and differentiation to compensate for lost or injured cells. Similar neuroprotective and regenerative functions of Epo have been described in the nervous systems of both vertebrates and invertebrates, indicating that tissue-protective Epo-like signaling has evolved prior to its erythropoietic function in the vertebrate lineage. Epo mediates its erythropoietic function through a homodimeric Epo receptor (EpoR) that is also widely expressed in the nervous system. However, identification of neuroprotective but non-erythropoietic Epo splice variants and Epo derivatives indicated the existence of other types of Epo receptors. In this review, we summarize evidence for potential Epo receptors that might mediate Epo’s tissue-protective function in non-hematopoietic tissue, with focus on the nervous system. In particular, besides EpoR, we discuss three other potential neuroprotective Epo receptors: (1) a heteroreceptor consisting of EpoR and common beta receptor (βcR), (2) the Ephrin (Eph) B4 receptor and (3) the human orphan cytokine receptor-like factor 3 (CRLF3). Full article
(This article belongs to the Special Issue Injury and Repair in the Nervous System)

Other

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Open AccessCase Report
Intraneural Platelet-Rich Plasma Injections for the Treatment of Radial Nerve Section: A Case Report
J. Clin. Med. 2018, 7(2), 13; https://doi.org/10.3390/jcm7020013
Received: 5 December 2017 / Revised: 9 January 2018 / Accepted: 16 January 2018 / Published: 29 January 2018
Cited by 1 | PDF Full-text (1188 KB) | HTML Full-text | XML Full-text
Abstract
The radial nerve is the most frequently injured nerve in the upper extremity. Numerous options in treatment have been described for radial nerve injury, such as neurolysis, nerve grafts, or tendon transfers. Currently, new treatment options are arising, such as platelet-rich plasma (PRP), [...] Read more.
The radial nerve is the most frequently injured nerve in the upper extremity. Numerous options in treatment have been described for radial nerve injury, such as neurolysis, nerve grafts, or tendon transfers. Currently, new treatment options are arising, such as platelet-rich plasma (PRP), an autologous product with proved therapeutic effect for various musculoskeletal disorders. We hypothesized that this treatment is a promising alternative for this type of nerve pathology. The patient was a healthy 27-year-old man who suffered a deep and long cut in the distal anterolateral region of the right arm. Forty-eight hours after injury, an end-to-end suture was performed without a microscope. Three months after the surgery, an electromyogram (EMG) showed right radial nerve neurotmesis with no tendency to reinnervation. Four months after the trauma, serial intraneural infiltrations of PRP were conducted using ultrasound guidance. The therapeutic effect was assessed by manual muscle testing and by EMG. Fourteen months after the injury and 11 months after the first PRP injection, functional recovery was achieved. The EMG showed a complete reinnervation of the musculature of the radial nerve dependent. The patient remains satisfied with the result and he is able to practice his profession. Conclusions: PRP infiltrations have the potential to enhance the healing process of radial nerve palsy. This case report demonstrates the therapeutic potential of this technology for traumatic peripheral nerve palsy, as well as the apt utility of US-guided PRP injections. Full article
(This article belongs to the Special Issue Injury and Repair in the Nervous System)
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J. Clin. Med. EISSN 2077-0383 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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