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      The fate of neurons after traumatic spinal cord injury in rats: A systematic review

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          To reach an evidence-based knowledge in the context of the temporal-spatial pattern of neuronal death and find appropriate time of intervention in order to preserve spared neurons and promote regeneration after traumatic spinal cord injury (TSCI).

          Materials and Methods:

          The study design was based on Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA)-guided systematic review. PubMed and EMBASE were searched (24 October, 2015) with no temporal or linguistic restrictions. Hand-search was performed in the bibliographies of relevant articles. Non-interventional animal studies evaluating time-dependent neuronal death following acute mechanical trauma to the spinal cord were included. We separately evaluated the fate of various populations of neurons including propriospinal neurons, ventral motor neurons, Clarke’s column neurons, and supraspinal neurons.


          We found 11,557 non-duplicated studies. Screening through the titles and abstracts led to 549 articles, 49 of which met the inclusion criteria. Both necrotic and apoptotic neuronal deaths occur after TSCI, though necrosis is the prominent mechanism. There are differences in the responses of intrinsic neurons of the spinal cord to the TSCI. Also, the extent of neuronal death in the supraspinal neurons depends on the anatomical location of their axons.


          In order to develop new therapies, selection of the injury model and time of intervention has a crucial role in the efficacy of therapy. In addition, examining the safety and efficacy of an intervention by reliable methods not confounded by the injury-related changes would promote translation of therapies to the clinical application.

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          Most cited references 66

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          Status of implementation of Framework Convention on Tobacco Control (FCTC) in Ghana: a qualitative study

          Background The Framework Convention on Tobacco Control (FCTC), a World Health Organization treaty, has now been ratified by over 165 countries. However there are concerns that implementing the Articles of the treaty may prove difficult, particularly in the developing world. In this study we have used qualitative methods to explore the extent to which the FCTC has been implemented in Ghana, a developing country that was 39th to ratify the FCTC, and identify barriers to effective FCTC implementation in low income countries. Methods Semi-structured interviews with 20 members of the national steering committee for tobacco control in Ghana, the official multi-disciplinary team with responsibility for tobacco control advocacy and policy formulation, were conducted. The Framework method for analysis and NVivo software were used to identify key issues relating to the awareness of the FCTC and the key challenges and achievements in Ghana to date. Results Interviewees had good knowledge of the content of the FCTC, and reported that although Ghana had no explicitly written policy on tobacco control, the Ministry of Health had issued several tobacco control directives before and since ratification. A national tobacco control bill has been drafted but has not been implemented. Challenges identified included the absence of a legal framework for implementing the FCTC, and a lack of adequate resources and prioritisation of tobacco control efforts, leading to slow implementation of the treaty. Conclusion Whilst Ghana has ratified the FCTC, there is an urgent need for action to pass a national tobacco control bill into law to enable it to implement the treaty, sustain tobacco control efforts and prevent Ghana's further involvement in the global tobacco epidemic.
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            Neuronal and glial apoptosis after traumatic spinal cord injury.

            Cell death was examined by studying the spinal cords of rats subjected to traumatic insults of mild to moderate severity. Within minutes after mild weight drop impact (a 10 gm weight falling 6.25 mm), neurons in the immediate impact area showed a loss of cytoplasmic Nissl substances. Over the next 7 d, this lesion area expanded and cavitated. Terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL)-positive neurons were noted primarily restricted to the gross lesion area 4-24 hr after injury, with a maximum presence at 8 hr after injury. TUNEL-positive glia were present at all stages studied between 4 hr and 14 d, with a maximum presence within the lesion area 24 hr after injury. However 7 d after injury, a second wave of TUNEL-positive glial cells was noted in the white matter peripheral to the lesion and extending at least several millimeters away from the lesion center. The suggestion of apoptosis was supported by electron microscopy, as well as by nuclear staining with Hoechst 33342 dye, and by examination of DNA prepared from the lesion site. Furthermore, repeated intraperitoneal injections of cycloheximide, beginning immediately after a 12.5 mm weight drop insult, produced a substantial reduction in histological evidence of cord damage and in motor dysfunction assessed 4 weeks later. Present data support the hypothesis that apoptosis dependent on active protein synthesis contributes to the neuronal and glial cell death, as well as to the neurological dysfunction, induced by mild-to-moderate severity traumatic insults to the rat spinal cord.
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              Activation of the caspase-3 apoptotic cascade in traumatic spinal cord injury.

              Traumatic spinal cord injury often results in complete loss of voluntary motor and sensory function below the site of injury. The long-term neurological deficits after spinal cord trauma may be due in part to widespread apoptosis of neurons and oligodendroglia in regions distant from and relatively unaffected by the initial injury. The caspase family of cysteine proteases regulates the execution of the mammalian apoptotic cell death program. Caspase-3 cleaves several essential downstream substrates involved in the expression of the apoptotic phenotype in vitro, including gelsolin, PAK2, fodrin, nuclear lamins and the inhibitory subunit of DNA fragmentation factor. Caspase-3 activation in vitro can be triggered by upstream events, leading to the release of cytochrome c from the mitochondria and the subsequent transactivation of procaspase-9 by Apaf-1. We report here that these upstream and downstream components of the caspase-3 apoptotic pathway are activated after traumatic spinal cord injury in rats, and occur early in neurons in the injury site and hours to days later in oligodendroglia adjacent to and distant from the injury site. Given these findings, targeting the upstream events of the caspase-3 cascade has therapeutic potential in the treatment of acute traumatic injury to the spinal cord.

                Author and article information

                Iran J Basic Med Sci
                Iran J Basic Med Sci
                Iranian Journal of Basic Medical Sciences
                Mashhad University of Medical Sciences (Iran )
                June 2018
                : 21
                : 6
                : 546-557
                [1 ]Pediatric Urology and Regenerative Medicine Research Center, Children’s Hospital Medical Center, Tehran University of Medical Sciences, Tehran, Iran
                [2 ]Sina Trauma and Surgery Research Center, Tehran University of Medical Sciences, Tehran, Iran
                [3 ]Department of Chemical and Biomolecular Engineering, University of Melbourne, Victoria 3010, Australia
                [4 ]Brain and Mind Center, University of Sydney, 94 Mallett St, Camperdown NSW 2050, Australia
                [5 ]Cochrane Schizophrenia Group, Institute of Mental Health, University of Nottingham, Nottingham, UK
                [6 ]Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, 635 Charles Young Drive, CA 90095, USA
                Author notes
                [* ] Corresponding author: Vafa Rahimi-Movaghar. Sina Trauma and Surgery Research Center, Tehran University of Medical Sciences, Tehran, Iran. Tel/Fax: +98-216 6757003; Email: v_rahimi@
                Copyright: © Iranian Journal of Basic Medical Sciences

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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