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      Semiquantitative Evaluation of Muscle Repair by Diffusion Tensor Imaging in Mice

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          ABSTRACT

          Muscle injury is one of the most common traumas in orthopedic and sports medicine. However, there are only a few treatment options with marginal clinical benefits for this condition. Muscle repair after injury involves multiple and complex processes, such as the inflammation phase, regeneration phase, and remodeling phase. To develop a treatment modality and to examine the efficacy of novel interventions and agents for patients with muscle injuries, it is essential to establish a reliable and sensitive method to monitor the changes in muscle structure and status during muscle repair. Diffusion‐weighted magnetic resonance imaging has been widely used to assess the diffusivity of water molecules in tissue. When it is used in combination with diffusion tensor imaging (DTI), the microstructure of muscle tissue can be indirectly depicted. In the present study, we evaluated the time‐course changes in the diffusivity and anisotropy in muscles by DTI and histology after injury in mice. We found that the diffusivity and anisotropy exhibit distinct kinetics during muscle repair and that these kinetics were significantly altered in mutant mice with a defect in muscle regeneration. Our data show that muscle repair processes can be readily evaluated and monitored by DTI technique and suggest that DTI can be clinically applied for assessing muscle injury and repair in humans. © 2018 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

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          Most cited references27

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          A hitchhiker's guide to diffusion tensor imaging

          Diffusion Tensor Imaging (DTI) studies are increasingly popular among clinicians and researchers as they provide unique insights into brain network connectivity. However, in order to optimize the use of DTI, several technical and methodological aspects must be factored in. These include decisions on: acquisition protocol, artifact handling, data quality control, reconstruction algorithm, and visualization approaches, and quantitative analysis methodology. Furthermore, the researcher and/or clinician also needs to take into account and decide on the most suited software tool(s) for each stage of the DTI analysis pipeline. Herein, we provide a straightforward hitchhiker's guide, covering all of the workflow's major stages. Ultimately, this guide will help newcomers navigate the most critical roadblocks in the analysis and further encourage the use of DTI.
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            Inducible lineage tracing of Pax7-descendant cells reveals embryonic origin of adult satellite cells.

            We have generated a mouse strain carrying a Cre-ER(T2) knock-in allele at the Pax7 locus, the Pax7(CE) allele (Lepper et al., 2009, Nature 460:627-631). Combining Pax7(CE) and the R26R(LacZ) Cre reporter allele, here we describe temporal-specific tamoxifen (tmx)-inducible lineage tracing of embryonic Pax7-expressing cells. In particular, we focus on the somitic lineage. Tmx-inducible Cre activity directed by the Pax7(CE) allele is similar to the endogenous Pax7 expression pattern. The somitic Pax7-expressing cells selectively marked at embryonic day 9.5 (E9.5) give rise to dorsal dermis and brown adipose tissue, in addition to dorsal aspects of trunk muscles and the diaphragm muscle. However, they do not contribute to ventral body wall and limb muscles. After E12.5, marked Pax7-expressing cells become lineage restricted to muscles. Descendants of these early marked Pax7-expressing cells begin to occupy sublaminal positions associated with the myofibers around E16.5, characteristic of embryonic satellite cells. Furthermore, they contribute to adult myofibers and regeneration competent satellite cells in the tibialis anterior muscle, providing evidence that some adult satellite cells are of embryonic origin. (c) 2010 Wiley-Liss, Inc.
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              Ectodomain shedding and ADAMs in development.

              Proteolytic enzymes belonging to the A Disintegin And Metalloproteinase (ADAM) family are able to cleave transmembrane proteins close to the cell surface, in a process referred to as ectodomain shedding. Substrates for ADAMs include growth factors, cytokines, chemokines and adhesion molecules, and, as such, many ADAM proteins play crucial roles in cell-cell adhesion, extracellular and intracellular signaling, cell differentiation and cell proliferation. In this Review, we summarize the fascinating roles of ADAMs in embryonic and adult tissue development in both vertebrates and invertebrates.
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                Author and article information

                Contributors
                keisukehoriuchi@gmail.com
                Journal
                JBMR Plus
                JBMR Plus
                10.1002/(ISSN)2473-4039
                JBM4
                JBMR Plus
                John Wiley and Sons Inc. (Hoboken )
                2473-4039
                05 March 2018
                July 2018
                : 2
                : 4 ( doiID: 10.1002/jbm4.v2.4 )
                : 227-234
                Affiliations
                [ 1 ] Department of Physiology Keio University School of Medicine Tokyo Japan
                [ 2 ] Central Institute for Experimental Animals Kanagawa Japan
                [ 3 ] Department of Orthopedic Surgery Keio University School of Medicine Tokyo Japan
                [ 4 ] Department of Orthopedics Tokyo Dental College Ichikawa General Hospital Ichikawa City Chiba Japan
                [ 5 ] Department of Radiological Sciences Tokyo Metropolitan University Tokyo Japan
                [ 6 ] Department of Pathology Keio University School of Medicine Tokyo Japan
                [ 7 ] Department of Orthopedic Surgery National Defense Medical College Saitama Japan
                Author notes
                [*] [* ] Address correspondence to: Keisuke Horiuchi, PhD, MD, Department of Orthopedic Surgery, National Defense Medical College, Namiki 3‐2, Tokorozawa, Saitama 359‐8513, Japan. E‐mail: keisukehoriuchi@ 123456gmail.com

                [†]

                JH and SM contributed equally to this work.

                Article
                JBM410040
                10.1002/jbm4.10040
                6124170
                69904206-49b2-4b32-9cbd-7d61db3c5ef7
                © 2018 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 18 October 2017
                : 24 January 2018
                : 04 February 2018
                Page count
                Figures: 5, Tables: 0, Pages: 8, Words: 4414
                Categories
                Original Article
                Original Articles
                Custom metadata
                2.0
                jbm410040
                July 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.4.7.1 mode:remove_FC converted:05.09.2018

                magnetic resonance imaging,diffusion tensor imaging,muscle injury,muscle repair,adam10

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