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      An Orthopedic-, Surgical-, and Epidemiological-Based Investigation of Leprosy, in the Tamil Nadu State of India

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          Abstract

          No other research paper has ever been written about leprosy in this manner. The orthopedic and surgical implications, as well as the functional debility caused by the disease, have not been previously explained by past research as they have in such a comprehensive manner in this paper. The results of this study have regional and global implications as they pertain to disease pathology, risk factor recognition/disease prevention, and treatment. This paper is a unique, in that it also serves as a combination of a review of the current medical literature, as well as an epidemiological survey of the disease in a region of the world which has never been researched in the past. Clinical data points to the possibility of a new strain of the disease. This information is of significance because it effects prevention and improved treatment of the disease, which leads to devastating sequela. This was a cross-sectional study involving subjects diagnosed with leprosy in the Chengalpet region of the Kancheepuram District, of the Tamil Nadu state of India. The study was performed at the Tamil Nadu Medical College Teaching Hospital and Research Center. This study included various physical examinations, observation and survey of lesions, questionnaires in regard the debilitating orthopedic and medical effects of the disease, as well as treatment options.

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          The Role of Neurotrophins in the Regulation of Myelin Development

          Junhua Xiao, Trevor J. Kilpatrick, Simon Murray (2009)
          Neurotrophins comprise a family of growth factors that are expressed in a variety of cell types, and which exert influences on a large range of cellular activities that are important for development and the maintenance of the nervous system, as well as in neurodegenerative and psychiatric disorders. More recently, neurotrophins have been implicated in influencing the dynamic and complex signals that occur between neurons and glial cells, including Schwann cells in the peripheral nervous system and oligodendrocytes in the central nervous system that regulate myelination. Here we review the recent studies that identify neurotrophins as important regulators of both peripheral and central myelination, highlight some of the many questions that remain to be answered, and identify possibilities for further research.
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            Neuron-glia signaling and the protection of axon function by Schwann cells.

            Klaus-Armin Nave, Susanne Quintes, Sandra Goebbels … (2010)
            The interaction between neurons and glial cells is a feature of all higher nervous systems. In the vertebrate peripheral nervous system, Schwann cells ensheath and myelinate axons thereby allowing rapid saltatory conduction and ensuring axonal integrity. Recently, some of the key molecules in neuron-Schwann cell signaling have been identified. Neuregulin-1 (NRG1) type III presented on the axonal surface determines the myelination fate of axons and controls myelin sheath thickness. Recent observations suggest that NRG1 regulates myelination via the control of Schwann cell cholesterol biosynthesis. This concept is supported by the finding that high cholesterol levels in Schwann cells are a rate-limiting factor for myelin protein production and transport of the major myelin protein P0 from the endoplasmic reticulum into the growing myelin sheath. NRG1 type III activates ErbB receptors on the Schwann cell, which leads to an increase in intracellular PIP3 levels via the PI3-kinase pathway. Surprisingly, enforced elevation of PIP3 levels by inactivation of the phosphatase PTEN in developing and mature Schwann cells does not entirely mimic NRG1 type III stimulated myelin growth, but predominantly causes focal hypermyelination starting at Schmidt-Lanterman incisures and nodes of Ranvier. This indicates that the glial transduction of pro-myelinating signals has to be under tight and life-long control to preserve integrity of the myelinated axon. Understanding the cross talk between neurons and Schwann cells will help to further define the role of glia in preserving axonal integrity and to develop therapeutic strategies for peripheral neuropathies such as CMT1A.
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              Mycobacterium leprae infection of human Schwann cells depends on selective host kinases and pathogen-modulated endocytic pathways.

              Jon Holy, Laís Carvalho Luma Bezerra, Lucineia Alves … (2004)
              Mycobacterium leprae, an obligate intracellular pathogen, shows a unique tropism for Schwann cells (SC). This leads to the peripheral neuropathy disorder observed in leprosy. In this study, we investigated signal transduction events and the intracellular fate of M. leprae during the interaction of the microorganism with SC. First, we demonstrated that the human schwannoma cell line ST88-14 readily phagocytized the bacteria as observed by time-lapse microscopy, actin staining and electron microscopy. The effect of specific kinase inhibitors on M. leprae internalization was then investigated showing that functional protein tyrosine kinase, calcium-dependent protein kinase and phosphatidylinositol 3-kinase, but not cAMP-dependent protein kinase are essential for phagocytosis of the bacteria. Similar results were obtained when irradiated and live bacteria were compared and when M. leprae was pre-coated with recombinant histone-like-protein/laminin binding protein, a bacterial adhesin. In addition, experiments were performed to analyze the bacterial trafficking within the endosomal network by labeling the acidified intracellular compartments of M. leprae-infected SC with the Lysotracker acidotrophic probe. Acidification of vesicles containing live M. leprae was minimal in both RAW murine macrophages and SC, although phagosomes containing heat-killed bacteria seem to follow normal endocytic maturation. These data indicate that the invading bacteria interfere with normal endocytic pathway maturation of bacteria-containing phagosomes within SC.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Adv Orthop
                Journal ID (iso-abbrev): Adv Orthop
                Journal ID (publisher-id): AOP
                Title: Advances in Orthopedics
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-3464
                ISSN (Electronic): 2090-3472
                Publication date (Print): 2012
                Publication date (Electronic): 17 May 2012
                Volume: 2012
                Electronic Location Identifier: 783853
                Affiliations
                1College of Osteopathic Medicine, Michigan State University, East Lansing, MI 48824, USA
                2College of Human Medicine, Michigan State University, East Lansing, MI 48824, USA
                3Oakland University, Rochester, MI 48309, USA
                4Department of Community Medicine, SRM Medical College, SRM University, Tamil Nadu, Kattankulathur 603 203, India
                5Michigan State University, Institute of International Health (MSU-IIH), B-319 West Fee Hall, East Lansing, MI 48824, USA
                Author notes

                Academic Editor: Masato Takao

                Article
                DOI: 10.1155/2012/783853
                PMC ID: 3362809
                PubMed ID: 22666605
                SO-VID: a1648de0-03c6-4370-9069-a9c44b8331bd
                Copyright © Copyright © 2012 Jason Samona et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 27 December 2011
                Date revision received : 23 February 2012
                Date accepted : 24 February 2012
                Categories
                Subject: Clinical Study

                ScienceOpen disciplines: Orthopedics
                Data availability:
                ScienceOpen disciplines: Orthopedics

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