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Tissues and organs have, although sometimes limited, the capacity for endogenous repair, which is aimed to re-establish integrity and homeostasis. Tissue repair involves pro- and anti-inflammatory processes, new tissue formation and remodelling. Depending on the local microenvironment, tissue repair results either in scar tissue formation or in regeneration. The latter aims to recapitulate the original tissue structure and architecture with the proper functionality. Although some organisms (such as planarians) have a high regenerative capacity throughout the body, in humans this property is more restricted to a few organs and tissues. Regeneration in the adult is possible in particular through the existence of tissue-resident pools of stem/progenitor cells. In response to tissue damage, these cells are activated, they proliferate and migrate, and differentiate into mature cells. Angiogenesis and neovascularization play a crucial role in tissue repair. Besides providing with oxygen and nutrients, angiogenesis generates a vascular niche (VN) consisting of different blood-derived elements and endothelial cells surrounded by basement membrane as well as perivascular cells. The newly generated VN communicates with the local stem/progenitor cells and contributes to tissue repair. For example, platelets, macrophages, neutrophils, perivascular cells and other VN components actively participate in the repair of skin, bone, muscle, tendon, brain, spinal cord, etc. Despite these observations, the exact role of the VN in tissue repair and the underlying mechanisms are still unclear and are awaiting further evidence that, indeed, will be required for the development of regenerative therapies for the treatment of traumatic injuries as well as degenerative diseases.

Angiogenesis --- Platelets and Platelets Lysate --- Blood Vessels and Endothelial Cells --- Granulocyte Colony Stimulating Factor (G-CSF) --- Pericytes --- Stem and Progenitor Cells --- Vascular Niche --- Tissue Repair and Regeneration --- Angiogenesis --- Platelets and Platelets Lysate --- Blood Vessels and Endothelial Cells --- Granulocyte Colony Stimulating Factor (G-CSF) --- Pericytes --- Stem and Progenitor Cells --- Vascular Niche --- Tissue Repair and Regeneration

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Interleukin-6. --- B cell differentiation factor-2 --- B cell stimulation factor-2 --- Hepatocyte-stimulating factor --- Hybridoma growth factor --- IL-6 (Biomolecule) --- MGI-2 (Biomolecule) --- Myeloid differentiation-inducing protein --- Myeloid growth inducer-2 --- Plasmacytoma growth factor --- Interleukins

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Interleukin-6 --- Cancer --- Neoplasms --- Cancers --- Carcinoma --- Malignancy (Cancer) --- Malignant tumors --- Tumors --- B cell differentiation factor-2 --- B cell stimulation factor-2 --- Hepatocyte-stimulating factor --- Hybridoma growth factor --- IL-6 (Biomolecule) --- MGI-2 (Biomolecule) --- Myeloid differentiation-inducing protein --- Myeloid growth inducer-2 --- Plasmacytoma growth factor --- Interleukins --- Pathophysiology --- Therapeutic use --- Evaluation --- Immunotherapy --- pharmacology. --- therapeutic use. --- drug therapy. --- Congresses --- Conferences - Meetings --- Immunotherapy&delete& --- Evaluation&delete& --- Pathophysiology&delete& --- Therapeutic use&delete& --- pharmacology --- therapeutic use --- drug therapy

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Multiple sclerosis (MS) is one of the most common neurological disorders in young adults. The etiology of MS is not known, but it is generally accepted that it is autoimmune in nature. Our knowledge of the pathogenesis of MS has increased tremendously in the past decade through clinical studies and the use of experimental autoimmune encephalomyelitis (EAE), a model that has been widely used for MS research. Major advances in the field, such as understanding the roles of pathogenic Th17 cells, myeloid cells, and B cells in MS/EAE, as well as cytokine and chemokine signaling that controls neuroinflammation, have led to the development of potential and clinically approved disease-modifying agents (DMAs). There are many aspects related to the initiation, relapse and remission, and progression of MS that are yet to be elucidated. For instance, what are the genetic and environmental risk factors that promote the initiation of MS, and how do these factors impact the immune system? What factors drive the progression of MS, and what are the roles of peripheral immune cells in disease progression? How do the CNS-infiltrated immune cells interact with the CNS-resident glial cells when the disease progresses? What is the role of microbiome in MS? Can we develop animal models that better represent subcategories of MS? Understanding the cellular and molecular mechanisms that govern the pathogenesis of MS will help to develop novel and more specific therapeutic strategies that will ultimately improve clinical outcomes of the treatments. This Special Issue of Cells has published original research articles, a retrospective clinical report, and review articles that investigate the cellular and molecular basis of MS.

Medicine --- neutrophils --- lymphocytes --- NLR --- multiple sclerosis --- disease activity --- inside-out --- outside-in --- oligodendrocytosis --- demyelination --- gliosis --- histology --- top-down proteomics --- bioinformatics --- mitochondria --- CD4+ T cells --- memory T cells --- autoimmune disease --- effector memory T cell --- central memory T cell --- tissue-resident T cell --- experimental autoimmune encephalomyelitis --- monocytes --- granulocyte-macrophage colony-stimulating factor --- S100B --- relapsing-remitting experimental autoimmune encephalomyelitis --- pentamidine --- NG2-glia --- progenitors --- lineage --- in utero electroporation --- morphometric analyses --- clonal analyses --- lesioned brain --- sphingosine-1-phosphate receptors --- glutamate synaptic dysfunction --- microglia --- T lymphocytes --- experimental autoimmune encephalomyelitis (EAE) --- pro-inflammatory cytokines --- neuroinflammation --- ozanimod --- AUY954 --- A971432 --- S1P1 --- S1P5 --- kynurenine pathway --- kynurenic acid --- oxidative stress --- quinolinic acid --- N-acetylserotonin --- IDO --- NAD+, multiple sclerosis --- laquinimod --- neutrophils --- lymphocytes --- NLR --- multiple sclerosis --- disease activity --- inside-out --- outside-in --- oligodendrocytosis --- demyelination --- gliosis --- histology --- top-down proteomics --- bioinformatics --- mitochondria --- CD4+ T cells --- memory T cells --- autoimmune disease --- effector memory T cell --- central memory T cell --- tissue-resident T cell --- experimental autoimmune encephalomyelitis --- monocytes --- granulocyte-macrophage colony-stimulating factor --- S100B --- relapsing-remitting experimental autoimmune encephalomyelitis --- pentamidine --- NG2-glia --- progenitors --- lineage --- in utero electroporation --- morphometric analyses --- clonal analyses --- lesioned brain --- sphingosine-1-phosphate receptors --- glutamate synaptic dysfunction --- microglia --- T lymphocytes --- experimental autoimmune encephalomyelitis (EAE) --- pro-inflammatory cytokines --- neuroinflammation --- ozanimod --- AUY954 --- A971432 --- S1P1 --- S1P5 --- kynurenine pathway --- kynurenic acid --- oxidative stress --- quinolinic acid --- N-acetylserotonin --- IDO --- NAD+, multiple sclerosis --- laquinimod

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Cellular Responses to Stress brings together a group of scientists who work on different but interrelated aspects of cellular stress responses. The book provides state-of-the-art information on the wide spectrum of ways in which cells can respond to different forms of stress induced by chemicals, oxidants, and DNA-damaging agents. Mechanisms are described that involve altered uptake and efflux of chemical agents, intracellular detoxification, and DNA damage responses. Many of these changes trigger a cascade of reactions mediated by stress-activated signaling pathways, which have the capacity to determine whether a cell will survive or die. The spectrum of topics covered in this book aims to provide a broad overview of our current knowledge of the different forms of adaptive response systems.It is hoped that this text will stimulate further research to establish the relative cellular role of specific response pathways and will enable us to gain a deeper understanding of the mechanisms that allow cells to live or die. This book will be valued by university researchers at all levels, industrial scientists in the pharmaceutical and biotechnology industries, and clinical researchers.Originally published in 1999.The Princeton Legacy Library uses the latest print-on-demand technology to again make available previously out-of-print books from the distinguished backlist of Princeton University Press. These editions preserve the original texts of these important books while presenting them in durable paperback and hardcover editions. The goal of the Princeton Legacy Library is to vastly increase access to the rich scholarly heritage found in the thousands of books published by Princeton University Press since its founding in 1905.

Stress (Physiology) --- Cell metabolism --- Cellular control mechanisms --- Cells --- Metabolism --- Regulation --- AMPK. --- ASK1. --- Actin. --- Activation. --- Angiogenesis. --- Antibody. --- Antigen. --- Apoptosis. --- Autoimmunity. --- Autophosphorylation. --- C-Fos. --- C-Jun N-terminal kinases. --- C-terminus. --- Cell Cycle Arrest. --- Cell Line, Transformed. --- Cell cycle. --- Cell membrane. --- Cell migration. --- Cell surface receptor. --- Cellular differentiation. --- Cellular stress response. --- Conformational change. --- Cytochrome P450. --- Cytokine receptor. --- Cytokine. --- Cytotoxicity. --- DNA-PKcs. --- Drug metabolism. --- Ectopic expression. --- Effector (biology). --- Endonuclease. --- Enzyme. --- Epidermal growth factor receptor. --- Epidermal growth factor. --- Extracellular signal–regulated kinases. --- Fibroblast growth factor. --- Gene expression. --- Gene therapy. --- Gene. --- Germinal center. --- Glutathione S-transferase. --- HMG-CoA reductase. --- Heat shock. --- Histidine kinase. --- Hormone-sensitive lipase. --- Hsp27. --- Immortalised cell line. --- Immunodeficiency. --- Immunoglobulins. --- Immunoprecipitation. --- In vitro. --- Inducer. --- Inflammation. --- Jurkat cells. --- Kinase. --- Lymphotoxin. --- Macrophage colony-stimulating factor. --- Mechanism of action. --- Mechanistic target of rapamycin. --- Metabolism. --- Mitogen-activated protein kinase kinase. --- Mitogen-activated protein kinase. --- Mitogen. --- Mitosis. --- Model organism. --- Neuropeptide. --- Neurotoxin. --- Osmotic shock. --- Oxidative phosphorylation. --- Oxidative stress. --- P38 mitogen-activated protein kinases. --- Pathogenesis. --- Peptide. --- Peroxidase. --- Phosphatase. --- Phosphoinositide 3-kinase. --- Phosphorylation cascade. --- Phosphorylation. --- Post-translational modification. --- Protease. --- Protein kinase. --- Protein phosphorylation. --- Protein synthesis inhibitor. --- Protein. --- Proteolysis. --- RNA interference. --- Receptor (biochemistry). --- Receptor tyrosine kinase. --- Repressor. --- Response element. --- Signal transduction. --- Ternary Complex Factors. --- Thrombin. --- Transcription factor. --- Transcriptional regulation. --- Transfection. --- Transposable element. --- Tumor necrosis factor superfamily. --- Turgor pressure. --- Vascular endothelial growth factor.