Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

Granulocyte colony-stimulating factor (G-CSF or GCSF) is a secreted glycoprotein that stimulates the proliferation and differentiation of granulocyte precursor cells, and induces mobilization of peripheral blood progenitor cells from the bone marrow. Development of recombinant human G-CSF has had a profound impact on the treatment of many diseases, including severe chronic neutropenia and cancer, and has enabled peripheral stem cell transplantation to supplant bone marrow transplantation in the autologous setting. This Milestones in Drug Therapy volume describes the experience of the last 20 years of treatment with recombinant human G-CSF, including the basic science, the use of recombinant human G-CSF in both the oncology and nononcology settings, and the safety and economics of its use. Many of the authors were the original investigators of recombinant human G-CSF and other authors are key researchers who provide their outlook for the next 20 years for use of and research with recombinant human G-CSF.

Drug abuse -- Etiology -- Handbooks, manuals, etc. --- Drug abuse -- Psychological aspects -- Handbooks, manuals, etc. --- Filgrastim --- Colony-Stimulating Factors --- Leukemia --- Neoplasms, Plasma Cell --- Receptors, Colony-Stimulating Factor --- Lymphoproliferative Disorders --- Hematologic Diseases --- Hemostatic Disorders --- Therapeutics --- Paraproteinemias --- Hemorrhagic Disorders --- Hematopoietic Cell Growth Factors --- Receptors, Cytokine --- Immunoproliferative Disorders --- Neoplasms by Histologic Type --- Analytical, Diagnostic and Therapeutic Techniques and Equipment --- Receptors, Growth Factor --- Hemic and Lymphatic Diseases --- Blood Protein Disorders --- Glycoproteins --- Vascular Diseases --- Cytokines --- Proteins --- Receptors, Peptide --- Neoplasms --- Receptors, Immunologic --- Diseases --- Immune System Diseases --- Cardiovascular Diseases --- Receptors, Cell Surface --- Amino Acids, Peptides, and Proteins --- Intercellular Signaling Peptides and Proteins --- Membrane Proteins --- Chemicals and Drugs --- Biological Factors --- Peptides --- Multiple Myeloma --- Granulocyte Colony-Stimulating Factor --- Drug Therapy --- Leukocyte Disorders --- Leukemia, Myeloid --- Receptors, Granulocyte Colony-Stimulating Factor --- Health & Biological Sciences --- Biology --- Pharmacy, Therapeutics, & Pharmacology --- Microbiology & Immunology --- Granulocyte-macrophage colony-stimulating factor. --- Colony-stimulating factors (Physiology) --- Granulocytes. --- Macrophages. --- Histiocytes --- Mononuclear phagocytes --- Granular leucocytes --- CSF-GM (Colony-stimulating factor) --- GM-CSF (Colony-stimulating factor) --- Histamine-producing cell-stimulating factor --- Medicine. --- Cancer research. --- Immunology. --- Pharmacology. --- Hematology. --- Cytokines. --- Growth factors. --- Biomedicine. --- Pharmacology/Toxicology. --- Cancer Research. --- Cytokines and Growth Factors. --- Antigen presenting cells --- Connective tissue cells --- Killer cells --- Phagocytes --- Reticulo-endothelial system --- Leucocytes --- Hematopoietic growth factors --- Toxicology. --- Oncology. --- Haematology --- Internal medicine --- Blood --- Cellular immunity --- Immune response --- Immunobiology --- Life sciences --- Serology --- Tumors --- Chemicals --- Medicine --- Pharmacology --- Poisoning --- Poisons --- Regulation --- Toxicology --- Cell growth factors --- Cellular growth factors --- Growth peptides --- Growth promoting substances --- Growth substances --- Peptide growth factors --- Peptide regulatory factors --- Polypeptide growth factors --- Cancer research --- Drug effects --- Medical pharmacology --- Medical sciences --- Chemotherapy --- Drugs --- Pharmacy --- Physiological effect

Choose an application

• Reference Manager
• EndNote
• RefWorks (Direct export to RefWorks)

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.

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 --- n/a --- relapsing-remitting experimental autoimmune encephalomyelitis