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Journal Article
The EMBO Journal, ISSN 0261-4189, 02/2007, Volume 26, Issue 4, pp. 1129 - 1139
Journal Article
Science, ISSN 0036-8075, 11/2008, Volume 322, Issue 5904, pp. 1101 - 1104
Journal Article
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, ISSN 0363-6135, 07/2019, Volume 317, Issue 1, pp. H124 - H140
Journal Article
Clinical Science, ISSN 0143-5221, 2014, Volume 126, Issue 3, pp. 207 - 221
COPD (chronic obstructive pulmonary disease) is caused by exposure to toxic gases and particles, most often CS (cigarette smoke), leading to emphysema, chronic... 
Inflammation | Mainstream | Chronic obstructive pulmonary disease (copd) | Neutrophil | Smoke | Sidestream | MEDICINE, RESEARCH & EXPERIMENTAL | HUMAN NEUTROPHILS | COLONY-STIMULATING FACTOR | mainstream | smoke | SIDESTREAM SMOKE | MECHANISMS | ENVIRONMENTAL TOBACCO-SMOKE | neutrophil | RAT LUNG | OBSTRUCTIVE PULMONARY-DISEASE | inflammation | chronic obstructive pulmonary disease (COPD) | sidestream | MICE | INDUCED EMPHYSEMA | Smoking - adverse effects | Inflammation - pathology | Lung - pathology | Cytokines - metabolism | Smoke - adverse effects | Mice, Inbred C57BL | Bronchoalveolar Lavage Fluid - immunology | Pulmonary Disease, Chronic Obstructive - pathology | Neutrophil Infiltration | Inflammation - metabolism | Animals | Smoking - pathology | Smoke - analysis | Female | Bronchoalveolar Lavage Fluid - cytology | Mice | Bronchoalveolar Lavage Fluid - chemistry | Pulmonary Disease, Chronic Obstructive - metabolism | Pulmonary Disease, Chronic Obstructive - immunology | Disease Models, Animal | Index Medicus | S3 | IL-1β, interleukin 1β | CS, cigarette smoke | S8 | COPD, chronic obstructive pulmonary disease | GM-CSF, granulocyte macrophage colony-stimulating factor | CO-Hb, carboxyhaemoglobin | MMP12, matrix metalloproteinase 12 | MIP, macrophage inflammatory protein | TPM, total particulate matter | TNF-α, tumour necrosis factor α | CC, carbonyl compounds | NE, neutrophil elastase | IFNβ, interferon β | MCP-1, monocyte chemoattractant protein-1 | PAH, polycyclic aromatic hydrocarbons | KC, keratinocyte chemoattractant | NF-κB, nuclear factor κB | Original Paper | HO, haem oxygenase | MMD, mass median diameter | H&E, haematoxylin and eosin | PM, particulate matter | DNPH, 2,4-dinitrophenylhydrazine | HPRT-1, hypoxanthine–guanine phosphoribosyltransferase | BAL, bronchoalveolar lavage | GC-SIM-MS, gas-chromatography with selective ion monitoring MS | LPS, lipopolysaccharide | CMD, count median diameter
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 2/2006, Volume 103, Issue 8, pp. 2770 - 2775
Journal Article
PLoS ONE, ISSN 1932-6203, 02/2014, Volume 9, Issue 2, pp. e89068 - e89068
Lymphocytic infiltration in the lamina propria (LP), which is primarily composed of CD4(+) Th1 cells and plasma cells, and increased numbers of intraepithelial... 
CXCL10 | INFLAMMATORY-BOWEL-DISEASE | EPITHELIAL-CELLS | AUTOIMMUNE-DISEASES | MULTIDISCIPLINARY SCIENCES | CHEMOKINE RECEPTOR CXCR3 | CHEMOATTRACTANTS | IMMUNOPATHOLOGY | EXPRESSION | PLASMA-CELLS | INTRAEPITHELIAL LYMPHOCYTES | Tumor Necrosis Factor-alpha - metabolism | Chemokine CXCL10 - blood | Intestinal Mucosa - metabolism | Receptors, CXCR3 - metabolism | Gene Expression Regulation - immunology | Humans | Interferon-gamma - metabolism | Celiac Disease - pathology | Signal Transduction - immunology | Chemokine CXCL10 - biosynthesis | Interferon-beta - metabolism | Celiac Disease - immunology | Intestinal Mucosa - immunology | Chemokine CXCL9 - metabolism | Celiac Disease - blood | Adult | T-Lymphocytes - immunology | Intestine, Small - metabolism | Chemokine CXCL11 - metabolism | Chemokine CXCL10 - metabolism | Child | Celiac Disease - metabolism | Intestine, Small - immunology | Plasma Cells - immunology | Celiac disease | B cells | RNA | T cells | Disease | Pathogenesis | Mucosa | Lymphocytes T | Arthritis | mRNA | Tissues | Small intestine | Recruitment | Signal transduction | Lymphocytes | Rodents | Gastroenterology | Gluten | Cytokines | Dendritic cells | Lamina propria | Inflammation | Poly (I:C) | CXCR3 protein | Permeability | Interleukin 15 | Gene expression | Epithelium | Patients | CD4 antigen | Signaling | Enterocytes | Biopsy | γ-Interferon | CXCL10 protein | Plasma cells | Ligands | Infiltration | CXCL11 protein | Autoimmune diseases | Chemokines | Index Medicus
Journal Article
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 2015, Volume 309, Issue 11, pp. H1883 - H1893
The activation of the calpain system is involved in the repair process following myocardial infarction (MI). However, the impact of the inhibition of calpain... 
Myocardial infarction | Calpastatin | Cardiac rupture | Lymphocytes | Calpain | Inflammation | Macrophages | Scar healing | SYSTEM | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | lymphocytes | THERAPEUTIC INTERVENTIONS | myocardial infarction | scar healing | HEART-FAILURE | calpastatin | DEFICIENCY | cardiac rupture | EXACERBATES CARDIAC DYSFUNCTION | calpain | macrophages | REPAIR | CALPAIN ACTIVATION | inflammation | ACUTE MYOCARDIAL-INFARCTION | PERIPHERAL VASCULAR DISEASE | INFLAMMATORY RESPONSE | Chemotaxis, Leukocyte | Myocardial Infarction - genetics | Up-Regulation | Calpain - metabolism | Myocardium - immunology | Ventricular Function, Left | Homeodomain Proteins - metabolism | Male | Wound Healing | Myocardial Infarction - immunology | CD4-Positive T-Lymphocytes - immunology | Ventricular Remodeling | Time Factors | Myocardial Infarction - pathology | Myocardium - metabolism | Ventricular Dysfunction, Left - pathology | Myocardial Infarction - physiopathology | Macrophages - immunology | Disease Models, Animal | Calcium-Binding Proteins - metabolism | Lymphocyte Activation | Mice, Inbred C57BL | CD4-Positive T-Lymphocytes - metabolism | Genotype | Myocardium - pathology | Myocardial Infarction - metabolism | Homeodomain Proteins - genetics | Ventricular Dysfunction, Left - physiopathology | Macrophage Activation | Mice, Knockout | Ventricular Dysfunction, Left - metabolism | Macrophages - metabolism | Phenotype | Animals | Heart Rupture, Post-Infarction - metabolism | Enzyme Activation | Heart Rupture, Post-Infarction - pathology | Heart Rupture, Post-Infarction - physiopathology | Calcium-Binding Proteins - genetics | Disease susceptibility | T cells | Mortality | Genetic aspects | Dosage and administration | Gene expression | Observations | Drug therapy | Health aspects | Heart attack | Statins | T cell receptors | Heart attacks | Protease inhibitors | Rodents | Index Medicus
Journal Article