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Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 04/2016, Volume 36, Issue 4, pp. 636 - 646
.... Echocardiography showed that Bsg mice showed less hypertrophy, less left ventricular dilatation, and preserved... 
heart failure | cytokines | hypertrophy | inflammation | angiotensin II | INHIBITS EMMPRIN | CHRONIC HEART-FAILURE | RECEPTOR | CANCER | METALLOPROTEINASE INDUCER EMMPRIN | PMA-INDUCED MACROPHAGES | ACTIVATES PLATELETS | PERIPHERAL VASCULAR DISEASE | CD147 | HEMATOLOGY | EXPRESSION | Oxidative Stress | Heart Failure - physiopathology | Male | Aortic Diseases - metabolism | Heart Failure - prevention & control | Hypertrophy, Left Ventricular - genetics | Time Factors | Ventricular Dysfunction, Left - genetics | Basigin - genetics | Myocardium - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Heart Failure - etiology | Disease Models, Animal | Fibroblasts - metabolism | Animals, Newborn | Angiotensin II - pharmacology | Hypertrophy, Left Ventricular - prevention & control | Rats | Heart Failure - genetics | Heart Failure - metabolism | Fibroblasts - pathology | Mice, Knockout | Ventricular Dysfunction, Left - metabolism | Myocytes, Cardiac - pathology | Aortic Diseases - genetics | Myocytes, Cardiac - drug effects | Fibroblasts - drug effects | Fibrosis | Myocytes, Cardiac - metabolism | Hypertrophy, Left Ventricular - physiopathology | Rats, Wistar | Ventricular Function, Left | JNK Mitogen-Activated Protein Kinases - metabolism | Extracellular Signal-Regulated MAP Kinases - metabolism | Blood Proteins - metabolism | Hypertrophy, Left Ventricular - pathology | Inflammation Mediators - metabolism | Ventricular Dysfunction, Left - pathology | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Cells, Cultured | Ventricular Dysfunction, Left - etiology | Myocardium - pathology | Heart Failure - pathology | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Mechanotransduction, Cellular | Aortic Diseases - physiopathology | Animals | Aortic Diseases - complications | Basigin - metabolism | Matrix Metalloproteinases - metabolism
Journal Article
Cardiovascular Research, ISSN 0008-6363, 12/2012, Volume 96, Issue 3, pp. 456 - 465
.... Doxorubicin treatment caused left ventricular dilatation and dysfunction within 6 days. Cardiomyocyte autophagy appeared to be activated in the doxorubicin group, based... 
Heart failure | Autophagy | Doxorubicin | MAMMALIAN TARGET | CARDIAC & CARDIOVASCULAR SYSTEMS | ACTIVATED PROTEIN-KINASE | INDUCED APOPTOSIS | PHOSPHORYLATION | MECHANISMS | CELL-DEATH | DEGENERATION | HEART | INHIBITION | 3-METHYLADENINE | AMP-Activated Protein Kinases - metabolism | Microtubule-Associated Proteins - genetics | Ventricular Function, Left | Microtubule-Associated Proteins - metabolism | Heart Failure - physiopathology | Green Fluorescent Proteins - genetics | Ventricular Dysfunction, Left - chemically induced | Autophagy - drug effects | Autophagy-Related Protein-1 Homolog | Starvation - metabolism | Heart Failure - prevention & control | Hypertrophy, Left Ventricular - chemically induced | Time Factors | Hypertrophy, Left Ventricular - pathology | Adenosine Triphosphate - metabolism | Ventricular Dysfunction, Left - pathology | Protein-Serine-Threonine Kinases - metabolism | Green Fluorescent Proteins - metabolism | Hypertrophy, Left Ventricular - metabolism | Hypertrophy, Left Ventricular - prevention & control | Cells, Cultured | Rats | Mice, Transgenic | Heart Failure - metabolism | Antibiotics, Antineoplastic | Heart Failure - pathology | Cathepsin D - metabolism | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Stroke Volume | Ventricular Dysfunction, Left - metabolism | Myocytes, Cardiac - pathology | Animals | Energy Metabolism | Myocytes, Cardiac - metabolism | Mice | Ventricular Pressure | Hypertrophy, Left Ventricular - physiopathology | Heart Failure - chemically induced | Starvation - complications | Index Medicus
Journal Article
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 07/2014, Volume 34, Issue 7, pp. 1399 - 1411
.... hBAC-S100 mice with CKD showed increased fibroblast growth factor 23 in the hearts, left ventricular hypertrophy, diastolic dysfunction, focal cartilaginous metaplasia, and calcification... 
renal insufficiency chronic | S100 proteins | glycosylation end products advanced | hypertrophy left ventricular | MORTALITY | PLASMA S100A12 LEVELS | renal insufficiency, chronic | VASCULAR CALCIFICATION | hypertrophy, left ventricular | ATHEROSCLEROSIS | RAGE | ARTERIAL CALCIFICATION | glycosylation end products, advanced | GROWTH-FACTOR 23 | HEMODIALYSIS-PATIENTS | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | EXPRESSION | SOLUBLE RECEPTOR | Calgranulin B - metabolism | Diastole | Humans | Calgranulin A - genetics | Renal Insufficiency, Chronic - complications | Sclerosis | S100A12 Protein | Fibroblast Growth Factors - metabolism | Inflammation - metabolism | S100 Proteins - genetics | Hypertrophy, Left Ventricular - genetics | Calcinosis - etiology | Time Factors | Myocardium - metabolism | Renal Insufficiency, Chronic - genetics | Receptor for Advanced Glycation End Products | Disease Models, Animal | Fibroblasts - metabolism | Signal Transduction | Receptors, Immunologic - deficiency | Genotype | Mice, Transgenic | S100 Proteins - metabolism | Mice, Knockout | Ventricular Dysfunction, Left - metabolism | Phenotype | Heart Valve Diseases - metabolism | Heart Valve Diseases - genetics | Mice | Hypertrophy, Left Ventricular - physiopathology | Receptors, Immunologic - genetics | Heart Valve Diseases - pathology | Ventricular Function, Left | Calgranulin A - metabolism | Leukocyte L1 Antigen Complex - metabolism | Aortic Valve - pathology | Renal Insufficiency, Chronic - metabolism | Inflammation - complications | Ventricular Remodeling | Inflammation Mediators - metabolism | Calgranulin B - genetics | Calcinosis - metabolism | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Mice, Inbred C57BL | Cells, Cultured | Ventricular Dysfunction, Left - etiology | Heart Valve Diseases - etiology | Aortic Valve - metabolism | Ventricular Dysfunction, Left - physiopathology | Animals | Inflammation - genetics | Leukocyte L1 Antigen Complex - genetics | Receptors, Immunologic - metabolism
Journal Article
Circulation, ISSN 0009-7322, 06/2019, Volume 139, Issue 24, pp. 2765 - 2777
Journal Article
Journal of the American Heart Association, ISSN 2047-9980, 01/2016, Volume 5, Issue 1, p. n/a
... of metabolic syndrome is metabolic heart disease (MHD), which is associated with left ventricular (LV) hypertrophy, diastolic dysfunction, and impaired cardiac energetics... 
metabolic heart disease | mitochondria | obesity | oxidative protein modifications | oxidative stress | Obesity | Oxidative stress | Metabolic heart disease | Mitochondria | Oxidative protein modifications | EXTREME OBESITY | CARDIAC & CARDIOVASCULAR SYSTEMS | UNCOUPLING PROTEINS | MECHANISMS | DIABETIC CARDIOMYOPATHY | SUCCINATE-DEHYDROGENASE | COMPLEX-II | PROTEIN S-GLUTATHIONYLATION | MICE | DYSFUNCTION | Mitochondrial Diseases - pathology | Mitochondria, Heart - metabolism | Reactive Oxygen Species - metabolism | Oxidative Stress | Ventricular Function, Left | Mitochondria, Heart - pathology | Mitochondrial Diseases - metabolism | Electron Transport Complex I - metabolism | Mitochondrial Diseases - etiology | Hypertrophy, Left Ventricular - genetics | Ventricular Dysfunction, Left - genetics | Hypertrophy, Left Ventricular - pathology | Adenosine Triphosphate - metabolism | Diet, High-Fat | Ventricular Dysfunction, Left - pathology | Dietary Sucrose | Disease Models, Animal | Mitochondrial Diseases - genetics | Mitochondrial Diseases - prevention & control | Electron Transport Complex II - genetics | Oxidation-Reduction | Catalase - genetics | Hypertrophy, Left Ventricular - etiology | Hypertrophy, Left Ventricular - metabolism | Hypertrophy, Left Ventricular - prevention & control | Mice, Inbred C57BL | Ventricular Dysfunction, Left - etiology | Mice, Transgenic | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Catalase - metabolism | Ventricular Dysfunction, Left - metabolism | Animals | Energy Metabolism | Electron Transport Complex II - metabolism | Protein Processing, Post-Translational | Hypertrophy, Left Ventricular - physiopathology | Mutation | Mitochondrial Diseases - physiopathology
Journal Article
Hypertension, ISSN 0194-911X, 06/2012, Volume 59, Issue 6, pp. 1170 - 1178
Chronic left ventricular failure causes pulmonary congestion with increased lung weight and type 2 pulmonary hypertension... 
Transverse aortic constriction | Pulmonary vascular morphology | Pulmonary hypertension | OVERLOAD | PRESSURE | HYPERTROPHY | OXIDATIVE STRESS | pulmonary hypertension | ARTERIAL-HYPERTENSION | transverse aortic constriction | PERIPHERAL VASCULAR DISEASE | EXTRACELLULAR-SUPEROXIDE DISMUTASE | EXPRESSION | pulmonary vascular morphology | Leukocytes - pathology | Lung Diseases - metabolism | Heart Failure - physiopathology | Hypertension, Pulmonary - physiopathology | Ventricular Dysfunction, Left - complications | Male | Pulmonary Edema - etiology | Lung Diseases - etiology | Pulmonary Edema - physiopathology | Collagen - genetics | Lung - metabolism | Pulmonary Edema - metabolism | Heart Failure - complications | Lung - pathology | Hypertrophy, Left Ventricular - metabolism | Mice, Inbred C57BL | Water - metabolism | Organ Size | Heart Failure - metabolism | Hypertension, Pulmonary - metabolism | Lung - physiopathology | Reverse Transcriptase Polymerase Chain Reaction | Constriction, Pathologic - complications | Blotting, Western | Ventricular Dysfunction, Left - physiopathology | Aorta - pathology | Ventricular Dysfunction, Left - metabolism | Collagen - metabolism | Animals | Transforming Growth Factor beta - genetics | Fibrosis - etiology | Hypertrophy, Left Ventricular - complications | Hypoxia - physiopathology | Lung Diseases - physiopathology | Mice | Hypertrophy, Left Ventricular - physiopathology | Hypertension, Pulmonary - etiology | Leukocytes - metabolism | Transforming Growth Factor beta - metabolism
Journal Article
Journal Article
Circulation Research, ISSN 0009-7330, 09/2011, Volume 109, Issue 7, pp. 783 - 793
...β in maintaining mitochondrial energy metabolism and contractile function in pressure overload hypertrophy... 
heart failure | cardiac hypertrophy | mitochondria | gene expression | TRANSCRIPTIONAL COACTIVATOR PGC-1-ALPHA | ACTIVATION | CARDIAC & CARDIOVASCULAR SYSTEMS | MITOCHONDRIAL | ENERGETICS | METABOLISM | FATTY-ACID OXIDATION | CARDIAC-HYPERTROPHY | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | MICE | CONTRACTILE FUNCTION | HEMATOLOGY | Blood Pressure | Mitochondria, Heart - metabolism | Oxidative Stress | Ventricular Function, Left | Heart Failure - physiopathology | Heart Failure - prevention & control | Ventricular Dysfunction, Left - genetics | Myocardium - metabolism | Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha | Trans-Activators - genetics | Ultrasonography | Aging | Heart Failure - diagnostic imaging | Energy Metabolism - genetics | Fatty Acids - metabolism | Heart Failure - etiology | Disease Models, Animal | Myocardial Contraction | Oxidation-Reduction | Gene Expression Regulation | Oxidative Phosphorylation | Ventricular Dysfunction, Left - etiology | Heart Failure - genetics | Heart Failure - metabolism | Disease Progression | Ventricular Dysfunction, Left - diagnostic imaging | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Mice, Knockout | Ventricular Dysfunction, Left - metabolism | Animals | Trans-Activators - deficiency | Hypertrophy, Left Ventricular - complications | Glucose - metabolism | Mice | Transcription Factors | Hypertrophy, Left Ventricular - physiopathology | Hexokinase - metabolism | Hypertrophy, Left Ventricular - diagnostic imaging
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2016, Volume 11, Issue 11, p. e0166845
.... The aim of this study was to determine whether treatment with atorvastatin for 4 weeks would lead to changes in collagen metabolism and ventricular remodeling in a rat model of MI... 
IN-VITRO | ACTIVATION | MULTIDISCIPLINARY SCIENCES | HEART-FAILURE | CARDIAC-HYPERTROPHY | MATRICELLULAR PROTEINS | EXTRACELLULAR-MATRIX | NF-KAPPA-B | MATRIX-METALLOPROTEINASE INHIBITION | EXPRESSION | RAT MODEL | Interleukin-1 - genetics | Gene Expression - drug effects | Rats, Wistar | Atorvastatin Calcium - pharmacology | Catheter Ablation | Male | NF-kappa B p50 Subunit - genetics | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Myocardial Infarction - pathology | Myocardium - metabolism | Atorvastatin Calcium - therapeutic use | Heart Ventricles - pathology | Disease Models, Animal | Myocardial Infarction - surgery | Interleukin-1 - metabolism | NF-kappa B p50 Subunit - metabolism | Rats | Myocardium - pathology | Collagen - metabolism | Animals | Anticholesteremic Agents - therapeutic use | Myocardial Infarction - drug therapy | Fibrosis | Hemodynamics - drug effects | Matrix Metalloproteinase 1 - metabolism | Ventricular Remodeling - drug effects | Anticholesteremic Agents - pharmacology | Physiological aspects | Drug therapy | Collagen | Analysis | Heart attack | Myocardial infarction | Heart | Heart attacks | Heart surgery | Collagens | Science | Kinases | Remodeling | Tissue inhibitor of metalloproteinase 1 | Proteins | Signal transduction | Ischemia | Rodents | Surgery | Atherosclerosis | Osteonectin | Interleukin 1 | Toll-like receptors | Fibroblasts | Physiology | Cardiology | Cross sections | Discipline | Drug dosages | Statins | Heart failure | NF-κB protein | Neutrophils | Coronary artery | Medical instruments | Inflammation | TLR4 protein | Saline solutions | Metabolism | Ostomy | Atorvastatin | Infarction | Ventricle | Laboratory animals | Hypertrophy
Journal Article
Cardiovascular Research, ISSN 0008-6363, 04/2012, Volume 94, Issue 1, pp. 96 - 104
.... We determined the role of GPR30 in the maintenance of left ventricular (LV) structure and diastolic function after the surgical loss of ovarian hormones in the female mRen2... 
Cardiac hypertrophy | GPR30 | Post-menopausal women | Diastolic dysfunction | mRen2.Lewis rat | mRen2 | CARDIAC & CARDIOVASCULAR SYSTEMS | PLUS PROGESTIN | CARDIAC MYOCYTES | RANDOMIZED CONTROLLED-TRIAL | HYPERTENSIVE POSTMENOPAUSAL WOMEN | BLOOD-PRESSURE | Lewis rat | REPLACEMENT THERAPY | COUPLED ESTROGEN-RECEPTOR | SEX-DIFFERENCES | CONTRACTILE FUNCTION | CORONARY-HEART-DISEASE | Renin - metabolism | Receptors, G-Protein-Coupled - metabolism | Calcium - metabolism | Natriuretic Peptide, Brain - metabolism | NADPH Oxidases - metabolism | Rats, Inbred Lew | Receptors, G-Protein-Coupled - agonists | Quinolines - administration & dosage | RNA, Messenger - metabolism | Quinolines - pharmacology | Renin - genetics | Time Factors | Ventricular Dysfunction, Left - genetics | Injections, Subcutaneous | Echocardiography, Doppler | Female | Blood Pressure - drug effects | Estrogens - metabolism | Cell Line | Angiotensin II - metabolism | Atrial Natriuretic Factor - metabolism | Ovariectomy | Rats, Transgenic | Hypertrophy, Left Ventricular - metabolism | Hypertrophy, Left Ventricular - prevention & control | Ventricular Function, Left - drug effects | Rats | Genotype | Cardiotonic Agents - pharmacology | Cyclopentanes - pharmacology | NADPH Oxidase 4 | Ventricular Dysfunction, Left - diagnostic imaging | Ventricular Dysfunction, Left - physiopathology | Ventricular Dysfunction, Left - prevention & control | Gene Expression Regulation - drug effects | Ventricular Dysfunction, Left - metabolism | Collagen - metabolism | Myocytes, Cardiac - pathology | Phenotype | Animals | Cardiotonic Agents - administration & dosage | Myocytes, Cardiac - drug effects | Myocytes, Cardiac - metabolism | Mice | Receptors, G-Protein-Coupled - genetics | Ventricular Remodeling - drug effects | Cyclopentanes - administration & dosage | Hypertrophy, Left Ventricular - diagnostic imaging | Original
Journal Article
Cardiovascular Research, ISSN 0008-6363, 01/2018, Volume 114, Issue 1, pp. 123 - 137
Journal Article
Cell Metabolism, ISSN 1550-4131, 12/2015, Volume 22, Issue 6, pp. 1020 - 1032
Chronic kidney disease (CKD) is a worldwide public health threat that increases risk of death due to cardiovascular complications, including left ventricular hypertrophy (LVH... 
KIDNEY-DISEASE | MORTALITY | KLOTHO | POINT MUTATION | SPECIFICITY | ENDOCRINOLOGY & METABOLISM | INHIBITOR | BLOCKADE | BINDING | EXPRESSION | FGF RECEPTOR | CELL BIOLOGY | Receptor, Fibroblast Growth Factor, Type 4 - metabolism | Humans | Glucuronidase - metabolism | Fibroblast Growth Factors - genetics | Male | Renal Insufficiency, Chronic - metabolism | Fibroblast Growth Factors - metabolism | Hypertrophy, Left Ventricular - pathology | HEK293 Cells | Receptor, Fibroblast Growth Factor, Type 4 - deficiency | Female | Receptor, Fibroblast Growth Factor, Type 4 - genetics | Disease Models, Animal | Phospholipase C gamma - metabolism | Mutagenesis, Site-Directed | Myocytes, Cardiac - cytology | Signal Transduction | Hypertrophy, Left Ventricular - metabolism | Mice, Inbred C57BL | NFATC Transcription Factors - metabolism | Cells, Cultured | Rats | Rats, Sprague-Dawley | Gene Knock-In Techniques | Mice, Knockout | Renal Insufficiency, Chronic - pathology | Animals | Glucuronidase - genetics | Myocytes, Cardiac - metabolism | Mice | Calcineurin - metabolism | Hypertension | Medical colleges | Chronic kidney failure | Heart enlargement | Stem cells | Physiological aspects | Fibroblast growth factors | Phospholipases | Drug discovery | T cells | Health aspects | Heart | Resveratrol | Development and progression | Kidney diseases | Cells
Journal Article