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Hepatology, ISSN 0270-9139, 02/2017, Volume 65, Issue 2, pp. 451 - 464
There is evidence that nonalcoholic fatty liver disease (NAFLD) is affected by gut microbiota. Therefore, we investigated its modifications in pediatric NAFLD... 
Pediatrics | Liver diseases | Volatile organic compounds--VOCs | Gas chromatography | Metabolomics | Obesity | Microbiota | rRNA 16S | Fatty liver | Butanol | Mass spectroscopy | Organic compounds
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2016, Volume 11, Issue 6, p. e0157246
Non-alcoholic fatty liver disease is one of the most important causes of liver-related morbidity in children. In non-alcoholic fatty liver disease, the... 
FIBROSIS | CONTROLLED-TRIAL | BILIARY TREE | DOCOSAHEXAENOIC ACID | REGENERATION | OMEGA-3-FATTY-ACIDS | MULTIDISCIPLINARY SCIENCES | MOUSE | DUCTULAR REACTION | STEATOHEPATITIS | CHILDREN | Wnt3A Protein - metabolism | Kupffer Cells - pathology | Non-alcoholic Fatty Liver Disease - pathology | Liver - pathology | Humans | Hepatocytes - pathology | Male | Hepatocytes - metabolism | Stem Cells - metabolism | Liver - drug effects | Anti-Inflammatory Agents - therapeutic use | Female | Kupffer Cells - metabolism | Phosphorylation - drug effects | Child | Hepatocytes - drug effects | Docosahexaenoic Acids - therapeutic use | Wnt3A Protein - genetics | Macrophages - pathology | Non-alcoholic Fatty Liver Disease - genetics | Signal Transduction | Liver - metabolism | Gene Expression Regulation | Non-alcoholic Fatty Liver Disease - metabolism | beta Catenin - metabolism | Disease Progression | beta Catenin - genetics | Kupffer Cells - drug effects | Non-alcoholic Fatty Liver Disease - drug therapy | Macrophages - metabolism | Biopsy | Adolescent | Stem Cells - drug effects | Stem Cells - pathology | Macrophages - drug effects | Macrophage Activation - drug effects | Immunohistochemistry | Polarization | Pediatrics | Phosphorylation | Wnt protein | Laboratories | Liver | Clinical trials | Activation | Macrophages | Docosahexaenoic acid | β-catenin | Body mass index | Cell activation | Ultrasonic imaging | Fatty liver | Rodents | Hepatology | Gastroenterology | Atherosclerosis | Children | Phenotypes | Liver diseases | Cytokines | Fatty acids | Progenitor cells | Morbidity | Children & youth | Hospitals | Acids | Orthopedics | Stem cells | Fibrosis | Cells (biology) | Insulin resistance | Immunofluorescence | Apoptosis
Journal Article
PLoS ONE, ISSN 1932-6203, 12/2016, Volume 11, Issue 12, p. e0168216
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2013, Volume 8, Issue 6, p. e67160
Journal Article
Oncotarget, ISSN 1949-2553, 2015, Volume 6, Issue 39, pp. 41434 - 41452
Lipopolysaccharide (LPS) is currently considered one of the major players in non-alcoholic fatty liver disease (NAFLD) pathogenesis and progression. Here, we... 
Pathology section | NAFLD | Inflammation | LITAF | LPS | Fibrosis | Liver Cirrhosis - immunology | Non-alcoholic Fatty Liver Disease - pathology | Up-Regulation | Liver - pathology | Humans | Hepatic Stellate Cells - metabolism | Male | Interleukin-1beta - genetics | Liver - immunology | Transfection | Hepatic Stellate Cells - immunology | Liver - drug effects | RNA Interference | Time Factors | Interleukin-1beta - metabolism | Inflammation Mediators - metabolism | Liver Cirrhosis - metabolism | Female | Transcription, Genetic | p38 Mitogen-Activated Protein Kinases - metabolism | Nuclear Proteins - genetics | Binding Sites | Cytokines - genetics | Liver Cirrhosis - genetics | Hepatic Stellate Cells - pathology | Hepatic Stellate Cells - drug effects | Cell Line | Liver Cirrhosis - drug therapy | Promoter Regions, Genetic | Cytokines - metabolism | Non-alcoholic Fatty Liver Disease - genetics | Signal Transduction | Liver - metabolism | Non-alcoholic Fatty Liver Disease - immunology | Nuclear Proteins - metabolism | Non-alcoholic Fatty Liver Disease - metabolism | Transcription Factors - genetics | Non-alcoholic Fatty Liver Disease - drug therapy | Transcription Factors - metabolism | Phenotype | Animals | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Liver Cirrhosis - pathology | Mice | Mice, Inbred BALB C | Protein Kinase Inhibitors - pharmacology
Journal Article
Cell Death and Differentiation, ISSN 1350-9047, 05/2017, Volume 24, Issue 5, pp. 889 - 902
Hepatocellular carcinoma (HCC) is the most common type of liver cancer in humans. The focal adhesion tyrosine kinase (FAK) is often over-expressed in human HCC... 
OVEREXPRESSION | METHYLATION | PROTEIN | INHIBITION | PATHWAY | BIOCHEMISTRY & MOLECULAR BIOLOGY | NUCLEAR FAK | MECHANISMS | HISTONE METHYLTRANSFERASE EZH2 | CANCER | EXPRESSION | CELL BIOLOGY | Focal Adhesion Kinase 1 - genetics | Neoplasm Transplantation | RNA, Small Interfering - genetics | E2F2 Transcription Factor - genetics | Apoptosis - drug effects | Humans | Gene Expression Regulation, Neoplastic | Apoptosis - genetics | Male | Receptor, Notch2 - genetics | E2F2 Transcription Factor - metabolism | Tumor Suppressor Protein p53 - genetics | Carcinoma, Hepatocellular - genetics | Liver Neoplasms - pathology | Focal Adhesion Kinase 1 - metabolism | Promoter Regions, Genetic | Enhancer of Zeste Homolog 2 Protein - genetics | Enhancer of Zeste Homolog 2 Protein - metabolism | Liver Neoplasms - genetics | Signal Transduction | Receptor, Notch2 - metabolism | Tumor Suppressor Protein p53 - metabolism | E2F3 Transcription Factor - genetics | G2 Phase Cell Cycle Checkpoints | Hep G2 Cells | Animals | Histones - genetics | Mice, Nude | Aminopyridines - pharmacology | Carcinoma, Hepatocellular - pathology | E2F3 Transcription Factor - metabolism | Liver Neoplasms - metabolism | Cell Line, Tumor | Cell Proliferation - drug effects | Mice | Histones - metabolism | Focal Adhesion Kinase 1 - antagonists & inhibitors | Carcinoma, Hepatocellular - metabolism | RNA, Small Interfering - metabolism | Original Paper
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2018, Volume 13, Issue 6, p. e0198490
Early life events are associated with the susceptibility to chronic diseases in adult life. Perturbations of endoplasmic reticulum (ER) homeostasis activate... 
INTRAUTERINE GROWTH-RETARDATION | INHIBITION | METABOLISM | FATTY LIVER-DISEASE | ER STRESS | MULTIDISCIPLINARY SCIENCES | CONSEQUENCES | ISCHEMIC-HEART-DISEASE | ENDOPLASMIC-RETICULUM STRESS | MODEL | THRIFTY PHENOTYPE HYPOTHESIS | Liver - pathology | Endoplasmic Reticulum - metabolism | Male | RNA, Messenger - metabolism | Heat-Shock Proteins - genetics | Leptin - blood | Fatty Acids, Nonesterified - blood | Female | Aspartate-Ammonia Ligase - metabolism | Disease Models, Animal | Glucose Tolerance Test | Unfolded Protein Response - genetics | Heat-Shock Proteins - metabolism | Liver - metabolism | Gene Expression Regulation | Aspartate-Ammonia Ligase - genetics | Metabolome | Rats | Fetal Growth Retardation - metabolism | Rats, Sprague-Dawley | Fetal Growth Retardation - pathology | Pregnancy | Animals | X-Box Binding Protein 1 - metabolism | X-Box Binding Protein 1 - genetics | Fetus | Cellular signal transduction | Models | Research | Gene expression | Growth retardation | Phosphorylation | Transcription factors | Disease | Liver | Genes | Homeostasis | Homology | mRNA | Activation | Glucose | Kinases | Proteins | Aspartate-ammonia ligase | Fatty liver | Protein folding | Rodents | Hepatology | Physiology | Lipogenesis | Gluconeogenesis | Medical research | Fetuses | Double-stranded RNA | Exposure | Metabolism | Steatosis | Glucose tolerance | Hypotheses | Hospitals | Ribonucleic acids | Protein kinase | Fibrosis | Asparagine | Insulin resistance | Diabetes | Gene therapy | Endoplasmic reticulum
Journal Article
Journal Article