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1. Full Text GLUTAMATE RECEPTOR-LIKE genes mediate leaf-to-leaf wound signalling
by Mousavi, Seyed A. R and Chauvin, Adeline and Pascaud, François and Kellenberger, Stephan and Farmer, Edward E
Nature, ISSN 0028-0836, 2013, Volume 500, Issue 7463, pp. 422 - 426
Wounded leaves communicate their damage status to one another through a poorly understood process of long-distance signalling. This stimulates the distal... 
RESPONSES | DEFENSE | ARABIDOPSIS-THALIANA | ATPASE ACTIVITY | HIGHER-PLANTS | JASMONIC ACID BIOSYNTHESIS | MULTIDISCIPLINARY SCIENCES | ACCUMULATION | POTENTIALS | INDUCTION | EXPRESSION | Receptors, Glutamate - metabolism | Genes, Plant | Herbivory - physiology | Plant Diseases - etiology | Electric Conductivity | Synaptic Transmission | Arabidopsis Proteins - metabolism | Synapses - metabolism | Models, Animal | Plant Diseases - genetics | Plant Leaves - drug effects | Nuclear Proteins - genetics | Arabidopsis Proteins - genetics | Arabidopsis - drug effects | Receptors, Glutamate - genetics | Nuclear Proteins - metabolism | Signal Transduction - genetics | Transcriptome - drug effects | Transcriptome - genetics | Cyclopentanes - pharmacology | Arabidopsis - metabolism | Isoleucine - metabolism | Arabidopsis - genetics | Oxylipins - metabolism | Gene Expression Regulation, Plant - drug effects | Animals | Plant Leaves - genetics | Plant Leaves - metabolism | Signal Transduction - drug effects | Isoleucine - analogs & derivatives | Oxylipins - pharmacology | Cyclopentanes - metabolism | Electrophysiological Phenomena | Mutation | Plant Growth Regulators - metabolism | Plant Growth Regulators - pharmacology | Electrodes | Plasma | Leaves | Gene expression
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2. Full Text Retinol-Binding Protein 4 and Insulin Resistance in Lean, Obese, and Diabetic Subjects
by Graham, Timothy E and Yang, Qin and Blüher, Matthias and Hammarstedt, Ann and Ciaraldi, Theodore P and Henry, Robert R and Wason, Christopher J and Oberbach, Andreas and Jansson, Per-Anders and Smith, Ulf and Kahn, Barbara B and Sahlgrenska akademin and Institute of Medicine, Department of Molecular and Clinical Medicine and Institutionen för medicin, avdelningen för molekylär och klinisk medicin and Göteborgs universitet and Gothenburg University and Sahlgrenska Academy
The New England Journal of Medicine, ISSN 0028-4793, 06/2006, Volume 354, Issue 24, pp. 2552 - 2563
In this study, serum levels of retinol-binding protein 4, a molecule secreted by adipocytes, correlated with the magnitude of insulin resistance in subjects... 
METABOLIC DEFECTS | MEDICINE, GENERAL & INTERNAL | PLASMA-CONCENTRATIONS | GLUCOSE | RETINOL-BINDING-PROTEIN | HYPERINSULINEMIA | ADIPOSITY | DYSLIPIDEMIA | CORONARY-HEART-DISEASE | FAT DISTRIBUTION | NIDDM | Cross-Sectional Studies | Glucose Transporter Type 4 - metabolism | Retinol-Binding Proteins, Plasma | Diabetes Mellitus, Type 2 - genetics | Humans | Middle Aged | Male | Diabetes Mellitus, Type 2 - metabolism | Obesity - blood | Thinness - metabolism | Obesity - metabolism | Metabolic Syndrome - blood | Diabetes Mellitus, Type 2 - blood | Retinol-Binding Proteins - metabolism | Insulin Resistance - physiology | Adipocytes - metabolism | Glucose Metabolism Disorders - metabolism | Thinness - blood | Glucose Metabolism Disorders - blood | Adult | Female | Exercise - physiology | Blood Glucose - metabolism | Insulin resistance | Diabetes | Glucose | Insulin | Rodents | Obesity/blood/metabolism | Blood Glucose/metabolism | Adipocytes/metabolism | Thinness/blood/metabolism | Exercise/physiology | MEDICIN OCH HÄLSOVETENSKAP | Diabetes Mellitus | Glucose Transporter Type 4/metabolism | Type 2/blood/genetics/metabolism | Glucose Metabolism Disorders/blood/metabolism | Insulin Resistance/physiology | Metabolic Syndrome X/blood | Retinol-Binding Proteins/metabolism | MEDICAL AND HEALTH SCIENCES
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3. Full Text Angiopoietin-like 4 (ANGPTL4, Fasting-induced Adipose Factor) Is a Direct Glucocorticoid Receptor Target and Participates in Glucocorticoid-regulated Triglyceride Metabolism
by Suneil K. Koliwad and Taiyi Kuo and Lauren E. Shipp and Nora E. Gray and Fredrik Backhed and Alex Yick-Lun So and Robert V. Farese, Jr and Jen-Chywan Wang and Sahlgrenska akademin and Institute of Medicine, Department of Molecular and Clinical Medicine and Institutionen för medicin, avdelningen för molekylär och klinisk medicin and Göteborgs universitet and Gothenburg University and Sahlgrenska Academy
Journal of Biological Chemistry, ISSN 0021-9258, 09/2009, Volume 284, Issue 38, pp. 25593 - 25601
Glucocorticoids are important regulators of lipid homeostasis, and chronically elevated glucocorticoid levels induce hypertriglyceridemia, hepatic steatosis,... 
OBESITY | PLASMA | GENE | CHROMATIN | ANGIOGENESIS | DIET | BIOCHEMISTRY & MOLECULAR BIOLOGY | HYPERLIPIDEMIA | MICE | TRANSCRIPTIONAL REGULATION | PROTEIN-4 | Transcription, Genetic - drug effects | Hypertriglyceridemia - genetics | Humans | Dexamethasone - adverse effects | Receptors, Glucocorticoid - metabolism | Hepatocytes - metabolism | Fatty Liver - chemically induced | Adipose Tissue - metabolism | Angiopoietin-like 4 Protein | Dexamethasone - pharmacology | Glucocorticoids - genetics | Glucocorticoids - metabolism | Response Elements - genetics | Lipoprotein Lipase - metabolism | Glucocorticoids - adverse effects | Fatty Liver - genetics | Angiopoietins - metabolism | Fatty Liver - metabolism | Lipoprotein Lipase - genetics | Liver - metabolism | Rats | Hypertriglyceridemia - metabolism | Mice, Knockout | Triglycerides - metabolism | Adipose Tissue, White | Hypertriglyceridemia - chemically induced | Animals | Receptors, Glucocorticoid - genetics | Cell Line, Tumor | Dexamethasone - metabolism | Glucocorticoids - pharmacology | Mice | Transcription, Genetic - genetics | Triglycerides - genetics | Angiopoietins - genetics | Index Medicus | Lipids and Lipoproteins | Metabolism, Regulation, and Signaling | Transcription | Dermatologi och venereologi | Dermatology and Venereal Diseases | Dexamethasone/adverse effects/metabolism/pharmacology | Hypertriglyceridemia/chemically induced/genetics/metabolism | Receptors | Adipose Tissue/metabolism | Liver/metabolism | Tumor | Adipose Tissue | Cell Line | Fatty Liver/chemically induced/genetics/metabolism | Triglycerides/genetics/ metabolism | Response Elements/genetics | Angiopoietins/genetics/ metabolism | Knockout | Lipoprotein Lipase/genetics/metabolism | White | Hepatocytes/metabolism | Genetic/drug effects/genetics | Glucocorticoids/adverse effects/genetics/ metabolism/pharmacology | Glucocorticoid/genetics/ metabolism
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4. Full Text Creatine biosynthesis and transport in health and disease
by Joncquel-Chevalier Curt, Marie and Voicu, Pia-Manuela and Fontaine, Monique and Dessein, Anne-Frédérique and Porchet, Nicole and Mention-Mulliez, Karine and Dobbelaere, Dries and Soto-Ares, Gustavo and Cheillan, David and Vamecq, Joseph
Biochimie, ISSN 0300-9084, 12/2015, Volume 119, pp. 146 - 165
Creatine is physiologically provided equally by diet and by endogenous synthesis from arginine and glycine with successive involvements of arginine glycine... 
GAMT | CRTR | SLC6A8 | AGAT | AMP activated protein kinase | Creatine | Secondary creatine disorders | GUANIDINOACETATE METHYLTRANSFERASE DEFICIENCY | OXIDATIVE STRESS | BIOCHEMISTRY & MOLECULAR BIOLOGY | OXYGEN SPECIES GENERATION | UREA CYCLE DISORDERS | MAGNETIC-RESONANCE-SPECTROSCOPY | RAT-KIDNEY TRANSAMIDINASE | LINKED MENTAL-RETARDATION | ACUTE MYOCARDIAL-INFARCTION | TERM-FOLLOW-UP | ARGININE-GLYCINE AMIDINOTRANSFERASE | Amino Acid Transport Systems, Basic - genetics | Humans | Nerve Tissue Proteins - deficiency | Movement Disorders - diagnosis | Amidinotransferases - genetics | Intellectual Disability - metabolism | Biological Transport, Active | Gyrate Atrophy - enzymology | Amino Acid Metabolism, Inborn Errors - genetics | Intellectual Disability - enzymology | Brain Diseases, Metabolic, Inborn - genetics | Hyperammonemia - diagnosis | Hyperammonemia - genetics | Creatine - genetics | Urea Cycle Disorders, Inborn - metabolism | Creatine - biosynthesis | Gyrate Atrophy - genetics | Plasma Membrane Neurotransmitter Transport Proteins - metabolism | Guanidinoacetate N-Methyltransferase - metabolism | Amidinotransferases - metabolism | Plasma Membrane Neurotransmitter Transport Proteins - genetics | Language Development Disorders - enzymology | Urea Cycle Disorders, Inborn - diagnosis | Energy Metabolism | Urea Cycle Disorders, Inborn - enzymology | Movement Disorders - genetics | Mutation | Ornithine - deficiency | Amino Acid Transport Systems, Basic - metabolism | Amino Acid Metabolism, Inborn Errors - enzymology | S-Adenosylmethionine - metabolism | AMP-Activated Protein Kinases - metabolism | Hyperammonemia - metabolism | Developmental Disabilities - metabolism | Guanidinoacetate N-Methyltransferase - genetics | Ornithine - genetics | Developmental Disabilities - genetics | Language Development Disorders - metabolism | Brain Diseases, Metabolic, Inborn - enzymology | Brain Diseases, Metabolic, Inborn - diagnosis | Intellectual Disability - genetics | Amino Acid Metabolism, Inborn Errors - diagnosis | Amino Acid Metabolism, Inborn Errors - metabolism | Mental Retardation, X-Linked - genetics | Mental Retardation, X-Linked - enzymology | Developmental Disabilities - enzymology | Language Development Disorders - diagnosis | Mental Retardation, X-Linked - diagnosis | Movement Disorders - enzymology | Creatine - metabolism | Hyperammonemia - enzymology | Creatine - deficiency | Gyrate Atrophy - diagnosis | Developmental Disabilities - diagnosis | Speech Disorders - diagnosis | Plasma Membrane Neurotransmitter Transport Proteins - deficiency | Speech Disorders - metabolism | Amidinotransferases - deficiency | Brain Diseases, Metabolic, Inborn - metabolism | Language Development Disorders - genetics | Ornithine - metabolism | Gyrate Atrophy - metabolism | Prenatal Diagnosis | Speech Disorders - genetics | Nerve Tissue Proteins - genetics | Nerve Tissue Proteins - metabolism | Amino Acid Transport Systems, Basic - deficiency | Movement Disorders - metabolism | Animals | Urea Cycle Disorders, Inborn - genetics | Guanidinoacetate N-Methyltransferase - deficiency | Intellectual Disability - diagnosis | Movement Disorders - congenital | Speech Disorders - enzymology | Methylation | Mental Retardation, X-Linked - metabolism | Antioxidants | Phosphates | Algorithms | Animal behavior | Physiological aspects | GABA | Glycine | Phosphotransferases | Medical research | Medicine, Experimental | Protein kinases | Life Sciences
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5. Full Text Programmed necrosis induced by asbestos in human mesothelial cells causes high-mobility group box 1 protein release and resultant inflammation
by Haining Yang and Zeyana Rivera and Sandro Jube and Masaki Nasu and Pietro Bertino and Chandra Goparaju and Guido Franzoso and Michael T. Lotze and Thomas Krausz and Harvey I. Pass and Marco E. Bianchi and Michele Carbone and Janet D. Rowley
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 7/2010, Volume 107, Issue 28, pp. 12611 - 12616
Asbestos carcinogenesis has been linked to the release of cytokines and mutagenic reactive oxygen species (ROS) from inflammatory cells. Asbestos is cytotoxic... 
Actinomycin | Asbestos | Cell death | Secretion | Plasma cells | Inflammation | Macrophages | Carcinogenesis | Necrosis | Apoptosis | Mesothelioma | Biomarker | Tumor necrosis factor-alpha | Chemoprevention | TRANSFORMATION | POLY(ADP-RIBOSE) POLYMERASE | MACROPHAGES | MULTIDISCIPLINARY SCIENCES | CROCIDOLITE ASBESTOS | HMGB1 | biomarker | MAMMALIAN-CELLS | tumor necrosis factor-alpha | PATHOGENESIS | chemoprevention | NECROTIC CELLS | carcinogenesis | TNF-ALPHA | INHIBITORS | mesothelioma | Tumor Necrosis Factor-alpha - metabolism | Asbestos - metabolism | Epithelial Cells - metabolism | Reactive Oxygen Species - metabolism | Humans | Reactive Oxygen Species - pharmacology | Adenosine Diphosphate Ribose - metabolism | Adenosine Diphosphate Ribose - pharmacology | Carcinogens - metabolism | Asbestos - pharmacology | Pleural Neoplasms - metabolism | Inflammation - metabolism | Carcinogens - pharmacology | Cell Nucleus - metabolism | HMGB Proteins - pharmacology | HMGB1 Protein - pharmacology | HMGB1 Protein - metabolism | Cell Death | Mesocricetus | Female | HMGB Proteins - metabolism | Poly Adenosine Diphosphate Ribose - pharmacology | Epithelium - drug effects | Cricetinae | Cytokines - metabolism | Epithelium - metabolism | Hydrogen Peroxide - pharmacology | Necrosis - metabolism | Hydrogen Peroxide - metabolism | Tumor Necrosis Factor-alpha - pharmacology | Macrophages - metabolism | Poly(ADP-ribose) Polymerases - metabolism | Animals | Mesothelioma - metabolism | Poly(ADP-ribose) Polymerases - pharmacology | Cells - metabolism | Mice | Mice, Inbred BALB C | Cytokines - pharmacology | Prevention | Mesothelium | Chromosomal proteins | Research | Chemical properties | Health aspects | Reactive oxygen species | Transformation | Deposits | Hydrogen peroxide | Cytokines | Cytotoxicity | HMGB1 protein | Nuclei | Carcinogens | Tumor necrosis factor-a | ATP | Cytoplasm | Biological Sciences
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6. Full Text Microtubules and Actin Microfilaments Regulate Lipid Raft/Caveolae Localization of Adenylyl Cyclase Signaling Components
by Brian P. Head and Hemal H. Patel and David M. Roth and Fiona Murray and James S. Swaney and Ingrid R. Niesman and Marilyn G. Farquhar and Paul A. Insel
Journal of Biological Chemistry, ISSN 0021-9258, 09/2006, Volume 281, Issue 36, pp. 26391 - 26399
Microtubules and actin filaments regulate plasma membrane topography, but their role in compartmentation of caveolae-resident signaling components, in... 
CYCLIC-AMP ACCUMULATION | S49 LYMPHOMA-CELLS | BIOCHEMISTRY & MOLECULAR BIOLOGY | CARDIAC MYOCYTES | CYTOSKELETAL ROLE | GTPASE-ACTIVATING PROTEIN | PLASMA-MEMBRANE | PROTEIN-TYROSINE-PHOSPHATASE | SMOOTH-MUSCLE CELLS | FOCAL ADHESIONS | PHOSPHORYLATED CAVEOLIN | Cell Fractionation | Nucleic Acid Synthesis Inhibitors - metabolism | Receptors, G-Protein-Coupled - metabolism | Membrane Microdomains - metabolism | Actins - metabolism | Cytochalasin D - metabolism | Male | Caveolins - metabolism | Caveolins - genetics | Microtubules - metabolism | Protein Isoforms - metabolism | Adrenergic beta-Agonists - metabolism | Tubulin Modulators - metabolism | Microfilament Proteins - metabolism | Contractile Proteins - metabolism | Receptors, Adrenergic, beta - metabolism | Cyclic AMP - metabolism | Sarcolemma - metabolism | Actin Cytoskeleton - metabolism | Caveolae - metabolism | Cells, Cultured | Isoproterenol - metabolism | Colchicine - metabolism | Rats | Adenylyl Cyclases - metabolism | Rats, Sprague-Dawley | Filamins | Mice, Knockout | Animals | Models, Biological | Sarcolemma - ultrastructure | Cytoskeleton - metabolism | Myocytes, Cardiac - metabolism | Signal Transduction - physiology | Mice | Adenylyl Cyclases - genetics | Myocytes, Cardiac - ultrastructure | Protein Isoforms - genetics
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7. Full Text Personal model-assisted identification of NAD(+) and glutathione metabolism as intervention target in NAFLD
by Mardinoglu, Adil and Bjornson, Elias and Zhang, Cheng and Klevstig, Martina and Söderlund, Sanni and Ståhlman, Marcus and Adiels, Martin and Hakkarainen, Antti and Lundbom, Nina and Kilicarslan, Murat and Hallström, Björn M and Lundbom, Jesper and Vergès, Bruno and Barrett, Peter Hugh R and Watts, Gerald F and Serlie, Mireille J and Nielsen, Jens and Uhlén, Mathias and Smith, Ulf and Marschall, Hanns-Ulrich and Taskinen, Marja-Riitta and Boren, Jan and Science for Life Laboratory, SciLifeLab and KTH and Centra
Molecular systems biology, ISSN 1744-4292, 2017, Volume 13, Issue 3, pp. 916 - n/a
To elucidate the molecular mechanisms underlying non-alcoholic fatty liver disease (NAFLD), we recruited 86 subjects with varying degrees of hepatic steatosis... 
serine | NAFLD | personalized genome‐scale metabolic modeling | glutathione | personalized genome-scale metabolic modeling | FATTY LIVER-DISEASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | MUSCLE | DRUG TARGETS | CANCER | AMINO-ACID-METABOLISM | HEPATOCELLULAR-CARCINOMA | INSULIN-RESISTANCE | ADIPOSE-TISSUE | GENOME-SCALE | REVEALS | Glycine - blood | Liver - enzymology | Non-alcoholic Fatty Liver Disease - genetics | Glutathione - metabolism | Serine - blood | Humans | Liver - metabolism | Middle Aged | Male | Non-alcoholic Fatty Liver Disease - metabolism | Patient-Specific Modeling | Metabolomics - methods | Gene Expression Regulation, Enzymologic | Serine - administration & dosage | Animals | Lipoproteins - metabolism | Female | Mice | Non-alcoholic Fatty Liver Disease - diet therapy | Genome | NAD - metabolism | Serine - therapeutic use | Disease Models, Animal | Genomes | Metabolites | Metabolism | Liver | Rodents | Serine | Lipids | Biosynthesis | Glycine | Body mass index | Fatty liver | Precursors | Supplementation | Glutathione | Level (quantity) | Liver diseases | Fasting | Demand analysis | Dietary supplements | Triglycerides | Fluxes | Apolipoproteins | Gene expression | Cholesterol | Steatosis | NAD | Molecular modelling | Insulin resistance | Plasma levels | Laboratory animals | Life Sciences | Biochemistry, Molecular Biology | Biological Sciences | Naturvetenskap | Biologiska vetenskaper | Natural Sciences
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8. Full Text No beneficial effects of resveratrol on the metabolic syndrome: A randomized placebo-controlled clinical trial
by Kjær, Thomas Nordstrøm and Ornstrup, Marie Juul and Poulsen, Morten Møller and Stødkilde-Jørgensen, Hans and Jessen, Niels and Jørgensen, Jens Otto Lunde and Richelsen, Bjørn and Pedersen, Steen Bønløkke
Journal of Clinical Endocrinology and Metabolism, ISSN 0021-972X, 05/2017, Volume 102, Issue 5, pp. 1642 - 1651
Context: Low-grade inflammation is associated with obesity and the metabolic syndrome (MetS). Preclinical evidence suggests that resveratrol (RSV) has... 
SUPPLEMENTATION | OBESE MEN | ALKALINE-PHOSPHATASE | INFLAMMATION | ENDOCRINOLOGY & METABOLISM | SECRETION | HEALTH | CORONARY-ARTERY-DISEASE | CHALLENGES | Blood Pressure | Body Composition | Stilbenes - therapeutic use | Humans | Leptin - metabolism | Middle Aged | Male | Metabolic Syndrome - metabolism | Muscle, Skeletal - metabolism | Adipose Tissue - immunology | Metabolic Syndrome - drug therapy | Fructosamine - metabolism | Adipose Tissue - metabolism | Muscle, Skeletal - immunology | Liver - diagnostic imaging | Quadriceps Muscle - immunology | Metabolic Syndrome - immunology | Real-Time Polymerase Chain Reaction | Double-Blind Method | Magnetic Resonance Spectroscopy | Cholesterol, HDL - metabolism | Liver - metabolism | Insulin Resistance | Cholesterol - metabolism | Intra-Abdominal Fat - metabolism | Absorptiometry, Photon | Blotting, Western | Triglycerides - metabolism | Receptors, Urokinase Plasminogen Activator - metabolism | Intra-Abdominal Fat - diagnostic imaging | Magnetic Resonance Imaging | Antioxidants - therapeutic use | Insulin - metabolism | Muscle, Skeletal - diagnostic imaging | Interleukin-6 - immunology | Cholesterol, LDL - metabolism | Blood Glucose - metabolism | Quadriceps Muscle - metabolism | C-Reactive Protein - immunology | C-reactive protein | Pressure effects | Liver | Interleukin | Medical services | Homeostasis | Clinical trials | Lipids | Standard error | Glucose | Metabolic syndrome | Composition effects | Blood | Body composition | Interleukin 6 | Body mass index | Urokinase | Glucose metabolism | Randomization | Body composition (biology) | Resveratrol | Blood pressure | Bioindicators | Lipid metabolism | Supplementation | Deposition | Middle age | Dietary supplements | Muscles | Inflammation | Gene expression | Metabolism | Low density lipoprotein | Cholesterol | Skeletal muscle | U-Plasminogen activator | Body mass | Biopsy | Body size | Men | Plasma levels | Metabolic disorders
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9. Full Text Antibody-aided clearance of extracellular α-synuclein prevents cell-to-cell aggregate transmission
by Bae, Eun-Jin and Lee, He-Jin and Rockenstein, Edward and Ho, Dong-Hwan and Park, Eun-Bi and Yang, Na-Young and Desplats, Paula and Masliah, Eliezer and Lee, Seung-Jae
Journal of Neuroscience, ISSN 0270-6474, 09/2012, Volume 32, Issue 39, pp. 13454 - 13469
Abnormal deposition and intercellular propagation of alpha-synuclein plays a central role in the pathogenesis of disorders such as Parkinson's Disease (PD) and... 
IMMUNIZATION | PROTEIN | PLASMA | BIOMARKER | ALZHEIMERS-DISEASE | MOUSE MODEL | PATHOLOGY | FC-GAMMA-RIIA | NEUROSCIENCES | NEURODEGENERATIVE DISEASES | PARKINSONS-DISEASE | Synaptic Transmission - physiology | Antibodies - metabolism | Lewy Body Disease - immunology | Humans | alpha-Synuclein - immunology | Extracellular Space - drug effects | Nerve Degeneration - genetics | Cell Communication - physiology | Culture Media, Conditioned - pharmacology | Phosphopyruvate Hydratase - metabolism | Amyloid - ultrastructure | Antigens, CD - metabolism | Neuroglia - drug effects | Brain - metabolism | Lewy Body Disease - genetics | Extracellular Space - metabolism | Amyloid - metabolism | Microfilament Proteins - metabolism | alpha-Synuclein - genetics | Disease Models, Animal | Calcium-Binding Proteins - metabolism | Cell Line | Microscopy, Electron, Transmission | Cytokines - metabolism | Mice, Transgenic | Nerve Degeneration - immunology | Cathepsin D - metabolism | Extracellular Space - immunology | Antibodies - pharmacology | Caveolin 1 - metabolism | Lewy Body Disease - metabolism | Platelet-Derived Growth Factor - metabolism | Animals | Analysis of Variance | Brain - pathology | Immunization, Passive | Neuroglia - metabolism | Mice | Chromatography, Gel | alpha-Synuclein - metabolism | Nerve Degeneration - drug therapy | Astrocytes - metabolism
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