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1. Full Text Alzheimer's disease: early alterations in brain DNA methylation at ANK1, BIN1, RHBDF2 and other loci
by De Jager, Philip L and Srivastava, Gyan and Lunnon, Katie and Burgess, Jeremy and Schalkwyk, Leonard C and Yu, Lei and Eaton, Matthew L and Keenan, Brendan T and Ernst, Jason and McCabe, Cristin and Tang, Anna and Raj, Towfique and Replogle, Joseph and Brodeur, Wendy and Gabriel, Stacey and Chai, High S and Younkin, Curtis and Younkin, Steven G and Zou, Fanggeng and Szyf, Moshe and Epstein, Charles B and Schneider, Julie A and Bernstein, Bradley E and Meissner, Alex and Ertekin-Taner, Nilufer and Chibnik, Lori B and Kellis, Manolis and Mill, Jonathan and Bennett, David A
Nature Neuroscience, ISSN 1097-6256, 08/2014, Volume 17, Issue 9, pp. 1156 - 1163
We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease... 
RELIGIOUS ORDERS | COMMON VARIANTS | GENETIC RISK | SUSCEPTIBILITY LOCI | AGING PROJECT | COGNITIVE IMPAIRMENT | WIDE ASSOCIATION | NEUROPATHOLOGY | RUSH MEMORY | NEUROSCIENCES | GENOME | Brain | Neurodegenerative diseases | RNA | DNA methylation | Nervous system | Alzheimer's disease | CpG islands | Humans | Middle Aged | Male | Brain - physiology | Alzheimer Disease - pathology | Protein Interaction Maps | Amyloidosis - epidemiology | Amyloidosis - genetics | Tumor Suppressor Proteins - genetics | Aged, 80 and over | Alzheimer Disease - epidemiology | Female | Genetic Predisposition to Disease - epidemiology | Nuclear Proteins - genetics | Genetic Predisposition to Disease - genetics | Genome-Wide Association Study | Amyloidosis - pathology | DNA Methylation - genetics | Carrier Proteins - genetics | Ankyrins - genetics | Adaptor Proteins, Signal Transducing - genetics | Brain - pathology | CpG Islands - genetics | Aged | Alzheimer Disease - genetics | Brain research | Genetic susceptibility | Genetic research | Development and progression | Genetic aspects | Research | Methylation | Index Medicus
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2. The Phenotype and Genotype of Mevalonate Kinase Deficiency: A Series of 114 Cases From the Eurofever Registry
by ter Haar, Nienke M and Jeyaratnam, Jerold and Lachmann, Helen J and Simon, Anna and Brogan, Paul A and Doglio, Matteo and Cattalini, Marco and Anton, Jordi and Modesto, Consuelo and Quartier, Pierre and Hoppenreijs, Esther and Martino, Silvana and Insalaco, Antonella and Cantarini, Luca and Lepore, Loredana and Alessio, Maria and Calvo Penades, Inmaculada and Boros, Christina and Consolini, Rita and Rigante, Donato and Russo, Ricardo and Pachlopnik Schmid, Jana and Lane, Thirusha and Martini, Alberto and Ruperto, Nicolino and Frenkel, Joost and Gattorno, Marco and Paediat Rheumatology Int Trials and Paediatric Rheumatology International Trials Organisation and Eurofever Project
Arthritis and Rheumatology, ISSN 2326-5191, 11/2016, Volume 68, Issue 11, pp. 2795 - 2805
ObjectiveMevalonate kinase deficiency (MKD) is a rare metabolic disease characterized by recurrent inflammatory episodes. This study was undertaken to describe... 
MVK | HYPER-IGD | PERIODIC FEVER SYNDROME | ACIDURIA | HYPERIMMUNOGLOBULINEMIA-D | AUTOINFLAMMATORY DISEASES | MUTATIONS | SPECTRUM | RHEUMATOLOGY | Kinases | Genotype & phenotype | Cerebellum | Headache | Interleukin 1 receptor antagonist | etanercept | Consumers | Data processing | Fatigue | Inflammation | Macrophages | Mental retardation | Fever | Heterozygosity | Nonsteroidal antiinflammatory drugs | Lymphadenopathy | Mevalonate kinase | Cell activation | Remission | Amyloidosis | Children | Mutation | Age | Metabolic disorders | Steroid hormones | Genotypes | Arthralgia - etiology | Uveitis - etiology | Humans | Child, Preschool | Lymphadenopathy - etiology | Male | Arthralgia - physiopathology | Arthritis - genetics | Stomatitis, Aphthous - genetics | Cerebellar Diseases - physiopathology | Amyloidosis - genetics | Skin Diseases - physiopathology | Amyloidosis - etiology | Child | Stomatitis, Aphthous - etiology | Infant, Newborn | Myalgia - physiopathology | Amyloidosis - physiopathology | Genotype | Headache - physiopathology | Vomiting - genetics | Phenotype | Diarrhea - genetics | Abdominal Pain - genetics | Adolescent | Age of Onset | Intellectual Disability - etiology | Uveitis - genetics | Vomiting - physiopathology | Conjunctivitis - etiology | Conjunctivitis - genetics | Arthritis - physiopathology | Headache - etiology | Skin Diseases - genetics | Mevalonate Kinase Deficiency - physiopathology | Myalgia - genetics | Cerebellar Diseases - etiology | Diarrhea - physiopathology | Infant | Mevalonate Kinase Deficiency - genetics | Intellectual Disability - genetics | Pharyngitis - genetics | Arthritis - etiology | Female | Registries | Retrospective Studies | Arthralgia - genetics | Pharyngitis - physiopathology | Abdominal Pain - etiology | Pharyngitis - etiology | Lymphadenopathy - genetics | Abdominal Pain - physiopathology | Myalgia - etiology | Phosphotransferases (Alcohol Group Acceptor) - genetics | Headache - genetics | Intellectual Disability - physiopathology | Skin Diseases - etiology | Cerebellar Diseases - genetics | Conjunctivitis - physiopathology | Mevalonate Kinase Deficiency - complications | Stomatitis, Aphthous - physiopathology | Vomiting - etiology | Diarrhea - etiology | Lymphadenopathy - physiopathology | Uveitis - physiopathology
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3. Full Text The Contribution of SAA1 Polymorphisms to Familial Mediterranean Fever Susceptibility in the Japanese Population
by Migita, Kiyoshi and Agematsu, Kazunaga and Masumoto, Junya and Ida, Hiroaki and Honda, Seiyo and Jiuchi, Yuka and Izumi, Yasumori and Maeda, Yumi and Uehara, Ritei and Nakamura, Yoshikazu and Koga, Tomohiro and Kawakami, Atsushi and Nakashima, Munetoshi and Fujieda, Yuichiro and Nonaka, Fumiaki and Eguchi, Katsumi and Furukawa, Hiroshi and Nakamura, Tadashi and Nakamura, Minoru and Yasunami, Michio
PLoS ONE, ISSN 1932-6203, 02/2013, Volume 8, Issue 2, pp. e55227 - e55227
Background/Aims: Familial Mediterranean Fever (FMF) has traditionally been considered to be an autosomal-recessive disease, however, it has been observed that... 
RHEUMATOID-ARTHRITIS | AA-AMYLOIDOSIS | FMF PATIENTS | SERUM AMYLOID A1 | INTERLEUKIN-1-BETA | MULTIDISCIPLINARY SCIENCES | DISEASE | INFLAMMASOME | SECONDARY | MUTATIONS | GENE POLYMORPHISMS | Disease | Interleukin | Single-nucleotide polymorphism | Family medical history | Population genetics | Proteins | Interleukin 1 | Population | Tumor necrosis factor-TNF | Genetic loci | Familial Mediterranean fever | Amyloid | Genotypes | Public health | Variant genotypes | Internal medicine | Inflammasomes | Interleukin 1 receptor antagonist | Rheumatology | Inflammation | Environmental factors | Patients | Amyloid proteins | Fever | Medicine | Studies | Polymerase chain reaction | Hospitals | Pyrin protein | Gene frequency | Rheumatoid arthritis | Alleles | Amyloidosis | Mutation | Gene Frequency - genetics | Genetic Predisposition to Disease | Demography | Humans | Japan | Asian Continental Ancestry Group - genetics | Familial Mediterranean Fever - genetics | Genetic Loci - genetics | Interleukin 1 Receptor Antagonist Protein - genetics | Male | Serum Amyloid A Protein - genetics | Interleukin-1beta - genetics | Mutation - genetics | Case-Control Studies | Polymorphism, Single Nucleotide - genetics | Adult | Female | Disease susceptibility | Genetic aspects | Single nucleotide polymorphisms | Interleukins | Genes | Index Medicus
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4. Full Text The Tumor-Necrosis-Factor Receptor–Associated Periodic Syndrome: New Mutations in TNFRSF1A, Ancestral Origins, Genotype-Phenotype Studies, and Evidence for Further Genetic Heterogeneity of Periodic Fevers
by Aksentijevich, Ivona and Galon, Jérôme and Soares, Miguel and Mansfield, Elizabeth and Hull, Keith and Oh, Hye-Hyun and Goldbach-Mansky, Raphaela and Dean, Jane and Athreya, Balu and Reginato, Antonio J and Henrickson, Michael and Pons-Estel, Bernardo and O’Shea, John J and Kastner, Daniel L
The American Journal of Human Genetics, ISSN 0002-9297, 2001, Volume 69, Issue 2, pp. 301 - 314
Mutations in the extracellular domain of the 55-kD tumor-necrosis factor (TNF) receptor (TNFRSF1A), a key regulator of inflammation, define a periodic-fever... 
TNF RECEPTOR | ENCODING MEVALONATE KINASE | LOCALIZATION | COMPLEX | CHROMOSOME 12P13 | DISEASES | FAMILIAL MEDITERRANEAN FEVER | AMYLOIDOSIS | GENETICS & HEREDITY | IDENTIFICATION | LINKAGE | Tumor necrosis factor receptors | TNFRSF1A gene | periodic-fever syndrome | Gene frequency | Amyloidosis | man | tumor necrosis factor receptor-associated periodic syndrome | Fever | Humans | Molecular Sequence Data | Male | Antigens, CD - genetics | Haplotypes - genetics | Ethnic Groups - genetics | DNA Mutational Analysis | Amyloidosis - genetics | Base Sequence | Female | Antigens, CD - chemistry | Receptors, Tumor Necrosis Factor - genetics | Protein Structure, Tertiary | Amino Acid Sequence | Receptors, Tumor Necrosis Factor - chemistry | Introns - genetics | Alternative Splicing - genetics | Receptors, Tumor Necrosis Factor, Type I | Familial Mediterranean Fever - genetics | Models, Molecular | Exons - genetics | Penetrance | Mutation - genetics | Genetic Heterogeneity | Microsatellite Repeats - genetics | Pedigree | Polymorphism, Single Nucleotide - genetics | Gene mutations | Tumor necrosis factor | Analysis | Physiological aspects | Genetic aspects | Genomes | Index Medicus
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5. Full Text Phenotypic and genotypic characteristics of cryopyrin-associated periodic syndrome: a series of 136 patients from the Eurofever Registry
by Levy, R and Gérard, L and Kuemmerle-Deschner, J and Lachmann, H J and Koné-Paut, I and Cantarini, L and Woo, P and Naselli, A and Bader-Meunier, B and Insalaco, A and Al-Mayouf, S M and Ozen, S and Hofer, M and Frenkel, J and Modesto, C and Nikishina, I and Schwarz, T and Martino, S and Meini, A and Quartier, P and Martini, A and Ruperto, N and Neven, B and Gattorno, M and Eurofever and PRINTO and for PRINTO and Eurofever
Annals of the Rheumatic Diseases, ISSN 0003-4967, 11/2015, Volume 74, Issue 11, pp. 2043 - 2049
ObjectiveTo evaluate genetic, demographic and clinical features in patients with cryopyrin-associated periodic syndrome (CAPS) from the Eurofever Registry,... 
ARTICULAR SYNDROME | NLRP3 MUTATION | LOW-LEVEL MOSAICISM | SYNDROMES CAPS | GENETIC-HETEROGENEITY | MUCKLE-WELLS-SYNDROME | COLD AUTOINFLAMMATORY SYNDROME | RHEUMATOLOGY | CIAS1 MUTATIONS | AA AMYLOIDOSIS | MULTISYSTEM INFLAMMATORY DISEASE | Demography | Exanthema | Neurological complications | Familial Mediterranean Fever | Data processing | Skin | Inflammation | Mutation | Fever Syndromes | Fever | Age | Hearing loss | Arthralgia - etiology | Uveitis - etiology | Conjunctivitis - genetics | Headache - etiology | Exanthema - genetics | Myalgia - genetics | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Child, Preschool | Infant | Male | Papilledema - genetics | Arthritis - genetics | Meningitis - etiology | Exanthema - etiology | Young Adult | Arthritis - etiology | Germ-Line Mutation | Adult | Female | Registries | Retrospective Studies | Arthralgia - genetics | Child | Cryopyrin-Associated Periodic Syndromes - complications | Meningitis - genetics | Severity of Illness Index | Cryopyrin-Associated Periodic Syndromes - genetics | Europe | Genotype | Myalgia - etiology | Hearing Loss, Sensorineural - genetics | Headache - genetics | Cryopyrin-Associated Periodic Syndromes - physiopathology | Carrier Proteins - genetics | Phenotype | Hearing Loss, Sensorineural - etiology | Adolescent | Alleles | Heterozygote | Uveitis - genetics | Conjunctivitis - etiology | Cohort Studies | Papilledema - etiology | Complications and side effects | Nervous system diseases | Care and treatment | Research | Cryopyrin-associated periodic syndromes | Studies | Genotype & phenotype | Statistical analysis | Disease | Cold | Meningitis | Family medical history | Hearing impairment | Chronic illnesses | Index Medicus
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6. Full Text Prediction of Aggregation-Prone Regions in Structured Proteins
by Tartaglia, Gian Gaetano and Pawar, Amol P and Campioni, Silvia and Dobson, Christopher M and Chiti, Fabrizio and Vendruscolo, Michele
Journal of Molecular Biology, ISSN 0022-2836, 2008, Volume 380, Issue 2, pp. 425 - 436
We present a method for predicting the regions of the sequences of peptides and proteins that are most important in promoting their aggregation and amyloid... 
Aggregation | Prion disease | Parkinson's disease | Misfolding | Alzheimer's disease | FIBRIL FORMATION | prion disease | EXPERIMENTAL CONSTRAINTS | SOLID-STATE NMR | PODOSPORA-ANSERINA | BIOCHEMISTRY & MOLECULAR BIOLOGY | aggregation | ALPHA-SYNUCLEIN | HUMAN CALCITONIN | misfolding | HEREDITARY RENAL AMYLOIDOSIS | HET-S PRION | A-BETA | HUMAN PRION PROTEIN | Amino acid sequence | Amyloid | Prealbumin - genetics | Humans | Myoglobin - genetics | Glucagon - genetics | Molecular Sequence Data | Myoglobin - chemistry | Amyloid - chemistry | Trans-Activators - chemistry | Transcriptional Elongation Factors | Amyloid beta-Peptides - genetics | Computer Simulation | Glucagon - chemistry | Trans-Activators - genetics | Prealbumin - chemistry | alpha-Synuclein - genetics | Insulin - genetics | Peptide Fragments - genetics | Amino Acid Sequence | Amyloid - genetics | Muramidase - chemistry | Calcitonin - chemistry | Muramidase - genetics | Models, Molecular | Calcitonin - genetics | Protein Folding | alpha-Synuclein - chemistry | Proteins - genetics | Peptide Fragments - chemistry | Animals | Islet Amyloid Polypeptide | Insulin - chemistry | Protein Conformation | Software | Amyloid beta-Peptides - chemistry | Proteins - chemistry | Polypeptides | Index Medicus
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7. Full Text Timing of acquisition of deletion 13 in plasma cell dyscrasias is dependent on genetic context
by Laura Chiecchio and Gian Paolo Dagrada and Ashraf H. Ibrahim and Elizabet Dachs Cabanas and Rebecca K.M. Protheroe and David M. Stockley and Kim H. Orchard and Nicholas C.P. Cross and Christine J. Harrison and Fiona M. Ross and UK Myeloma Forum and on behalf of the UK Myeloma Forum
Haematologica, ISSN 0390-6078, 12/2009, Volume 94, Issue 12, pp. 1708 - 1713
Background Multiple myeloma, monoclonal gammopathy of undetermined significance and smoldering multiple myeloma harbor common chromosomal abnormalities but the... 
Deletion 13 | Genetic context | Plasma cell dyscrasias | MULTIPLE-MYELOMA | MONOSOMY-13 | TRANSLOCATIONS | 14Q32 | deletion 13 | CLASSIFICATION | plasma cell dyscrasias | PATHOGENESIS | AMYLOIDOSIS | genetic context | UNDETERMINED SIGNIFICANCE | MONOCLONAL GAMMOPATHY | CHROMOSOMAL-ABNORMALITIES | HEMATOLOGY | Chromosomes, Human, Pair 13 - genetics | Translocation, Genetic | Monoclonal Gammopathy of Undetermined Significance - genetics | Humans | Middle Aged | Paraproteinemias - genetics | Chromosomes, Human, Pair 4 - genetics | Chromosomes, Human, Pair 17 - genetics | Tumor Suppressor Protein p53 - genetics | Paraproteinemias - pathology | Time Factors | Aged, 80 and over | Adult | Chromosomes, Human, Pair 16 - genetics | Chromosome Deletion | In Situ Hybridization, Fluorescence | Chromosomes, Human, Pair 11 - genetics | Chromosomes, Human, Pair 6 - genetics | Multiple Myeloma - pathology | Monoclonal Gammopathy of Undetermined Significance - pathology | Gene Rearrangement | Aged | Cyclin D - genetics | Chromosomes, Human, Pair 14 - genetics | Immunoglobulin Heavy Chains - genetics | Multiple Myeloma - genetics | Index Medicus
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8. Full Text New Mutations of CIAS1 That Are Responsible for Muckle-Wells Syndrome and Familial Cold Urticaria: A Novel Mutation Underlies Both Syndromes
by Dodé, Catherine and Le Dû, Nathalie and Cuisset, Laurence and Letourneur, Frank and Berthelot, Jean-Marie and Vaudour, Gérard and Meyrier, Alain and Watts, Richard A and David Scott, G.I and Nicholls, Anne and Granel, Brigitte and Frances, Camille and Garcier, François and Edery, Patrick and Boulinguez, Serge and Domergues, Jean-Paul and Delpech, Marc and Grateau, Gilles
The American Journal of Human Genetics, ISSN 0002-9297, 2002, Volume 70, Issue 6, pp. 1498 - 1506
Mutations of CIAS1 have recently been shown to underlie familial cold urticaria (FCU) and Muckle-Wells syndrome (MWS), in three families and one family,... 
PROTEIN | DOMINANT PERIODIC FEVER | CROHNS-DISEASE | SUSCEPTIBILITY | GENETICS & HEREDITY | CHROMOSOME 1Q44 | DEAFNESS | IDENTIFICATION | ARTHRITIS | AUTOINFLAMMATORY SYNDROME | AA AMYLOIDOSIS | NLR Family, Pyrin Domain-Containing 3 Protein | Humans | Middle Aged | Urticaria - genetics | Urticaria - physiopathology | Child, Preschool | Molecular Sequence Data | Infant | Male | Haplotypes - genetics | Blood Proteins - genetics | DNA Mutational Analysis | Base Sequence | Adult | Female | Arthralgia - genetics | Child | Infant, Newborn | Amino Acid Sequence | Exons - genetics | Mutation - genetics | Syndrome | Carrier Proteins - genetics | Phenotype | Pedigree | Adolescent | Age of Onset | Alleles | Fever - genetics | Polymorphism, Single Nucleotide - genetics | Genetic research | Genetic aspects | Urticaria | Analysis | Index Medicus
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9. Full Text Amyloid fibril proteins and amyloidosis: chemical identification and clinical classification International Society of Amyloidosis 2016 Nomenclature Guidelines
by Sipe, Jean D and Benson, Merrill D and Buxbaum, Joel N and Ikeda, Shu-ichi and Merlini, Giampaolo and Saraiva, Maria J. M and Westermark, Per and Medicinska fakulteten and Medicinska och farmaceutiska vetenskapsområdet and Institutionen för immunologi, genetik och patologi and Uppsala universitet and Klinisk och experimentell patologi
Amyloid, ISSN 1350-6129, 10/2016, Volume 23, Issue 4, pp. 209 - 213
The Nomenclature Committee of the International Society of Amyloidosis (ISA) met during the XVth Symposium of the Society, 3 July-7 July 2016, Uppsala, Sweden,... 
inclusion body | nomenclature | amyloidosis | Amyloid fibril | amyloid protein | MEDICINE, RESEARCH & EXPERIMENTAL | BIOCHEMISTRY & MOLECULAR BIOLOGY | TRANSTHYRETIN AMYLOIDOSIS | MEDICINE, GENERAL & INTERNAL | TRANSMISSION | SEMEN | DISEASE | SENILE SYSTEMIC AMYLOIDOSIS | Staining and Labeling - methods | Prealbumin - genetics | Guidelines as Topic | Apolipoprotein C-III - chemistry | Protein Precursors - chemistry | Humans | Apolipoprotein C-III - metabolism | tau Proteins - metabolism | Amyloidosis - diagnosis | Amyloidogenic Proteins - chemistry | Apolipoprotein C-III - genetics | Apolipoprotein C-II - genetics | tau Proteins - chemistry | Sequence Analysis, Protein | tau Proteins - genetics | Amyloidosis - genetics | Amyloidosis - classification | Prealbumin - chemistry | alpha-Synuclein - genetics | Apolipoprotein C-II - chemistry | Amyloidogenic Proteins - genetics | Biomarkers - metabolism | Gene Expression | Protein Precursors - genetics | Amyloidosis - pathology | Terminology as Topic | Protein Precursors - metabolism | alpha-Synuclein - chemistry | Amyloidogenic Proteins - metabolism | Prealbumin - metabolism | Apolipoprotein C-II - metabolism | Birefringence | Congo Red - chemistry | alpha-Synuclein - metabolism | Coloring Agents - chemistry | Index Medicus | Basic Medicine | Medical and Health Sciences | Medicin och hälsovetenskap | Medicinska och farmaceutiska grundvetenskaper | Cell and Molecular Biology | Cell- och molekylärbiologi
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10. Full Text Mice with alopecia, osteoporosis, and systemic amyloidosis due to mutation in Zdhhc13, a gene coding for palmitoyl acyltransferase
by Saleem, Amir N and Chen, Yen-Hui and Baek, Hwa Jin and Hsiao, Ya-Wen and Huang, Hong-Wen and Kao, Hsiao-Jung and Liu, Kai-Ming and Shen, Li-Fen and Song, I-wen and Tu, Chen-Pei D and Wu, Jer-Yuarn and Kikuchi, Tateki and Justice, Monica J and Yen, Jeffrey J. Y and Chen, Yuan-Tsong
PLoS Genetics, ISSN 1553-7390, 06/2010, Volume 6, Issue 6, pp. 1 - 15
Protein palmitoylation has emerged as an important mechanism for regulating protein trafficking, stability, and protein protein interactions; however, its... 
FIBRIL FORMATION | SURFACTANT PROTEIN | MUTAGENESIS IDENTIFIES MICE | DISEASE | MOUSE | GENETICS & HEREDITY | TRAFFICKING | HIP14 | HUNTINGTIN | NF-KAPPA-B | EXPRESSION | Animal models | Nonsense mutation | Exons | Lipids | mRNA | Single-nucleotide polymorphism | Palmitic acid | Osteoporosis | Protein folding | Coding | Post-translation | Amyloid | Zinc finger proteins | Protein transport | Hair | Neurodegenerative diseases | Acyltransferase | Fatty acids | Polymerase chain reaction | Molecular modelling | chromosome 7 | Alopecia | Mutagenesis | Life span | Bone mineral density | Skin | Amyloidosis | Protein interaction | Gene mapping | palmitoylation | Immunohistochemistry | Amyloidosis - pathology | Gene Expression Regulation | Acyltransferases - metabolism | Organ Specificity | Acyltransferases - genetics | Alopecia - pathology | Alopecia - metabolism | Phenotype | Animals | Alopecia - genetics | Osteoporosis - metabolism | Osteoporosis - pathology | Amyloidosis - genetics | Base Sequence | Aging | Osteoporosis - genetics | Mice | Mutation | Amyloidosis - metabolism | Care and treatment | Baldness | Physiological aspects | Genetic aspects | Models | DNA binding proteins | Research | Risk factors | Index Medicus | Proteins | Bone density | Genes
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11. Full Text Loss of LR11/SORLA Enhances Early Pathology in a Mouse Model of Amyloidosis: Evidence for a Proximal Role in Alzheimer's Disease
by Dodson, Sara E and Andersen, Olav M and Karmali, Vinit and Fritz, Jason J and Cheng, Dongmei and Peng, Junmin and Levey, Allan I and Willnow, Thomas E and Lah, James J
Journal of Neuroscience, ISSN 0270-6474, 11/2008, Volume 28, Issue 48, pp. 12877 - 12886
Alzheimer's disease (AD) is the most prevalent form of dementia, resulting in progressive neuronal death and debilitating damage to brain loci that mediate... 
LR11 | Transgenic mouse | APOE | Alzheimer's disease | SORL1 | SORLA | β-amyloid | PRECURSOR PROTEIN APP | SORLA/LR11 | GENETIC-VARIANTS | transgenic mouse | NEUROSCIENCES | BETA | beta-amyloid | IN-VIVO | GENOME-WIDE | SORTILIN-RELATED RECEPTOR | ASSOCIATION | TRANSGENIC MICE | Brain | Up-Regulation | Genetic Predisposition to Disease | Neurons | Humans | Receptors, LDL | Gene Expression Regulation | Mice, Transgenic | Gene Dosage | Alzheimer Disease | Mice, Knockout | Index Medicus | Plaque, Amyloid | Animals | Membrane Transport Proteins | Amyloid beta-Peptides | Amyloidosis | Mice | Sorl1 protein, mouse | Amyloid beta-Protein Precursor | Disease Models, Animal | Neurons - pathology | Brain - metabolism | Membrane Transport Proteins - genetics | Amyloidosis - genetics | Amyloid beta-Peptides - metabolism | Amyloid beta-Protein Precursor - metabolism | Neurons - metabolism | Gene Dosage - genetics | Receptors, LDL - genetics | Alzheimer Disease - physiopathology | Genetic Predisposition to Disease - genetics | Plaque, Amyloid - pathology | Gene Expression Regulation - genetics | Brain - physiopathology | Amyloidosis - physiopathology | Up-Regulation - genetics | Plaque, Amyloid - genetics | Alzheimer Disease - metabolism | Plaque, Amyloid - metabolism | Alzheimer Disease - genetics | Amyloidosis - metabolism
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