Search results for "Phenotype"

showing 10 items of 1875 documents

GENETIC BASIS OF THE TRADE-OFF BETWEEN OFFSPRING NUMBER AND QUALITY IN THE BANK VOLE

2004

One of the main tenets of modern life-history theory is the negative relationship (trade-off) between the number and quality of offspring produced. Theory predicts a negative genetic correlation between these traits since both are closely related to fitness of individuals. However, the genetic basis of the trade-off has only been tested to a limited extent in natural populations. We examined whether size and quality of offspring are negatively related to litter size in the bank vole Clethrionomys glareolus. First, we found a significant negative phenotypic correlation between the number and size of offspring at birth in both laboratory and field populations of the bank vole. Second, a large…

Litter (animal)Litter SizeOffspringZoologyBiologyQuantitative trait locusTrade-offGenetic correlationQuantitative Trait HeritableGeneticsAnimalsSexual MaturationFinlandEcology Evolution Behavior and SystematicsGeneticsAnalysis of VarianceArvicolinaeReproductionbiology.organism_classificationBank volePhenotypeNegative relationshipBody ConstitutionFemaleAnalysis of varianceGeneral Agricultural and Biological SciencesEvolution
researchProduct

In vitro evidences of epithelial to mesenchymal transition in low cell-density cultured human fetal hepatocytes

2017

Abstract Culturing fetal hepatocytes in high cell-density allowed stabilization of the hepatocyte phenotype up to 8 weeks, including the maintenance of liver-specific functions. On the other hand, when cultured at low cell-density, fetal hepatocytes underwent morphological modifications and acquired fibroblastic morphology. Since a switch from E-cadherin to vimentin expression accompanied these changes, we hypothesized the occurrence of epithelial-to-mesenchymal transition when fetal hepatocytes were cultured at low cell-density. Changes in gene expressionsuch as up-regulation of fibrosis-related geneswere also observed, suggesting that the low cell-density culture system promoted the acqui…

Liver Cirrhosis0301 basic medicineEpithelial-Mesenchymal TransitionLiver fibrosisLiver fibrosisCell Culture TechniquesBiophysicsCell CountBiologyPrimary culturesBiochemistry03 medical and health sciencesFetal hepatocytesmedicineHumansEpithelial–mesenchymal transitionMolecular BiologyGeneCells CulturedEpithelial to mesenchymal transitionFetusTransition (genetics)Cell BiologyPhenotypeIn vitroCell biology030104 developmental biologymedicine.anatomical_structureLiverHepatocyteImmunologyHepatocytesBiochemical and Biophysical Research Communications
researchProduct

Dendritic cells in liver injury and fibrosis: shortcomings and promises.

2013

SummaryThe phenotype and function of liver dendritic cells (LDCs) are poorly understood. This Snapshot summarizes our current knowledge on LDCs in the healthy and injured liver, and their role in fibrosis progression and reversal. It also draws attention to various pitfalls in the current experimental design and conclusions based on available data.

Liver CirrhosisLiver dendritic cellsPlasmacytoid dendritic cellBiologyCCL2MiceFMS-like tyrosine kinase 3 ligandFibrosismedicineAnimalsHumansAntigen-presenting cellLiver injuryHepatologyFlt3LDendritic Cellsmedicine.diseaseCD11c-DTRDisease Models Animalmedicine.anatomical_structurePhenotypeLiverImmunologyHepatic stellate cellDisease ProgressionBone marrowToleranceJournal of hepatology
researchProduct

Liver Fibrosis and Metabolic Alterations in Adults With alpha-1-antitrypsin Deficiency Caused by the Pi*ZZ Mutation

2019

Background & Aims Alpha-1 antitrypsin deficiency (AATD) is among the most common genetic disorders. Severe AATD is caused by a homozygous mutation in the SERPINA1 gene that encodes the Glu342Lys substitution (called the Pi*Z mutation, Pi*ZZ genotype). Pi*ZZ carriers may develop lung and liver diseases. Mutation-associated lung disorders have been well studied, but less is known about the effects in liver. We assessed the liver disease burden and associated features in adults with this form of AATD. Methods We collected data from 554 Pi*ZZ adults (403 in an exploratory cohort, 151 in a confirmatory cohort), in 9 European countries, with AATD who were homozygous for the Pi*Z mutation, and 234…

Liver CirrhosisMale0301 basic medicineALTLiver diseasechemistry.chemical_compound0302 clinical medicineLiver Function TestsRisk FactorsGenotypeRare Liver DiseaseAlpha 1-antitrypsin deficiencyHomozygoteAge FactorsGastroenterologyMiddle AgedEuropeEditorial CommentaryPhenotypemedicine.anatomical_structureLiverElasticity Imaging TechniquesFemale030211 gastroenterology & hepatologyTEAdultmedicine.medical_specialty610Mice Transgenic03 medical and health sciencesSex Factorsalpha 1-Antitrypsin DeficiencyInternal medicinemedicinePiAnimalsHumansGenetic Predisposition to DiseaseASTAgedLungHepatologyTriglyceridebusiness.industryLipid Metabolismmedicine.diseaseFatty Liver030104 developmental biologyEndocrinologychemistryCase-Control Studiesalpha 1-AntitrypsinMutationSteatosisTransient elastographybusinessGastroenterology
researchProduct

The MBOAT7-TMC4 Variant rs641738 Increases Risk of Nonalcoholic Fatty Liver Disease in Individuals of European Descent

2016

Background & Aims Nonalcoholic fatty liver disease (NAFLD) is a leading cause of liver damage and is characterized by steatosis. Genetic factors increase risk for progressive NAFLD. A genome-wide association study showed that the rs641738 C>T variant in the locus that contains the membrane bound O-acyltransferase domain-containing 7 gene (MBOAT7, also called LPIAT1) and transmembrane channel-like 4 gene (TMC4) increased the risk for cirrhosis in alcohol abusers. We investigated whether the MBOAT7-TMC4 is a susceptibility locus for the development and progression of NAFLD. Methods We genotyped rs641738 in DNA collected from 3854 participants from the Dallas Heart Study (a multi-ethnic…

Liver CirrhosisMale0301 basic medicineCirrhosisBiopsyProton Magnetic Resonance SpectroscopyPhosphatidylinositolsTriglycerideSeverity of Illness IndexGastroenterologyLiver disease0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseMembrane Proteineducation.field_of_studyArachidonic Acidmedicine.diagnostic_testNASHGastroenterologyTexasEuropePhenotypeLiverLiver biopsyFemale030211 gastroenterology & hepatologyTexaCase-Control StudiePhosphatidylinositolHumanmedicine.medical_specialtyAcyltransferaseLiver CirrhosiEuropean Continental Ancestry GroupPopulationTM6SF2White PeopleArticle03 medical and health sciencesArachidonic Acid; NASH; PNPLA3; TM6SF2; Acetyltransferases; Acyltransferases; Biopsy; Case-Control Studies; Cross-Sectional Studies; Europe; European Continental Ancestry Group; Female; Genetic Predisposition to Disease; Genome-Wide Association Study; Humans; Liver; Liver Cirrhosis; Male; Membrane Proteins; Non-alcoholic Fatty Liver Disease; Phenotype; Phosphatidylinositols; Proton Magnetic Resonance Spectroscopy; Risk Factors; Severity of Illness Index; Texas; Triglycerides; Polymorphism GeneticGeneticAcetyltransferasesInternal medicineAcetyltransferasemedicineHumansGenetic Predisposition to DiseasePolymorphismeducationPNPLA3TriglyceridesCross-Sectional StudiePolymorphism GeneticHepatologybusiness.industryRisk FactorCase-control studyMembrane Proteinsmedicine.diseaseCross-Sectional Studies030104 developmental biologyEndocrinologyCase-Control StudiesSteatosisbusinessAcyltransferasesGenome-Wide Association StudyTM6SF2Gastroenterology
researchProduct

Genetic susceptibility of increased intestinal permeability is associated with progressive liver disease and diabetes in patients with non-alcoholic …

2020

Abstract Background and aim Increased intestinal permeability plays a key role in the pathogenesis of fat deposition in the liver. The aim of our study was to assess whether a single nucleotide polymorphism of protein tyrosine phosphatase non-receptor type 2 (PTPN2) (rs2542151 T→G), involved in intestinal permeability, may be associated with non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM). Methods and results We recruited a prospective cohort of NAFLD subjects and matched controls. Clinical data, PTPN2 genotype and laboratory data were collected for each patient. Results were stratified according to liver histology and diabetes. We enrolled 566 cases and 377 co…

Liver CirrhosisMaleEndocrinology Diabetes and MetabolismMedicine (miscellaneous)030204 cardiovascular system & hematologySeverity of Illness IndexGastroenterologyLiver disease0302 clinical medicineNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseasePrevalenceProspective StudiesProtein Tyrosine Phosphatase Non-Receptor Type 2Nutrition and Dieteticsmedicine.diagnostic_testFatty liverMiddle AgedPhenotypeItalyLiver biopsyFemaleCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtySettore MED/12 - GASTROENTEROLOGIA030209 endocrinology & metabolismIntestinal permeabilityPolymorphism Single NucleotideRisk AssessmentPermeability03 medical and health sciencesInternal medicineDiabetes mellitusmedicineGenetic susceptibilityHumansNonalcoholic fatty liver diseaseGenetic Predisposition to DiseaseGenetic Association Studiesbusiness.industryType 2 Diabetes Mellitusmedicine.diseaseCross-Sectional StudiesDiabetes Mellitus Type 2Intestinal AbsorptionCase-Control StudiesSteatosisSteatohepatitisbusiness
researchProduct

Increased hepatic fibrosis and JNK2-dependent liver injury in mice exhibiting hepatocyte-specific deletion of cFLIP.

2012

Chronic liver disease promotes hepatocellular injury involving apoptosis and triggers compensatory regeneration that leads to the activation of quiescent stellate cells in the liver. The deposition of extracellular matrix from activated myofibroblasts promotes hepatic fibrosis and the progression to cirrhosis with deleterious effects on liver physiology. The role of apoptosis signaling pathways in the development of fibrosis remains undefined. The aim of the current study was to determine the involvement of the caspase-8 homologue cellular FLICE-inhibitory protein (cFLIP) during the initiation and progression of fibrosis. Liver injury and fibrosis from carbon tetrachloride (CCl4) and thioa…

Liver CirrhosisMalePathologymedicine.medical_specialtyTime FactorsGenotypePhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBiologyThioacetamideChronic liver diseaseMicePhysiology (medical)medicineAnimalsMitogen-Activated Protein Kinase 9PhosphorylationExtracellular Signal-Regulated MAP KinasesCarbon TetrachlorideCompensatory regenerationLiver injuryMice KnockoutHepatologyCaspase 3Gastroenterologymedicine.diseaseCaspase 9Enzyme ActivationDisease Models Animalmedicine.anatomical_structurePhenotypeLiverApoptosisHepatocyteHepatic stellate cellCancer researchDisease ProgressionHepatocytesHepatocellular injuryChemical and Drug Induced Liver InjuryHepatic fibrosisSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
researchProduct

Hepatocyte-Specific Smad7 Expression Attenuates TGF-β–Mediated Fibrogenesis and Protects Against Liver Damage

2008

Background & Aims The profibrogenic role of transforming growth factor (TGF)-β in liver has mostly been attributed to hepatic stellate cell activation and excess matrix synthesis. Hepatocytes are believed to contribute to increased rates of apoptosis. Methods Primary hepatocyte outgrowths and AML12 cells were used as an in vitro model to detect TGF-β effects on the cellular phenotype and expression profile. Furthermore, a transgenic mouse model was used to determine the outcome of hepatocyte-specific Smad7 expression on fibrogenesis following CCl 4 -dependent damage. Samples from patients with chronic liver diseases were assessed for (partial) epithelial-to-mesenchymal transition (EMT) in h…

Liver CirrhosisMaleTime FactorsCell SurvivalApoptosisMice TransgenicBiologyCell LineSmad7 ProteinMiceTransforming Growth Factor betaFibrosismedicineAnimalsHumansSchistosomiasisEpithelial–mesenchymal transitionCarbon TetrachlorideCells CulturedOligonucleotide Array Sequence AnalysisR-SMADHepatologyGene Expression ProfilingGastroenterologyHepatitis Bmedicine.diseaseHepatic stellate cell activationMice Inbred C57BLCTGFDisease Models AnimalPhenotypemedicine.anatomical_structureHepatocyteCell TransdifferentiationHepatocytesCancer researchHepatic stellate cellCollagenTransforming growth factorGastroenterology
researchProduct

Genetic association of interleukin-6 polymorphism (-174 G/C) with chronic liver diseases and hepatocellular carcinoma

2012

Interleukin-6 (IL-6) is a pleiotropic cytokine which is expressed in many inflammatory cells in response to different types of stimuli, regulating a number of biological processes. The IL-6 gene is polymorphic in both the 5’ and 3’ flanking regions and more than 150 single nucleotide polymorphisms have been identified so far. Genetic polymorphisms of IL-6 may affect the outcomes of several diseases, where the presence of high levels of circulating IL-6 have been correlated to the stage and/or the progression of the disease itself. The -174 G/C polymorphism is a frequent polymorphism, that is located in the upstream regulatory region of the IL-6 gene and affects IL-6 production. However, the…

Liver Cirrhosismedicine.medical_specialtyCarcinoma HepatocellularHepatitis C virusSingle-nucleotide polymorphismBiologyChronic liver diseasemedicine.disease_causePolymorphism Single NucleotideGastroenterologyHepatitis B ChronicNon-alcoholic Fatty Liver DiseaseRisk FactorsChronic hepatitis Hepatocellular carcinoma Interleukin-6 Liver cirrhosis Single nucleotide polymorphismsInternal medicineGenotypemedicineHumansGenetic Predisposition to DiseaseTopic HighlightLiver Diseases AlcoholicInterleukin-6Liver NeoplasmsFatty liverGastroenterologyGeneral MedicineHepatitis C ChronicHepatitis Bmedicine.diseaseFatty LiverHepatitis AutoimmunePhenotypeHepatocellular carcinomaImmunologySteatohepatitisWorld Journal of Gastroenterology
researchProduct

Is processing speed a valid neurocognitive endophenotype in bipolar disorder? Evidence from a longitudinal, family study.

2021

[Background] Substantial evidence supports the existence of neurocognitive endophenotypes in bipolar disorder (BD), but very few longitudinal studies have included unaffected relatives. In a 5-year, follow-up, family study, we have recently suggested that deficits in manual motor speed and visual memory could be endophenotype candidates for BD. We aimed to explore whether this also applies to processing speed.

Longitudinal studyEndophenotypesBipolar disorderNeuropsychological TestsCognitionVisual memoryHumansMedicineLongitudinal StudiesBipolar disorderBiological Psychiatrybusiness.industryCognitionmedicine.diseaseFamily studyPsychiatry and Mental healthEndophenotypeMoodEndophenotypeDigit symbol substitution testLongitudinal studyCognition DisordersbusinessProcessing speedNeurocognitiveClinical psychology
researchProduct