Search results for "Hep"

showing 10 items of 12243 documents

Hyperammonemia alters the mismatch negativity in the auditory evoked potential by altering functional connectivity and neurotransmission

2020

Minimal hepatic encephalopathy (MHE) is a neuropsychiatric syndrome produced by central nervous system dysfunction subsequent to liver disease. Hyperammonemia and inflammation act synergistically to alter neurotransmission, leading to the cognitive and motor alterations in MHE, which are reproduced in rat models of chronic hyperammonemia. Patients with MHE show altered functional connectivity in different neural networks and a reduced response in the cognitive potential mismatch negativity (MMN), which correlates with attention deficits. The mechanisms by which MMN is altered in MHE remain unknown. The objectives of this work are as follows: To assess if rats with chronic hyperammonemia rep…

0301 basic medicineMalehippocampusPopulationMismatch negativityNeurotransmissionStimulus (physiology)Auditory cortexBiochemistrySynaptic Transmissionbehavioral disciplines and activitiesmetabolic diseases03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineNeural PathwaysmedicineAnimalsHyperammonemiaEvoked potentialRats Wistareducationeducation.field_of_studybusiness.industryGlutamate receptorBrainHyperammonemiamedicine.diseaseencephalopathyRats030104 developmental biologyHepatic EncephalopathyEvoked Potentials AuditorybusinessNeuroscience030217 neurology & neurosurgerypsychological phenomena and processes
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Nonacidic Farnesoid X Receptor Modulators.

2017

As a cellular bile acid sensor, farnesoid X receptor (FXR) participates in regulation of bile acid, lipid and glucose homeostasis, and liver protection. Clinical results have validated FXR as therapeutic target in hepatic and metabolic diseases. To date, potent FXR agonists share a negatively ionizable function that might compromise their pharmacokinetic distribution and behavior. Here we report the development and characterization of a high-affinity FXR modulator not comprising an acidic residue.

0301 basic medicineMalemedicine.drug_classPyridinesPeroxisome proliferator-activated receptorReceptors Cytoplasmic and NuclearATP-binding cassette transporterCholesterol 7 alpha-hydroxylase01 natural sciencesRats Sprague-Dawley03 medical and health sciencesStructure-Activity RelationshipDrug StabilityDrug DiscoverymedicineGlucose homeostasisAnimalsHumansPPAR alphaReceptorCholesterol 7-alpha-HydroxylaseATP Binding Cassette Transporter Subfamily B Member 11chemistry.chemical_classificationBile acid010405 organic chemistryChemistryHEK 293 cellsImidazolesMembrane Transport ProteinsHep G2 Cells0104 chemical sciencesMolecular Docking SimulationZolpidem030104 developmental biologyHEK293 CellsBiochemistryMolecular MedicineFarnesoid X receptorATP-Binding Cassette TransportersSterol Regulatory Element Binding Protein 1HeLa CellsJournal of medicinal chemistry
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Angiotensin II type II receptors and colonic dysmotility in 2,4-dinitrofluorobenzenesulfonic acid-induced colitis in rats

2016

Background: Angiotensin II (Ang II), the main peptide of the renin-angiotensin system (RAS), has been suggested to be involved in inflammatory bowel diseases. Since RAS has emerged as gut motility regulator, and dysmotility is associated with intestinal inflammation, our objective was to investigate in rat 2,4-dinitrobenzenesulfonic acid (DNBS)-induced colitis the functionality of RAS and its contribution to colonic motor alterations. Methods: The effects of Ang II on the longitudinal colonic muscular contractility of control and DNBS-treated rats were characterized in vitro. Transcripts encoding for Ang II receptors were investigated by RT-PCR. Key Results: Inflamed preparations showed a l…

0301 basic medicineMalemedicine.medical_specialtyAngiotensin receptormedicine.drug_classColonPhysiologyInflammationAT2 receptorReceptor Angiotensin Type 2Bowel inflammationEndocrine and Autonomic SystemContractilityRenin-Angiotensin System03 medical and health sciences0302 clinical medicineInternal medicinemedicineAnimalsRats WistarReceptorAngiotensin II receptor type 1Endocrine and Autonomic SystemsChemistryAT1 receptorAngiotensin IIMuscle contractilityGastroenterologyMuscle SmoothNitric oxideReceptor antagonistColitisAngiotensin II030104 developmental biologyEndocrinologyLosartancardiovascular system030211 gastroenterology & hepatologyDinitrofluorobenzenemedicine.symptomGastrointestinal Motilityhormones hormone substitutes and hormone antagonistsmedicine.drugMuscle Contraction
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Elevated Fatty Liver Index as a Risk Factor for All‐Cause Mortality in Human Immunodeficiency Virus–Hepatitis C Virus–Coinfected Patients (ANRS CO13 …

2020

International audience; Background and aims: Human immunodeficiency virus (HIV)-hepatitis C virus (HCV)-coinfected patients are at high risk of metabolic complications and liver-related events, which are both associated with hepatic steatosis and its progressive form, nonalcoholic steatohepatitis, a known risk factor for mortality. The fatty liver index (FLI), a noninvasive steatosis biomarker, has recently drawn attention for its clinical prognostic value, although its capacity to predict mortality risk in HIV-HCV-coinfected patients has never been investigated. Using a Cox proportional hazards model for mortality from all causes, with data from the French National Agency for Research on A…

0301 basic medicineMalemedicine.medical_specialtyCirrhosisHepatitis C virusmedicine.medical_treatment[SDV]Life Sciences [q-bio]HIV InfectionsLiver transplantationmedicine.disease_causeGastroenterologyAntiviral AgentsCohort Studies03 medical and health sciences0302 clinical medicineRisk Factors[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesInternal medicineCause of DeathmedicineHumansRisk factorComputingMilieux_MISCELLANEOUSHepatologybusiness.industryCoinfectionHazard ratioFatty liverHepatitis C ChronicMiddle Agedmedicine.disease3. Good healthFatty Liver[SDV] Life Sciences [q-bio]030104 developmental biology[SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases030211 gastroenterology & hepatologyFemaleFranceSteatosisViral hepatitisbusiness
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Hepatitis C virus intrinsic molecular determinants may contribute to the development of cholestatic hepatitis after liver transplantation

2018

Cholestatic hepatitis C (CHC) is a severe form of hepatitis C virus (HCV) infection recurrence that leads to high graft loss rates early after liver transplantation (LT). To investigate the pathogenic mechanisms of CHC, we analysed HCV quasispecies in CHC patients compared to a control group (mild hepatitis C recurrence) by deep pyrosequencing. At the time of LT, NS5B quasispecies complexity was similar between the two groups but, after LT, it decreased more sharply in CHC patients than in the control group. Interestingly, the major variant before LT propagated efficiently and remained as the dominant sequence after LT in 62 % of CHC patients versus 11 % of controls (P=0.031). Sequence anal…

0301 basic medicineMalemedicine.medical_specialtyGenotypeDeep sequencingSequence analysismedicine.medical_treatmentHepatitis C virus030106 microbiologyViral quasispeciesHepacivirusLiver transplantationBiologyViral Nonstructural ProteinsGraft lossmedicine.disease_causeGastroenterology03 medical and health scienceschemistry.chemical_compoundVirologyInternal medicinemedicineHumansNS5BAgedLiver transplantationHepatitis C virusHigh-Throughput Nucleotide SequencingHepatitis CHepatitis C ChronicMiddle Agedmedicine.diseaseVirologyCholestatic hepatitis CLiver TransplantationJaundice ObstructiveQuasispecies030104 developmental biologychemistryCholestatic hepatitisFemale
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Heterozygous carriage of the alpha1-antitrypsin Pi*Z variant increases the risk to develop liver cirrhosis.

2018

ObjectiveHomozygous alpha1-antitrypsin (AAT) deficiency increases the risk for developing cirrhosis, whereas the relevance of heterozygous carriage remains unclear. Hence, we evaluated the impact of the two most relevant AAT variants (‘Pi*Z’ and ‘Pi*S’), present in up to 10% of Caucasians, on subjects with non-alcoholic fatty liver disease (NAFLD) or alcohol misuse.DesignWe analysed multicentric case–control cohorts consisting of 1184 people with biopsy-proven NAFLD and of 2462 people with chronic alcohol misuse, both cohorts comprising cases with cirrhosis and controls without cirrhosis. Genotyping for the Pi*Z and Pi*S variants was performed.ResultsThe Pi*Z variant presented in 13.8% of p…

0301 basic medicineMalemedicine.medical_specialtyHeterozygoteCirrhosisMedizinSingle-nucleotide polymorphismDiseaseGastroenterologyPolymorphism Single NucleotideRisk Assessment03 medical and health sciences0302 clinical medicineAge DistributionLiver Cirrhosis AlcoholicNon-alcoholic Fatty Liver DiseaseInternal medicineGermanymedicinePiConfidence IntervalsOdds RatioHumansGenetic Predisposition to DiseaseRisk factorSex DistributionGenotypingLiver injurybusiness.industryGenetic Carrier ScreeningIncidenceFatty liverBiopsy NeedleGastroenterologyGenetic Variationmedicine.diseasePrognosisImmunohistochemistry030104 developmental biologyAustriaCase-Control Studiesalpha 1-Antitrypsin030211 gastroenterology & hepatologyFemalebusinessGut
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Recombinant human hepatocyte growth factor provides protective effects in cerulein-induced acute pancreatitis in mice.

2018

Acute pancreatitis is a multifactorial disease associated with profound changes of the pancreas induced by release of digestive enzymes that lead to increase in proinflammatory cytokine production, excessive tissue necrosis, edema, and bleeding. Elevated levels of hepatocyte growth factor (HGF) and its receptor c-Met have been observed in different chronic and acute pancreatic diseases including experimental models of acute pancreatitis. In the present study, we investigated the protective effects induced by the recombinant human HGF in a mouse model of cerulein-induced acute pancreatitis. Pancreatitis was induced by 8 hourly administrations of supramaximal cerulein injections (50 µg/kg, ip…

0301 basic medicineMalemedicine.medical_specialtyNecrosisPhysiologyClinical BiochemistryInflammationApoptosismedicine.disease_causeProtective AgentsAntioxidantsProinflammatory cytokine03 medical and health sciencesMiceInternal medicineEdemamedicineAnimalsHumansbusiness.industryHepatocyte Growth FactorCell BiologyProto-Oncogene Proteins c-metmedicine.diseaseGlutathioneSurvival AnalysisRecombinant ProteinsDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyPancreatitisAcute pancreatitisPancreatitisHepatocyte growth factormedicine.symptombusinessOxidative stressCeruletidemedicine.drugSignal TransductionJournal of cellular physiology
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Lysosomal acid lipase deficiency: Expanding differential diagnosis.

2016

The differential diagnoses for metabolic liver diseases may be challenging in clinical settings, which represents a critical issue for disorders such as lysosomal acid lipase deficiency (LAL-D). LAL-D is caused by deficient activity of the LAL enzyme, resulting in the accumulation of cholesteryl esters and triglycerides throughout the body, predominately in the liver, spleen, gastrointestinal tract, and blood vessel walls. LAL-D is a progressive, multi-organ disease with early mortality and significant morbidity characterized by a combination of hepatic dysfunction and dyslipidemia. Evidence suggests LAL-D may be substantially underdiagnosed or misdiagnosed, which is critical given that dis…

0301 basic medicineMalemedicine.medical_specialtyPathologyAdolescentEndocrinology Diabetes and MetabolismDiseaseLysosomal acid lipase deficiencyBiochemistryGastroenterologyDiagnosis Differential03 medical and health sciences0302 clinical medicineEndocrinologyInternal medicineGeneticsmedicineLysosomal storage diseaseHumansChildMolecular BiologyTriglyceridesNiemann-Pick DiseasesGaucher Diseasebusiness.industryWolman DiseaseInfantEnzyme replacement therapySterol Esterasemedicine.diseaseClinical trial030104 developmental biologyEarly DiagnosisSebelipase alfaDisease Progression030211 gastroenterology & hepatologyFemaleCholesterol EstersDifferential diagnosisbusinessDyslipidemiaMolecular genetics and metabolism
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Overactivation of the endocannabinoid system alters the antilipolytic action of insulin in mouse adipose tissue.

2017

Evidence has accumulated that obesity-related metabolic dysregulation is associated with overactivation of the endocannabinoid system (ECS), which involves cannabinoid receptor 1 (CB1R), in peripheral tissues, including adipose tissue (AT). The functional consequences of CB1R activation on AT metabolism remain unclear. Since excess fat mobilization is considered an important primary event contributing to the onset of insulin resistance, we combined in vivo and in vitro experiments to investigate whether activation of ECS could alter the lipolytic rate. For this purpose, the appearance of plasma glycerol was measured in wild-type and CB1R−/− mice after acute anandamide administration or inh…

0301 basic medicineMalemedicine.medical_specialtyPhysiologyEndocrinology Diabetes and Metabolismmedicine.medical_treatmentAdipose tissue030209 endocrinology & metabolismBiologyFatty Acids NonesterifiedCANNABINOID RECEPTOR 103 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineInsulin resistanceDownregulation and upregulationReceptor Cannabinoid CB1Physiology (medical)Internal medicineinsulin resistancemedicineLipolysisAnimalsInsulinendocannabinoid systemInsulinHydrolysis[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismmedicine.diseaseEndocannabinoid systemUp-RegulationJZL195Mice Inbred C57BLcannabinoid receptor 1030104 developmental biologyEndocrinologychemistryAdipose TissuelipolysisJZL195Endocannabinoids
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Infant Formula Feeding Increases Hepatic Cholesterol 7α Hydroxylase (CYP7A1) Expression and Fecal Bile Acid Loss in Neonatal Piglets.

2018

BACKGROUND: During the postnatal feeding period, formula-fed infants have higher cholesterol synthesis rates and lower circulating cholesterol concentrations than their breastfed counterparts. Although this disparity has been attributed to the uniformly low dietary cholesterol content of typical infant formulas, little is known of the underlying mechanisms associated with this altered cholesterol metabolism phenotype. OBJECTIVE: We aimed to determine the molecular etiology of diet-associated changes in early-life cholesterol metabolism with the use of a postnatal piglet feeding model. METHODS: Two-day-old male and female White-Dutch Landrace piglets were fed either sow milk (Sow group) or d…

0301 basic medicineMalemedicine.medical_specialtymedicine.drug_classSwineMedicine (miscellaneous)030209 endocrinology & metabolismCholesterol 7 alpha-hydroxylaseReal-Time Polymerase Chain ReactionGene Expression Regulation EnzymologicBile Acids and Salts03 medical and health scienceschemistry.chemical_compoundFecesRandom Allocation0302 clinical medicineBlood serumInternal medicinemedicineAnimalsHumansCholesterol 7-alpha-HydroxylaseEnterohepatic circulationNutrition and DieteticsBile acidCholesterolReverse Transcriptase Polymerase Chain ReactionInfantFGF19Infant Formula030104 developmental biologyEndocrinologyMilkchemistryInfant formulaAnimals NewbornLiverFemaleSoybeansNutrient Physiology Metabolism and Nutrient-Nutrient InteractionsBreast feedingThe Journal of nutrition
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