Search results for "onset."

showing 10 items of 478 documents

Investigating fibrosis and inflammation in an ex vivo NASH murine model.

2020

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease, characterized by excess fat accumulation (steatosis). Nonalcoholic steatohepatitis (NASH) develops in 15–20% of NAFLD patients and frequently progresses to liver fibrosis and cirrhosis. We aimed to develop an ex vivo model of inflammation and fibrosis in steatotic murine precision-cut liver slices (PCLS). NASH was induced in C57Bl/6 mice on an amylin and choline-deficient l-amino acid-defined (CDAA) diet. PCLS were prepared from steatohepatitic (sPCLS) and control (cPCLS) livers and cultured for 48 h with LPS, TGFβ1, or elafibranor. Additionally, C57Bl/6 mice were placed on CDAA diet for 12 wk to receive elafibranor…

0301 basic medicineLipopolysaccharidesLiver CirrhosisMalePhysiologyHEPATOCYTESLiver diseaseMice0302 clinical medicineChalconesFibrosisNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseCells CulturedINSULIN-RESISTANCEGastroenterologyElafibranorTGF-BETALiver030211 gastroenterology & hepatologyCHOLINE-DEFICIENT DIETEXPRESSIONmedicine.medical_specialtyEARLY-ONSETIn Vitro TechniquesCollagen Type IProinflammatory cytokineTransforming Growth Factor beta103 medical and health sciencesIn vivoPhysiology (medical)Internal medicinemedicineAnimalsHEPATIC STEATOSISFATTY LIVER-DISEASEInflammationPRECISION-CUT LIVERHepatologybusiness.industrymedicine.diseaseLipid MetabolismDietMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyPROLIFERATOR-ACTIVATED RECEPTORSSteatosisPropionatesbusinessTranscriptomeEx vivoAmerican journal of physiology. Gastrointestinal and liver physiology
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PI3K inhibition reduces murine and human liver fibrogenesis in precisioncut liver slices

2019

Background: Liver fibrosis results from continuous inflammation and injury. Despite its high prevalence worldwide, no approved antifibrotic therapies exist. Omipalisib is a selective inhibitor of the PI3K/mTOR pathway that controls nutrient metabolism, growth and proliferation. It has shown antifibrotic properties in vitro. While clinical trials for idiopathic pulmonary fibrosis have been initiated, an in-depth preclinical evaluation is lacking. We evaluated omipalisib's effects on fibrogenesis using the ex vivo model of murine and human precision-cut tissue slices (PCTS).Methods: Murine and human liver and jejunum PCTS were incubated with omipalisib up to 10 mu M for 48 h. PI3K pathway act…

0301 basic medicineLiver CirrhosisMalePrecision-cut tissue slicesPROGRESSIONPharmacologyBILIARYBiochemistryPI3KGSK2126458JejunumMicePhosphatidylinositol 3-Kinases0302 clinical medicineAdenosine TriphosphateFibrosisFIBROSIShealth care economics and organizationsPhosphoinositide-3 Kinase InhibitorsSulfonamidesPyridazinesmedicine.anatomical_structureJejunumTARGET030220 oncology & carcinogenesisToxicityQuinolinesPhosphorylationmedicine.symptomATP Binding Cassette Transporter Subfamily BLiver fibrosisEARLY-ONSETInflammation03 medical and health sciencesmedicineAnimalsHumansOmipalisibProtein kinase BPI3K/AKT/mTOR pathwayPharmacologybusiness.industryCUT LIVERmedicine.diseaseMice Inbred C57BLMODEL030104 developmental biologybusinessMATRIXEx vivoBiochemical Pharmacology
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Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification

2020

International audience; Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromo…

0301 basic medicineMaleCerebellumPathology[SDV]Life Sciences [q-bio]recessive brain calcificationMice0302 clinical medicineCognitive declineAge of OnsetChildGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSBrain Diseasesprimary familial brain calcificationMalalties neurodegenerativesBrainFahr diseaseCalcinosisOCLNNeurodegenerative DiseasesHuman brainMiddle AgedPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structureKnockout mouseFemalemedicine.symptomAdultmedicine.medical_specialtyAdolescentGenes RecessiveNeuropathologyBiologyCalcificacióCalcification03 medical and health sciencesBasal Ganglia DiseasesReportGeneticsmedicineAnimalsHumansAllelesSLC20A2Cerebellar ataxiaknock out mouse modelmedicine.diseaseJAM2030104 developmental biologyFahr disease; familial idiopathic basal ganglia calcification; JAM2; JAM3; knock out mouse model; MYORG; OCLN; primary familial brain calcification; recessive brain calcification; SLC20A2familial idiopathic basal ganglia calcificationJAM3MYORGXenotropic and Polytropic Retrovirus ReceptorCell Adhesion Molecules030217 neurology & neurosurgeryCalcification
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Autosomal-Recessive Mutations in AP3B2, Adaptor-Related Protein Complex 3 Beta 2 Subunit, Cause an Early-Onset Epileptic Encephalopathy with Optic At…

2016

International audience; Early-onset epileptic encephalopathy (EOEE) represents a heterogeneous group of severe disorders characterized by seizures, interictal epileptiform activity with a disorganized electroencephalography background, developmental regression or retardation, and onset before 1 year of age. Among a cohort of 57 individuals with epileptic encephalopathy, we ascertained two unrelated affected individuals with EOEE associated with developmental impairment and autosomal-recessive variants in AP3B2 by means of whole-exome sequencing. The targeted sequencing of AP3B2 in 86 unrelated individuals with EOEE led to the identification of an additional family. We gathered five addition…

0301 basic medicineMaleMicrocephalyDevelopmental DisabilitiesPostnatal microcephalycopper-metabolismEpilepsy0302 clinical medicineexpansionhermansky-pudlak-syndromeddc:576.5Age of OnsetChilddisordersGenetics (clinical)seizuresGeneticsMEDNIK syndromeSyndrome3. Good healthPedigreeintellectual disabilityChild Preschoolmednik syndromeMicrocephalyFemaleDevelopmental regressionAdaptor Protein Complex 3Genes RecessiveBiologyAP3B103 medical and health sciencesAtrophyReport[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansAdaptor Protein Complex beta SubunitsmousediseaseEpilepsyap-4 deficiencyInfant NewbornInfantmedicine.diseaseOptic Atrophy030104 developmental biologyMutationHermansky–Pudlak syndrome030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Skeletal alterations, developmental delay and new mutations in juvenile-onset Pompe disease.

2018

Abstract Pompe disease is an autosomal recessive disorder caused by a deficiency of acid α-glucosidase. In addition to the severe infantile form with cardiac involvement, late-onset variants can affect older children, adolescents (aged >1 year old) or adults. Patients with juvenile (a subgroup of late-onset type) Pompe disease typically do not have cardiac alterations e.g. hypertrophic cardiomyopathy, and the diagnosis is often difficult because it can clinically resemble myriad other neuromuscular disorders. A high level of clinical suspicion is necessary for a timely and accurate diagnosis. We describe 3 interesting cases of patients with juvenile-onset Pompe disease who presented some un…

0301 basic medicineMalePediatricsmedicine.medical_specialtyAdolescentDevelopmental DisabilitiesDisease03 medical and health sciences0302 clinical medicinemedicineJuvenileHumansMuscle SkeletalGenetics (clinical)business.industryGlycogen Storage Disease Type IIGenetic variantsalpha-Glucosidases030104 developmental biologyJuvenile onsetNeurologyPediatrics Perinatology and Child HealthMutationNeurology (clinical)Glucan 14-alpha-Glucosidasebusiness030217 neurology & neurosurgeryNeuromuscular disorders : NMD
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Mediterranean diet and knee osteoarthritis outcomes: A longitudinal cohort study.

2018

Objectives: Mediterranean diet has several beneficial effects on health, but data regarding the association between Mediterranean diet and knee osteoarthritis (OA) are limited mainly to cross-sectional studies. We investigated whether higher Mediterranean diet adherence is prospectively associated with lower risk of radiographic OA (ROA), radiographic symptomatic knee OA (SxOA) and pain worsening in North American people at high risk or having knee OA. Methods: Adherence to the Mediterranean diet was evaluated using a validated Mediterranean diet score (aMED), categorized in five categories (Q1 to Q5, higher values reflecting higher adherence to Mediterranean diet). Knee OA outcomes include…

0301 basic medicineMalemedicine.medical_specialtyMediterranean diet*Osteoarthritis initiative030209 endocrinology & metabolismOsteoarthritisCritical Care and Intensive Care MedicineLower riskDiet MediterraneanArticleknee osteoarthritisNew onset03 medical and health sciencessymbols.namesake0302 clinical medicine*Mediterranean diet*Knee osteoarthritis*PainInternal medicineMediterranean dietMedicineHumanspainPoisson regressionLongitudinal StudiesLongitudinal cohort030109 nutrition & dieteticsNutrition and Dieteticsbusiness.industryMiddle AgedOsteoarthritis Kneemedicine.disease*OsteoarthritisArthralgiaosteoarthritisagedKnee painOsteoarthritis InitiativeRelative risksymbolsDisease ProgressionosteoarthritiFemalemedicine.symptom*Agedbusiness
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Formin 2 links neuropsychiatric phenotypes at young age to an increased risk for dementia

2017

Age-associated memory decline is due to variable combinations of genetic and environmental risk factors. How these risk factors interact to drive disease onset is currently unknown. Here we begin to elucidate the mechanisms by which post-traumatic stress disorder (PTSD) at a young age contributes to an increased risk to develop dementia at old age. We show that the actin nucleator Formin 2 (Fmn2) is deregulated in PTSD and in Alzheimer's disease (AD) patients. Young mice lacking the Fmn2 gene exhibit PTSD-like phenotypes and corresponding impairments of synaptic plasticity, while the consolidation of new memories is unaffected. However, Fmn2 mutant mice develop accelerated age-associated me…

0301 basic medicineMalememoriaAginggenetics [Stress Disorders Post-Traumatic]Diseasegenetics [Neuronal Plasticity]BioinformaticsdemenciaStress Disorders Post-TraumaticMice0302 clinical medicineRisk FactorsNews & ViewsAge of OnsetMice KnockoutNeuronal PlasticitybiologyGeneral NeuroscienceMicrofilament ProteinsNuclear Proteinsgenetics [Nuclear Proteins]FearadultoMiddle AgedAlzheimer's diseasephysiology [Aging]Phenotype3. Good healthPhenotypemiedoFormin 2Forminsgenetics [Aging]estres postraumaticoepidemiology [Stress Disorders Post-Traumatic]AdultHDAC inhibidorpsychology [Dementia]alzheimerForminsNerve Tissue Proteinsepidemiology [Dementia]Affect (psychology)General Biochemistry Genetics and Molecular Biology03 medical and health sciencesHDAC inhibitorMemorygenetics [Dementia]ddc:570medicineDementiaAnimalsHumansenvejecimientoMolecular Biologyphysiology [Memory]General Immunology and MicrobiologyPost-traumatic stress disordermedicine.diseaseYoung age030104 developmental biologyformin 2 protein mouseCase-Control StudiesSynaptic plasticitybiology.proteinDementiagenetics [Microfilament Proteins]complications [Stress Disorders Post-Traumatic]030217 neurology & neurosurgeryHomeostasis
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miRNomic Signature in Very Low Birth-Weight Neonates Discriminates Late-Onset Gram-Positive Sepsis from Controls

2021

Background and Objectives. Neonatal sepsis is a serious condition with a high rate of mortality and morbidity. Currently, the gold standard for sepsis diagnosis is a positive blood culture, which takes 48–72 h to yield results. We hypothesized that identifying differentially expressed miRNA pattern in neonates with late-onset Gram-positive sepsis would help with an earlier diagnosis and therapy. Methods. This is a prospective observational study in newborn infants with late-onset Gram positive bacterial sepsis and non-septic controls. Complementary to blood culture, an aliquot of 0.5 mL of blood was used to determine small non-coding RNA expression profiling using the GeneChip miRNA 4.0 Arr…

0301 basic medicineMedicine (General)neonatal sepsisvery low birth-weight neonatesClinical BiochemistryArticleSepsis03 medical and health sciencesR5-9200302 clinical medicineImmune system030225 pediatricsmicroRNAmedicineBlood cultureNeonatal sepsismedicine.diagnostic_testbusiness.industrylate-onset Gram-positive sepsisGold standard (test)medicine.diseaseLow birth weight030104 developmental biologymiRNomic signatureImmunologyGene chip analysismedicine.symptomsepsis neonatalbusinessDiagnostics
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Ebola Virus Disease Complicated by Late-Onset Encephalitis and Polyarthritis, Sierra Leone

2016

To the Editor: Ebola virus (EBOV) disease is usually an acute illness, but increasing evidence exists of persistent infections and post-Ebola syndromes. We report a case of EBOV encephalitis.

0301 basic medicineMicrobiology (medical)LetterEpidemiologyExpeditedencephalitisviruseslcsh:MedicineEbola virus diseaseLate onsetDiseasemedicine.disease_causepolyarthritislcsh:Infectious and parasitic diseasesSierra LeoneSierra leoneviral persistenceAcute illnessEbola Virus Disease Complicated by Late-Onset Encephalitis and Polyarthritis Sierra LeoneEbola virus03 medical and health sciences0302 clinical medicinemedicinelcsh:RC109-216viruses030212 general & internal medicineLetters to the EditorEbola virusbusiness.industrylcsh:Rvirus diseasesmedicine.diseaseVirology030104 developmental biologyInfectious DiseasesImmunologyPolyarthritisViral persistencebusinessEncephalitisEmerging Infectious Diseases
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Usefulness of current candidate genetic markers to identify childhood cancer patients at risk for platinum-induced ototoxicity: Results of the Europe…

2020

Background Irreversible sensorineural hearing loss is a common side effect of platinum treatment with the potential to significantly impair the neurocognitive, social and educational development of childhood cancer survivors. Genetic association studies suggest a genetic predisposition for cisplatin-induced ototoxicity. Among other candidate genes, thiopurine methyltransferase (TPMT) is considered a critical gene for susceptibility to cisplatin-induced hearing loss in the FDA drug label and a pharmacogenetic guideline. The aim of this cross-sectional cohort study was to confirm the genetic associations in a large pan-European population and to evaluate the diagnostic accuracy of the genetic…

0301 basic medicineOncologyMaleCancer ResearchCandidate genePharmacogenomic VariantsCancer survivorsCHILDRENAnti-neoplastic drugsVARIANTSOCT2Carboplatin0302 clinical medicineHearingRisk FactorsNeoplasmsTPMTHearing / drug effectsProspective StudiesAge of OnsetChild610 Medicine & healthPREDICTORSmedia_commonHearing Loss Sensorineural / physiopathologyeducation.field_of_studyddc:618Thiopurine methyltransferasebiologycarboplatin [Cisplatin]Neoplasms / drug therapyOrganic Cation Transporter 2EuropeOncologyCisplatin: carboplatinCisplatin / adverse effects030220 oncology & carcinogenesisChild PreschoolOrganic Cation Transporter 2 / geneticsFemaleSENSITIVITYChildhood cancer360 Social problems & social servicesCohort studyDrug-induced ototoxicitymedicine.medical_specialtyINDUCED HEARING-LOSSAdolescentMulticenter cohort studyHearing Loss SensorineuralPopulationAdverse drug reactionAntineoplastic AgentsPolymorphism Single NucleotideRisk AssessmentHearing Loss Sensorineural / chemically inducedCarboplatin / adverse effects03 medical and health sciencesACYP2OtotoxicitySDG 3 - Good Health and Well-beingInternal medicinemedicineGenetic predispositionmedia_common.cataloged_instanceHumansGenetic Predisposition to DiseaseCISPLATIN-INDUCED OTOTOXICITYEuropean unioneducationGenetic Association StudiesGenetic associationRetrospective Studiesbusiness.industryAntineoplastic Agents / adverse effectsInfant NewbornInfantOdds ratioGuidelinemedicine.diseaseOtotoxicityCOMTPharmacogenomic Testing030104 developmental biologyCross-Sectional StudiesPharmacogeneticsbiology.proteinGenetic markersHearing Loss Sensorineural / geneticsCisplatinbusinessPharmacogenetics
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