Search results for "script"

showing 10 items of 5143 documents

In vitro assessment of competitive and time-dependent inhibition of the nevirapine metabolism by nortriptyline in rats

2018

Abstract Nevirapine (NVP) is a non-nucleoside reverse transcriptase inhibitor of human immunodeficiency virus type 1 (HIV-1) widely used as a component of High Active Antiretroviral Therapy (HAART) since it is inexpensive, readily absorbed after oral administration and non-teratogenic. In the present work, the mechanism of a previously described pharmacokinetic interaction between NVP and the antidepressant drug nortriptyline (NT) was studied using rat hepatic microsomes. The obtained results showed a competitive inhibition of the NVP metabolism by NT. The three main NVP metabolites (2-OH-NVP, 3-OH-NVP and 12-OH-NVP) where competitively inhibited with similar inhibitory constant values (Ki …

Male0301 basic medicineTime FactorsMetabolite030106 microbiologyNortriptylineAntidepressive Agents TricyclicPharmacologyBinding Competitive030226 pharmacology & pharmacyBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNon-competitive inhibitionimmune system diseasesOral administrationIn vivomedicineAnimalsNevirapineRats WistarPharmacologyReverse-transcriptase inhibitorChemistryvirus diseasesRatsMicrosomes LiverMicrosomeReverse Transcriptase InhibitorsNortriptylineDrug metabolismmedicine.drugBiochemical Pharmacology
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Astrocytic Calcium Waves Signal Brain Injury to Neural Stem and Progenitor Cells

2017

Summary Brain injuries, such as stroke or trauma, induce neural stem cells in the subventricular zone (SVZ) to a neurogenic response. Very little is known about the molecular cues that signal tissue damage, even over large distances, to the SVZ. Based on our analysis of gene expression patterns in the SVZ, 48 hr after an ischemic lesion caused by middle cerebral artery occlusion, we hypothesized that the presence of an injury might be transmitted by an astrocytic traveling calcium wave rather than by diffusible factors or hypoxia. Using a newly established in vitro system we show that calcium waves induced in an astrocytic monolayer spread to neural stem and progenitor cells and increase th…

Male0301 basic medicineTime FactorsNotch signaling pathwaySubventricular zonechemistry.chemical_elementBiologyCalciumcalcium signalingBiochemistryArticleMice03 medical and health sciencesAdenosine TriphosphateNeural Stem CellsDownregulation and upregulationCell MovementGeneticsmedicineAnimalsCell Self RenewalProgenitor celllcsh:QH301-705.5Cells CulturedCalcium signalinglcsh:R5-920Gene Expression ProfilingastrocytesGap JunctionsCell DifferentiationCell BiologyAnatomyHypoxia (medical)strokeNeural stem cellDisease Models Animal030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)chemistryBrain InjuriesCalciummedicine.symptomFunction and Dysfunction of the Nervous Systemlcsh:Medicine (General)TranscriptomeNeurosciencenotchDevelopmental BiologyStem Cell Reports
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Pancreatic Protein Tyrosine Phosphatase 1B Deficiency Exacerbates Acute Pancreatitis in Mice

2016

Acute pancreatitis (AP) is a common and devastating gastrointestinal disorder that causes significant morbidity. The disease starts as local inflammation in the pancreas that may progress to systemic inflammation and complications. Protein tyrosine phosphatase 1B (PTP1B) is implicated in inflammatory signaling, but its significance in AP remains unclear. To investigate whether PTP1B may have a role in AP, we used pancreas PTP1B knockout (panc-PTP1B KO) mice and determined the effects of pancreatic PTP1B deficiency on cerulein- and arginine-induced acute pancreatitis. We report that PTP1B protein expression was increased in the early phase of AP in mice and rats. In addition, histological an…

Male0301 basic medicineWistarSystemic inflammationMedical and Health SciencesOral and gastrointestinalMicePathology2.1 Biological and endogenous factorsAetiologyNon-Receptor Type 1CancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 1Pancreatitis Acute NecrotizingReverse Transcriptase Polymerase Chain ReactionRegular Articlemedicine.anatomical_structureAcute NecrotizingGastrointestinal disorderAcute pancreatitisTumor necrosis factor alphamedicine.symptomPancreashormones hormone substitutes and hormone antagonistsmedicine.medical_specialtyKnockoutInflammationPathology and Forensic MedicineProinflammatory cytokinePancreatic Cancer03 medical and health sciencesRare DiseasesInternal medicinemedicineAnimalsRats WistarAnimalbusiness.industrymedicine.diseaseRatsDisease Models Animal030104 developmental biologyEndocrinologyPancreatitisDisease ModelsPancreatitisProtein Tyrosine PhosphataseDigestive DiseasesbusinessThe American Journal of Pathology
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NFIB Haploinsufficiency Is Associated with Intellectual Disability and Macrocephaly

2018

The nuclear factor I (NFI) family of transcription factors play an important role in normal development of multiple organs. Three NFI family members are highly expressed in the brain, and deletions or sequence variants in two of these, NFIA and NFIX, have been associated with intellectual disability (ID) and brain malformations. NFIB, however, has not previously been implicated in human disease. Here, we present a cohort of 18 individuals with mild ID and behavioral issues who are haploinsufficient for NFIB. Ten individuals harbored overlapping microdeletions of the chromosomal 9p23-p22.2 region, ranging in size from 225 kb to 4.3 Mb. Five additional subjects had point sequence variations c…

Male0301 basic medicinechromosome 9p23Medical and Health SciencesCorpus CallosumCohort StudiesMice2.1 Biological and endogenous factorsMegalencephalyAetiologyChildAgenesis of the corpus callosumGenetics (clinical)PediatricGenetics & HeredityCerebral CortexMice KnockoutGeneticsSingle Nucleotidenuclear factor IBiological SciencesNFIBNFIXdevelopmental delayMental HealthNFIBCodon NonsenseNFIAintellectual disabilityChild Preschoolchromosome 9p22.3NeurologicalSpeech delayFemalemedicine.symptomHaploinsufficiencyAdultAdolescentKnockoutIntellectual and Developmental Disabilities (IDD)[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBiologymacrocephalyPolymorphism Single NucleotideArticleYoung Adult03 medical and health sciencesRare DiseasesBehavioral and Social ScienceGeneticsmedicinemegalencephalyAnimalsHumansPolymorphismCodonPreschoolNeurosciencesMacrocephalymedicine.diseaseBrain DisordershaploinsufficiencyNFI Transcription Factors030104 developmental biologyNonsense[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsbiology.proteinagenesis of the corpus callosumAmerican journal of human genetics
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The SGLT2 inhibitor empagliflozin improves the primary diabetic complications in ZDF rats

2017

Hyperglycemia associated with inflammation and oxidative stress is a major cause of vascular dysfunction and cardiovascular disease in diabetes. Recent data reports that a selective sodium-glucose co-transporter 2 inhibitor (SGLT2i), empagliflozin (Jardiance®), ameliorates glucotoxicity via excretion of excess glucose in urine (glucosuria) and significantly improves cardiovascular mortality in type 2 diabetes mellitus (T2DM). The overarching hypothesis is that hyperglycemia and glucotoxicity are upstream of all other complications seen in diabetes. The aim of this study was to investigate effects of empagliflozin on glucotoxicity, β-cell function, inflammation, oxidative stress and endothel…

Male0301 basic medicineendocrine system diseasesDiabetic CardiomyopathiesFPS-ZM1 RAGE inhibitorClinical BiochemistryAorta ThoracicRAGE receptor for AGEICAM-1 intercellular adhesion molecule-1ECL enhanced chemiluminescence030204 cardiovascular system & hematologyDPP-4 dipeptidyl peptidase-4medicine.disease_causeTNF-α tumor necrosis factor-αBiochemistryeNOS endothelial •NO synthase (type 3)0302 clinical medicineGlucosidesecSOD extracellular superoxide dismutaseInsulin-Secreting CellsCCL-2 see MCP-1HyperlipidemiaHyperinsulinemiaGTN glyceryl trinitrate (nitroglycerin)IFN-γ interferon-γDHE dihydroethidineEndothelial dysfunctionEndothelial dysfunctionIL-6 interleukin-6lcsh:QH301-705.5HO-1 heme oxygenase-1lcsh:R5-920ICAM-1NG normoglycemiaDiabetesNox catalytic subunit of NADPH oxidaseSGLT2 inhibitorβ-cell contentL-012 8-amino-5-chloro-7-phenylpyrido[34-d]pyridazine-14-(2H3H)dione sodium saltChIP chromatin immunoprecipitationC-Reactive ProteinCRP C-reactive proteinAGE advanced glycation end productsHbA1c glycohemoglobinlcsh:Medicine (General)Research PaperZucker diabetic fatty ratsmedicine.medical_specialtyDMSO dimethylsulfoxideMCP-1 monocyte-chemoattractant-protein-1qRT-PCR quantitative reverse transcription polymerase chain reactionZDF Zucker diabetic fatty (rat)Low-grade inflammation03 medical and health sciencesROS reactive oxygen speciesSodium-Glucose Transporter 2Physiology (medical)Internal medicineDiabetes mellitusPKC protein kinase CEmpagliflozinmedicineAnimalsHypoglycemic AgentsBenzhydryl CompoundsCOX2 cyclooxygenase-2SGLT2i SGLT2 inhibitorSodium-Glucose Transporter 2 InhibitorsGlycated HemoglobinACh acetylcholinebusiness.industryOrganic Chemistrynutritional and metabolic diseasesType 2 Diabetes Mellitusmedicine.diseaseH2K9me2 histone3 lysine9 dimethylationRatsRats ZuckerDHFR dihydrofolate reductaseSGLT2 sodium-glucose co-transporter-2Oxidative StresssGC soluable guanylyl cyclaseGlucose030104 developmental biologyEndocrinologylcsh:Biology (General)ALDH-2 mitochondrial aldehyde dehydrogenaseEndothelium VascularAGE/RAGE signalingHG hyperglycemiabusinessOxidative stressRedox Biology
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Bainbridge-Ropers syndrome caused by loss-of-function variants in ASXL3: a recognizable condition

2016

International audience; Truncating ASXL3 mutations were first identified in 2013 by Bainbridge et al. as a cause of syndromic intellectual disability in four children with similar phenotypes using whole-exome sequencing. The clinical features - postulated by Bainbridge et al. to be overlapping with Bohring-Opitz syndrome - were developmental delay, severe feeding difficulties, failure to thrive and neurological abnormalities. This condition was included in OMIM as 'Bainbridge-Ropers syndrome' (BRPS, #615485). To date, a total of nine individuals with BRPS have been published in the literature in four reports (Bainbridge et al., Dinwiddie et al, Srivastava et al. and Hori et al.). In this re…

Male0301 basic medicinemedicine.medical_specialtyMicrocephalyfamilyAdolescentphenotypeDevelopmental DisabilitiesSevere muscular hypotoniaMedizinTrigonocephaly030105 genetics & heredityBiologyArticle03 medical and health sciencesIntellectual disabilityGeneticsmedicineHumansCraniofacial[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsnovo frameshift mutationgenedisordersGenetics (clinical)GeneticsInfantSyndromemedicine.diseaseDermatologyFailure to Thrive030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsintellectual disabilityChild Preschoolbohring-opitz syndromeMutationFailure to thriveMedical geneticsFemalemedicine.symptomBohring–Opitz syndromeTranscription Factors
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Cholesterol burden in the liver induces mitochondrial dynamic changes and resistance to apoptosis

2018

Non-alcoholic fatty liver disease (NAFLD) encompasses a broad spectrum of histopathological changes ranging from non-inflammatory intracellular fat deposition to non-alcoholic steatohepatitis (NASH), which may progress into hepatic fibrosis, cirrhosis, or hepatocellular carcinoma. Recent data suggest that impaired hepatic cholesterol homeostasis and its accumulation are relevant to the pathogenesis of NAFLD/NASH. Despite a vital physiological function of cholesterol, mitochondrial dysfunction is an important consequence of dietary-induced hypercholesterolemia and was, subsequently, linked to many pathophysiological conditions. The aim in the current study was to evaluate the morphological a…

Male0301 basic medicinemedicine.medical_specialtyTime FactorsCirrhosisPhysiologyClinical BiochemistryApoptosisMitochondria LiverMitochondrionDiet High-Fatmedicine.disease_causeMitochondrial DynamicsCholesterol Dietary03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNon-alcoholic Fatty Liver DiseaseInternal medicinemedicineAnimalsCells CulturedCell ProliferationCholesterolbusiness.industryFatty liverCell Biologymedicine.diseaseMice Inbred C57BLDisease Models AnimalOxidative Stress030104 developmental biologymedicine.anatomical_structureEndocrinologyGene Expression RegulationLiverchemistry030220 oncology & carcinogenesisHepatocyteHepatocytesSteatohepatitisTranscriptomeHepatic fibrosisbusinessOxidative stressJournal of Cellular Physiology
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Neuropeptide FF increases M2 activation and self-renewal of adipose tissue macrophages

2017

The quantity and activation state of adipose tissue macrophages (ATMs) impact the development of obesity-induced metabolic diseases. Appetite-controlling hormones play key roles in obesity; however, our understanding of their effects on ATMs is limited. Here, we have shown that human and mouse ATMs express NPFFR2, a receptor for the appetite-reducing neuropeptide FF (NPFF), and that NPFFR2 expression is upregulated by IL-4, an M2-polarizing cytokine. Plasma levels of NPFF decreased in obese patients and high-fat diet-fed mice and increased following caloric restriction. NPFF promoted M2 activation and increased the proliferation of murine and human ATMs. Both M2 activation and increased ATM…

Male0301 basic medicinemedicine.medical_specialty[SDV.BIO]Life Sciences [q-bio]/BiotechnologyUbiquitin-Protein LigasesAdipose tissue macrophagesMafB Transcription FactorAdipose tissueMice TransgenicReceptors Cell SurfaceSelf renewalMice03 medical and health sciencesClinical investigationInternal medicinemedicineAnimalsNeuropeptide FFTranscription factorAdaptor Proteins Signal TransducingCell ProliferationSTAT62. Zero hungerArginasebiologybusiness.industryChemistryMacrophagesProteinsSciences du Vivant [q-bio]/BiotechnologiesGeneral MedicineMacrophage ActivationInterleukin-10Ubiquitin ligaseCell biologyEndocrinology030104 developmental biologyAdipose TissueMAFBbiology.proteinInterleukin-4CorrigendumbusinessOligopeptidesMacrophage proliferationResearch ArticleJournal of Clinical Investigation
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Childhood Dietary Intake in Italy: The Epidemiological "MY FOOD DIARY" Survey

2019

Promoting a healthy lifestyle during the first years of life is a key strategy for controlling obesity risk in later life

Male0301 basic medicinemedicine.medical_specialtydescriptive observational study; dietary pattern; epidemiology; food record; health; infants; nutrient intake; obesity; survey; toddlersToddlerEpidemiologyDietary pattern030209 endocrinology & metabolismReference rangelcsh:TX341-641Child Nutritional Physiological PhenomenaFood recordDiet RecordsArticle03 medical and health sciences0302 clinical medicineNutrientEnvironmental healthEpidemiologymedicineHumansEarly childhoodObesitytoddlersChildSurveyDietary Reference Values030109 nutrition & dieteticsNutrition and Dieteticsbusiness.industryinfantsInfantFeeding BehaviorNutrientsmedicine.diseaseObesityNutrient intakeDiet RecordsDietDescriptive observational studyItalyHealthChild PreschoolFemaleChild Nutritional Physiological PhenomenaEnergy Intakebusinesslcsh:Nutrition. Foods and food supplyFood Science
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Poor transcript-protein correlation in the brain: negatively correlating gene products reveal neuronal polarity as a potential cause

2018

Transcription, translation, and turnover of transcripts and proteins are essential for cellular function. The contribution of those factors to protein levels is under debate, as transcript levels and cognate protein levels do not necessarily correlate due to regulation of translation and protein turnover. Here we propose neuronal polarity as a third factor that is particularly evident in the CNS, leading to considerable distances between somata and axon terminals. Consequently, transcript levels may negatively correlate with cognate protein levels in CNS regions, i.e., transcript and protein levels behave reciprocally. To test this hypothesis, we performed an integrative inter-omics study a…

Male0301 basic medicineneuronal polarityintegrative omics[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyBiologynegative transcript|protein correlationProteomicsBiochemistryRats Sprague-DawleyTranscriptome03 medical and health sciencesCellular and Molecular Neurosciencetranscriptomics0302 clinical medicineproteomicsTranscription (biology)[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]AnimalsRNA MessengerGeneNeuronsProtein turnoverBrainCell PolarityProteinsRatsTransport proteinCell biology030104 developmental biologySuperior olivary complexprotein transportFemaleDNA microarray030217 neurology & neurosurgery
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