Search results for "Transcription"

showing 10 items of 2278 documents

MRI findings and genotype analysis in patients with childhood onset growth hormone deficiency--correlation with severity of hypopituitarism.

2007

Aim: To evaluate the relationship between pituitary size, PIT1 and PROP1 genotype, and the severity of childhood onset growth hormone deficiency (coGHD). Patients: Forty-four patients with coGHD (34 M; 9.7 ± 4.1 years): severe isolated (SI) GHD (n = 14); partial isolated (PI) GHD (n = 13); multiple pituitary hormone deficiencies (MPHD) (n=17). Results: Pituitary abnormalities were found in 7/14 patients with SIGHD (50%), 16/17 patients with MPHD (94.1%), and no patient with PIGHD. Mean pituitary height (PHT SDS) was significantly lower in MPHD than in SIGHD and PIGHD. Pituitary height SDS and pituitary volume (PV) SDS correlated with IGF-I SDS and stimulated GH peaks in the SIGHD and MPHD g…

Malemedicine.medical_specialtyAdolescentGenotypeEndocrinology Diabetes and MetabolismGenotype AnalysisHypopituitarismHypopituitarismGrowth hormone deficiencyCorrelationEndocrinologyInternal medicineAge Determination by SkeletonGenotypemedicineHumansIn patientAge of OnsetChildDwarfism PituitaryRetrospective StudiesHomeodomain Proteinsbusiness.industrymedicine.diseaseMagnetic Resonance ImagingBody HeightEndocrinologyChild PreschoolPituitary GlandPediatrics Perinatology and Child HealthPituitary hormonesDisease ProgressionFemalebusinessTranscription Factor Pit-1Mri findingsJournal of pediatric endocrinologymetabolism : JPEM
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Gene Transcription Alterations Associated with Decrease of Ethanol Intake Induced by Naltrexone in the Brain of Wistar Rats

2006

Preclinical and clinical studies suggest that the administration of the opioid antagonist naltrexone decreases the intake of ethanol. However, the neuroplastic adaptations in the brain associated to reduction of ethanol consumption remains to be elucidated. The aim of the study was to identify gene transcription alterations underlying the attenuation of voluntary ethanol intake by administration of naltrexone in rats. Increasing doses of naltrexone (0.7 mg/kg, 4 days and 1.4 mg/kg/day, 4 days) to rats with acquired high preferring ethanol consumption (>3.5 g of ethanol/kg/day) decreased voluntary ethanol intake (50%). Voluntary ethanol consumption altered mu-opioid receptor function in the …

Malemedicine.medical_specialtyAlcohol DrinkingTranscription Geneticmedicine.drug_classNarcotic AntagonistsNucleus accumbensPharmacologyNaltrexoneInternal medicineImage Processing Computer-AssistedmedicineAnimalsRats WistarOpioid peptideIn Situ HybridizationBrain ChemistryPharmacologyEthanolTyrosine hydroxylaseChemistryOlfactory tubercleCentral Nervous System DepressantsEnkephalin Ala(2)-MePhe(4)-Gly(5)-NaltrexoneRatsAnalgesics OpioidVentral tegmental areaPsychiatry and Mental healthmedicine.anatomical_structureEndocrinologynervous systemGuanosine 5'-O-(3-Thiotriphosphate)HypothalamusAutoradiographyOpioid antagonistmedicine.drugNeuropsychopharmacology
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Acetylcholine leads to signal transducer and activator of transcription 1 (STAT-1) mediated oxidative/nitrosative stress in human bronchial epithelia…

2013

AbstractThe induction of nitric oxide synthase (iNOS) expression via the signal transducer and activator of transcription 1 (STAT-1) is involved in the mechanism of oxidative/nitrosative stress. We investigated whether acetylcholine (ACh) generates oxidative/nitrosative stress in bronchial epithelial cells during airway inflammation of COPD and evaluated the effects of Tiotropium, a once-daily antimuscarinic drug, and Olodaterol, a long-acting β2-agonist on these mechanisms. Human bronchial epithelial cells (16-HBE) were stimulated (4h, 37°C) with induced sputum supernatants (ISSs) from healthy controls (HC) (n=10), healthy smokers (HS) (n=10) or COPD patients (n=10), as well as with ACh (f…

Malemedicine.medical_specialtyBlotting WesternNitric Oxide Synthase Type IIBronchiOxidative phosphorylationCholinergic AgonistsFlow cytometrychemistry.chemical_compoundPulmonary Disease Chronic ObstructiveWestern blotInternal medicinemedicineHumansRNA Small InterferingMolecular BiologyCells Culturedchemistry.chemical_classificationReactive oxygen speciesbiologymedicine.diagnostic_testNitrotyrosineEpithelial CellsMiddle AgedAcetylcholinerespiratory tract diseasesEpithelial cellNitric oxide synthaseOxidative StressEndocrinologySTAT1 Transcription FactorchemistrySTAT proteinbiology.proteinOxidative/nitrosative stressTyrosineMolecular MedicineSTAT-1FemaleReactive Oxygen SpeciesAcetylcholinemedicine.drugBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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Mediterranean Diet Reduces the Adverse Effect of the TCF7L2-rs7903146 Polymorphism on Cardiovascular Risk Factors and Stroke Incidence

2013

OBJECTIVE Transcription factor 7-like 2 (TCF7L2) polymorphisms are strongly associated with type 2 diabetes, but controversially with plasma lipids and cardiovascular disease. Interactions of the Mediterranean diet (MedDiet) on these associations are unknown. We investigated whether the TCF7L2-rs7903146 (C>T) polymorphism associations with type 2 diabetes, glucose, lipids, and cardiovascular disease incidence were modulated by MedDiet. RESEARCH DESIGN AND METHODS A randomized trial (two MedDiet intervention groups and a control group) with 7,018 participants in the PREvención con DIetaMEDiterránea study was undertaken and major cardiovascular events assessed. Data were analyzed at b…

Malemedicine.medical_specialtyCardiovascular and Metabolic RiskMediterranean dietEndocrinology Diabetes and MetabolismPopulationType 2 diabetesDiet MediterraneanGastroenterologylaw.inventionRandomized controlled triallawRisk FactorsDiabetes mellitusInternal medicineInternal MedicinemedicineOdds RatioHumanseducationTriglyceridesOriginal ResearchAgedAdvanced and Specialized Nursingeducation.field_of_studyPolymorphism Geneticbusiness.industryIncidenceHazard ratioOdds ratioFastingMiddle Agedmedicine.diseaseStrokeEndocrinologyDiabetes Mellitus Type 2Cardiovascular DiseasesFemalebusinessTCF7L2Transcription Factor 7-Like 2 ProteinDiabetes Care
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Pgc-1α and Nr4a1 Are Target Genes of Circadian Melatonin and Dopamine Release in Murine Retina

2015

Purpose The neurohormones melatonin and dopamine mediate clock-dependent/circadian regulation of inner retinal neurons and photoreceptor cells and in this way promote their functional adaptation to time of day and their survival. To fulfill this function they act on melatonin receptor type 1 (MT1 receptors) and dopamine D4 receptors (D4 receptors), respectively. The aim of the present study was to screen transcriptional regulators important for retinal physiology and/or pathology (Dbp, Egr-1, Fos, Nr1d1, Nr2e3, Nr4a1, Pgc-1α, Rorβ) for circadian regulation and dependence on melatonin signaling/MT1 receptors or dopamine signaling/D4 receptors. Methods This was done by gene profiling using qu…

Malemedicine.medical_specialtyDopamineDNA Mutational AnalysisBiologyMelatonin receptorRetinaMelatoninMiceDopamineInternal medicinemedicineNuclear Receptor Subfamily 4 Group A Member 1AnimalsCircadian rhythmReceptorMelatoninRegulation of gene expressionDNAAdaptation PhysiologicalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaeye diseasesCircadian RhythmMice Inbred C57BLEndocrinologyGene Expression RegulationDopamine receptorMutationFemalesense organsSignal transductionhormones hormone substitutes and hormone antagonistsmedicine.drugSignal TransductionTranscription Factors
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Evaluation of the therapeutic potential of PPARalpha agonists for X-linked adrenoleukodystrophy.

2003

Adrenoleukodystrophy protein (ABCD1), a peroxisomal membrane protein, is mutated in patients affected by X-linked adrenoleukodystrophy (X-ALD). Adrenoleukodystrophy-related protein (ABCD2) is the closest relative of ABCD1. Pharmacological induction of ABCD2 gene expression has been proposed as a novel therapy strategy for X-ALD. Fibrates induce peroxisome proliferation and Abcd2 expression in rodent liver. Here we evaluate the possibility of using peroxisome proliferator-activated receptor alpha (PPARalpha) agonists for pharmacological induction of ABCD2 expression. In the liver of PPARalpha-deficient mice, both the constitutive and the fenofibrate-inducible Abcd2 gene expression was found …

Malemedicine.medical_specialtyEndocrinology Diabetes and MetabolismMolecular Sequence DataDrug Evaluation PreclinicalPeroxisome ProliferationReceptors Cytoplasmic and NuclearBiologySulfidesATP Binding Cassette Transporter Subfamily DResponse ElementsBiochemistrychemistry.chemical_compoundMiceEndocrinologyInternal medicineGene expressionGeneticsmedicineAnimalsAdrenoleukodystrophyMolecular BiologyGenePhenylurea CompoundsTetradecylthioacetic acidBrainmedicine.diseaseMolecular biologyIntronsMice Mutant StrainsSterol regulatory element-binding proteinDNA-Binding ProteinsMice Inbred C57BLButyratesSterolsEndocrinologychemistryGene Expression RegulationLiverCCAAT-Enhancer-Binding ProteinsSterol Regulatory Element Binding Protein 1AdrenoleukodystrophyATP-Binding Cassette TransportersSterol regulatory element-binding protein 2Sterol Regulatory Element Binding Protein 1Sterol Regulatory Element Binding Protein 2Transcription FactorsMolecular genetics and metabolism
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Polymorphism in the peroxisome proliferator-activated receptor ? gene influences the risk for Alzheimer?s disease

2003

The peroxisome proliferator-activated receptor alpha (PPAR-alpha) is a member of the steroid hormone super family of ligand-inducible transcription factors, involved in glucose and lipid metabolism. We screened for polymorphisms in the PPAR-alpha gene and detected two known polymorphisms located in exon 5 and intron 7. These polymorphisms were investigated for their possible association with Alzheimer's disease (AD) and for their effect in carriers of an insulin gene (INS) polymorphism. The PPAR-alpha C --G polymorphism in exon 5 (L162V) was associated with AD, in that the V-allele was more frequent in AD patients than in healthy subjects. Further data analysis revealed that carriers of an …

Malemedicine.medical_specialtyGenotypemedicine.medical_treatmentDNA Mutational AnalysisReceptors Cytoplasmic and NuclearBiologyExonGene FrequencyAlzheimer DiseaseInternal medicineGenotypemedicineHumansInsulinGenetic Predisposition to DiseaseGenetic TestingAlleleReceptorAllele frequencyBiological PsychiatryAgedAged 80 and overAmyloid beta-PeptidesPolymorphism GeneticExonsMiddle Agedmedicine.diseasePsychiatry and Mental healthSteroid hormoneEndocrinologyAmino Acid SubstitutionNeurologyFemaleNeurology (clinical)Peroxisome proliferator-activated receptor alphaAlzheimer's diseaseTranscription FactorsJournal of Neural Transmission
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Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy

2011

Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associated signaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1 (regulated in development and DNA damage responses) that increased seven- to eightfold and was associated with muscle atrophy in diabetes. The diabetes-induced increase in REDD1 was confirmed at the protein level. …

Malemedicine.medical_specialtyMAP Kinase Signaling SystemPhysiologyEndocrinology Diabetes and MetabolismFOXO1P70-S6 Kinase 1MyostatinBiologyMiceRandom Allocation03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicinemedicineAnimalsRNA MessengerPhosphorylationMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathwayOligonucleotide Array Sequence Analysis030304 developmental biology0303 health sciencesForkhead Box Protein O1Gene Expression ProfilingTOR Serine-Threonine KinasesUbiquitinationForkhead Transcription FactorsOrgan SizeMyostatinProtein ubiquitinationMuscle atrophyMuscular AtrophyDNA Repair EnzymesDiabetes Mellitus Type 1EndocrinologyGene Expression Regulationbiology.proteinPhosphorylationmedicine.symptomProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryTranscription FactorsAmerican Journal of Physiology-Endocrinology and Metabolism
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Sex differences in nucleus accumbens transcriptome profiles associated with susceptibility versus resilience to subchronic variable stress

2015

Depression and anxiety disorders are more prevalent in females, but the majority of research in animal models, the first step in finding new treatments, has focused predominantly on males. Here we report that exposure to subchronic variable stress (SCVS) induces depression-associated behaviors in female mice, whereas males are resilient as they do not develop these behavioral abnormalities. In concert with these different behavioral responses, transcriptional analysis of nucleus accumbens (NAc), a major brain reward region, by use of RNA sequencing (RNA-seq) revealed markedly different patterns of stress regulation of gene expression between the sexes. Among the genes displaying sex differe…

Malemedicine.medical_specialtyMethyltransferaseStreRepression PsychologyNucleus accumbensBiologyAnxietyMotor ActivityGene Expression Regulation EnzymologicNucleus AccumbensDNA Methyltransferase 3ATranscriptomeMiceInternal medicineGene expressionmedicineTranscriptional regulationAnimalsNucleus accumbenEpigeneticsDNA (Cytosine-5-)-MethyltransferasesGene Knock-In TechniquesSwimmingGeneticsMice KnockoutSex CharacteristicsBehaviorNeuroscience (all)DepressionGeneral NeuroscienceEpigeneticFeeding BehaviorArticlesResilience PsychologicalSex differenceMice Inbred C57BLEndocrinologyChronic DiseaseBrain stimulation rewardFemaleTranscriptomeStress PsychologicalSex characteristics
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Down-regulation of the expression of endothelial NO synthase is likely to contribute to glucocorticoid-mediated hypertension.

1999

Hypertension is a side effect of systemically administered glucocorticoids, but the underlying molecular mechanism remains poorly understood. Ingestion of dexamethasone by rats telemetrically instrumented increased blood pressure progressively over 7 days. Plasma concentrations of Na + and K + and urinary Na + and K + excretion remained constant, excluding a mineralocorticoid-mediated mechanism. Plasma NO 2 − /NO 3 − (the oxidation products of NO) decreased to 40%, and the expression of endothelial NO synthase (NOS III) was found down-regulated in the aorta and several other tissues of glucocorticoid-treated rats. The vasodilator response of resistance arterioles was tested by intravital m…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIDown-RegulationVasodilationBiologyEndothelial NOSRats Inbred WKYUmbilical veinDexamethasonechemistry.chemical_compoundInternal medicinemedicineAnimalsRNA MessengerPromoter Regions GeneticAortaCells CulturedNitritesDNA PrimersMultidisciplinaryNitratesBase SequenceAntiglucocorticoidNitric Oxide Synthase Type IIIBiological SciencesRatsNitric oxide synthaseVasodilationEndocrinologychemistryHypertensionbiology.proteinEndothelium VascularNitric Oxide SynthaseGlucocorticoidIntravital microscopymedicine.drugTranscription FactorsProceedings of the National Academy of Sciences of the United States of America
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