Search results for "Base Sequence"

showing 10 items of 1146 documents

Glucocorticoids as modulators of expression and activity of Antithrombin (At): potential clinical relevance.

2014

Abstract Introduction An inverse relationship has been reported between decreased postoperative Antithrombin (AT) plasmatic levels and the incidence of complications. We hypothesized that Nuclear Hormone Receptors could modulate the expression of SERPINC1 , encoding AT, through a Hormone Regulatory Element present in its promoter, and thus hormone analogs could be a pharmacological complement in surgical procedures to activate endogenous AT synthesis. Materials and Methods The expression of SERPINC1 was analyzed in HepG2 cells by quantitative RT-PCR and Western Blot. Two studies were conducted with (a) patients submitted to cardiac surgery with cardiopulmonary bypass receiving (n =17) or no…

Malemedicine.medical_specialtyMolecular Sequence DataReceptors Cytoplasmic and NuclearRetinoid X receptorLigandsAntithrombinsCohort StudiesRetinoidsInternal medicinemedicineHumansGlucocorticoidsDexamethasoneAgedCardiopulmonary BypassBase Sequencebusiness.industryAntithrombinRNA-Binding ProteinsHematologyHep G2 CellsIsoxazolesMiddle AgedEndocrinologyRetinoid X ReceptorsTreatment OutcomeMethylprednisoloneNuclear receptorHemostasisFemaleCortisonebusinessHormonemedicine.drugThrombosis research
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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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The oxytocin receptor system: structure, function, and regulation.

2001

The neurohypophysial peptide oxytocin (OT) and OT-like hormones facilitate reproduction in all vertebrates at several levels. The major site of OT gene expression is the magnocellular neurons of the hypothalamic paraventricular and supraoptic nuclei. In response to a variety of stimuli such as suckling, parturition, or certain kinds of stress, the processed OT peptide is released from the posterior pituitary into the systemic circulation. Such stimuli also lead to an intranuclear release of OT. Moreover, oxytocinergic neurons display widespread projections throughout the central nervous system. However, OT is also synthesized in peripheral tissues, e.g., uterus, placenta, amnion, corpus lut…

Malemedicine.medical_specialtyPhysiologyOxytocin receptor bindingCentral nervous systemMolecular Sequence DataBiologyOxytocinPosterior pituitaryPhysiology (medical)Internal medicineNeoplasmsSequence Homology Nucleic AcidmedicineAnimalsHumansAmino Acid SequenceReceptorMolecular BiologyBehaviorBase SequenceBehavior AnimalSequence Homology Amino AcidGeneral MedicineOxytocin receptorBiological EvolutionEndocrinologymedicine.anatomical_structureOxytocinReceptors OxytocinMagnocellular cellFemaleSignal transductionSequence Alignmentmedicine.drugSignal TransductionPhysiological reviews
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Ontogeny of bradykinin B2 receptors in the rat kidney: Implications for segmental nephron maturation

1997

Ontogeny of bradykinin B 2 receptors in the rat kidney: Implications for segmental nephron maturation. Kinins modulate renal function, yet their role in the developing kidney is largely unknown. To explore the developmental role of the kallikrein-kinin system, we examined the postnatal ontogeny and intrarenal localization of B 2 receptors in the rat. Northern blot analysis and RT-PCR documented the expression of B 2 receptor mRNA in the kidney and extrarenal tissues of fetal, neonatal and adult animals. The abundance of B 2 receptor mRNA is 10- to 30-fold higher in neonatal than adult tissues in the following order: kidney > heart > aorta > lung > brain. Receptor autoradiography revealed a …

Malemedicine.medical_specialtyReceptor Bradykinin B2Receptor expressionMolecular Sequence DataBradykininNephronBiologyBradykininKidneyPolymerase Chain ReactionRats Sprague-Dawleychemistry.chemical_compoundParacrine signallingInternal medicinemedicineAnimalsTissue DistributionAmino Acid SequenceRNA MessengerNorthern blotReceptorBradykinin Receptor AntagonistsDNA PrimersKidneyBase Sequenceurogenital systemReceptors BradykininGene Expression Regulation DevelopmentalNephronsKininImmunohistochemistryPeptide FragmentsRatsmedicine.anatomical_structureEndocrinologyAnimals NewbornchemistryNephrologyAutoradiographyKidney International
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Single nucleotide polymorphisms (SNPs) of pro-inflammatory/anti-inflammatory and thrombotic/fibrinolytic genes in patients with acute ischemic stroke…

2011

Abstract Background The genetic basis of complex diseases like ischemic stroke probably consists of several predisposing risk factors, such as genes involved in inflammation and thrombotic pathways. On this basis the aim of our study was to evaluate the role of SNPs (single nucleotide polymorphisms) of some pro-inflammatory/anti-inflammatory and coagulation/fibrinolytic genes in patients with acute ischemic stroke. Methods The study population consisted of 144 consecutive Caucasian adult patients who were hospitalized in the Internal Medicine Department at the University of Palermo between November 2006 and January 2008, and who met inclusion criteria. The cases were patients admitted with …

Malemedicine.medical_specialtymedicine.medical_treatmentImmunologySingle-nucleotide polymorphismDiseaseBiochemistryPolymorphism Single NucleotideBrain IschemiaBrain ischemiaInternal medicineFibrinolysisGenotypeImmunology and AllergyMedicineSettore MED/05 - Patologia ClinicaHumansAlleleMolecular BiologyCytokineAllelesAgedDNA PrimersGeneticsAged 80 and overBase Sequencebusiness.industryFibrinolysisHaplotypeSingle nucleotide polymorphisms (SNPs)Hematologymedicine.diseaseStrokeHaplotypesAcute DiseasePopulation studyFemalebusinessCytokine
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A new heterozygous mutation (D196N) in the Gs alpha gene as a cause for pseudohypoparathyroidism type IA in a boy who had gallstones

2011

Background Pseudohypoparathyroidism (PHP) is characterized by hypocalcemia and hyperphosphatemia in association with an increased secretion of parathyroid hormone (PTH) due to decreased target tissue responsiveness to PTH. Patients with PHP type Ia are not only resistant to PTH, but also to other hormones that bind to receptors coupled to stimulatory G protein (Gsalpha). PHP Ia and Albright hereditary osteodystrophy (AHO) are caused by a reduced activity of the Gsalpha protein. Heterozygous inactivating Gs alpha (GNAS) gene mutations have been identified in these patients. Methods We studied a boy with PHP Ia. During follow-up the patient developed elevated liver enzyme serum levels and abd…

Malemusculoskeletal diseasesHeterozygotemedicine.medical_specialtyErythrocytesFoot Deformities CongenitalEndocrinology Diabetes and MetabolismMutation MissenseParathyroid hormoneGallstonesGene mutationHyperphosphatemiaEndocrinologyInternal medicineChromograninsGTP-Binding Protein alpha Subunits GsGNAS complex locusHumansMedicineMissense mutationnatural sciencesAmino Acid SequenceChildConserved SequencePseudohypoparathyroidismBase SequenceSequence Homology Amino Acidbiologybusiness.industryDNAExonsGallstonesmedicine.diseasePedigreeCholesterolEndocrinologyAmino Acid SubstitutionPseudohypoparathyroidismPediatrics Perinatology and Child Healthbiology.proteinbusinessHand Deformities CongenitalHormoneJournal of Pediatric Endocrinology and Metabolism
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Targeting transcription factor Stat4 uncovers a role for interleukin-18 in the pathogenesis of severe lupus nephritis in mice

2011

Polymorphisms in the transcription factor Stat4 gene have been implicated as risk factors for systemic lupus erythematosus. Although some polymorphisms have a strong association with autoantibodies and nephritis, their impact on pathophysiology is still unknown. To explore this further we used signal transducers and activators of transcription 4 (Stat4) knockout MRL/MpJ-Fas(lpr)/Fas(lpr) (MRL-Fas(lpr)) mice and found that they did not differ in survival or renal function from Stat4-intact MRL-Fas(lpr) mice. Circulating interleukin (IL)-18 levels, however, were elevated in Stat4-deficient compared to Stat4-intact mice, suggesting that this interleukin might contribute to the progression of l…

Malemusculoskeletal diseasesMice Inbred MRL lprchronic inflammationLupus nephritisKidneyInterleukin-23ArticleProinflammatory cytokineOligodeoxyribonucleotides AntisenseGene Knockout TechniquesInterferon-gammaMiceimmune system diseasesmedicineAnimalsskin and connective tissue diseasesSTAT4DNA PrimersAutoimmune diseaseMice Knockoutlupus nephritisMice Inbred BALB CBase Sequencebusiness.industryGene Transfer TechniquesInterleukin-18InterleukinGlomerulonephritishemic and immune systemsSTAT4 Transcription Factormedicine.diseaseInterleukin-12chronic glomerulonephritisNephrologyImmunologyInterleukin 18FemalebusinessNephritisKidney International
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Expanded CTG repeats trigger miRNA alterations in Drosophila that are conserved in myotonic dystrophy type 1 patients

2013

Myotonic dystrophy type 1 (DM1) is caused by the expansion of CTG repeats in the 3' untranslated region of the DMPK gene. Several missplicing events and transcriptional alterations have been described in DM1 patients. A large number of these defects have been reproduced in animal models expressing CTG repeats alone. Recent studies have also reported miRNA dysregulation in DM1 patients. In this work, a Drosophila model was used to investigate miRNA transcriptome alterations in the muscle, specifically triggered by CTG expansions. Twenty miRNAs were differentially expressed in CTG-expressing flies. Of these, 19 were down-regulated, whereas 1 was up-regulated. This trend was confirmed for thos…

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesDown-RegulationGene ExpressionBiologyMyotonic dystrophyLife ExpectancyGeneticsmedicineAnimalsDrosophila ProteinsHumansMyotonic DystrophyMuscle SkeletalMolecular BiologyCells CulturedGenetics (clinical)Oligonucleotide Array Sequence AnalysisGeneticsBase SequenceLife spanNuclear ProteinsGeneral Medicinemedicine.diseaseMicroRNAsDrosophila melanogasterGene Expression RegulationFemaleTranscriptomeTrinucleotide Repeat Expansion
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Duchenne muscular dystrophy and idiopathic hyperCKemia segregating in a family

1995

A 7-month-old boy with gross motor delay and failure to thrive presented with rhabdomyolysis following an acute asthmatic episode. During hospitalization an electrocardiographic conversion to a Wolff-Parkinson-White type 1 (WPW) pattern took place. Duchenne muscular dystrophy (DMD) was suspected based on elevated creatine kinase (CK) serum levels, muscle biopsy, and family history. The diagnosis was confirmed by molecular analysis, which documented a deletion corresponding to cDNA probe 1-2a in the dystrophin gene, in the propositus and in an affected male cousin of his mother. "Idiopathic" hyperCKemia was found in the propositus, his father, and 5 of his relatives. We suggest that the unus…

Malemusculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesPediatricsmedicine.medical_specialtyDuchenne muscular dystrophyMolecular Sequence DataGene mutationPolymerase Chain ReactionMuscular DystrophiesGenomic ImprintingPrenatal DiagnosisInternal medicinemedicineHumansFamily historyCreatine KinaseGenetics (clinical)X-linked recessive inheritanceDNA PrimersGenes DominantMuscle biopsyBase Sequencebiologymedicine.diagnostic_testGenetic Carrier ScreeningInfantExonsmedicine.diseasePedigreeEndocrinologyMutationFailure to thrivebiology.proteinFemaleCreatine kinasemedicine.symptomDystrophinMetabolism Inborn ErrorsAmerican Journal of Medical Genetics
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Failure to detect genomic viral sequences in pancreatic tissues from two children with acute-onset diabetes mellitus.

1994

Two cases of fatal, acute-onset, insulin-dependent diabetes mellitus (IDDM) in children were diagnosed. Epidemiologic and serologic studies, as well as histologic analysis of pancreatic tissue in fatal viral infections, support the contention that a viral infection could cause beta cell destruction, leading to IDDM. The presence of nucleic acid sequences from viral agents considered to be potentially diabetogenic, specifically, cytomegalovirus and mumps, rubella, and coxsackie viruses, were investigated in the pancreatic tissues by reverse transcription followed by polymerase chain reaction (RT-PCR) and Southern blot hybridization. Total pancreatic RNAs extracted from five children who died…

MalevirusesMolecular Sequence DataCytomegalovirusMumps virusBiologymedicine.disease_causeRubellaVirologyDiabetes mellitusmedicineHumansPancreasEnterovirusType 1 diabetesBase SequenceInfantRubella virusmedicine.diseaseVirologyReverse transcriptaseInfectious DiseasesDiabetes Mellitus Type 1Mumps virusChild PreschoolImmunologyAcute DiseaseVirusesRNA ViralFemaleViral diseaseBeta cellRubella virusJournal of medical virology
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