Search results for " Type 3"

showing 10 items of 19 documents

The DNA methylation profile of human spermatogonia at single-cell- and single-allele-resolution refutes its role in spermatogonial stem cell function…

2019

Human spermatogonial stem cells (hSSCs) have potential in fertility preservation of prepubertal boys or in treatment of male adults suffering from meiotic arrest. Prior to therapeutic application, in vitro propagation of rare hSSCs is mandatory. As the published data points to epigenetic alterations in long-term cell culture of spermatogonia (SPG), an initial characterisation of their DNA methylation state is important. Testicular biopsies from five adult normogonadotropic patients were converted into aggregate-free cell suspensions. FGFR3-positive (FGFR3+) SPG, resembling a very early stem cell state, were labelled with magnetic beads and isolated in addition to unlabelled SPG (FGFR3-). DN…

0301 basic medicineHomeobox protein NANOGMaleEmbryologyBiologyEpigenesis Genetic03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansReceptor Fibroblast Growth Factor Type 3EpigeneticsSpermatogenesisMolecular BiologyAllelesMEG3030219 obstetrics & reproductive medicineKCNQ1OT1Stem CellsObstetrics and GynecologyCell DifferentiationCell BiologyMethylationDNA MethylationMolecular biologySpermatozoaSpermatogonia030104 developmental biologymedicine.anatomical_structureReproductive MedicineDNA methylationGenomic imprintingGerm cellDevelopmental BiologyMolecular human reproduction
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Neuroprotective potential of antihyperglycemic drug metformin in streptozocin-induced rat model of sporadic Alzheimer's disease.

2020

Abstract The earliest hallmarks of sporadic Alzheimer's disease (sAD) are impaired glucose metabolism, chronic neuroinflammation, diminished synaptic plasticity and subsequent cognitive decline. The safest antidiabetic drug metformin has shown both glucose metabolism-improving and cognition-enhancing action in type 2 diabetes patients and diabetic model animals. However, metformin has not been previously studied in intracerebroventricular streptozocin (STZ)-induced model of sAD. Therefore, our aim was to assess the preventive action of metformin in sAD model-rats. Firstly, the actions of metformin (75 and 100 mg/kg) on cognitive functions and sociability were examined. Secondly, we wanted t…

0301 basic medicineMaleendocrine system diseasesNerve Tissue ProteinsType 2 diabetesPharmacologyGPI-Linked ProteinsNeuroprotectionStreptozocin03 medical and health sciencesGlycogen Synthase Kinase 30302 clinical medicineCognitionAlzheimer DiseaseMorris Water Maze TestMedicineAnimalsHypoglycemic AgentsCognitive declineRats WistarSocial BehaviorNeuroinflammationInjections IntraventricularPharmacologyGlucose Transporter Type 1Behavior AnimalGlucose Transporter Type 3business.industrydigestive oral and skin physiologyGlucose transporternutritional and metabolic diseasesBrainmedicine.diseaseMetforminMetforminAstrogliosisDisease Models Animal030104 developmental biologyGlucoseNeuroprotective AgentsSynaptic plasticityAcetylcholinesterasebusinessNeuroglia030217 neurology & neurosurgerymedicine.drugEuropean journal of pharmacology
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The MC3 receptor binding affinity of melanocortins correlates with the nitric oxide production inhibition in mice brain inflammation model

2006

Melanocortins possess strong anti-inflammatory effects acting in the central nervous system via inhibition of the production of nitric oxide (NO) during brain inflammation. To shed more light into the role of melanocortin (MC) receptor subtypes involved we synthesized and evaluated some novel peptides, modified in the melanocyte-stimulating hormone (MSH) core structure, natural MCs and known MC receptor selective peptides - MS05, MS06. Since the study included both selective, high affinity binders and the novel peptides, it was possible to do the correlation analysis of binding activities and the NO induction-related anti-inflammatory effect of the peptides. beta-MSH, gamma1-MSH, gamma2-MSH…

Central Nervous SystemLipopolysaccharidesMalemedicine.medical_specialtyInsectaLipopolysaccharidePhysiologyAnti-Inflammatory AgentsInflammationBiologyNitric OxideBiochemistryNitric oxideMiceCellular and Molecular Neurosciencechemistry.chemical_compoundEndocrinologyMelanocortin receptorInternal medicinemedicineAnimalsReceptorMelanocortinsInflammationMice Inbred ICRintegumentary systemReceptors MelanocortinElectron Spin Resonance SpectroscopyCell biologyEndocrinologychemistryForebrainmedicine.symptomMelanocortinPeptideshormones hormone substitutes and hormone antagonistsProtein BindingReceptor Melanocortin Type 3Peptides
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Effects of SCA40 on human isolated bronchus and human polymorphonuclear leukocytes: comparison with rolipram, SKF94120 and levcromakalim

1996

1. SCA40 (0.1 nM-0.1 mM) produced concentration-dependent suppression of the spontaneous tone of human isolated bronchus (-log EC50 = 6.85 +/- 0.09; n = 10) and reached a maximal relaxation similar to that of theophylline (3 mM). The potency (-log EC50 values) of SCA40 compared to other relaxants was rolipram (7.44 +/- 0.12; n = 9) > SCA40 > or = levcromakalim (6.49 +/- 0.04; n = 6) > SKF94120 (5.87 +/- 0.10; n = 9). 2. When tested against the activity of the isoenzymes of cyclic nucleotide phosphodiesterase (PDE) isolated from human bronchus, SCA40 proved highly potent against PDE III (-log IC50 = 6.47 +/- 0.16; n = 4). It was markedly less potent against PDE IV (4.82 +/- 0.18; n = 4) and …

Cromakalimmedicine.medical_specialtyCardiotonic AgentsNeutrophilsLeukotriene B4Muscle Relaxationchemistry.chemical_elementBronchiIn Vitro TechniquesCalciumPharmacologyLeukotriene B4chemistry.chemical_compound3'5'-Cyclic-GMP PhosphodiesterasesSuperoxidesInternal medicinemedicineHumansBenzopyransPyrrolesRolipramCyclic Nucleotide Phosphodiesterases Type 5PharmacologyCyclic nucleotide phosphodiesterasePhosphoric Diester HydrolasesSuperoxideAnti-Inflammatory Agents Non-SteroidalElastaseImidazolesN-Formylmethionine leucyl-phenylalanineCyclic Nucleotide Phosphodiesterases Type 3PyrrolidinonesBronchodilator AgentsCyclic Nucleotide Phosphodiesterases Type 4N-Formylmethionine Leucyl-PhenylalanineEndocrinologychemistry3'5'-Cyclic-AMP PhosphodiesterasesPyrazinesCalciumLeukocyte ElastaseRolipramCromakalimResearch Articlemedicine.drugBritish Journal of Pharmacology
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A novel mutation in FGFR-3 disrupts a putative N-glycosylation site and results in hypochondroplasia

2000

Winterpacht, Andreas, Katja Hilbert, Christiane Stelzer, Thorsten Schweikardt, Heinz Decker, Hugo Segerer, Jürgen Spranger, and Bernhard Zabel. A novel mutation in FGFR-3 disrupts a putative N-glycosylation site and results in hypochondroplasia. Physiol. Genomics 2: 9–12, 2000.—Fibroblast growth factor receptor 3 (FGFR3) is a glycoprotein that belongs to the family of tyrosine kinase receptors. Specific mutations in the FGFR3 gene are associated with autosomal dominant human skeletal disorders such as hypochondroplasia, achondroplasia, and thanatophoric dysplasia. Hypochondroplasia (HCH), the mildest form of this group of short-limbed dwarfism disorders, results in ∼60% of cases from a mut…

GlycosylationGlycosylationPhysiologyDNA Mutational AnalysisHypochondroplasiaOsteochondrodysplasiasReceptor tyrosine kinaseMicechemistry.chemical_compoundGeneticsmedicineAnimalsHumansPoint MutationReceptor Fibroblast Growth Factor Type 3N-Glycosylation SiteGeneticschemistry.chemical_classificationBinding SitesBase SequencebiologyInfantDNAProtein-Tyrosine Kinasesmedicine.diseaseReceptors Fibroblast Growth FactorMolecular biologyProtein Structure TertiaryMice Inbred C57BLAmino Acid SubstitutionchemistryFibroblast growth factor receptorMutationbiology.proteinFemaleGlycoproteinNovel mutationPhysiological Genomics
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Beta-MSH inhibits brain inflammation via MC(3)/(4) receptors and impaired NF-kappaB signaling.

2005

The anti-inflammatory effects of melanocortin peptides have been demonstrated in different inflammation models. This is the first report describing the molecular mechanisms for the beta-MSH-induced suppression of bacterial lipopolisaccharide (LPS)-caused brain inflammation. We found that beta-MSH suppresses LPS-induced nuclear translocation of the transcription factor NF-kappaB, and inhibits the expression of inducible nitric oxide synthase, and the following nitric oxide overproduction in the brain, in vivo. Moreover, administering the preferentially MC(4) receptor selective antagonist HS014 blocked completely these effects, suggesting a tentative MC(4) receptor mediated mechanism of actio…

LipopolysaccharidesMalemedicine.medical_specialtyImmunologyNitric Oxide Synthase Type IIInflammationElectrophoretic Mobility Shift AssayNitric OxidePeptides CyclicNitric oxidechemistry.chemical_compoundMiceInternal medicinebeta-MSHmedicineImmunology and AllergyAnimalsDrug InteractionsReceptorBrain ChemistryMice Inbred ICRbiologyDose-Response Relationship DrugImmunochemistryElectron Spin Resonance SpectroscopyNF-kappa BNF-κBHormonesCell biologyNitric oxide synthaseDisease Models AnimalEndocrinologyNeurologyMechanism of actionchemistrybiology.proteinEncephalitisReceptor Melanocortin Type 4Neurology (clinical)medicine.symptomMelanocortinSignal transductionhormones hormone substitutes and hormone antagonistsReceptor Melanocortin Type 3Signal TransductionJournal of neuroimmunology
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17β-Hydroxysteroid dehydrogenase-3 deficiency: From pregnancy to adolescence

2009

OBJECTIVE: Aim of this study is to report on basal clinical phenotype and follow up after diagnosis, of patients with 17beta-hydroxysteroid-dehydrogenase type 3 (17beta-HSD3) deficiency in Italy. SETTING: Pediatric Endocrine Departments, University Hospitals. PATIENTS: The cases of 5 Italian subjects affected by 17beta-HSD3 deficiency are presented in this study. INTERVENTIONS: Laboratory and genetic assessment. Gonadectomy and female sex assignment (4 patients) or GnRH analog therapy to regress puberty and gender identity disorder (1 patient). RESULTS: Presentation lasted from pregnancy (pre-natal diagnosis of a 46,XY fetus with female external genitalia) to infancy (inguinal hernia contai…

MaleGender Identity DisorderPediatricsmedicine.medical_specialty17-Hydroxysteroid DehydrogenasesEndocrinology Diabetes and MetabolismSex assignmentPrenatal diagnosisGene mutationBiologyClitoromegalyAdolescence pregnancy 17beta-Hydroxysteroid dehydrogenase-3 deficiencySettore MED/38 - Pediatria Generale E SpecialisticaEndocrinologyPregnancyPrenatal DiagnosismedicineHumansDisorders of sex developmentDISORDERS OF SEX DEVELOPMENTTestosterone17-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE 3 GENEGynecologyPregnancyPubertymedicine.diseaseFemaleMALE/FEMALE SEX REVERSALTESTOSTERONE/D4-ANDROSTENEDIONE RATIO17-BETA-HYDROXYSTEROID DEHYDROGENASE TYPE 3 DEFICIENCYmedicine.symptomJournal of Endocrinological Investigation
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Familial seborrhoeic keratosis associated with multiple 'pure reticulated acanthomas' and infundibulocystic basal cell carcinomas.

2017

Background A variety of genodermatoses with multiple cutaneous tumors with germline genetic alterations such as Gorlin syndrome with PTCH1 gene mutations have been described. Other cutaneous syndromes have been associated with somatic gene mutations, such as FGFR3 in familial seborrhoeic keratosis. Objective We describe the clinical, dermoscopic, and histopathological features of multiple cutaneous lesions, mostly infundibulocystic basal cell carcinomas and pure reticulated acanthomas, present in a family affected by familial seborrhoeic keratosis. In addition, we tested for possible germline alterations in the FGFR3 and PTCH1 genes. Methods Ten members of one family were clinically examine…

MalePathologymedicine.medical_specialtySkin NeoplasmsKeratosisDermoscopyDermatologyGene mutationBiologyGermline030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicinemedicineHumansReceptor Fibroblast Growth Factor Type 3Keratosis SeborrheicGerm-Line MutationAgedPolymorphism Geneticmedicine.diagnostic_testApocrinePTCH1 GeneMiddle Agedmedicine.diseaseDermatologyPedigreePatched-1 ReceptorPTCH1Carcinoma Basal Cell030220 oncology & carcinogenesisAcanthomaSkin biopsyFemaleAcanthoma
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Phenotypic expression of the fibroblast growth factor receptor 3 (FGFR3) mutation P250R in a large craniosynostosis family.

1997

The craniosynostosis syndromes are a heterogeneous group of sporadic, autosomal dominant disorders with significant clinical overlap. Recently, we described a large family with autosomal dominant craniosynostosis suggestive of Saethre-Chotzen syndrome, in which linkage to the Saethre-Chotzen syndrome loci on 7p had been excluded. We now report the presence of a mutation in the fibroblast growth factor receptor 3 (FGFR3) in this family. The mutation, P250R, had been previously reported in 10 patients with non-syndromic craniosynostosis. Variable expression of this mutation is evident especially in two additional members of this family, one of whom is severely affected with pancraniosynostosi…

MaleTurkish populationGenetic LinkageBiologyMuenke syndromeCraniosynostosisVariable ExpressionCraniosynostosesGenetic linkageGeneticsmedicineHumansReceptor Fibroblast Growth Factor Type 3Genetics (clinical)GeneticsGenetic heterogeneityInfant NewbornInfantProtein-Tyrosine KinasesFibroblast growth factor receptor 3medicine.diseaseReceptors Fibroblast Growth FactorPedigreePhenotypeMutationMutation (genetic algorithm)FemaleResearch ArticleJournal of Medical Genetics
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Fibroblast growth factor-2 and its receptor expression in proliferating precursor cells of the subventricular zone in the adult rat brain

2008

Several findings have suggested the existence in the subventricular zone (SVZ) from sagittal sections of adult rat brain of a trophic mechanism, mediated by fibroblast growth factor-2 (FGF-2) and its multiple high-affinity FGF receptors (FGFRs), regulating neurogenesis mainly by controlling precursor cell proliferation. However, no clear data are available on the expression of FGF-2 and FGFRs in proliferating precursor cells of the SVZ. To address these questions we examined FGF-2 mRNA and its FGFR mRNA expression in proliferating precursor cells of the SVZ by using a double labeling procedure, combining in situ hybridization for FGF-2 and its FGFR mRNA with immunohistochemistry for bromode…

Maleanimal diseasesReceptor expressionGene ExpressionFGF-2Subventricular zoneSVZBiologySettore BIO/09 - FisiologiaCerebral Ventricleschemistry.chemical_compoundPrecursor cellmedicineAnimalsReceptor Fibroblast Growth Factor Type 3RNA MessengerReceptor Fibroblast Growth Factor Type 1Rats WistarReceptor Fibroblast Growth Factor Type 2BrdUCell ProliferationFGF receptorGeneral NeuroscienceFibroblast growth factor receptor 1NeurogenesisBrainPrecursor cellsFibroblast growth factor receptor 4RatsCell biologyAdult Stem CellsFGF receptorsmedicine.anatomical_structureBromodeoxyuridinenervous systemchemistryFibroblast growth factor receptorFibroblast Growth Factor 2NeuroscienceBromodeoxyuridineBrdU; FGF receptors; FGF-2Neuroscience Letters
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