Search results for "Androgen"

showing 10 items of 326 documents

Evolution of yolk androgens in birds: development, coloniality and sexual dichromatism

2007

18 pages; International audience; Current theory recognizes the adaptive value of maternal effects in shaping offspring phenotypes in response to selective pressures and vindicates the value of these traits in fostering adaptation and speciation. Yolk androgens in birds are a relatively well-known maternal effect and have been linked to adaptations related to development, coloniality life, and sexual selection. We tested whether interspecific patterns of yolk androgen levels (androstenedione and testosterone) were related to interspecific variation in development, sexual selection, and coloniality. First, we found no relationship between androgen levels and duration of development as reflec…

0106 biological sciencesMaleEmbryo Nonmammalian01 natural sciencesyolk androgensandrostenedioneTestosteronePhylogenyComputingMilieux_MISCELLANEOUS0303 health sciencesSex CharacteristicsMaternal effectEgg YolkPhenotypecolonialitySexual selectiondichromatism.maternal effectsFemalemedicine.medical_specialty[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]food.ingredientmedicine.drug_classZoologyEmbryonic DevelopmentBiologydichromatism010603 evolutionary biologyBirds03 medical and health sciencesfoodInternal medicineYolkmedicineAnimalsAndrostenedione[ SDV.OT ] Life Sciences [q-bio]/Other [q-bio.OT]Social BehaviorEcology Evolution Behavior and Systematics030304 developmental biologyDichromatism[SDV.OT] Life Sciences [q-bio]/Other [q-bio.OT]AndrogenMating system[SDE.ES]Environmental Sciences/Environmental and Society[SDE.BE] Environmental Sciences/Biodiversity and EcologyEndocrinologytestosterone[SDE.ES] Environmental Sciences/Environmental and Society[SDE.BE]Environmental Sciences/Biodiversity and Ecology
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Testosterone-Mediated Effects on Fitness-Related Phenotypic Traits and Fitness

2009

International audience; The physiological and behavioral mechanisms underlying life-history trade-offs are a continued source of debate. Testosterone (T) is one physiological factor proposed to mediate the trade-off between reproduction and survival. We use phenotypic engineering and multiple laboratory and field fitness-related phenotypic traits to test the effects of elevated T between two bank vole Myodes glareolus groups: dominant and subordinate males. Males with naturally high T levels showed higher social status (laboratory dominance) and mobility (distance between capture sites) than low-T males, and the effect of T on immune response was also T group specific, suggesting that behav…

0106 biological sciencesMalemedicine.medical_specialtymedicine.drug_class[SDE.MCG]Environmental Sciences/Global ChangesRadioimmunoassayZoologySpatial BehaviorHierarchy SocialTrade-off010603 evolutionary biology01 natural sciencesAntibodies03 medical and health sciencesImmune systemSpecies SpecificityInternal medicinemedicineAgonistic behaviourAnimalsTestosteroneEcology Evolution Behavior and SystematicsFinland030304 developmental biology0303 health sciencesbiologyReproductive successAggressionArvicolinaePhenotypic traitbiology.organism_classificationAndrogenSurvival AnalysisBank voleEndocrinologyPhenotypeImmunoglobulin GLinear Modelsmedicine.symptom
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Long-term fitness consequences of high yolk androgen levels: sons pay the costs

2012

Summary 1. Early growth conditions, for example hormonal environment during embryonic development, may have long-lasting effects on behaviour and phenotype, with subsequent fitness consequences. Yolk androgens have been shown to affect various offspring traits in the short-term, but fitness consequences for either offspring or parents, a prerequisite for studying the adaptiveness of this maternal effect, are poorly known in the wild. 2. We experimentally elevated yolk androgen levels of whole clutches in a wild population of collared flycatchers (Ficedula albicollis) and investigated the long-term effects of yolk androgens on offspring local recruitment, parental return rate, and timing and…

0106 biological sciencesmedicine.medical_specialtyfood.ingredientmedicine.drug_classOffspringPopulationZoologyBiology010603 evolutionary biology01 natural sciencesSexual conflictfoodInternal medicineYolkmedicine0501 psychology and cognitive sciences050102 behavioral science & comparative psychologyeducationEcology Evolution Behavior and SystematicsTestosteroneeducation.field_of_study05 social sciencesMaternal effectAndrogenEndocrinologyembryonic structuresParent–offspring conflictFunctional Ecology
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Kinetics of the early development of uniparental human haploid embryos

2016

Objective: To describe morphokinetically the early development of human haploid parthenotes and androgenotes and to compare them with euploid embryos. Design: Experimental study of kinetics. Setting: University-affiliated private fertility center. Patient(s): Experimental haploid parthenotes and androgenotes. Intervention(s): Kinetic study of early development (up to eight cells) of 8 parthenotes, 10 androgenotes, and 20 euploid embryos. Main Outcome Measure(s): Timing of the first seven cleavages determined according to embryo origin, then calculation of the duration of the second and third cell cycles (cc2 and cc3) of whole embryos and individual cells. Result(s): Parthenotes and androgen…

0301 basic medicineAdultanimal structuresAdolescentmedicine.medical_treatmentEmbryonic DevelopmentBiologyHaploidyIntracytoplasmic sperm injectionAndrology03 medical and health sciencesYoung Adult0302 clinical medicinemedicineHumansSperm Injections IntracytoplasmichumanGenetics030219 obstetrics & reproductive medicineOutcome measuresObstetrics and GynecologyEmbryoOocyte activationAndrogenoteAneuploidyKineticshaploid030104 developmental biologyReproductive Medicinemorphokineticparthenoteembryonic structuresPloidy
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Non-classic congenital adrenal hyperplasia due to 21-hydroxylase deficiency revisited: an update with a special focus on adolescent and adult women.

2016

Background Non-classic congenital hyperplasia (NCAH) due to 21-hydroxylase deficiency is a common autosomal recessive disorder characterized by androgen excess. Objective and rationale We conducted a systematic review and critical assessment of the available evidence pertaining to the epidemiology, pathophysiology, diagnosis and management of NCAH. A meta-analysis of epidemiological data was also performed. Search methods Peer-reviewed studies evaluating NCAH published up to October 2016 were reviewed. Multiple databases were searched including MEDLINE, EMBASE, Cochrane, ERIC, EBSCO, dissertation abstracts, and current contents. Outcomes The worldwide prevalence of NCAH amongst women presen…

0301 basic medicineAdultmedicine.medical_specialtyPediatricsHirsutismAdolescentGenetic counseling030209 endocrinology & metabolismDiseaseMiscarriage03 medical and health sciences0302 clinical medicinemedicineHumansCongenital adrenal hyperplasiahirsutismMenstruation DisturbancesGynecologyPregnancyAdrenal Hyperplasia Congenitalbusiness.industry17-alpha-HydroxyprogesteroneHyperandrogenismObstetrics and GynecologyAndrogen Antagonistsmedicine.diseasePolycystic ovary030104 developmental biologyReproductive MedicineFemalebusinessInfertility FemaleHuman reproduction update
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Effects of Nandrolone Stimulation on Testosterone Biosynthesis in Leydig Cells

2016

Anabolic androgenic steroids (AAS) are among the drugs most used by athletes for improving physical performance, as well as for aesthetic purposes. A number of papers have showed the side effects of AAS in different organs and tissues. For example, AAS are known to suppress gonadotropin‐releasing hormone, luteinizing hormone, and follicle‐stimulating hormone. This study investigates the effects of nandrolone on testosterone biosynthesis in Leydig cells using various methods, including mass spectrometry, western blotting, confocal microscopy and quantitative real‐time PCR. The results obtained show that testosterone levels increase at a 3.9 μM concentration of nandrolone and return to the ba…

0301 basic medicineEnzymologicMalePhysiologyClinical BiochemistryAndrogenAnabolic Agents; Androgens; Animals; Cell Line; Cell Survival; Dose-Response Relationship Drug; Gene Expression Regulation Enzymologic; Leydig Cells; Male; Nandrolone; Phosphoproteins; Rats; Steroid 17-alpha-Hydroxylase; Testosterone; Physiology; Clinical Biochemistry; Cell BiologyAnabolic AgentsOriginal Research ArticlesNandroloneTestosteroneOriginal Research ArticleTestosteroneAnabolic Agents; Androgens; Animals; Cell Line; Cell Survival; Dose-Response Relationship Drug; Gene Expression Regulation Enzymologic; Leydig Cells; Male; Nandrolone; Phosphoproteins; Rats; Steroid 17-alpha-Hydroxylase; Testosterone; Clinical Biochemistry; Cell Biology; Physiology; Medicine (all)Steroidogenic acute regulatory proteinMedicine (all)Leydig CellsSteroid 17-alpha-HydroxylaseCYP17A1PhosphoproteinAndrogensDrugLuteinizing hormonemedicine.drugAnabolic Agents; Androgens; Animals; Cell Line; Cell Survival; Dose-Response Relationship Drug; Gene Expression Regulation Enzymologic; Leydig Cells; Male; Nandrolone; Phosphoproteins; Rats; Steroid 17-alpha-Hydroxylase; TestosteroneLeydig Cellendocrine systemmedicine.medical_specialtyCell SurvivalBiologyGene Expression Regulation EnzymologicCell LineDose-Response Relationship03 medical and health sciencesDownregulation and upregulationIn vivoInternal medicinemedicineAnimalsDose-Response Relationship DrugAnimalCell BiologyPhosphoproteinsRats030104 developmental biologyEndocrinologyGene Expression RegulationNandroloneAnabolic AgentRatHormone
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Clinical and hormonal characteristics in heterozygote carriers of congenital adrenal hyperplasia

2020

Abstract Non-classical congenital adrenal hyperplasia (NC-CAH) includes a group of genetic disorders due to a broad class of CYP21A2 variants identifying a disease-causing ‘C’ genotype. The heterozygous carriers of CYP21 mutations are at increased risk of developing clinically evident hyperandrogenism, even though clinical and laboratory characteristics are still underestimated. With the aim of obtaining a more accurate delineation of the phenotype of heterozygous carrier of CAH, we analyzed clinical, biochemical and molecular characteristics in a cohort of Sicilian subjects. Fifty-seven females with biallelic and monoallelic CYP21A2 variants classifying NC-CAH (24) and heterozygous carrier…

0301 basic medicineHirsutismHydrocortisoneendocrine system diseasesEndocrinology Diabetes and MetabolismClinical BiochemistryPhysiologyOverweighturologic and male genital diseasesBiochemistrySettore MED/13 - Endocrinologia0302 clinical medicineEndocrinologySettore BIO/10 - BiochimicaGenotypeMedicineChildhirsutismPolycystic ovaryfemale genital diseases and pregnancy complications030220 oncology & carcinogenesisCohortMolecular MedicineFemalemedicine.symptomAdultHeterozygotecongenital hereditary and neonatal diseases and abnormalitiesAdolescentYoung Adult03 medical and health sciencesHumansCongenital adrenal hyperplasiaMolecular BiologyHeterozygous carrierAdrenal Hyperplasia Congenitalbusiness.industryHyperandrogenismCongenital adrenal hyperplasianutritional and metabolic diseasesHeterozygote advantageCell BiologyOverweightmedicine.diseaseOligomenorrhea17OHProgesterone deficiency030104 developmental biologyMutationSteroid 21-HydroxylaseHyperandrogenismbusinessThe Journal of Steroid Biochemistry and Molecular Biology
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The maternal hormone in the male brain: Sexually dimorphic distribution of prolactin signalling in the mouse brain.

2018

Research of the central actions of prolactin is highly focused on females, but this hormone has also documented roles in male physiology and behaviour. Here, we provide the first description of the pattern of prolactin-derived signalling in the male mouse brain, employing the immunostaining of phosphorylated signal transducer and activator of transcription 5 (pSTAT5) after exogenous prolactin administration. Next, we explore possible sexually dimorphic differences by comparing pSTAT5 immunoreactivity in prolactin-supplemented males and females. We also assess the role of testosterone in the regulation of central prolactin signalling in males by comparing intact with castrated prolactin-supp…

0301 basic medicineMaleCell signalingPeptide HormonesSignal transductionBiochemistrychemistry.chemical_compoundMice0302 clinical medicineArcuate NucleusSTAT5 Transcription FactorMedicine and Health SciencesMorphogenesisTestosteroneLipid HormonesPhosphorylationTestosteroneNeuronsSex CharacteristicsMultidisciplinarySexual DifferentiationCerebrumReproductionQRBrainHormones esteroidesSTAT signalingmedicine.anatomical_structureCervell Localització de funcionsHypothalamusAndrogensMedicineFemaleAnatomyhormones hormone substitutes and hormone antagonistsResearch Articlemedicine.medical_specialtyendocrine systemCell biologyScienceHypothalamusBiologyResearch and Analysis MethodsAmygdala03 medical and health sciencesInternal medicinemedicineAnimalsCastrationImmunohistochemistry TechniquesSexual DimorphismProlactin receptorBiology and Life SciencesProlactinHormonesProlactinSexual dimorphismHistochemistry and Cytochemistry Techniques030104 developmental biologyEndocrinologyCastrationchemistryImmunologic Techniques030217 neurology & neurosurgeryHormoneDevelopmental BiologyPloS one
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Repurposing of the Antiepileptic Drug Levetiracetam to Restrain Neuroendocrine Prostate Cancer and Inhibit Mast Cell Support to Adenocarcinoma

2021

A relevant fraction of castration-resistant prostate cancers (CRPC) evolve into fatal neuroendocrine (NEPC) tumors in resistance to androgen deprivation and/or inhibitors of androgen receptor pathway. Therefore, effective drugs against both CRPC and NEPC are needed. We have previously described a dual role of mast cells (MCs) in prostate cancer, being capable to promote adenocarcinoma but also to restrain NEPC. This finding suggests that a molecule targeting both MCs and NEPC cells could be effective against prostate cancer. Using an in silico drug repurposing approach, here we identify the antiepileptic drug levetiracetam as a potential candidate for this purpose. We found that the protein…

0301 basic medicineMaleLevetiracetammast cellsneuroendocrine differentiationNeuroendocrine differentiationCell DegranulationAndrogen deprivation therapyProstate cancer0302 clinical medicineTumor Cells CulturedImmunology and AllergySV2AOriginal ResearchMembrane Glycoproteinsdrug repurposingCell Differentiationprostate cancerGene Expression Regulation NeoplasticMatrix Metalloproteinase 9030220 oncology & carcinogenesisAdenocarcinomaAnticonvulsantsLevetiracetammedicine.druglcsh:Immunologic diseases. AllergyImmunologyAntineoplastic AgentsMice TransgenicNerve Tissue Proteins03 medical and health sciencesmedicineAnimalsHumanstumor microenvironmentmouse modelsHigh-grade prostatic intraepithelial neoplasiadrug repurposing; mast cells; mouse models; neuroendocrine differentiation; prostate cancer; tumor microenvironmentCell Proliferationbusiness.industryDrug RepositioningProstatic NeoplasmsNeoplasms Experimentalmedicine.diseaseCarcinoma Neuroendocrinedrug repurposing mast cells mouse models neuroendocrine differentiation prostate cancer tumor microenvironmentAndrogen receptorMice Inbred C57BL030104 developmental biologyCancer researchlcsh:RC581-607business
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Am J Hum Genet

2019

ZMIZ1 is a coactivator of several transcription factors, including p53, the androgen receptor, and NOTCH1. Here, we report 19 subjects with intellectual disability and developmental delay carrying variants in ZMIZ1. The associated features include growth failure, feeding difficulties, microcephaly, facial dysmorphism, and various other congenital malformations. Of these 19, 14 unrelated subjects carried de novo heterozygous single-nucleotide variants (SNVs) or single-base insertions/deletions, 3 siblings harbored a heterozygous single-base insertion, and 2 subjects had a balanced translocation disrupting ZMIZ1 or involving a regulatory region of ZMIZ1. In total, we identified 13 point mutat…

0301 basic medicineMaleMicrocephaly[SDV]Life Sciences [q-bio]Developmental DisabilitiesAucunBiology030226 pharmacology & pharmacyTransactivation03 medical and health sciencesMiceNeurodevelopmental disorder0302 clinical medicineReportIntellectual DisabilityCoactivatormedicineGeneticsAnimalsHumansPoint MutationAlleleChildExomeGenetics (clinical)Alleles030304 developmental biologyGenetics0303 health sciencesPoint mutationCorrectionInfantSyndromemedicine.diseaseAndrogen receptor030104 developmental biologyChild PreschoolFemale030217 neurology & neurosurgeryTranscription Factors
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