Search results for "Press"

showing 10 items of 15058 documents

A novel microglial subset plays a key role in myelinogenesis in developing brain.

2017

Microglia are resident macrophages of the central nervous system that contribute to homeostasis and neuroinflammation. Although known to play an important role in brain development, their exact function has not been fully described. Here, we show that in contrast to healthy adult and inflammation-activated cells, neonatal microglia show a unique myelinogenic and neurogenic phenotype. A CD11c(+) microglial subset that predominates in primary myelinating areas of the developing brain expresses genes for neuronal and glial survival, migration, and differentiation. These cells are the major source of insulin-like growth factor 1, and its selective depletion from CD11c(+) microglia leads to impa…

0301 basic medicineAgingmedicine.medical_treatmentNews & ViewsInsulin-Like Growth Factor IMyelin SheathCell AggregationNeural PlateMicrogliaACTIVATED MICROGLIAGeneral NeuroscienceExperimental autoimmune encephalomyelitisNeurogenesisIGF1BrainGene Expression Regulation DevelopmentalADULT BRAINUp-RegulationALZHEIMERS-DISEASEmedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMyelinogenesisGROWTHFemaleMicrogliaCNSEncephalomyelitis Autoimmune ExperimentalNeurogenesisCentral nervous systemCD11cBiologyGeneral Biochemistry Genetics and Molecular BiologyDEPENDENT MANNER03 medical and health sciencesmedicinePOSTNATAL-DEVELOPMENTAnimalsMolecular BiologyNeuroinflammationGeneral Immunology and MicrobiologyCD11cGrowth factorGene Expression ProfilingCENTRAL-NERVOUS-SYSTEMmedicine.diseaseGALECTIN-1CD11c AntigenMice Inbred C57BL030104 developmental biologynervous systemAnimals NewbornImmunologymyelinogenesisNeuroscienceBiomarkersThe EMBO journal
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Estrogenic regulation of skeletal muscle proteome : a study of premenopausal women and postmenopausal MZ cotwins discordant for hormonal therapy

2017

Female middle age is characterized by a decline in skeletal muscle mass and performance, predisposing women to sarcopenia, functional limitations, and metabolic dysfunction as they age. Menopausal loss of ovarian function leading to low circulating level of 17b-estradiol has been suggested as a contributing factor to aging-related muscle deterioration. However, the underlying molecular mechanisms remain largely unknown and thus far androgens have been considered as a major anabolic hormone for skeletal muscle. We utilized muscle samples from 24 pre- and postmenopausal women to establish proteome-wide profiles, associated with the difference in age (30–34 years old vs. 54– 62 years old), men…

0301 basic medicineAgingnaisetlabel‐free protein quantitationProteomeAnabolismvaihdevuodetmedicine.medical_treatmentTwinsmenopausenano‐LC‐HD‐MSElihakset0302 clinical medicineSTRENGTHBRAIN315 Sport and fitness sciencesta315luustoINHIBITORHormone replacement therapy (menopause)ta3142MITOCHONDRIAL BIOGENESISMiddle AgedPostmenopauseMenopauseREPLACEMENThormone replacement therapyEditorialmedicine.anatomical_structurehormonihoitoHormonal therapyOriginal ArticleFemalemuscleswomenAdultestrogeenitnano-LC-HD-MSEEXPRESSIONmedicine.medical_specialtyBiologyestrogenic regulation03 medical and health sciencesmitochondrial functionInternal medicinemedicineHumansMuscle Skeletallabel-free protein quantitationmuscle proteomeAgedSkeletal muscleEstrogenslabel-free proteinquantitationOriginal ArticlesCell Biologyfunctional annotationmedicine.diseaseMiddle ageMONOZYGOTIC TWIN PAIRS030104 developmental biologyEndocrinologyPremenopauselihasmassaSarcopeniaCELLS3111 BiomedicineEnergy Metabolismfemale muscle030217 neurology & neurosurgeryskeletal musclesHormone
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Longevity-related molecular pathways are subject to midlife “switch” in humans

2019

Emerging evidence indicates that molecular aging may follow nonlinear or discontinuous trajectories. Whether this occurs in human neuromuscular tissue, particularly for the noncoding transcriptome, and independent of metabolic and aerobic capacities, is unknown. Applying our novel RNA method to quantify tissue coding and long noncoding RNA (lncRNA), we identified ~800 transcripts tracking with age up to ~60 years in human muscle and brain. In silico analysis demonstrated that this temporary linear “signature” was regulated by drugs, which reduce mortality or extend life span in model organisms, including 24 inhibitors of the IGF‐1/PI3K/mTOR pathway that mimicked, and 5 activators that oppos…

0301 basic medicineAgingved/biology.organism_classification_rank.speciesMuscle Fibers SkeletallihaksetTranscriptome0302 clinical medicineGene expressionGene Regulatory NetworksRNA-Seqmedia_commonCerebral CortexNeuronsreactive oxygen speciesihoTOR Serine-Threonine Kinasesmitochondrial complex 1LongevityBrainNon-coding RNAAlzheimer'sECSITCell biologytranskriptio (biologia)mTORRNA Long NoncodingOriginal ArticleaivotSignal TransductionAdultTranscriptional ActivationskinIn silicomedia_common.quotation_subjectLongevityBiology03 medical and health sciencesHumanslong noncoding RNAskeletal muscleModel organismGeneSirolimusved/biologyagingRNACell BiologyTwins MonozygoticOriginal Articles030104 developmental biologyikääntyminenRNATranscriptome030217 neurology & neurosurgery
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Muscarinic type-1 receptors contribute to I-K,I-ACh in human atrial cardiomyocytes and are upregulated in patients with chronic atrial fibrillation

2018

Background: Basal and acetylcholine-gated inward-rectifier K+-currents (I-K1 and I-K,I-ACh, respectively) are altered in atrial fibrillation (AF). G(i)-protein-coupled muscarinic (M) receptors type-2 are considered the predominant receptors activating I-K,I-ACh. Although a role for G(q)-coupled non-M-2-receptor subtypes has been suggested, the precise regulation of I-K,I-ACh by multiple M-receptor subtypes in the human atrium is unknown. Here, we investigated M-1-receptor-mediated I-K,I-ACh regulation and its remodeling in chronic AF (cAF). Methods and results: M-1-receptor mRNA and protein abundance were increased in atrial cardiomyocyte fractions and atrial homogenates from cAF patients, …

0301 basic medicineAgonistEXPRESSIONmedicine.medical_specialtyCarbacholmedicine.drug_classMedizin030204 cardiovascular system & hematologyPertussis toxinSUBTYPES03 medical and health sciences0302 clinical medicineInternal medicineMuscarinic acetylcholine receptormedicinePROTEIN-KINASE-CReceptorAcetylcholine receptorK+-CURRENTACETYLCHOLINE-RECEPTORSCHANNELSCONGESTIVE-HEART-FAILUREbusiness.industryMuscarinic receptor subtypesInward-rectifier K+-channelELECTROPHYSIOLOGYPirenzepineAtrial fibrillationDEPENDENT REGULATIONPOTASSIUM CURRENTS030104 developmental biologyEndocrinologyCardiology and Cardiovascular MedicinebusinessAcetylcholinemedicine.drug
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Subchronic vortioxetine treatment -but not escitalopram- enhances pyramidal neuron activity in the rat prefrontal cortex.

2017

Abstract Vortioxetine (VOR) is a multimodal antidepressant drug. VOR is a 5-HT 3 -R, 5-HT 7 -R and 5-HT 1D -R antagonist, 5-HT 1B -R partial agonist, 5-HT 1A -R agonist, and serotonin transporter (SERT) inhibitor. VOR shows pro-cognitive activity in animal models and beneficial effects on cognitive dysfunction in major depressive patients. Here we compared the effects of 14-day treatments with VOR and escitalopram (ESC, selective serotonin reuptake inhibitor) on neuronal activity in the medial prefrontal cortex (mPFC). Ten groups of rats (5 standard, 5 depleted of 5-HT with p -chlorophenylalanine -pCPA-, used as model of cognitive impairment) were fed with control food or with two doses of …

0301 basic medicineAgonistMalegenetic structuresmedicine.drug_classSerotonin reuptake inhibitorAction PotentialsPrefrontal CortexPharmacologyCitalopramSulfidesPartial agonistPiperazines03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicinePremovement neuronal activityAnimalsRats WistarSerotonin transporterPharmacologyVortioxetinebiologyPyramidal CellsAntagonistAntidepressive AgentsRats030104 developmental biologybiology.proteinAntidepressantVortioxetinesense organsPsychologyNeuroscience030217 neurology & neurosurgerySelective Serotonin Reuptake InhibitorsNeuropharmacology
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Estradiol, acting through ERα, induces endothelial non-classic renin-angiotensin system increasing angiotensin 1–7 production

2016

Intracellular renin-angiotensin system (RAS) can operate independently of the circulating RAS. Estrogens provide protective effects by modulating the RAS. Our aim was to investigate the effect of estradiol (E2) on angiotensin converting enzymes (ACE) 1 and ACE2 expression and activities in human endothelial cells (HUVEC), and the role of estrogen receptors (ER). The results confirmed the presence of active intracellular RAS in HUVEC. Physiological concentrations of E2 induced a concentration-dependent increase of ACE1 and ACE2 mRNA expression and ACE1, but not ACE2, protein levels. ACE1 and ACE2 enzymatic activities were also induced with E2. These effects were mediated through ERα activati…

0301 basic medicineAgonistmedicine.medical_specialtymedicine.drug_classEstrogen receptorPeptidyl-Dipeptidase A030204 cardiovascular system & hematologyBiologyBiochemistryEstrogen Receptor AntagonistsCiencias Biológicas03 medical and health sciences0302 clinical medicineEndocrinologyPiperidinesInternal medicineRenin–angiotensin systemHuman Umbilical Vein Endothelial CellsmedicineHumansFulvestrantMolecular BiologyESTROGEN RECEPTORDose-Response Relationship DrugEstradiolEstrogen Receptor alphaANGIOTENSIN CONVERTING ENZYMESBioquímica y Biología MolecularRENIN ANGIOTENSIN SYSTEMPeptide FragmentsEndothelial stem cellESTROGEN030104 developmental biologyEndocrinologyGene Expression RegulationEstrogenENDOTHELIAL CELLPyrazolesAngiotensin-Converting Enzyme 2Estrogen Receptor AntagonistsAngiotensin IEstrogen receptor alphaCIENCIAS NATURALES Y EXACTAShormones hormone substitutes and hormone antagonistsIntracellularMolecular and Cellular Endocrinology
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Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension

2020

Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidati…

0301 basic medicineAircraftmedicine.medical_treatmentClinical BiochemistryBlood Pressure1308 Clinical Biochemistrymedicine.disease_causeBiochemistryMice0302 clinical medicineMedicineEndothelial dysfunctionlcsh:QH301-705.5lcsh:R5-920NADPH oxidasebiologyCytokineHypertensionmedicine.symptomlcsh:Medicine (General)Arterial hypertensionmedicine.medical_specialtyArticles from the Special Issue on Impact of environmental pollution and stress on redox signaling and oxidative stress pathways; Edited by Thomas Münzel and Andreas Daiber10208 Institute of Neuropathology610 Medicine & healthInflammation03 medical and health sciencesInternal medicineEnvironmental noise exposureAnimalsNeuroinflammationInflammationbusiness.industryOrganic ChemistryEndothelial functionmedicine.diseaseAngiotensin IIMice Inbred C57BLOxidative Stress030104 developmental biologyEndocrinologyBlood pressurelcsh:Biology (General)Vascular oxidative stressbiology.protein570 Life sciences; biologyEndothelium Vascularbusiness030217 neurology & neurosurgeryOxidative stress1605 Organic ChemistryRedox Biology
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Distinctive Histogenesis and Immunological Microenvironment Based on Transcriptional Profiles of Follicular Dendritic Cell Sarcomas

2017

Abstract Follicular dendritic cell (FDC) sarcomas are rare mesenchymal tumors with variable clinical, morphologic, and phenotypic characteristics. Transcriptome analysis was performed on multiple FDC sarcomas and compared with other mesenchymal tumors, microdissected Castleman FDCs, and normal fibroblasts. Using unsupervised analysis, FDC sarcomas clustered with microdissected FDCs, distinct from other mesenchymal tumors and fibroblasts. The specific endowment of FDC-related gene expression programs in FDC sarcomas emerged by applying a gene signature of differentially expressed genes (n = 1,289) between microdissected FDCs and fibroblasts. Supervised analysis comparing FDC sarcomas with mi…

0301 basic medicineAlgorithms; B7-H1 Antigen; Castleman Disease; Chromatin; Cluster Analysis; Dendritic Cell Sarcoma Follicular; Gene Expression Profiling; Gene Expression Regulation Neoplastic; Humans; Programmed Cell Death 1 Ligand 2 Protein; Programmed Cell Death 1 Receptor; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Up-Regulation; Gene Regulatory Networks; Molecular Biology; Oncology; Cancer ResearchCancer ResearchProgrammed Cell Death 1 ReceptorDendritic Cell Sarcoma FollicularBiologyT-Lymphocytes RegulatoryB7-H1 AntigenTranscriptome03 medical and health sciencesmedicineCluster AnalysisHumansGene Regulatory NetworksMolecular BiologyRegulation of gene expressionCluster AnalysiGene Regulatory NetworkFollicular dendritic cellsCastleman DiseaseGene Expression ProfilingMesenchymal stem cellT-Lymphocytes Helper-InducerProgrammed Cell Death 1 Ligand 2 Proteinmedicine.diseaseChromatinUp-RegulationAlgorithmGene Expression Regulation NeoplasticGene expression profiling030104 developmental biologyOncologyCancer researchImmunohistochemistrySarcomaAlgorithmsHumanSignal TransductionExtracellular matrix organizationMolecular Cancer Research
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Mechanisms of the Development of Allergy (MeDALL) : Introducing novel concepts in allergy phenotypes

2017

Asthma, rhinitis, and eczema are complex diseases with multiple genetic and environmental factors interlinked through IgE-associated and non–IgE-associated mechanisms. Mechanisms of the Development of ALLergy (MeDALL; EU FP7-CP-IP; project no: 261357; 2010-2015) studied the complex links of allergic diseases at the clinical and mechanistic levels by linking epidemiologic, clinical, and mechanistic research, including in vivo and in vitro models. MeDALL integrated 14 European birth cohorts, including 44,010 participants and 160 cohort follow-ups between pregnancy and age 20 years. Thirteen thousand children were prospectively followed after puberty by using a newly standardized MeDALL Core Q…

0301 basic medicineAllergyGenome-wide association studyComorbidityImmunoglobulin Emedicine.disease_causeCohort StudiesTranslational Research Biomedical0302 clinical medicineAllergenREGULATORY B-CELLSPRECISION MEDICINEMedicineBIRTH COHORT INFANTSATOPIC-DERMATITISImmunology and Allergy[SDV.IMM.ALL]Life Sciences [q-bio]/Immunology/AllergologyChildmedia_commonbiologyatopic dermatitisAtopic dermatitis3. Good healthEuropeMulticenter StudyCHRONIC RESPIRATORY-DISEASESrhinitiPhenotypeINNER-CITY CHILDRENBiomarker (medicine)Femaleatopic dermatitiAdolescentEUROPEAN INNOVATION PARTNERSHIPImmunologyreview03 medical and health sciencesEARLY-LIFEYoung AdultrhinitisAllergy ; Asthma ; Atopic Dermatitis ; RhinitisHypersensitivityJournal Articlemedia_common.cataloged_instanceAnimalsHumansEuropean unionAsthmaMOUNTAIN CEDAR POLLINOSISbusiness.industryGene Expression ProfilingCHILDHOOD ASTHMAAllergensImmunoglobulin Emedicine.diseaseallergyAsthma030104 developmental biology030228 respiratory systemImmunologybiology.proteinImmunizationbusinessGenome-Wide Association StudyJournal of Allergy and Clinical Immunology
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Expression of Alpha-Enolase (ENO1), Myc Promoter-Binding Protein-1 (MBP-1) and Matrix Metalloproteinases (MMP-2 and MMP-9) Reflect the Nature and Agg…

2019

Breast cancer is a complex and heterogeneous disease: Several molecular alterations cause cell proliferation and the acquisition of an invasive phenotype. Extracellular matrix (ECM) is considered essential for sustaining tumor growth and matrix metalloproteinases (MMPs) have been identified as drivers of many aspects of the tumor phenotype. Mounting evidence indicates that both &alpha

0301 basic medicineAlpha-enolaseENO1Kaplan-Meier EstimateMatrix metalloproteinasemedicine.disease_causeMetastasisExtracellular matrixlcsh:Chemistry0302 clinical medicineSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopybiologyMMP-2General MedicineComputer Science ApplicationsDNA-Binding ProteinsGene Expression Regulation NeoplasticMatrix Metalloproteinase 9030220 oncology & carcinogenesisDisease ProgressionMatrix Metalloproteinase 2FemaleMMP-9Breast NeoplasmsCatalysisArticleInorganic Chemistry03 medical and health sciencesBreast cancerbreast cancerCell Line TumormedicineBiomarkers TumorHumansPhysical and Theoretical ChemistryMBP-1Molecular BiologyCell ProliferationTumor Suppressor ProteinsOrganic ChemistryCancermedicine.diseaseSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Phosphopyruvate HydrataseCancer cellbiology.proteinCancer researchCarcinogenesisInternational Journal of Molecular Sciences
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