Search results for "DOC"

showing 10 items of 14105 documents

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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5-year analysis of neoadjuvant pertuzumab and trastuzumab in patients with locally advanced, inflammatory, or early-stage HER2-positive breast cancer…

2016

Summary Background In the primary analysis of the NeoSphere trial, patients given neoadjuvant pertuzumab, trastuzumab, and docetaxel showed a significantly improved pathological complete response compared with those given trastuzumab and docetaxel after surgery. Here, we report 5-year progression-free survival, disease-free survival, and safety. Methods In this multicentre, open-label, phase 2 randomised trial in hospitals and medical clinics, treatment-naive adults with locally advanced, inflammatory, or early-stage HER2-positive breast cancer were randomly assigned (1:1:1:1) to receive four neoadjuvant cycles of trastuzumab (8 mg/kg loading dose, followed by 6 mg/kg every 3 weeks) plus do…

0301 basic medicineAdultmedicine.medical_specialtyTime FactorsAdolescentReceptor ErbB-2PopulationAntibodies Monoclonal HumanizedGastroenterologyGroup B03 medical and health sciencesYoung Adult0302 clinical medicineInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumanseducationSurvival rateAgedNeoplasm StagingAged 80 and overeducation.field_of_studybusiness.industryMiddle AgedTrastuzumabmedicine.diseasePrognosisNeoadjuvant TherapySurgerySurvival Rate030104 developmental biologyOncologyDocetaxelTolerabilityChemotherapy Adjuvant030220 oncology & carcinogenesisFemaleInflammatory Breast NeoplasmsPertuzumabNeoplasm Recurrence LocalbusinessFebrile neutropeniamedicine.drugEpirubicinFollow-Up StudiesThe Lancet. Oncology
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Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions.

2020

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin i…

0301 basic medicineAdvanced glycation end product (AGE)AMP-activated protein kinase (AMPK)endocrine system diseasesglycerol 3-phosphate dehydrogenase (GPD)Clinical Biochemistrytype 1 diabetes (T1D)Type 2 diabetesmTORC1Review Articleelectron transport chain (ETC)PharmacologyMitochondrionmedicine.disease_causeBiochemistry0302 clinical medicineLeukocytesCREB-binding protein (CBP)inner mitochondrial membrane (IMM)lcsh:QH301-705.5lcsh:R5-920cAMP response element-binding (CREB)glucagon-like peptide 1 (GLP-1)type 2 diabetes (T2D)Type 2 diabetesMetforminMetforminMitochondriamedicine.anatomical_structurereactive nitrogen species (RNS)reactive oxygen species (ROS)sirtuin (SIRT)medicine.symptomlcsh:Medicine (General)cardiovascular diseases (CVD)medicine.drugEndotheliumnitric oxide synthase (NOS)polycystic ovary syndrome (PCOS)Pathophysiologyinsulin resistance (IR)superoxide dismutase (SOD)03 medical and health sciencesglycated haemoglobin (HbA1c)medicineorganic cation transporter (OCT)HumansEndotheliumintercellular adhesion molecule-1 (ICAM-1)business.industryoxidative phosphorylation (OXPHOS)Organic Chemistryperoxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)AMPKmedicine.diseaseAtherosclerosisvascular cell adhesion molecule-1 (VCAM-1)Treatment030104 developmental biologylcsh:Biology (General)Mechanism of actionDiabetes Mellitus Type 2Oxidative stressbusinessinsulin receptor substrate (IRS)030217 neurology & neurosurgeryOxidative stress
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IGF-1 Haploinsufficiency Causes Age-Related Chronic Cochlear Inflammation and Increases Noise-Induced Hearing Loss

2021

This article belongs to the Collection Insulin-Like Growth Factors in Development, Cancers and Aging.

0301 basic medicineAgingApoptosisHaploinsufficiencyMice0302 clinical medicineBiology (General)Insulin-Like Growth Factor ICell DeathapoptosisGeneral Medicine3. Good healthCochleaCytokinesmedicine.symptomHaploinsufficiencyNoise-induced hearing lossmedicine.medical_specialtyHeterozygoteHearing lossQH301-705.5InflammationArticleARHLProinflammatory cytokine03 medical and health sciencesInternal medicinemedicineotorhinolaryngologic diseasesAnimalsRNA MessengerProtein kinase BCochleaInflammationbusiness.industryGene Expression ProfilingAKTTGFβ1Auditory Thresholdmedicine.diseaseOxidative Stress030104 developmental biologyEndocrinologyGene Expression RegulationHearing Loss Noise-InducedAgeingSynapsesIL1βJNKbusinessNoise030217 neurology & neurosurgeryBiomarkersNIHL
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The Role of Chemokines in Alzheimer's Disease

2019

Objective: The most common multifactorial neurodegenerative disorder occurring in old age is Alzheimer’s disease. The neuropathological hallmarks of that disorder are amyloid plaques with the presence of β -amyloid aggregates, intraneuronal tau protein tangles, and chronic inflammation. Brain cells such as microglia and astrocytes are inflammatory cells associated with Alzheimer’s disease and involved in the production of inflammatory mediators, such as cytokines and chemokines. Chemokines consist of a large family of protein mediators with low molecular weight, which able to control the migration and residence of all immune cells. In pathological conditions, such as Alzheimer’s disease, c…

0301 basic medicineAgingChemokineAmyloidEndocrinology Diabetes and MetabolismTau protein030209 endocrinology & metabolismInflammation03 medical and health sciences0302 clinical medicineImmune systemAlzheimer DiseaseAmyloid precursor proteinAnimalsHumansImmunology and AllergyMedicineSenile plaquesInflammationbiologyMicrogliabusiness.industryBrainOxidative Stress030104 developmental biologymedicine.anatomical_structureImmunologybiology.proteinReceptors ChemokineChemokinesmedicine.symptombusinessEndocrine, Metabolic & Immune Disorders - Drug Targets
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Targeting the Endoplasmic Reticulum Unfolded Protein Response to Counteract the Oxidative Stress-Induced Endothelial Dysfunction

2017

In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the U…

0301 basic medicineAgingProgrammed cell deathendocrine systemOxidative phosphorylationReview Articlemedicine.disease_causeEndoplasmic ReticulumBiochemistryINITIATION-FACTOR 2-ALPHA03 medical and health sciencesProgrammed cell-deathSELECTIVE-INHIBITIONProgrammed cell-death;TXNIP/NLRP3 INFLAMMASOME ACTIVATION; MITOCHONDRIAL ELECTRON-TRANSPORT; SPONTANEOUSLY HYPERTENSIVE-RATS; INITIATION-FACTOR 2-ALPHA; CORONARY-ARTERY FUNCTION; ER STRESS; SELECTIVE-INHIBITION; MESSENGER-RNA; TRANSMEMBRANE PROTEINmedicineHumansEndothelial dysfunctionlcsh:QH573-671TXNIP/NLRP3 INFLAMMASOME ACTIVATIONSPONTANEOUSLY HYPERTENSIVE-RATSEndothelial Cellbusiness.industrylcsh:CytologyEndoplasmic reticulumfungiEndothelial CellsOxidative StreCell BiologyGeneral MedicineAdaptive responseMITOCHONDRIAL ELECTRON-TRANSPORTER STRESSmedicine.diseaseCell biologyOxidative Stress030104 developmental biologyProteostasisTRANSMEMBRANE PROTEINUnfolded protein responseUnfolded Protein ResponsebusinessMESSENGER-RNAOxidative stressCORONARY-ARTERY FUNCTIONHumanOxidative Medicine and Cellular Longevity
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Decreased bioavailability of nitric oxide in aorta from ovariectomized senescent mice. Role of cyclooxygenase.

2015

This study investigates the effects of aging and/or ovariectomy on vascular reactivity to thromboxane A2 (TXA2) receptor stimulation with U46619, and the modulation by nitric oxide (NO) and cyclooxygenase (COX) in aorta from female senescence-accelerated mice (SAMP8) and from senescence resistant mice (SAMR1). Five-month-old female SAMR1 and SAMP8 were divided into three groups: sham-operated, ovariectomized and ovariectomized plus estradiol. Twenty-eight days after surgery, thoracic aortic rings were mounted for isometric recording of tension and concentration-response curves for U46619 (10(-10)-3 × 10(-7) M) were performed in the absence and in the presence of the NO synthase inhibitor N(…

0301 basic medicineAgingReceptors ThromboxaneAorta Thoracic030204 cardiovascular system & hematologyBiochemistrychemistry.chemical_compoundThromboxane A2Mice0302 clinical medicineEndocrinologySuperoxidesThoracic aortaVasoconstrictor AgentsbiologyEstradiolSuperoxideEstrogen Replacement TherapyAge FactorsOvariectomized ratFemaleMenopauseSignal Transductionmedicine.medical_specialtymedicine.drug_classOvariectomyDown-RegulationNitric OxideNitric oxide03 medical and health sciencesThromboxane A2medicine.arteryInternal medicineGeneticsmedicineAnimalsCyclooxygenase InhibitorsMolecular BiologyAortaDose-Response Relationship Drugbusiness.industryCell BiologyEnzyme ActivationOxidative Stress030104 developmental biologyEndocrinologychemistryEstrogenProstaglandin-Endoperoxide SynthasesVasoconstrictionbiology.proteinCyclooxygenaseNitric Oxide SynthasebusinessExperimental gerontology
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“Pro-youthful” factors in the “labyrinth” of cardiac rejuvenation

2016

IF 3.350; International audience; The mechanisms of aging and senescence include various endogenous and exogenous factors. Among cardiovascular diseases, heart failure is a typical age-related disease. New strategies to restore cardiomyocyte cells have been reported: endogenous substances that can regenerate the heart's cardiomyocytes have been described: follistatin like 1 (FSTL1), growth-differentiation factor 11 (GDF11) and insulin-like growth factor 1 (IGF-I). Manipulation of the different anti and pro-pathways is essential to discover new approaches to regenerative therapies. (C) 2016 Elsevier Inc. All rights reserved.

0301 basic medicineAgingStem-Cellsmedicine.medical_treatmentEndogenyCardiovascular-DiseaseBioinformaticsBiochemistryEndocrinologyFollistatin-Like 1Myocytes CardiacInsulin-Like Growth Factor Ibiology[SDV.MHEP.GEG]Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyGrowth differentiation factorGrowth-Factor-I3. Good healthIGF-IGrowth Differentiation FactorsBone Morphogenetic ProteinsCardiacMouse HeartSenescencemedicine.medical_specialtyFollistatin-Related ProteinsGene-Expression[ SDV.MHEP.GEG ] Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontologyFSTL1Mammalian Heart03 medical and health sciencesMyocardial-InfarctionInternal medicineGeneticsmedicineHumansRegenerationRejuvenationMolecular BiologyHeart FailureYoung BloodTelomerase ExpressionRegeneration (biology)Growth factorCell Biologymedicine.disease030104 developmental biologyEndocrinologyHeart failureGDF11GDF11biology.proteinFollistatin
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Interactive effects of aging and aerobic capacity on energy metabolism-related metabolites of serum, skeletal muscle, and white adipose tissue

2021

ABSTRACTAerobic capacity is a strong predictor of longevity. With aging, aerobic capacity decreases concomitantly with changes in whole body metabolism leading to increased disease risk. To address the role of aerobic capacity, aging and their interaction on metabolism, we utilized rat models of low and high intrinsic aerobic capacity (LCRs/HCRs) and assessed the metabolomics of serum, muscle, and white adipose tissue (WAT). We compared LCRs and HCRs at two time points: Young rats were sacrificed at 9 months, and old rats were sacrificed at 21 months. Targeted and semi-quantitative metabolomics analysis was performed on ultra-pressure Liquid Chromatography Tandem Mass Spectrometry (UPLC-MS)…

0301 basic medicineAgingWhite adipose tissue030204 cardiovascular system & hematologychemistry.chemical_compound0302 clinical medicineTandem Mass SpectrometryMetabolitesaineenvaihduntametabolitesALL-CAUSE MORTALITY2. Zero hungerchemistry.chemical_classification0303 health sciencesmetabolomicsAmino acidmedicine.anatomical_structureCARDIOVASCULAR-DISEASEOBESITYaerobinen suorituskykyOriginal ArticleCARDIORESPIRATORY FITNESSARTIFICIAL SELECTIONmedicine.medical_specialtyAdipose Tissue WhiteEXERCISErasva-aineenvaihdunta03 medical and health sciencesMetabolomicsFATNESSAerobic capacityInternal medicinemedicineAnimalsMetabolomicsBeta (finance)Muscle SkeletalAerobic capacity030304 developmental biologyAMINO-ACID-METABOLISMFatty acid metabolismagingSkeletal muscleLipid metabolismCardiorespiratory fitnessMetabolismRatsaerobic capacityikääntyminen030104 developmental biologyEndocrinologyPHYSICAL-ACTIVITYchemistryFUEL SELECTIONaineenvaihduntatuotteet3111 Biomedicinekoe-eläinmallitGeriatrics and GerontologyEnergy MetabolismChromatography Liquid
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Characterization of NO-Induced Nitrosative Status in Human Placenta from Pregnant Women with Gestational Diabetes Mellitus

2017

Dysregulation of NO production is implicated in pregnancy-related diseases, including gestational diabetes mellitus (GDM). The role of NO and its placental targets in GDM pregnancies has yet to be determined. S-Nitrosylation is the NO-derived posttranslational protein modification that can modulate biological functions by forming NO-derived complexes with longer half-life, termed S-nitrosothiol (SNO). Our aim was to examine the presence of endogenous S-nitrosylated proteins in cysteine residues in relation to antioxidant defense, apoptosis, and cellular signal transduction in placental tissue from control (n=8) and GDM (n=8) pregnancies. S-Nitrosylation was measured using the biotin-switch …

0301 basic medicineAgingendocrine system diseasesPlacentaNitric Oxide Synthase Type IIExpressionApoptosisBiochemistryBody Mass Index0302 clinical medicineNitric-oxidePregnancyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyCaspase 3lcsh:CytologyNitrosylationP38General MedicineCatalaseCaspase 9TrophoblastsGestational diabetesmedicine.anatomical_structureCatalase030220 oncology & carcinogenesisFemaleResearch ArticleAdultmedicine.medical_specialtyArticle SubjectNitrosationNitric OxidePathophysiology03 medical and health sciencesErk1/2Internal medicinePlacentamedicineHumanslcsh:QH573-671Protein kinase BPregnancyFetusNitratesS-NitrosothiolsCesarean SectionCell BiologyPeroxiredoxinsmedicine.diseaseProtein s-nitrosylationDiabetes Gestational030104 developmental biologyEndocrinologyOxidative stressCase-Control Studiesbiology.proteinPeroxiredoxinProto-Oncogene Proteins c-aktOxidative Medicine and Cellular Longevity
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