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Predictors of Hepatitis B Surface Antigen Titers two decades after vaccination in a cohort of students and post-graduates of the Medical School at th…

2017

Introduction and objective. The introduction of a vaccine against hepatitis B virus (HBV) for newborn babies in Italy in 1991, extended to 12-year-old children for the first 12 years of application, has been a major achievement in terms of the prevention of HBV infection. The objective of this study was to analyse the long-term immunogenicity and effectiveness of HBV vaccination among healthcare students with different working seniorities. Materials and method. A cross-sectional observational study of undergraduate and postgraduate students attending the Medical School of the University of Palermo was conducted from January 2014 – July 2016. HBV serum markers were performed with commercial …

0301 basic medicineMaleHBsAgSettore MED/07 - Microbiologia E Microbiologia ClinicaStudents Medicalmedicine.disease_causeLogistic regressionCohort Studies0302 clinical medicine030212 general & internal medicineChildWaste Management and DisposalHBV infectionlcsh:Environmental sciencesSchools Medicallcsh:GE1-350Anti-HBs titreHepatitis BVaccinationCohortFemaleAdultmedicine.medical_specialtyHepatitis B virusAdolescent030106 microbiologyHBV infection HBV vaccination Anti-HBs titre Healthcare students postgraduate medical studentsHealthcare studentslcsh:Agriculture03 medical and health sciencesYoung AdultInternal medicinemedicineHumansHepatitis B VaccinesHepatitis B AntibodiesStudentsEcology Evolution Behavior and SystematicsHBV vaccinationHepatitis B virusHepatitis B Surface Antigensbusiness.industrySettore MED/44 - Medicina Del Lavorolcsh:SPublic Health Environmental and Occupational HealthOdds ratioConfidence intervalpostgraduate medical studentsCross-Sectional StudiesImmunologyObservational studybusinessBiomarkersFollow-Up Studies
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Generation of a disease-specific iPS cell line derived from a patient with Charcot-Marie-Tooth type 2K lacking functional GDAP1 gene

2016

Human CMT2-FiPS4F1 cell line was generated from fibroblasts of a patient with Charcot-Marie-Tooth disease harbouring the following mutations in the GDAP1 gene in heterozygosis: p.Q163X/p.T288NfsX3. This patient did not present mutations in the PM22, MPZ or GJB genes. Human reprogramming factors OCT3/4, KLF4, SOX2 and C-MYC were delivered using a non-integrative methodology that involves the use of Sendai virus.

0301 basic medicineMaleHeterozygoteCellular differentiationCèl·lulesDNA Mutational AnalysisGenetic VectorsInduced Pluripotent Stem CellsKaryotypeNerve Tissue ProteinsBiologyPolymorphism Single NucleotideSendai virusCell Line03 medical and health sciencesKruppel-Like Factor 4stomatognathic systemCharcot-Marie-Tooth DiseaseHumansInduced pluripotent stem cellGeneTranscription factorMedicine(all)GeneticsBase SequenceHeterozygote advantageCell DifferentiationCell BiologyGeneral MedicineFibroblastsbiology.organism_classificationCellular ReprogrammingSendai virus030104 developmental biologyMicroscopy FluorescenceKLF4embryonic structuresSistema nerviós MalaltiesReprogrammingDevelopmental BiologyTranscription Factors
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Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations

2016

This work was supported by Spanish Ministry of Economy and Competitiveness (MINECO) Grants SAF2010-16044 and SAF2013-46663-R (to V.A.), SAF2011-30312 and SAF2014-58286-C2-1-R (to L.H.-M.), SAF2011-30088 (to E.D.), and SAF2014-52413-R (to C.L.-O.) and Fondo de Investigación Sanitaria del Instituto de Salud Carlos III Grants RD12/0042/0028 (to V.A.), RD12/0042/0011 (to J.T.), and RD12/0042/0002 (to L.H.-M.), with cofunding from the Fondo Europeo de Desarrollo Regional and the Progeria Research Foundation. J.A.G. is the recipient of a U-Mobility Grant from the Marie Curie cofunding of Regional, National and International Programme (Grant 246550). The Instituto Universitario de Oncología is sup…

0301 basic medicineMaleHutchinson–Gilford progeria syndrome calcium handling connexin43 prelamin A progerinElectrònica en cardiologia030204 cardiovascular system & hematologyPathogenesisCiencias Biomedicas0302 clinical medicineProgeriaCardiac Conduction System DiseasefisiologiapatologíaTecnología médicaChildCiencias médicasMice KnockoutProgeriaprelamin AMultidisciplinaryintegumentary systemMetalloendopeptidasesHeartProgerinHutchinson-Gilford progeria syndrome3. Good health:Enginyeria biomèdica::Electrònica biomèdica::Electrònica en cardiologia [Àrees temàtiques de la UPC]Sarcoplasmic Reticulummedicine.anatomical_structurePNAS PlusChild Preschoolcardiovascular systemNuclear laminaFemalemedicine.symptomBradycardiaAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentBiology03 medical and health sciencesQRS complexYoung AdultElectrònica mèdicaInternal medicinemedicineAnimalsHumansPR intervalHutchinson–Gilford progeria syndromeNuclear LaminaMyocardiumMembrane Proteinsnutritional and metabolic diseasesArrhythmias Cardiacmedicine.diseaseMedical electronicsconnexin43Mice Inbred C57BL030104 developmental biologyEndocrinologyVentricleprogerinConnexin 43calcium handlingsistema cardiovascularCalcium
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The Effect of a Novel c.820C>T (Arg274Trp) Mutation in the Mitofusin 2 Gene on Fibroblast Metabolism and Clinical Manifestation in a Patient

2017

Charcot-Marie-Tooth disease type 2A (CMT2A) is an autosomal dominant axonal peripheral neuropathy caused by mutations in the mitofusin 2 gene (MFN2). Mitofusin 2 is a GTPase protein present in the outer mitochondrial membrane and responsible for regulation of mitochondrial network architecture via the fusion of mitochondria. As that fusion process is known to be strongly dependent on the GTPase activity of mitofusin 2, it is postulated that the MFN2 mutation within the GTPase domain may lead to impaired GTPase activity, and in turn to mitochondrial dysfunction. The work described here has therefore sought to verify the effects of MFN2 mutation within its GTPase domain on mitochondrial and e…

0301 basic medicineMaleHydrolasesMutantMFN2lcsh:MedicineGTPaseMitochondrionmedicine.disease_causeEndoplasmic ReticulumBiochemistryGTP Phosphohydrolases0302 clinical medicineMental RetardationAnimal CellsCharcot-Marie-Tooth DiseaseMedicine and Health SciencesMissense mutationlcsh:ScienceEnergy-Producing OrganellesCells CulturedConnective Tissue CellsGeneticsMutationMultidisciplinarySecretory PathwayOrganic CompoundsMonosaccharidesTryptophanMitochondrial DNACell biologyMitochondriaEnzymesNucleic acidsChemistryNeurologyConnective TissueCell ProcessesPhysical SciencesCellular Structures and OrganellesCellular TypesAnatomyResearch ArticleForms of DNACarbohydratesMutation MissenseBiologyBioenergeticsArgininePolymorphism Single NucleotideMitochondrial Proteins03 medical and health sciencesMitofusin-2Young AdultmedicineGeneticsHumansEndoplasmic reticulumlcsh:ROrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsCell BiologyDNAFibroblastsGuanosine Triphosphatase030104 developmental biologyBiological TissueGlucoseAmino Acid SubstitutionCase-Control StudiesMutationEnzymologylcsh:Q030217 neurology & neurosurgeryPLoS ONE
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Disease severity in patients with visceral leishmaniasis is not altered by co-infection with intestinal parasites

2017

Visceral leishmaniasis (VL) is a neglected tropical disease that affects the poorest communities and can cause substantial morbidity and mortality. Visceral leishmaniasis is characterized by the presence of Leishmania parasites in the spleen, liver and bone marrow, hepatosplenomegaly, pancytopenia, prolonged fever, systemic inflammation and low body mass index (BMI). The factors impacting on the severity of VL are poorly characterized. Here we performed a cross-sectional study to assess whether co-infection of VL patients with intestinal parasites influences disease severity, assessed with clinical and haematological data, inflammation, cytokine profiles and BMI. Data from VL patients was s…

0301 basic medicineMaleIMPACTPhysiologyHepatosplenomegalySystemic inflammationPathology and Laboratory MedicineTHERAPYSeverity of Illness IndexBody Mass Index0302 clinical medicineIntestinal ParasitesBone MarrowZoonosesImmune PhysiologyMedicine and Health SciencesIntestinal Diseases ParasiticHELMINTH INFECTIONSLeishmaniasisImmune ResponseInnate Immune SystembiologyCoinfectionlcsh:Public aspects of medicineASCARIASIS11 Medical And Health SciencesHematologyPancytopenia3. Good healthInfectious DiseasesCytokinesLeishmaniasis Visceralmedicine.symptomLife Sciences & BiomedicineHepatomegalyResearch ArticleNeglected Tropical DiseasesAdultlcsh:Arctic medicine. Tropical medicineAdolescentlcsh:RC955-962030231 tropical medicineImmunology03 medical and health sciencesYoung AdultSigns and SymptomsDONOVANIDiagnostic MedicineTropical MedicineHOOKWORMSeverity of illnessmedicineParasitic DiseasesAnimalsHumansParasitesInflammationScience & TechnologyProtozoan InfectionsINTERFERON-GAMMAbusiness.industryPublic Health Environmental and Occupational HealthTropical diseaseBiology and Life SciencesLeishmaniasislcsh:RA1-127006 Biological SciencesMolecular DevelopmentINTERLEUKIN-10Leishmaniabiology.organism_classificationmedicine.diseaseTropical Diseases030104 developmental biologyVisceral leishmaniasisCross-Sectional StudiesLogistic ModelsCase-Control StudiesCo-InfectionsImmune SystemImmunologySplenomegalyUNDERNUTRITIONParasitologyEthiopiabusinessParasitic Intestinal DiseasesSpleenDevelopmental Biology
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Inflammasome activation in Ankylosing Spondylitis is associated to gut dysbiosis

2021

Objective: We undertook this study to evaluate the activation and functional relevance of inflammasome pathways in ankylosing spondylitis (AS) patients and rodent models and their relationship to dysbiosis. Methods: An inflammasome pathway was evaluated in the gut and peripheral blood from 40 AS patients using quantitative reverse transcriptase–polymerase chain reaction (qRT-PCR), immunohistochemistry (IHC), flow cytometry, and confocal microscopy, and was compared to that of 20 healthy controls and 10 patients with Crohn’s disease. Bacteria was visualized using silver stain in human samples, and antibiotics were administered to HLA–B27–transgenic rats. The NLRP3 inhibitor MCC950 was admini…

0301 basic medicineMaleInflammasomesmedicine.medical_treatmentInterleukin-1betaInterleukin-23Mice0302 clinical medicineCrohn DiseaseNLRC4Interleukin 23Immunology and AllergyIleitisHLA-B27 AntigenSulfonamidesReverse Transcriptase Polymerase Chain ReactionCaspase 1Interleukin-17Interleukin-18InflammasomeIleitisMiddle AgedImmunohistochemistryAnti-Bacterial AgentsDNA-Binding ProteinsCytokineIndenesFemaleInterleukin 17Rats Transgenicmedicine.drugAdultAdolescentImmunologyReceptors Cell Surface03 medical and health sciencesAIM2Young AdultRheumatologyIleumNLR Family Pyrin Domain-Containing 3 ProteinmedicineAnimalsHumansSpondylitis AnkylosingFurans030203 arthritis & rheumatologybusiness.industryCalcium-Binding Proteinsmedicine.diseaseGastrointestinal MicrobiomeRatsCARD Signaling Adaptor Proteins030104 developmental biologyCase-Control StudiesImmunologyDysbiosisJointsbusinessDysbiosis
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No pre-zygotic isolation mechanisms between Schistosoma haematobium and Schistosoma bovis parasites: From mating interactions to differential gene ex…

2021

Species usually develop reproductive isolation mechanisms allowing them to avoid interbreeding. These preventive barriers can act before reproduction, “pre-zygotic barriers”, or after reproduction, “post-zygotic barriers”. Pre-zygotic barriers prevent unfavourable mating, while post-zygotic barriers determine the viability and selective success of the hybrid offspring. Hybridization in parasites and the underlying reproductive isolation mechanisms maintaining their genetic integrity have been overlooked. Using an integrated approach this work aims to quantify the relative importance of pre-zygotic barriers in Schistosoma haematobium x S. bovis crosses. These two co-endemic species cause sch…

0301 basic medicineMaleIntrogressionRC955-962Gene ExpressionBiochemistryTransmembrane Transport Proteins0302 clinical medicineMedical ConditionsCricetinaeArctic medicine. Tropical medicineMedicine and Health SciencesMatingSchistosoma haematobiumGeneticsMammalsbiologyMosaicism[SDV.BID.EVO]Life Sciences [q-bio]/Biodiversity/Populations and Evolution [q-bio.PE]ReproductionEukaryotaReproductive isolationGenomicsInfectious DiseasesMate choiceVertebratesHamstersSchistosomaFemalePublic aspects of medicineRA1-1270Transcriptome AnalysisResearch ArticleEvolutionary ProcessesReproductive IsolationGenetic Speciation030231 tropical medicineIntrogressionRodents03 medical and health sciencesHelminthsGeneticsParasitic DiseasesAnimalsGeneSchistosomaEvolutionary BiologyHost (biology)Public Health Environmental and Occupational HealthOrganismsBiology and Life SciencesComputational BiologyProteinsbiology.organism_classificationGenome AnalysisInvertebratesSchistosoma Haematobium030104 developmental biologyGene Expression RegulationAmniotesZoologyPLoS Neglected Tropical Diseases
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Effectiveness of the physical activity intervention program in the PREDIMED-Plus study: a randomized controlled trial

2018

[Background] The development and implementation of effective physical activity (PA) intervention programs is challenging, particularly in older adults. After the first year of the intervention program used in the ongoing PREvención con DIeta MEDiterránea (PREDIMED)-Plus trial, we assessed the initial effectiveness of the PA component.

0301 basic medicineMaleMediterranean diethumanosrestricción calóricaMyocardial InfarctionMedicine (miscellaneous)physical activitycardiovascular-diseaseejercicio físicoDiet MediterraneanPersones granslaw.inventionmissing data0302 clinical medicineClinical trialsRandomized controlled trialpreventionlawSurveys and QuestionnairesClinical endpoint030212 general & internal medicineolder-adultsStrokeGeneralized estimating equationlcsh:RC620-627mediana edadolder adultsBody mass index2. Zero hungerancianoNutrition and Dieteticssobrepesodietaresultado del tratamientolcsh:Public aspects of medicinehealthMiddle Agedwaist circumference3. Good healthlcsh:Nutritional diseases. Deficiency diseasesTreatment Outcomeestilo de vidaOlder adultsWaist circumferenceFemalewomenpérdida de pesometaanalysisRandomized control trialmedicine.medical_specialtyWaistPes corporalPhysical Therapy Sports Therapy and RehabilitationExercicibody mass indexClinical nutrition03 medical and health sciencesWeight LossmedicineHumansIntervention programObesityLife StyleobesidadExerciseinfarto de miocardioAgedCaloric Restriction030109 nutrition & dieteticsperímetro abdominalbusiness.industrybehaviorPhysical activityResearchíndice de masa corporallcsh:RA1-1270OverweightBody weightmedicine.diseaserandomized control trialDiettamaño de la muestraintervention programSample SizePhysical therapyOlder peoplebusinessBody mass indexAssaigs clínicsInternational Journal of Behavioral Nutrition and Physical Activity
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Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy.

2019

Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxi…

0301 basic medicineMaleMice 129 StrainTime FactorsHeart DiseasesNitric Oxide Synthase Type IIIPhysiology030204 cardiovascular system & hematologyPharmacology03 medical and health sciences0302 clinical medicineEnosPhysiology (medical)medicineCyclic AMPCyclic GMP-Dependent Protein KinasesAnimalsDoxorubicinMyocytes CardiacCalcium SignalingRats WistarProtein kinase BCyclic GMPCells CulturedSimendanCardioprotectionMice KnockoutCardiotoxicityAntibiotics AntineoplasticbiologyDose-Response Relationship DrugChemistryCalcium-Binding ProteinsMammary Neoplasms ExperimentalCardiovascular AgentsLevosimendanbiology.organism_classificationCyclic AMP-Dependent Protein KinasesMyocardial ContractionCardiotoxicityPhospholambanMice Inbred C57BL030104 developmental biologyDoxorubicinMilrinoneFemaleCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-aktmedicine.drugCardiovascular research
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PRRT2 gene variant in a child with dysmorphic features, congenital microcephaly, and severe epileptic seizures: genotype-phenotype correlation?

2019

Abstract Background Mutations in Proline-rich Transmembrane Protein 2 (PRRT2) have been primarily associated with individuals presenting with infantile epilepsy, including benign familial infantile epilepsy, benign infantile epilepsy, and benign myoclonus of early infancy, and/or with dyskinetic paroxysms such as paroxysmal kinesigenic dyskinesia, paroxysmal non-kinesigenic dyskinesia, and exercise-induced dyskinesia. However, the clinical manifestations of this disorder vary widely. PRRT2 encodes a protein expressed in the central nervous system that is mainly localized in the pre-synaptic neurons and is involved in the modulation of synaptic neurotransmitter release. The anomalous functio…

0301 basic medicineMaleMicrocephalyMutation MissenseCase ReportNerve Tissue ProteinsBioinformaticsRisk AssessmentSeverity of Illness Index03 medical and health sciences0302 clinical medicineRare DiseasesSeizuresmedicineHumansGenetic Predisposition to DiseaseGenetic TestingExome sequencingGenetic Association StudiesBenign familial infantile epilepsyDysmorphic featuresbusiness.industryEpileptic encephalopathylcsh:RJ1-570InfantMembrane Proteinslcsh:PediatricsParoxysmal dyskinesiamedicine.diseaseBody Dysmorphic DisordersPrognosisPRRT2 mutationMagnetic Resonance Imaging030104 developmental biologyDyskinesiaMicrocephalymedicine.symptomPRRT2 mutation Dysmorphic features Microcephaly Epileptic encephalopathybusinessMyoclonus030217 neurology & neurosurgeryPRRT2Benign infantile epilepsy
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