Search results for " Genotype"

showing 10 items of 205 documents

Apoe genotypes and brain imaging classes in normal cognition, mild cognitive impairment, and alzheimer’s disease: A longitudinal study

2020

Objective: To evaluate in 419 stroke-free cognitively normal subjects (CN) aged 45-82 years covering during a long prospective study (11.54 ± 1.47 years) the preclinical to dementia spectrum: 1) the distribution of small vessel disease (V) and brain atrophy (A) aggregated as following: V−/A−, V−/A+, V+/A−, V+/A+; 2) the relationship of these imaging classes with individual apolipoprotein E (APOE) genotypes; 3) the risk of progression to Alzheimer Disease (AD) of the individual APOE genotypes. Methods: Participants underwent one baseline (t0), and 4 clinical and neuropsychological assessments (t1,t2,t3, and t4). Brain MRI was performed in all subjects at t0, t2, t3 and t4.. White matter hyp…

MaleApolipoprotein Emedicine.medical_specialtyGenotypeApolipoprotein E4NeuroimagingNeuropsychological TestsAPOE genotypes Brain imaging classes Caudate atrophy Global cerebral atrophy Lacunes White matter hyperintensities Aged Aged 80 and over Alzheimer Disease Apolipoprotein E4 Apolipoproteins E Brain Case-Control Studies Cognitive Dysfunction Disease Progression Female Genotype Humans Longitudinal Studies Magnetic Resonance Imaging Male Middle Aged Neuroimaging Neuropsychological Tests Risk Factorsbrain imaging classesApolipoproteins EAtrophyNeuroimagingAlzheimer DiseaseRisk FactorsInternal medicineGlobal brain atrophymedicineHumansDementiaCognitive DysfunctionLongitudinal Studiescaudate atrophyAgedglobal cerebral atrophyAged 80 and overAPOE genotypesbusiness.industryNeuropsychologyBrainMiddle Agedwhite matter hyperintensitiesmedicine.diseaseMagnetic Resonance ImagingHyperintensityNeurologyCase-Control StudiesDisease ProgressionCardiologyFemaleNeurology (clinical)Alzheimer's diseasebusiness
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Epidemiological and clinical scenario of chronic liver diseases in Italy: Data from a multicenter nationwide survey

2016

The last Italian prevalence survey on chronic liver diseases (CLD) was performed in 2001. The present study evaluated the changes occurring over thirteen years. Background The last Italian prevalence survey on chronic liver diseases (CLD) was performed in 2001. The present study evaluated the changes occurring over thirteen years. Methods We enrolled 2,557 CLD consecutive patients in 16 Italian liver units in 2014. Results HBV etiology accounted for 513 (20.2%) cases, alone in 439 and associated with HCV and/or alcohol abuse in 74. Of these 513, 11.9% were anti-HDV-positive and 7.2% HBeAg-positive. HCV alone was responsible for 50.3% of CLD and with alcohol abuse for 5.9%. HCV RNA was detec…

MaleCirrhosisAlcohol abuseGastroenterology0302 clinical medicineNon-alcoholic Fatty Liver DiseaseSurveys and QuestionnairesEpidemiologyOutpatients80 and overSurveys and QuestionnaireChronic hepatitis; Chronic liver diseases; HCC; Liver cirrhosis; Adolescent; Adult; Aged; Aged 80 and over; Alcoholism; Carcinoma Hepatocellular; Female; Genotype; Hepatitis B; Hepatitis C; Humans; Inpatients; Italy; Liver Cirrhosis; Liver Neoplasms; Male; Middle Aged; Non-alcoholic Fatty Liver Disease; Outpatients; Surveys and Questionnaires; Young Adult; Hepatology; Gastroenterology030212 general & internal medicineYoung adultHCCChronic liver diseasesChronic hepatitisAged 80 and overMedicine (all)Liver NeoplasmsChronic liver diseaseGastroenterologyvirus diseasesOutpatientHepatitis CHepatitis BMiddle AgedHepatitis BHepatitis CAlcoholismItalyLiver Neoplasm030211 gastroenterology & hepatologyFemaleInpatientHumanAdultmedicine.medical_specialtyCarcinoma HepatocellularAdolescentGenotypeLiver CirrhosiChronic hepatitis; Chronic liver diseases; HCC; Liver cirrhosis; Medicine (all); Hepatology; Gastroenterology03 medical and health sciencesYoung AdultInternal medicinemedicineHumansAgedInpatientsHepatologybusiness.industryCarcinomaHepatocellularHepatologymedicine.diseasedigestive system diseasesLiver cirrhosisEtiologyChronic hepatitibusiness
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Factors that predict response of patients with hepatitis C virus infection to boceprevir

2012

Background & Aims Little is known about factors associated with a sustained virologic response (SVR) among patients with hepatitis C virus (HCV) infection to treatment with protease inhibitors. Methods Previously untreated patients (from the Serine Protease Inhibitor Therapy 2 [SPRINT-2] trial) and those who did not respond to prior therapy (from the Retreatment with HCV Serine Protease Inhibitor Boceprevir and PegIntron/Rebetol 2 [RESPOND-2] trial) received either a combination of peginterferon and ribavirin for 48 weeks or boceprevir, peginterferon, and ribavirin (triple therapy) after 4 weeks of peginterferon and ribavirin (total treatment duration, 28–48 wk). A good response to interfer…

MaleCirrhosisMESH: Logistic ModelsHepacivirusMESH: Risk AssessmentGastroenterologyPolyethylene GlycolsMESH: Recombinant ProteinsMESH: Genotype0302 clinical medicineOdds RatioProspective StudiesMESH: Treatment OutcomeResponse to Therapy0303 health sciencesMESH: Polymorphism Single NucleotideGastroenterologyvirus diseases3. Good healthMESH: RNA ViralHCVDrug Therapy Combination030211 gastroenterology & hepatologyClinical Trial; Genetic; Prognostic Factors; Response to Therapy; Adult; Antiviral Agents; Biomarkers; Canada; Drug Therapy Combination; Europe; Female; Genotype; Hepacivirus; Hepatitis C; Humans; Interferon-alpha; Interleukins; Logistic Models; Male; Multivariate Analysis; Odds Ratio; Phenotype; Polyethylene Glycols; Polymorphism Single Nucleotide; Proline; Prospective Studies; RNA Viral; Recombinant Proteins; Ribavirin; Risk Assessment; Risk Factors; Time Factors; Treatment Outcome; United States; Viral Load; GastroenterologyViral loadmedicine.medical_specialtyMESH: InterleukinsGenotypeProlineInterferon alpha-2MESH: PhenotypeAntiviral AgentsRisk Assessment03 medical and health sciencesDrug TherapyGeneticMESH: RibavirinMESH: CanadaBoceprevirHumansPolymorphismMESH: ProlineMESH: HumansPrognostic FactorsInterleukinsMESH: AdultOdds ratiomedicine.diseaseUnited Statesdigestive system diseasesClinical trialLogistic ModelschemistryImmunologyMESH: FemaleBiomarkersTime Factorsmedicine.disease_causechemistry.chemical_compoundRisk FactorsInterferonMESH: Risk FactorsMESH: HepacivirusViralSingle NucleotideViral LoadHepatitis CClinical TrialRecombinant ProteinsEuropePhenotypeTreatment OutcomeCombinationRNA ViralFemaleMESH: Interferon-alphaMESH: Viral Loadmedicine.drugAdultMESH: Antiviral AgentsCanadaHepatitis C virusPolymorphism Single NucleotideMESH: Multivariate AnalysisInternal medicineRibavirinmedicineMESH: United States030304 developmental biologyMESH: Hepatitis CHepatologybusiness.industryRibavirinMESH: Time FactorsMESH: Biological MarkersInterferon-alpha[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMESH: Prospective StudiesMESH: MaleMESH: Odds RatioMESH: Drug Therapy CombinationMESH: Polyethylene GlycolsMultivariate AnalysisRNAInterferonsMESH: Europebusiness
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Detection of drug resistance mutations at low plasma HIV-1 RNA load in a European multicentre cohort study

2011

Background and objectives: Guidelines indicate a plasma HIV-1 RNA load of 500-1000 copies/mL as the minimal threshold for antiretroviral drug resistance testing. Resistance testing at lower viral load levels may be useful to guide timely treatment switches, although data on the clinical utility of this remain limited. We report here the influence of viral load levels on the probability of detecting drug resistance mutations (DRMs) and other mutations by routine genotypic testing in a large multicentre European cohort, with a focus on tests performed at a viral load <1000 copies/mL. Methods: A total of 16511 HIV-1 reverse transcriptase and protease sequences from 11492 treatment-experienced …

MaleDrug ResistanceHIV InfectionsDrug resistanceCohort Studies0302 clinical medicineGenotypeHIV InfectionPharmacology (medical)030212 general & internal medicineViral0303 health sciencesProteolytic enzymesGenotypic testing; HIV; Viral load; Adult; Anti-HIV Agents; CD4 Lymphocyte Count; Cohort Studies; Europe; Female; Genotype; HIV Infections; HIV-1; Humans; Male; RNA Viral; Viral Proteins; Drug Resistance Viral; Mutation Missense; Viral Load; Pharmacology; Pharmacology (medical); Infectious DiseasesViral LoadGenotypic testing3. Good healthEuropeInfectious DiseasesCohortRNA ViralFemaleViral loadCohort studyHumanMicrobiology (medical)AdultGenotypeAnti-HIV AgentsMutation MissenseBiologySettore MED/17 - MALATTIE INFETTIVE03 medical and health sciencesViral ProteinsSDG 3 - Good Health and Well-beingDrug Resistance ViralHumansViral ProteinPharmacology030306 microbiologyHIVAnti-HIV AgentVirologyReverse transcriptaseCD4 Lymphocyte CountRegimenHIV; genotypic testing; viral loadGenotypic testing; HIV; Viral load; Adult; Anti-HIV Agents; CD4 Lymphocyte Count; Cohort Studies; Drug Resistance Viral; Europe; Female; Genotype; HIV Infections; HIV-1; Humans; Male; Mutation Missense; RNA Viral; Viral Load; Viral ProteinsImmunologyMutationHIV-1RNAMissenseCohort Studie
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Presence of calreticulin mutations in JAK2-negative polycythemia vera

2014

Abstract Calreticulin (CALR) mutations have recently been reported in JAK2- and MPL-negative Myeloproliferative Neoplasms (MPN), particularly essential thrombocythemia (ET) and primary myelofibrosis (PMF).The clinical course of sporadic CALR-mutated patients seems to be more indolent than that of JAK2-mutated patients. In contrast, no CALR mutation has been found in the 647 published cases of Polycythemia Vera (PV) patients tested. Consequently, CALR mutations were considered exclusive to JAK2 and MPL mutations. Since 98% of PV patients harbor a JAK2 mutation (mostly the V617F mutation in exon 14 and more rarely, in exon 12), the absence of CALR mutations in PV seemed logical. Here, we desc…

MaleErythrocytesMESH: Thrombocytosismedicine.disease_causeMESH: Polycythemia VeraBiochemistryMESH: Janus Kinase 2MESH: GenotypeHemoglobinsMESH: Aged 80 and overPolycythemia verahemic and lymphatic diseasesPolycythemia VeraMESH: HeterozygoteAged 80 and overThrombocytosisMESH: AgedMutation[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyJanus kinase 2biologyMESH: ErythrocytesExonsHematologyLeukemiaMESH: HemoglobinsMESH: Primary MyelofibrosisThrombocythemia EssentialHeterozygoteMESH: MutationGenotypeMESH: CalreticulinImmunologyContext (language use)medicineHumansMyelofibrosisAllelesAgedMESH: HumansEssential thrombocythemiabusiness.industryMESH: AllelesCell BiologyJanus Kinase 2medicine.diseaseMESH: MalePrimary MyelofibrosisMESH: Gene DeletionMutationImmunologybiology.proteinCancer researchMESH: Thrombocythemia EssentialCalreticulinMESH: ExonsbusinessCalreticulinGene Deletion[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyBlood
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A novel DFNB1 deletion allele supports the existence of a distant cis-regulatory region that controls GJB2 and GJB6 expression

2010

Contains fulltext : 87760_1.pdf (author's version ) (Open Access) Contains fulltext : 87760_2.pdf (Publisher’s version ) (Closed access) Eleven affected members of a large German-American family segregating recessively inherited, congenital, non-syndromic sensorineural hearing loss (SNHL) were found to be homozygous for the common 35delG mutation of GJB2, the gene encoding the gap junction protein Connexin 26. Surprisingly, four additional family members with bilateral profound SNHL carried only a single 35delG mutation. Previously, we demonstrated reduced expression of both GJB2 and GJB6 mRNA from the allele carried in trans with that bearing the 35delG mutation in these four persons. Usin…

MaleGenetics and epigenetic pathways of disease [NCMLS 6][SDV]Life Sciences [q-bio]PenetranceMESH: Base SequenceRegulatory Sequences Nucleic Acidsensorineural hearing lossConnexinsMESH: GenotypeMESH: Hearing Loss Sensorineural/diagnosisMESH: PenetranceGenotypeCopy-number variationGenetics (clinical)Sequence DeletionGeneticsComparative Genomic Hybridization0303 health sciencesMESH: Genetic TestingMESH: Gene Expression Regulation*030305 genetics & heredityPenetranceGJB2PedigreeConnexin 26MESH: Sequence Deletion*MESH: Hearing Loss Sensorineural/geneticsFemaleChromosome DeletionFunctional Neurogenomics [DCN 2]GJB6GenotypeMESH: PedigreeMESH: Chromosome DeletionHearing Loss SensorineuralMolecular Sequence Dataconnexin 26connexin 30DFNB1gene expression regulationGJB2GJB6sensorineural hearing losssequence deletionBiologyMESH: Connexin 30MESH: Connexins/genetics*MESH: Sequence Homology Nucleic AcidArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesMonoallelic MutationGJB6MESH: Connexin 26Sequence Homology Nucleic AcidConnexin 30otorhinolaryngologic diseasesGeneticsHumansGenetic TestingAlleleGeneMESH: Regulatory Sequences Nucleic Acid/genetics*AllelesDFNB1030304 developmental biologyFamily HealthMESH: HumansMESH: Molecular Sequence DataBase SequenceChromosomes Human Pair 13MESH: AllelesBreakpointMESH: MaleMESH: Comparative Genomic HybridizationGene Expression RegulationMESH: Family Healthbiology.proteinHuman medicineMESH: Chromosomes Human Pair 13/geneticsMESH: FemaleClinical Genetics
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A novel KCNQ3 mutation in familial epilepsy with focal seizures and intellectual disability

2015

Mutations in the KCNQ2 gene encoding for voltage-gated potassium channel subunits have been found in patients affected with early onset epilepsies with wide phenotypic heterogeneity, ranging from benign familial neonatal seizures (BFNS) to epileptic encephalopathy with cognitive impairment, drug resistance, and characteristic electroencephalography (EEG) and neuroradiologic features. By contrast, only few KCNQ3 mutations have been rarely described, mostly in patients with typical BFNS. We report clinical, genetic, and functional data from a family in which early onset epilepsy and neurocognitive deficits segregated with a novel mutation in KCNQ3 (c.989G>T; p.R330L). Electrophysiological stu…

MaleGenotype-phenotype correlationmedicine.medical_specialtyNeurologyBenign familial neonatal seizuresMutantGenotype-phenotype correlationsmedicine.disease_causeMutagenesiKCNQ3 Potassium ChannelEpilepsyKCNQBenign Familial Neonatal Seizures KCNQ cognitive impairment voltage-gated potassium channels epilepsy mutagenesis genotype-phenotype correlationsSeizuresSettore M-PSI/08 - Psicologia ClinicaIntellectual DisabilityIntellectual disabilitymedicineHumansKCNQ2 Potassium ChannelVoltage-gated potassium channelBenign familial neonatal seizuresGenetic Predisposition to DiseaseGenetic TestingChildGenetic testingGeneticsMutationEpilepsymedicine.diagnostic_testGenetic heterogeneitybusiness.industryMedicine (all)Benign familial neonatal seizures; Cognitive impairment; Epilepsy; Genotype-phenotype correlations; KCNQ; Mutagenesis; Voltage-gated potassium channels; Child; Female; Genetic Testing; Humans; Intellectual Disability; KCNQ2 Potassium Channel; KCNQ3 Potassium Channel; Male; Mutation; Pedigree; Seizures; Genetic Predisposition to Disease; Neurology (clinical); Neurology; Medicine (all)Benign familial neonatal seizuremedicine.diseaseSeizureSettore MED/39 - Neuropsichiatria InfantilePedigreeCognitive impairmentNeurologyMutagenesisMutationFemaleNeurology (clinical)businessVoltage-gated potassium channelsHuman
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Add-on peginterferon alfa-2a to nucleos(t)ide analogue therapy for Caucasian patients with hepatitis B ‘e’ antigen-negative chronic hepatitis B genot…

2019

Nucleos(t)ide analogues (NAs) and peginterferon have complementary effects in chronic hepatitis B, but it is unclear whether combination therapy improves responses in genotype D-infected patients. We conducted an open-label study of peginterferon alfa-2a 180 μg/week added to ongoing NA therapy in hepatitis B e antigen (HBeAg)-negative, genotype D-infected patients with HBV DNA <20 IU/mL. The primary endpoint was proportion of patients with ≥50% decline in serum HBsAg by the end of the 48-week add-on phase. Seventy patients received treatment, 11 were withdrawn at week 24 for no decrease in HBsAg, and 14 withdrew for other reasons. Response rate (per-protocol population) was 67.4% (29/43) at…

MaleHBsAgGastroenterologyPolyethylene Glycolschronic hepatitis B; HBeAg-negative; nucleos(t)ide analogues; peginterferon; treatment; Hepatology; Infectious Diseases; Virology0302 clinical medicineInterferonGenotypeHBVHepatitis B e Antigenspeginterferonchronic hepatitis b; hbeag-negative; nucleos(t)ide analogues; peginterferon; treatment; adult; antiviral agents; drug administration schedule; drug therapy combination; female; genotype; hepatitis b e antigens; hepatitis b virus; hepatitis b chronic; humans; interferon-alpha; male; middle aged; nucleosides; polyethylene glycols; recombinant proteins; treatment outcomeeducation.field_of_studytreatmentnucleos(t)ide analoguesvirus diseasesNucleosidesMiddle AgedRecombinant ProteinsTreatment OutcomeInfectious Diseasesnucleos(t)ide analogueHBeAg030220 oncology & carcinogenesisDrug Therapy CombinationFemale030211 gastroenterology & hepatologyPeginterferon alfa-2amedicine.drugAdultHepatitis B virusmedicine.medical_specialtyGenotypeCombination therapyPopulationHBeAg-negativeInfectious DiseaseHBeAg-negative; chronic hepatitis B; nucleos(t)ide analogues; peginterferon; treatmentchronic hepatitis B; HBeAg-negative; nucleos(t)ide analogues; peginterferon; treatmentAntiviral AgentsDrug Administration Schedule03 medical and health sciencesHepatitis B ChronicInternal medicineVirologymedicineHumanschronic hepatitis BeducationHepatologybusiness.industryInterferon-alphaConfidence intervalbusiness
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Clinical features and comorbidity pattern of HCV infected migrants compared to native patients in care in Italy: A real-life evaluation of the PITER …

2021

Background: Direct-acting antivirals are highly effective for the treatment of hepatitis C virus (HCV) infection, regardless race/ethnicity. We aimed to evaluate demographic, virological and clinical data of HCV-infected migrants vs. natives consecutively enrolled in the PITER cohort. Methods: Migrants were defined by country of birth and nationality that was different from Italy. Mann-Whitney U test, Chi-squared test and multiple logistic regression were used. Results: Of 10,669 enrolled patients, 301 (2.8%) were migrants: median age 47 vs. 62 years, (p &lt; 0.001), females 56.5% vs. 45.3%, (p &lt; 0.001), HBsAg positivity 3.8% vs. 1.4%, (p &lt; 0.05). Genotype 1b was prevalent in both gro…

MaleHCV genotypesEthnic groupLinked-to-care patientComorbidityHepacivirusLogistic regressionmedicine.disease_causeComorbidities; Direct acting antivirals; HCV Cohort; Linked-to-care patients; Aged; Antiviral Agents; Coinfection; Comorbidity; Female; Hepacivirus; Hepatitis C Chronic; Humans; Italy; Male; Middle Aged; Transients and MigrantsComorbidities0302 clinical medicineMedicineComorbidities; Direct acting antivirals; HCV Cohort; Linked-to-care patientsChronicTransients and MigrantsCoinfectionGastroenterologyvirus diseasesMiddle AgedHepatitis CLife evaluationItaly030220 oncology & carcinogenesisLinked-to-care patientsCohort030211 gastroenterology & hepatologyFemaleComorbiditieHumanHepatitis C virusSettore MED/12 - GASTROENTEROLOGIAAntiviral AgentsDirect acting antivirals03 medical and health sciencesDisease severityHumansAgedAntiviral AgentHepaciviruHepatologybusiness.industrySettore MED/09 - MEDICINA INTERNAHepatitis C Chronicmedicine.diseaseComorbiditydigestive system diseasesDirect acting antiviralHCV CohortbusinessDemography
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Yersinia pestis DNA from Skeletal Remains from the 6th Century AD Reveals Insights into Justinianic Plague

2013

Yersinia pestis, the etiologic agent of the disease plague, has been implicated in three historical pandemics. These include the third pandemic of the 19th and 20th centuries, during which plague was spread around the world, and the second pandemic of the 14th–17th centuries, which included the infamous epidemic known as the Black Death. Previous studies have confirmed that Y. pestis caused these two more recent pandemics. However, a highly spirited debate still continues as to whether Y. pestis caused the so-called Justinianic Plague of the 6th–8th centuries AD. By analyzing ancient DNA in two independent ancient DNA laboratories, we confirmed unambiguously the presence of Y. pestis DNA in…

MaleHistoryYersinia pestis590Social and Behavioral SciencesPandemicBiology (General)16th CenturyPhylogenyHistory 15th CenturybiologyBacterialHistory 19th Century20th CenturyBiological AnthropologyHistory 16th Century17th CenturyFemaleBase Sequence; Bone and Bones; DNA Bacterial; Female; Genotype; History 15th Century; History 16th Century; History 17th Century; History 19th Century; History 20th Century; History Medieval; Humans; Male; Molecular Sequence Data; Pandemics; Yersinia pestis; Phylogeny; PlagueMedievalResearch ArticleDNA BacterialGenotypeQH301-705.5ImmunologyMolecular Sequence DataPlague (disease)MicrobiologyBone and BonesNOHistory 17th CenturyVirologyGeneticsHumansBase sequenceMolecular BiologyPandemicsBiologyPlague bacillus19th CenturyPlagueBase SequenceDNARC581-607History 20th Centurybiology.organism_classificationVirologyHistory Medieval15th CenturyAncient DNAYersinia pestisAnthropologyYersinia pestis DNAParasitologyImmunologic diseases. Allergy
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