Search results for "Sang"

showing 10 items of 428 documents

Hemostatic function in young subjects with central obesity: relationship with left ventricular function.

1995

This study was designed to evaluate coagulation and fibrinolysis activity and their relationship with left ventricular function in young obese subjects with central fat distribution. We assessed coagulation and fibrinolysis activity by evaluation of factor VII activity, fibrinogen and plasminogen, plasminogen activator inhibitor (PAI), and tissue plasminogen activator antigen basally (tPA1) and after venous occlusion (tPA2). These measures were evaluated in young (< 40 years) obese subjects with central fat distribution (n = 19) and in comparable lean subjects (n = 20). Blood glucose, triglycerides, total and high-density lipoprotein (HDL) cholesterol, apolipoprotein (apo) A1 and apo B, fas…

AdultBlood GlucoseMalemedicine.medical_specialtySettore MED/09 - Medicina InternaApolipoprotein BEndocrinology Diabetes and Metabolismmedicine.medical_treatmentFibrinogenVentricular Function LeftSettore MED/15 - Malattie Del Sanguechemistry.chemical_compoundEndocrinologyWaist–hip ratioInternal medicineFibrinolysismedicineHumansInsulinObesityHemostatic functionBlood CoagulationApolipoproteins ATriglyceridesApolipoproteins BHemostasisbiologybusiness.industryCholesterolCholesterol HDLFibrinogenCentral obesity Hemostatic function left ventricular functionPlasminogenFactor VIISettore MED/11 - Malattie Dell'Apparato CardiovascolarePlasminogen InactivatorsEndocrinologychemistrybiology.proteinBody ConstitutionRegression AnalysisFemalebusinessPlasminogen activatormedicine.drugLipoproteinMetabolism: clinical and experimental
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Role of APOBEC3H in the Viral Control of HIV Elite Controller Patients

2017

Background APOBEC3H (A3H) gene presents variation at 2 positions (rs139297 and rs79323350) leading to a non-functional protein. So far, there is no information on the role played by A3H in spontaneous control of HIV. The aim of this study was to evaluate the A3H polymorphisms distribution in a well-characterized group of Elite Controller (EC) subjects. Methods We analyzed the genotype distribution of two different SNPs (rs139297 and rs79323350) of A3H in 30 EC patients and compared with 11 non-controller (NC) HIV patients. Genotyping was performed by PCR, cloning and Sanger sequencing. Both polymorphisms were analyzed jointly in order to adequately attribute the active or inactive status of…

AdultCD4-Positive T-LymphocytesMalers139297HIV InfectionsSingle-nucleotide polymorphismBiologyVirus ReplicationPolymorphism Single NucleotideAPOBEC3H polymorphisms03 medical and health sciencessymbols.namesake0302 clinical medicineGene FrequencyAminohydrolasesGenotypeHumansAlleleGenotypingGeneSanger sequencingCloningelite controllers.HaplotypeHIVGeneral MedicineMiddle AgedCross-Sectional StudiesHaplotypesImmunologyrs79323350symbolsFemaleResearch Paper030215 immunologyInternational Journal of Medical Sciences
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The obsolescent renal glomerulus ? Collapse, sclerosis, hyalinosis, fibrosis

1977

By light and electron microscopical examination it is shown that four structural components can contribute to obsolescent glomeruli: capillary basement membranes, enriched mesangium matrix, “vascular” hyalin and collagen fibers. Each of these components can bring about glomerular damage alone. One non-reactive form — a glomerular collapse with only basement membrane remnants — can be separated from three reactive forms: the accumulation of mesangium matrix (sclerosis or matrix-sclerosis), deposition of vascular hyalin (hyalinosis in the narrow sense), and fiber development within the former urinary space (fibrosis or fibro-sclerosis). The use of the term “fibrinoid” in place of the descript…

AdultHyalinPathologymedicine.medical_specialtyHistologyRenal glomerulusKidney GlomerulusBasement MembranePathology and Forensic MedicineFibrosismedicineHumansChildMolecular BiologyCollapse (medical)HyalineBasement membraneMesangium matrixSclerosisUrinary spaceGlomerulosclerosis Focal SegmentalChemistryBiopsy NeedleGlomerulosclerosisCell BiologyGeneral MedicineAnatomymedicine.diseaseMicroscopy Electronmedicine.anatomical_structureCollagenAnatomymedicine.symptomVirchows Archiv A Pathological Anatomy and Histology
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Homozygous variants in the gene SCAPER cause syndromic intellectual disability

2019

The S-Phase Cyclin A Associated Protein In The ER (SCAPER) gene is a ubiquitously expressed gene with unknown function in the brain. Recently, biallelic SCAPER variants were described in four patients from three families with retinitis pigmentosa (RP) and intellectual disability (ID). Here, we expand the spectrum of pathogenic variants in SCAPER and report on 10 further patients from four families with ID, RP, and additional dysmorphic features carrying homozygous variants in SCAPER. The variants found comprise frameshift, nonsense, and missense variants as well as an intragenic homozygous deletion, which spans SCAPER exons 15 and 16 and introduces a frameshift and a premature stop codon. A…

AdultMale0301 basic medicineAdolescentmedia_common.quotation_subjectCyclin ANonsenseGene Expression030105 genetics & heredityFrameshift mutationConsanguinityMice03 medical and health sciencesExonNeural Stem CellsIntellectual DisabilityRetinitis pigmentosaGene expressionGeneticsmedicineAnimalsHumansMissense mutationFamilyChildGeneGenetics (clinical)media_commonCerebral CortexNeuronsGeneticsbiologyHomozygoteSyndromemedicine.diseasePedigree030104 developmental biologyMutationbiology.proteinFemaleCarrier ProteinsRetinitis PigmentosaAmerican Journal of Medical Genetics Part A
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Whole genome paired-end sequencing elucidates functional and phenotypic consequences of balanced chromosomal rearrangement in patients with developme…

2019

BackgroundBalanced chromosomal rearrangements associated with abnormal phenotype are rare events, but may be challenging for genetic counselling, since molecular characterisation of breakpoints is not performed routinely. We used next-generation sequencing to characterise breakpoints of balanced chromosomal rearrangements at the molecular level in patients with intellectual disability and/or congenital anomalies.MethodsBreakpoints were characterised by a paired-end low depth whole genome sequencing (WGS) strategy and validated by Sanger sequencing. Expression study of disrupted and neighbouring genes was performed by RT-qPCR from blood or lymphoblastoid cell line RNA.ResultsAmong the 55 pat…

AdultMale0301 basic medicineCandidate geneAdolescentDNA Copy Number VariationsDevelopmental Disabilities030105 genetics & heredityGenomeTranslocation GeneticStructural variationChromosome BreakpointsStructure-Activity RelationshipYoung Adult03 medical and health sciencessymbols.namesakeposition effectGeneticsHumansChildGeneGenetic Association StudiesGenetics (clinical)Paired-end tagComputingMilieux_MISCELLANEOUSchromosomal rearrangementsChromosome AberrationsGene RearrangementWhole genome sequencingGeneticsSanger sequencingwhole genome sequencingbiologystructural variationInfantNFIXPhenotype030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsintellectual disabilityChild Preschoolbiology.proteinsymbolsFemaleBiomarkers
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Identification of a novel LMF1 nonsense mutation responsible for severe hypertriglyceridemia by targeted next-generation sequencing

2016

Background Severe hypertriglyceridemia (HTG) may result from mutations in genes affecting the intravascular lipolysis of triglyceride (TG)-rich lipoproteins. Objective The aim of this study was to develop a targeted next-generation sequencing panel for the molecular diagnosis of disorders characterized by severe HTG. Methods We developed a targeted customized panel for next-generation sequencing Ion Torrent Personal Genome Machine to capture the coding exons and intron/exon boundaries of 18 genes affecting the main pathways of TG synthesis and metabolism. We sequenced 11 samples of patients with severe HTG (TG&gt;885 mg/dL–10 mmol/L): 4 positive controls in whom pathogenic mutations had pre…

AdultMale0301 basic medicineCandidate geneEndocrinology Diabetes and MetabolismDNA Mutational AnalysisNonsense mutationPanel-based NGS sequencing030204 cardiovascular system & hematologyBiologymedicine.disease_causeDNA sequencing03 medical and health sciencessymbols.namesakeExon0302 clinical medicineNutrition and DieteticInternal MedicinemedicineHumansGeneHypertriglyceridemiaSanger sequencingGeneticsMutationNutrition and DieteticsLMF1 geneNonsense mutationHigh-Throughput Nucleotide SequencingInfantMembrane ProteinsIon semiconductor sequencingMiddle AgedIon torrent PGM sequencingPhenotype030104 developmental biologyChild PreschoolsymbolsFemaleCardiology and Cardiovascular MedicineJournal of Clinical Lipidology
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Phenotype and natural history of inherited neuropathies caused byHSJ1c.352+1G&gt;A mutation

2015

Mutations in the HSJ1 ( Heat-Shock Protein J1 ) gene, also called DNAJB2 (DnaJ (Hsp40) homologue, subfamily B, member 2), have been recently described as a cause of hereditary neuropathies. The HSJ1 c.352+1G>A mutation in homozygote state has been reported as the causative mutation in a single family with autosomal recessive distal hereditary motor neuropathy (dHMN).1 Since then, two other families with different HSJ1 mutations have been described: one with a dHMN phenotype and the other with a Charcot-Marie-Tooth disease type 2 (CMT2) phenotype.2 We identified the HSJ1 c.352+1G>A mutation in 10 patients who underwent long-lasting follow-up. We describe their phenotype and clinical evolutio…

AdultMale0301 basic medicineNeural ConductionCell Cycle ProteinsNeurological examinationDisease03 medical and health sciencessymbols.namesake0302 clinical medicineCharcot-Marie-Tooth DiseasemedicineHumansGeneHeat-Shock ProteinsExome sequencingAdaptor Proteins Signal TransducingGenetic testingGeneticsSanger sequencingmedicine.diagnostic_testbusiness.industryNuclear ProteinsMiddle AgedPhenotypePsychiatry and Mental healthPhenotype030104 developmental biologySpainMutationMutation (genetic algorithm)symbolsFemaleSurgeryNeurology (clinical)Hereditary Sensory and Motor Neuropathybusiness030217 neurology & neurosurgeryJournal of Neurology, Neurosurgery &amp; Psychiatry
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Hereditary angioedema with a mutation in the plasminogen gene

2017

Background Hereditary angioedema (HAE) with normal C1-INH (HAEnCI) may be linked to specific mutations in the coagulation factor 12 (FXII) gene (HAE-FXII) or functional mutations in other genes that are still unknown. We sought to identify and characterize a hitherto unknown type of HAE with normal C1-INH and without mutation in the F12 gene. Methods The study comprised analysis of whole-exome sequencing, Sanger sequencing, and clinical data of patients. Results We detected a mutation in the plasminogen (PLG) gene in patients with HAEnCI. The mutation c.9886A>G was located in exon 9 leading to the missense mutation p.Lys330Glu (K330E) in the kringle 3 domain of the PLG protein. The mutation…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyAdolescentImmunologyMutation MissenseGene mutationBiologyYoung Adult03 medical and health sciencesExonsymbols.namesake0302 clinical medicineGermanyExome SequencingmedicineHumansImmunology and AllergyMissense mutationChildExome sequencingAgedSanger sequencingAngioedemas HereditaryAutosomal dominant traitPlasminogenMiddle Agedmedicine.disease030104 developmental biology030228 respiratory systemChild PreschoolMutationMutation (genetic algorithm)Hereditary angioedemasymbolsFemaleAllergy
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Renal disease associated with myeloproliferative neoplasms and myelodysplastic syndrome/myeloproliferative neoplasms

2020

Aims Renal changes in patients with myeloproliferative neoplasms (MPNs) or myelodysplastic syndrome (MDS)/MPNs have been addressed by few, respectively no, reports. The aim of this study was to focus on a systematic evaluation of renal biopsies in patients with MPNs or MDS/MPNs. Methods and results The cohort comprised 29 patients (23 men) aged 67 ± 11 years (mean ± standard deviation), diagnosed with chronic myeloid leukaemia (n = 5), polycythaemia vera (n = 9), primary myelofibrosis (n = 5), essential thrombocythaemia (n = 2), or chronic myelomonocytic leukaemia (n = 4), as well as MPNs or MDS/MPNs not otherwise specified (n = 4). Patients manifested with proteinuria (93%), partially in t…

AdultMale0301 basic medicinemedicine.medical_specialtyPolycythaemiaHistologyThrombotic microangiopathy610 MedizinRenal functionMesangial hypercellularityGastroenterologyPathology and Forensic MedicineNephropathyCohort Studies03 medical and health sciencesGlomerulonephritis0302 clinical medicineRisk FactorsNeoplasmshemic and lymphatic diseasesInternal medicine610 Medical sciencesmedicineHumansddc:610MyelofibrosisAgedAged 80 and overMyeloproliferative DisordersProteinuriaThrombotic Microangiopathiesbusiness.industryGlomerulonephritisGeneral MedicineMiddle Agedmedicine.diseaseMyelodysplastic-Myeloproliferative Diseases030104 developmental biologyMyelodysplastic Syndromes030220 oncology & carcinogenesisFemaleKidney Diseasesmedicine.symptombusiness
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Quizartinib versus salvage chemotherapy in relapsed or refractory FLT3-ITD acute myeloid leukaemia (QuANTUM-R): a multicentre, randomised, controlled…

2019

Background Patients with relapsed or refractory FLT3 internal tandem duplication (FLT3-ITD)-positive acute myeloid leukaemia have a poor prognosis, including high frequency of relapse, poorer response to salvage therapy, and shorter overall survival than those with FLT3 wild-type disease. We aimed to assess whether single-agent quizartinib, an oral, highly potent and selective type II FLT3 inhibitor, improves overall survival versus salvage chemotherapy. Methods QuANTUM-R is a randomised, controlled, phase 3 trial done at 152 hospitals and cancer centres in 19 countries. Eligible patients aged 18 years or older with ECOG performance status 0-2 with relapsed or refractory (duration of first …

AdultMale0301 basic medicinemedicine.medical_specialtyPopulationSalvage therapy/Gastroenterology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicinemedicineHumansBenzothiazoleseducationSurvival rateAgedQuizartinibSalvage Therapyeducation.field_of_studybusiness.industryPhenylurea CompoundsMiddle Agedmedicine.diseaseFludarabineSurvival RateTransplantationLeukemia Myeloid AcuteSettore MED/15 - MALATTIE DEL SANGUE030104 developmental biologyfms-Like Tyrosine Kinase 3OncologychemistryTandem Repeat Sequences030220 oncology & carcinogenesisCytarabineFemaleNeoplasm Recurrence LocalbusinessFebrile neutropeniamedicine.drug
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