0000000000172063

AUTHOR

Marina D’addedda

showing 3 related works from this author

Factor V Leiden Is Associated with Repeated and Recurrent Unexplained Fetal Losses

1997

SummaryActivated protein C resistance (APCR) is responsible for most cases of familial thrombosis. The factor V missense mutation Arg506>Gln (FV Leiden) has been recognized as the commonest cause of this condition. Recently, it has been suggested that APCR is associated with second trimester fetal loss. We investigated the distribution of FV Leiden in a sample (n = 43) of Caucasian women with a history of two or more unexplained fetal losses. A group (n = 118) of parous women with uneventful pregnancies from the same ethnical background served as control. We found the mutation in 7 cases (16.28%) and 5 controls (4.24%; p = 0.011). A statistically significant difference between women with…

medicine.medical_specialtyFetusPregnancybiologybusiness.industryFactor VCase-control studyHematologymedicine.diseaseGastroenterologyEndocrinologyInternal medicineFactor V LeidenmedicineCoagulopathybiology.proteinMissense mutationActivated protein C resistancebusinessThrombosis and Haemostasis
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PAI-1 plasma levels in a general population without clinical evidence of atherosclerosis: relation to environmental and genetic determinants.

1998

Abstract —Plasminogen activator inhibitor-1 (PAI-1) plasma levels have been consistently related to a polymorphism (4G/5G) of the PAI-1 gene. The renin-angiotensin pathway plays a role in the regulation of PAI-1 plasma levels. An insertion ( I )/deletion ( D ) polymorphism of the angiotensin-converting enzyme (ACE) gene has been related to plasma and cellular ACE levels. In 1032 employees (446 men and 586 women; 22 to 66 years old) of a hospital in southern Italy, we investigated the association between PAI-1 4G/5G and the ACE I/D gene variants and plasma PAI-1 antigen levels. None of the individuals enrolled had clinical evidence of atherosclerosis. In univariate analysis, PAI-1 levels we…

AdultMaleAgingmedicine.medical_specialtyAlcohol DrinkingGenotypePopulationPeptidyl-Dipeptidase ABody Mass Indexchemistry.chemical_compoundInsulin resistanceGene FrequencyInternal medicinePlasminogen Activator Inhibitor 1Blood plasmaGenotypemedicineHumanseducationAllele frequencyTriglyceridesAgedSex Characteristicseducation.field_of_studyPolymorphism GeneticbiologySmokingAngiotensin-converting enzymeMiddle Agedmedicine.diseaseCholesterolEndocrinologychemistryPlasminogen activator inhibitor-1Hypertensionbiology.proteinFemaleCardiology and Cardiovascular MedicineBody mass indexGene Deletion
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Identifying human platelet glycoproteins IIb and IIIa by capillary electrophoresis.

1998

Glanzmann thrombasthenia (GT) is an inherited hemorrhagic defect due to a failure of the platelet membrane glycoprotein (GP) IIb–IIIa complex. Capillary electrophoresis (CE) analysis of solubilized platelet membranes from normal individuals showed the presence of two peaks with a migration time of 27 and 29 min, respectively. An excellent run-to-run and day-to-day reproducibility of the technique (< 1% variation of the retention time) was documented. Using an automated Ferguson method, the apparent molecular masses were 100.0 kDa and 138.5 kDa, respectively. Immunoprecipitation with monoclonal antibodies anti-GP IIIa (B59.2.1) and anti-IIb (61.9.1.3) showed the two peaks as IIIa and IIb, re…

Blood PlateletsMaleClinical BiochemistryPlatelet Glycoprotein GPIIb-IIIa ComplexPlatelet membrane glycoproteinBiochemistryAnalytical ChemistryCapillary electrophoresisThrombastheniamedicineHumansPlateletChildPolyacrylamide gel electrophoresischemistry.chemical_classificationMembrane GlycoproteinsGlanzmann's thrombastheniaCell MembraneElectrophoresis Capillarymedicine.diseaseFlow CytometryMolecular biologyPrecipitin TestsPlatelet Glycoprotein GPIIb-IIIa ComplexchemistryGlycoproteinThrombastheniaElectrophoresis
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