Search results for "Homozygote"

showing 8 items of 138 documents

Effective hemostasis during minor surgery in a case of hereditary combined deficiency of vitamin K-dependent clotting factors.

2009

Combined deficiency of the vitamin K-dependent clotting factors (VKCFD) is a rare bleeding disorder involving defective gamma-carboxylation of coagulation factors II , VII, IX and X as well as natural anticoagulants protein C and protein S. The disease is characterized by a cluster of different, often life threatening, bleeding symptoms occurring both spontaneously and in a surgical setting. In the present paper we describe two different treatment modalities to be used both in a programmed surgical procedure and in an emergency scenario. As this disease is a natural model that resembles oral anticoagulation, our experience discloses a possible rationale in the use of recombinant activated …

VitaminAdultmedicine.medical_specialtyVitamin KBiopsyFactor VII DeficiencyHereditary Combined Deficiency of Vitamin K-dependent Clotting FactorsBlood Loss SurgicalDiseaseFactor VIIaGastroenterologyMixed Function Oxygenaseschemistry.chemical_compoundBlood Coagulation Disorders InheritedInternal medicineVitamin K Epoxide ReductasesGastroscopymedicineHumansRare Inherited Bleeding disorders Minor SurgeryOral anticoagulationClotting factorbusiness.industryHomozygoteWarfarinHematologyGeneral MedicineFactor VIIHemostasis SurgicalRecombinant ProteinsSurgeryCoagulationchemistryHemostasisTooth ExtractionFemaleBlood Coagulation TestsbusinessProtein Cmedicine.drugClinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
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α-Tocopherol Modulates Phosphatidylserine Externalization in Erythrocytes

2006

Objective— The aim of the present study was to assess the effect of α-tocopherol, the main vitamin E isomer on phosphatidylserine (PS) exposure at the surface of circulating erythrocytes, and to determine consequences on erythrocyte properties. Methods and Results— In vitro α-tocopherol enrichment of isolated erythrocytes significantly decreased PS externalization as assessed by lower Annexin V-fluorescein isothiocyanate labeling. Plasma phospholipid transfer protein (PLTP) transfers vitamin E, and both α-and γ-tocopherol accumulated in circulating erythrocytes from PLTP-deficient homozygous (PLTP −/− ) mice as compared with wild-type mice. In agreement with in vitro studies, vitamin E–enr…

Vitaminmedicine.medical_specialtyErythrocytesWhole Blood Coagulation Timemedicine.medical_treatmentalpha-TocopherolPhospholipidCell SeparationPhosphatidylserinesBiologyFibrin Fibrinogen Degradation ProductsMicechemistry.chemical_compoundAnnexinIn vivoPhospholipid transfer proteinInternal medicinemedicineAnimalsTocopherolPhospholipid Transfer ProteinsBlood CoagulationMice KnockoutVitamin EErythrocyte MembraneHomozygotePhosphatidylserinePhenotypeEndocrinologychemistryBiochemistryCardiology and Cardiovascular MedicineOxidation-ReductionBiomarkersArteriosclerosis, Thrombosis, and Vascular Biology
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Runs of homozygosity in the Italian goat breeds: impact of management practices in low-input systems

2021

Abstract Background Climate and farming systems, several of which are considered as low-input agricultural systems, vary between goat populations from Northern and Southern Italy and have led to different management practices. These processes have impacted genome shaping in terms of inbreeding and regions under selection and resulted in differences between the northern and southern populations. Both inbreeding and signatures of selection can be pinpointed by the analysis of runs of homozygosity (ROH), which provides useful information to assist the management of this species in different rural areas. Results We analyzed the ROH distribution and inbreeding (FROH) in 902 goats from the Italia…

adaptation; body size; climate change; ecological impact; farming system; goat; inbreeding; management practiceClimateecological impactadaptationQH426-470Runs of homozygosityPolymorphism Single NucleotideSF1-1100GeneticsAnimalsfarming systemsInbreedingPolymorphismEcology Evolution Behavior and SystematicsbiodiversityGenomeSettore AGR/17 - ZOOTECNICA GENERALE E MIGLIORAMENTO GENETICOlocal breedsAnimalGoatsROHHomozygoteGeneral MedicineSingle NucleotideAnimal cultureclimate changeAnimals; Genome; Homozygote; Inbreeding; Goats; Polymorphism Single Nucleotidelocal breeds biodiversity SNPs inbreedingGoatfarming systemRuns of homozygosity ROH Goat signatures of selection low-input system Climate farming systemsAnimal Science and Zoologybody sizeGoat signatures of selectionlow-input systemmanagement practiceResearch ArticleSNPs
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Complement C6 deficiency protects against diet-induced atherosclerosis in rabbits.

1998

Abstract —Low-density lipoprotein (LDL) can be transformed to an atherogenic moiety by nonoxidative, enzymatic degradation. Enzymatically degraded LDL induces macrophage foam cell formation, provokes release of cytokines, and also activates complement. To determine whether complement activation may contribute to atherogenesis, 6 pairs of homozygous C6-deficient rabbits and their non–C6-deficient heterozygous siblings were fed a cholesterol-rich diet for 14 weeks. Cholesterol levels and plasma lipoprotein profiles of the animals in the C6-competent and C6-deficient groups did not significantly differ, and the high density lipoprotein and LDL cholesterol ratios at the end of the experiment w…

medicine.medical_specialtyHeterozygoteArteriosclerosisBiologyPathogenesisCholesterol Dietarychemistry.chemical_compoundHigh-density lipoproteinInternal medicinemedicine.arterymedicineMacrophageAnimalsComplement ActivationFoam cellAortaCholesterolHomozygoteComplement systemComplement C6EndocrinologychemistryImmunologyDiet AtherogenicRabbitsCardiology and Cardiovascular MedicineLipoproteinArteriosclerosis, thrombosis, and vascular biology
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Long-term efficacy of lipoprotein apheresis and lomitapide in the treatment of homozygous familial hypercholesterolemia (HoFH): a cross-national retr…

2021

Abstract Background Homozygous familial hypercholesterolemia (HoFH) is a rare life-threatening condition that represents a therapeutic challenge. The vast majority of HoFH patients fail to achieve LDL-C targets when treated with the standard protocol, which associates maximally tolerated dose of lipid-lowering medications with lipoprotein apheresis (LA). Lomitapide is an emerging therapy in HoFH, but its place in the treatment algorithm is disputed because a comparison of its long-term efficacy versus LA in reducing LDL-C burden is not available. We assessed changes in long-term LDL-C burden and goals achievement in two independent HoFH patients’ cohorts, one treated with lomitapide in Ita…

medicine.medical_specialtySettore MED/09 - Medicina Interna[SDV]Life Sciences [q-bio]LipoproteinsGenetic diseaseTherapeuticsFamilial hypercholesterolemiaDiseaseLipoprotein apheresiLDLHyperlipoproteinemia Type IIchemistry.chemical_compoundLipoprotein apheresisRetrospective surveyInternal medicineCholesterol burden; Genetic disease; Homozygous hypercholesterolemia; LDL; Lipoprotein apheresis; Lomitapide; Therapeutics; Benzimidazoles; Homozygote; Humans; Lipoproteins; Retrospective Studies; Anticholesteremic Agents; Blood Component Removal; Hyperlipoproteinemia Type IImedicineHumansPharmacology (medical)Genetics (clinical)Retrospective Studiesmedicine.diagnostic_testbusiness.industryResearchAnticholesteremic AgentsHomozygous hypercholesterolemiaHomozygoteRGeneral Medicinemedicine.diseaseLomitapideLomitapidecholesterol burden; genetic disease; homozygous hypercholesterolemia; LDL; lipoprotein apheresis; lomitapide; therapeuticsCholesterol burdenchemistryCohortBlood Component RemovalMedicineTherapeutics.BenzimidazolesLipid profilebusinessLipoprotein apheresisCross nationalOrphanet Journal of Rare Diseases
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Neonatal Respiratory Insufficiency Caused by an (Homozygous) ABCA3-Stop Mutation: a Systematic Evaluation of Therapeutic Options

2014

Background Autosomal recessive ABCA3 (ATP-binding cassette protein A3) gene mutations have been associated with neonatal respiratory distress and pediatric interstitial lung disease. The clinical course of the disease depends on the underlying mutations. Therefore, knowledge of course, symptoms and treatment of the disease is important. Patient and methods A term newborn suffered from progressive respiratory insufficiency, which led to death at the age of 4.8 months. The girl developed interstitial lung disease. Infections as well as structural and functional disorders of the lung were systematically excluded. A homozygous c.4681C > T (Arg 1561 Stop) mutation of the ABCA3 gene was identifie…

medicine.medical_specialtymedicine.medical_treatmentGenes RecessiveDiseaseGene mutationABCA3Fatal OutcomeAdrenal Cortex HormonesInternal medicinemedicineHumansLung transplantationTreatment FailureIntensive care medicineChromosome AberrationsRespiratory Distress Syndrome NewbornLungbiologybusiness.industryHomozygoteInfant NewbornInterstitial lung diseaseInfantHydroxychloroquinemedicine.diseasePathophysiologymedicine.anatomical_structureMutationPediatrics Perinatology and Child HealthCodon Terminatorbiology.proteinATP-Binding Cassette TransportersFemaleMacrolidesLung Diseases InterstitialRespiratory InsufficiencybusinessHydroxychloroquinemedicine.drugKlinische Pädiatrie
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A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA b…

2002

The Cockayne syndrome B (CSB) gene product is involved in the repair of various types of base modifications in actively transcribed DNA sequences. To investigate its significance for the repair of endogenous oxidative DNA damage, homozygous csb(-/-)/ogg1(-/-) double knockout mice were generated. These combine the deficiency of CSB with that of OGG1, a gene coding for the mammalian repair glycosylase that initiates the base excision repair of 7,8-dihydro-8-oxoguanine (8-oxoG). Compared to ogg1(-/-) mice, csb(-/-)/ogg1(-/-) mice were found to accumulate with age severalfold higher levels of oxidited purine modifications in hepatocytes, splenocytes and kidney cells. In contrast, the basal (ste…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA RepairTranscription GeneticDNA damageDNA repairBiologyGene productMicechemistry.chemical_compoundGeneticsAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneDNA PrimersMice KnockoutBase SequenceHomozygoteDNA HelicasesDeoxyguanosinenutritional and metabolic diseasesBase excision repairMolecular biologyOxidative StressDNA Repair EnzymesBiochemistrychemistry8-Hydroxy-2'-DeoxyguanosineDNA glycosylaseDNADNA DamageNucleotide excision repairOncogene
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Variants of human CLDN9 cause mild to profound hearing loss

2021

Hereditary deafness is clinically and genetically heterogeneous. We investigated deafness segregating as a recessive trait in two families. Audiological examinations revealed an asymmetric mild to profound hearing loss with childhood or adolescent onset. Exome sequencing of probands identified a homozygous c.475G>A;p.(Glu159Lys) variant of CLDN9 (NM_020982.4) in one family and a homozygous c.370_372dupATC;p.(Ile124dup) CLDN9 variant in an affected individual of a second family. Claudin 9 (CLDN9) is an integral membrane protein and constituent of epithelial bicellular tight junctions that form semi-permeable, paracellular barriers between inner ear perilymphatic and endolymphatic compartment…

tight junctionsAdolescentclaudin 9In situ hybridizationDeafnessBiologyArticleFrameshift mutationMiceotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansPakistanInner earNonsyndromic deafnessChildClaudinGenetics (clinical)Exome sequencingnonsyndromic deafnessTight junctionGenetic heterogeneityclaudin 9; exome sequencing; Morocco; nonsyndromic deafness; Pakistan; tight junctionsHomozygotemedicine.diseaseMolecular biologyPedigreeMoroccomedicine.anatomical_structureClaudinsMutationexome sequencingHeLa CellsHuman Mutation
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