Search results for "MUTATION"

showing 10 items of 2830 documents

A 4-year study of the efficacy and tolerability of enzyme replacement therapy with agalsidase alfa in 36 women with Fabry disease

2009

Although Fabry disease is X linked and considered to affect primarily male hemizygotes, female heterozygotes may experience all the signs and symptoms of this metabolic disorder. This prospective, single-center, open-label, clinical trial was performed to evaluate the long-term response of female patients with Fabry disease to enzyme replacement therapy.Symptomatic women (average age = 47 years) enrolled in this 4-year study were treated with agalsidase alfa (Replagal, Shire HGT, Inc.) at a dose of 0.2 mg/kg, every other week for 4 years (N = 36). Clinical and biochemical assessments were conducted at 12-month intervals.The Mainz Severity Score Index, a measure of total disease burden, was …

Adultmedicine.medical_specialtyTreatment outcomeSeverity of Illness IndexDrug Administration ScheduleYoung Adultstomatognathic systemInternal medicineSeverity of illnessLeukocytesmedicineHumansProspective StudiesProspective cohort studyGenetics (clinical)AgedAnalysis of Variancebusiness.industryvirus diseasesEnzyme replacement therapyMiddle Agedmedicine.diseaseFabry diseaseRecombinant Proteinsdigestive system diseasesIsoenzymesClinical trialTreatment OutcomeTolerabilityalpha-GalactosidaseMutationPhysical therapyFabry DiseaseFemalebusinessAgalsidase alfaGlomerular Filtration RateGenetics in Medicine
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VITAMIN K-INDUCED MODIFICATION OF COAGULATION PHENOTYPE IN VKORC1 HOMOZYGOUS DEFICIENCY

2008

Summary.  Background: Combined vitamin K-dependent clotting factor (VKCF) deficiency type 2 (VKCFD2) is a rare bleeding disorder caused by mutated vitamin K 2,3-epoxide reductase complex subunit 1 (VKORC1) gene. Methods and results: An Italian patient with moderate to severe bleeding tendency was genotyped, and found to be homozygous for the unique VKORC1 mutation (Arg98Trp) so far detected in VKCFD2. The activity levels of VKCFs were differentially reduced, and inversely related to the previously estimated affinity of procoagulant factor propeptides for the γ-carboxylase. The normal (factor IX) or reduced antigen levels (other VKCFs) produced a gradient in specific activities. Vitamin K su…

Adultmedicine.medical_specialtycoagulation factor levelsVitamin KProtein SMixed Function OxygenasesTissue factorchemistry.chemical_compoundInternal medicineVitamin K Epoxide ReductasesmedicineVKCFD2HumansFactor IXClotting factorCoagulation factor levels; Thrombin generation; Vitamin K supplementation; VKCFD2; VKORC1 mutation;biologyFactor VIIChemistryFactor XHomozygotevitamin K supplementationHematologyBlood Coagulation DisordersEndocrinologyTreatment OutcomeCoagulationthrombin generationImmunologyMutationbiology.proteinFemaleBlood Coagulation TestsVKCFD2 VKORC1 mutation coagulation factor levels thrombin generation vitamin K supplementationProtein Cmedicine.drugHalf-LifeVKORC1 mutation
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Characterization of epitopes recognized by Candida factor 1 and 9 antisera by use of Saccharomyces cerevisiae mnn mutants

1993

The use of Saccharomyces cerevisiae mnn mutants has facilitated the study of the epitopes recognized by antisera against several antigenic factors of the genus Candida (Candida Check; Iatron Laboratories, Tokyo, Japan). We have taken advantage of the very well characterized structure of the mannans of the different mnn mutants to compare their reactivities with the factor antisera used in the identification of different species of the genus Candida. The results of this study provide evidence that one of the antigenic determinants recognized by factor 1 antisera is the O-linked mannose chains of the cell wall mannoproteins, while that recognized by factor 9 antiserum is the alpha 1-6-linked …

AgglutinationAntigenicityAntigens FungalMolecular Sequence DataImmunologyMutantSaccharomyces cerevisiaeMannoseEnzyme-Linked Immunosorbent AssaySaccharomyces cerevisiaeBiologyMicrobiologyEpitopeMicrobiologyMannansEpitopeschemistry.chemical_compoundAntigenAnimalsAntibodies FungalCandidaMannanAntiserumImmune Serabiology.organism_classificationInfectious DiseasesCarbohydrate SequenceBiochemistrychemistryMutationParasitologyRabbitsResearch ArticleInfection and Immunity
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Repair of oxidatively generated DNA damage in Cockayne syndrome

2013

Defects in the repair of endogenously (especially oxidatively) generated DNA modifications and the resulting genetic instability can potentially explain the clinical symptoms of Cockayne syndrome (CS), a hereditary disease characterized by developmental defects and neurological degeneration. In this review, we describe the evidence for the involvement of CSA and CSB proteins, which are mutated in most of the CS patients, in the repair and processing of DNA damage induced by reactive oxygen species and the implications for the induction of cell death and mutations. Taken together, the data demonstrate that CSA and CSB, in addition to their established role in transcription-coupled nucleotide…

AgingDNA RepairTranscription GeneticDNA damageDNA repairBiologymedicine.disease_causeCockayne syndromemedicineAnimalsHumansCockayne SyndromePoly-ADP-Ribose Binding ProteinsMutationDNA HelicasesBase excision repairmedicine.diseaseMolecular biologyCell biologyDNA Repair EnzymesMitochondrial DNA repairMutationDNA mismatch repairOxidation-ReductionDNA DamageTranscription FactorsDevelopmental BiologyNucleotide excision repairMechanisms of Ageing and Development
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Cannabinoid receptor 1 deficiency in a mouse model of Alzheimer's disease leads to enhanced cognitive impairment despite of a reduction in amyloid de…

2012

Alzheimer's disease (AD) is characterized by amyloid-beta deposition in amyloid plaques, neurofibrillary tangles, inflammation, neuronal loss, and cognitive deficits. Cannabinoids display neuromodulatory and neuroprotective effects and affect memory acquisition. Here, we studied the impact of cannabinoid receptor type 1 (CB1) deficiency on the development of AD pathology by breeding amyloid precursor protein (APP) Swedish mutant mice (APP23), an AD animal model, with CB1-deficient mice. In addition to the lower body weight of APP23/CB1(-/-) mice, most of these mice died at an age before typical AD-associated changes become apparent. The surviving mice showed a reduced amount of APP and its …

Agingmedicine.medical_specialtyPathologyCannabinoid receptormedicine.medical_treatmentMutantMice TransgenicInflammationDiseaseNeuroprotectionAmyloid beta-Protein PrecursorMiceReceptor Cannabinoid CB1Alzheimer DiseaseCell Line TumorInternal medicinemental disordersmedicineAmyloid precursor proteinAnimalsHumansMaze LearningCognitive impairmentAmyloid beta-Peptidesbiologybusiness.industryGeneral NeuroscienceBody WeightAge FactorsBrainPeptide FragmentsDisease Models AnimalEndocrinologyGene Expression RegulationMutationbiology.proteinlipids (amino acids peptides and proteins)MicrogliaNeurology (clinical)CannabinoidGeriatrics and Gerontologymedicine.symptomCognition DisordersbusinessDevelopmental BiologyNeurobiology of Aging
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Na+ ions binding to the bradykinin B2 receptor suppress agonist-independent receptor activation.

1996

Control of the balance between receptor activation and inactivation is a prerequisite for seven transmembrane domain (7TM) receptor function. We asked for a mechanism to stabilize the inactive receptor conformation which prevents agonist-independent receptor activation. Na+ ions have reciprocal effects on agonist versus antagonist interaction with various 7TM receptors. To investigate the Na+ dependence of receptor activation we chose the bradykinin B2 receptor as a prototypic 7TM receptor. Decrease of the intracellular Na+ content from 40 mM to 10 mM of COS-1 cells transiently expressing rat B2 receptors activated the B2 receptor in the absence of agonist as shown by a 3-fold increase in t…

AgonistIntracellular FluidIntrinsic activityReceptor Bradykinin B2medicine.drug_classInositol PhosphatesBradykininIn Vitro TechniquesBradykininLigandsBiochemistryCell Linechemistry.chemical_compoundmedicineAnimalsHumansPoint MutationBradykinin receptorPhosphorylationReceptorG protein-coupled receptorReceptors BradykininSodiumRatschemistryCOS CellsBiophysicsMutagenesis Site-DirectedAlpha-4 beta-2 nicotinic receptorIntracellularBiochemistry
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Altered atypical coupling of γ-aminobutyrate type A receptor agonist and convulsant binding sites in subunit-deficient mouse lines

2001

We searched for subunit correlations for GABA(A) receptor-associated atypically GABA-insensitive [35S]TBPS binding. The homomeric beta3 subunit receptors could be excluded, as GABA-insensitive [35S]TBPS binding was present in beta3-/- mice. Localization of GABA-insensitive [35S]TBPS binding correlated best with those of delta, alpha4 and alpha6 subunit mRNAs. The amounts of GABA-insensitive [35S]TBPS binding components were increased in delta-/- mice, but dramatically reduced in alpha6-/- mice, suggesting a role for alpha6 but excluding delta subunits.

Agonistmedicine.medical_specialtymedicine.drug_classProtein subunitMolecular Sequence DataConvulsantsBiologySulfur Radioisotopesmedicine.disease_causeMiceRadioligand AssayCellular and Molecular NeuroscienceInternal medicinemedicineAnimalsHomomericRNA MessengerBinding siteReceptorGABA AgonistsMolecular BiologyBrain ChemistryMice KnockoutMutationBinding SitesGABAA receptorBridged Bicyclo Compounds HeterocyclicReceptors GABA-AMolecular biologyEndocrinologynervous systemConvulsantMolecular Brain Research
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Finitary shadows of compact subgroups of $$S(\omega )$$

2020

AbstractLet LF be the lattice of all subgroups of the group $$SF(\omega )$$SF(ω) of all finitary permutations of the set of natural numbers. We consider subgroups of $$SF(\omega )$$SF(ω) of the form $$C\cap SF(\omega )$$C∩SF(ω), where C is a compact subgroup of the group of all permutations. In particular, we study their distribution among elements of LF. We measure this using natural relations of orthogonality and almost containedness. We also study complexity of the corresponding families of compact subgroups of $$S(\omega )$$S(ω).

Algebra and Number TheoryCompact groups of permutationsDistribution (number theory)Group (mathematics)010102 general mathematicsLattice (group)Almost containednessNatural number0102 computer and information sciences01 natural sciencesOmegaMeasure (mathematics)CombinatoricsOrthogonality010201 computation theory & mathematicsOrthogonality of finitary subgroupsFinitary0101 mathematicsMartin’s axiom.MathematicsAlgebra universalis
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L'eau et les territoires sahariens en Algérie, Mutations et enjeux

2007

International audience; Les rapports complexes et multiformes que les territoires entretiennent avec la question hydraulique prennent au Sahara une dimension toute particulière. Les mutations territoriales du XXe siècle qui l'ont caractérisé – urbanisation, accroissement démographique, intégration territorial... – ont remis en cause le fragile équilibre qui s'était institué depuis des siècles entre l'homme et son environnement. Ces mutations complexes ont engendré de nombreuses interrogations quant à la gestion actuelle et future de la question hydraulique au sein des territoires sahariens. Nous nous proposons ici de mettre en lumière quelques éléments permettant d'appréhender cette questio…

AlgérieMutations territorialesRessources hydrauliquesGestion territoriale[SHS.GEO] Humanities and Social Sciences/Geography[SHS.GEO]Humanities and Social Sciences/GeographySahara[ SHS.GEO ] Humanities and Social Sciences/Geography
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MGMT: Key node in the battle against genotoxicity, carcinogenicity and apoptosis induced by alkylating agents

2007

O(6)-methylguanine-DNA methyltransferase (MGMT) plays a crucial role in the defense against alkylating agents that generate, among other lesions, O(6)-alkylguanine in DNA (collectively termed O(6)-alkylating agents [O(6)AA]). The defense is highly important, since O(6)AA are common environmental carcinogens, are formed endogenously during normal cellular metabolism and possibly inflammation, and are being used in cancer therapy. O(6)AA induced DNA damage is subject to repair, which is executed by MGMT, AlkB homologous proteins (ABH) and base excision repair (BER). Although this review focuses on MGMT, the mechanism of repair by ABH and BER will also be discussed. Experimental systems, in wh…

Alkylating AgentsMethyltransferaseAlkylationDNA RepairDNA repairDNA damageGene ExpressionApoptosisIn Vitro TechniquesBiologyDNA Mismatch RepairModels BiologicalBiochemistryNecrosisO(6)-Methylguanine-DNA MethyltransferaseNeoplasmsAnimalsHumansDNA Modification MethylasesneoplasmsMolecular BiologyCarcinogenChromosome AberrationsGeneticsTumor Suppressor ProteinsO-6-methylguanine-DNA methyltransferaseDNACell BiologyBase excision repairdigestive system diseasesDNA Repair EnzymesMutationCancer researchDNA mismatch repairSister Chromatid ExchangeDNA DamageAlkyltransferaseDNA Repair
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