Search results for "Perl"

showing 10 items of 383 documents

Clinical experience of lomitapide therapy in patients with homozygous familial hypercholesterolaemia.

2014

The microsomal triglyceride transfer protein (MTP) inhibitor lomitapide is a licenced adjunct to a low-fat diet and other lipid-lowering medication, with or without low-density lipoprotein apheresis, for the treatment of adults with homozygous familial hypercholesterolaemia (HoFH). In a recently published phase 3 study, patients with HoFH received lomitapide in addition to maximally tolerated lipid-lowering therapy. Treatment with lomitapide resulted in a mean approximate 50% reduction in LDL-C levels after 26 weeks compared with baseline levels (p < 0.0001). This decrease in LDL-C was maintained at Weeks 56 and 78 (44% [p < 0.0001] and 38% [p = 0.0001], respectively). This paper offers cli…

AdultMalemedicine.medical_specialtySettore MED/09 - Medicina InternaPhases of clinical researchMicrosomal triglyceride transfer proteinHyperlipoproteinemia Type IIchemistry.chemical_compoundYoung AdultInternal medicineHo-FH lomitapide MTPInternal MedicinemedicineEffective treatmentHumansIn patientAdverse effectbiologymedicine.diagnostic_testbusiness.industryAnticholesteremic AgentsHomozygoteGeneral MedicineCholesterol LDLMiddle AgedLomitapideEndocrinologyApheresisTreatment Outcomechemistrybiology.proteinBenzimidazolesFemaleCardiology and Cardiovascular MedicinebusinessLiver function testsAtherosclerosis. Supplements
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Association of simvastatin and hyperlipidemia with periodontal status and bone metabolism markers.

2014

Background: The objective of this study is to determine whether simvastatin consumption and hyperlipidemia are associated with a worse periodontal condition and specific bone activity biomarkers. Methods: This cross-sectional and analytic study includes 73 patients divided into three groups: 1) simvastatin-treated patients with hyperlipidemia (n = 29); 2) patients with hyperlipidemia treated by diet alone (n = 28); and 3) normolipidemic patients (controls, n = 16). The periodontal clinical variables of all participants were gathered, a blood sample was drawn from each to determine the lipid profile (total cholesterol, triglycerides, low-density lipoprotein, and high-density lipoprotein), se…

AdultMalemedicine.medical_specialtySimvastatinAlcohol DrinkingOsteocalcinHyperlipidemiasBlood SedimentationCollagen Type IBone remodelingN-terminal telopeptideInternal medicineHyperlipidemiaPeriodontal Attachment LossmedicineHumansTriglyceridesAgedHypolipidemic AgentsPeriodontitismedicine.diagnostic_testbusiness.industryCholesterol HDLSmokingOsteoprotegerinnutritional and metabolic diseasesCholesterol LDLMiddle Agedmedicine.diseasePeptide FragmentsEndocrinologyC-Reactive ProteinCholesterolCross-Sectional StudiesClinical attachment lossSimvastatinErythrocyte sedimentation ratePeriodonticsFemaleHydroxymethylglutaryl-CoA Reductase InhibitorsPeriodontal IndexbusinessLipid profilePeptidesBiomarkersProcollagenmedicine.drugJournal of periodontology
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Distinct patterns of heparin affinity chromatography VLDL1 and VLDL2 subfractions in the different dyslipidaemias

2007

Very low density lipoprotein (VLDL) 1 and 2 were fractionated by heparin affinity chromatography into a bound and an unbound fraction and the different subfractions were quantified in 17 normolipidaemic (NL), 13 hypercholesterolaemic (HC), 10 hypertriglyceridaemic (HTG) and 11 combined hyperlipidaemic subjects (CHL). Unbound VLDL1 and VLDL2 were, respectively, 1.9- and 2.2-fold richer in triglycerides than bound VLDL1 and VLDL2. In HTG and CHL the concentration of all the VLDL subfractions was increased and plasma triglyceride level was correlated to unbound VLDL1 and to bound VLDL1 (respectively, r=0.86 (p<0.001) and r=0.77 (p<0.01) in HTG and r=0.73 (p<0.001) and r=0.62 (p<0.05) in CHL). …

AdultMalemedicine.medical_specialtyVery low-density lipoproteinHypercholesterolemiaHyperlipidemia Familial CombinedLipoproteins VLDLChromatography AffinityGlycosaminoglycanchemistry.chemical_compoundAffinity chromatographyInternal medicinemedicineHumansApolipoproteins BDyslipidemiasHypertriglyceridemiaTriglycerideHeparinCholesterolHypertriglyceridemiaAnticoagulantsHeparinMiddle Agedmedicine.diseaseEndocrinologychemistryFemaleCardiology and Cardiovascular MedicineUltracentrifugationProtein BindingLipoproteinmedicine.drugAtherosclerosis
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Efficacy and safety of lomitapide in familial chylomicronaemia syndrome

2022

Familial chylomicronaemia syndrome (FCS) is a rare autosomal recessive disorder, resulting in elevated triglycerides (TGs), abdominal pain and pancreatitis. Treatment options are limited. Lomitapide, a microsomal triglyceride transfer protein inhibitor, is approved for the treatment of homozygous familial hypercholesterolaemia. Whether its therapeutic use may be extended to FCS remains unknown. The aim of this study was to evaluate the efficacy and safety of lomitapide in adult patients with FCS.The open-label, single-arm 'LOCHNES' study of lomitapide in FCS enrolled patients18 years with genetically confirmed FCS, elevated fasting TG ≥ 750 mg/dL and history of pancreatitis. Patients were a…

AdultPancreatitiSettore MED/09 - Medicina InternaTriglycerideBenzimidazoleLomitapideAbdominal PainPancreatitisHyperlipoproteinemia Type I.HumansBenzimidazolesHyperlipoproteinemia Type ICardiology and Cardiovascular MedicineTriglyceridesFamilial chylomicronaemia syndromeHuman
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Wilms' tumor in patients with 9q22.3 microdeletion syndrome suggests a role for PTCH1 in nephroblastomas

2012

Nephroblastoma (Wilms' tumor; WT) is the most common renal tumor of childhood. To date, several genetic abnormalities predisposing to WT have been identified in rare overgrowth syndromes. Among them, abnormal methylation of the 11p15 region, GPC3 and DIS3L2 mutations, which are responsible for Beckwith-Wiedemann, Simpson-Golabi-Behmel and Perlman syndromes, respectively. However, the underlying cause of WT remains unknown in the majority of cases. We report three unrelated patients who presented with WT in addition to a constitutional 9q22.3 microdeletion and dysmorphic/overgrowth syndrome. The size of the deletions was variable (ie, from 1.7 to 8.9 Mb) but invariably encompassed the PTCH1 …

AdultPatched Receptorsmedicine.medical_specialtyPathologyPTCH1AdolescentNonsense mutationCNVShort ReportReceptors Cell SurfaceBiologymedicine.disease_causeWilms’ tumorWilms TumorFetal MacrosomiaSettore MED/38 - Pediatria Generale E SpecialisticaPregnancyInternal medicineGeneticsmedicineHumansPerlman syndromeChildovergrowthGenetics (clinical)MutationComparative Genomic HybridizationWilms' tumorPTCH1 GeneMicrodeletion syndromeFANCC nephroblastomamedicine.diseaseKidney NeoplasmsPatched-1 ReceptorEndocrinologyPTCH1Settore MED/03 - Genetica MedicaOvergrowth syndromeMutationFemaleChromosome DeletionChromosomes Human Pair 9Comparative genomic hybridization
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Six novel mutations of the LDL receptor gene in FH kindred of Sicilian and Paraguayan descent

2006

Familial hypercholesterolemia (FH) is an autosomal dominant inherited disease caused by mutations in the gene coding for the low density lipoprotein receptor (LDL-R). It is characterized by a high concentration of low density lipoprotein (LDL), which frequently gives rise to premature coronary artery disease. We studied the probands of five FH Sicilian families with 'definite' FH and one proband of Paraguayan descent with homozygous FH who has been treated with an effective living-donor liver transplantation. In order to seek the molecular defect in these six families, we used direct sequencing to define the molecular defects of the LDL-R gene responsible for the disease. We described three…

AdultProbandhypercholesterolemia LDL receptor gene mutation analysis direct sequencing splicing living-donor transplantationSettore MED/09 - Medicina InternaDNA Mutational AnalysisDirect sequencingHypercholesterolemiaFamilial hypercholesterolemiaBiologyGene mutationSplicingmedicine.disease_causeFrameshift mutationHyperlipoproteinemia Type IIExonGeneticsmedicineHumansMissense mutationRNA MessengerChildSicilyCells CulturedLiving-donor transplantationLDL receptor geneGeneticsMutationIntronExonsGeneral MedicineMiddle Agedmedicine.diseaseLipidsMolecular biologyPedigreeDirect sequencing; Hypercholesterolemia; LDL receptor gene; Living-donor transplantation; Mutation analysis; SplicingMutation analysisReceptors LDLParaguayChild PreschoolMutationBiological Assay
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A new PCSK9 gene promoter variant affects gene expression and causes autosomal dominant hypercholesterolemia.

2008

Autosomal dominant hypercholesterolemia (ADH) is a genetic disorder characterized by increased low-density lipoprotein (LDL)-cholesterol levels, leading to high risk of premature cardiovascular disease. More than 900 mutations in LDL receptor, six in APOB and 10 in PCSK9 have been identified as a cause of the disease in different populations. All known mutations in PCSK9 causing hypercholesterolemia produce an increase in the enzymatic activity of this protease. Up to now, there are data about the implication of PCSK9 in ADH in a low number of populations, not including a Spanish population.The objective of the study was to study the prevalence of PCSK9 mutations in ADH Spanish population.W…

Adultmedicine.medical_specialtyApolipoprotein BEndocrinology Diabetes and MetabolismClinical BiochemistryGene ExpressionTransfectionBiochemistryPolymorphism Single NucleotideHyperlipoproteinemia Type IIPCSK9 GeneMiceEndocrinologyGene FrequencyInternal medicinemedicineAnimalsHumansPromoter Regions GeneticAllele frequencyGeneCells CulturedGeneticsbiologyBase SequencePCSK9Biochemistry (medical)Serine EndopeptidasesGenetic disorderHyperlipoproteinemia Type IIaMiddle Agedmedicine.diseaseEndocrinologySpainCase-Control StudiesLDL receptorbiology.proteinNIH 3T3 Cellslipids (amino acids peptides and proteins)Mutant ProteinsProprotein ConvertasesProprotein Convertase 9The Journal of clinical endocrinology and metabolism
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Extracorporeal circuit heparinization in selective low density lipoprotein apheresis: changes in patient hemostasis and low molecular weight heparin …

1993

Treatment by low density lipoprotein (LDL) apheresis using dextran sulfate columns (DSC) leads to hemostasis alterations with prolonged activated partial thromboplastin time (APTT) of more than 120 seconds. In order to explain this hypocoagulability, we studied hemostasis parameters both in patients and in the extracorporeal circulation (ECC). Hemostasis changes are first related to unfractionated heparin (UFH)—needed to avoid circuit coagulation—which leads to high residual heparinemia in the patient (more than 3 times the recommended level for therapeutic use). Second, the hypocoagulability is induced by a coagulation factor decrease (primarily factors V, VIH, and X) mainly due to an adso…

Adultmedicine.medical_specialtyExtracorporeal Circulationmedicine.drug_classLow molecular weight heparinHyperlipoproteinemia Type IIInternal medicinemedicineHumansHemostasismedicine.diagnostic_testbusiness.industryExtracorporeal circulationAnticoagulantDextran SulfateNadroparinHematologyGeneral MedicineHeparinMiddle AgedBlood Coagulation FactorsSurgeryLipoproteins LDLApheresisLDL apheresisHemostasisCardiologyBlood Component RemovalbusinessPartial thromboplastin timemedicine.drugJournal of clinical apheresis
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Spectrum of mutations and phenotypic expression in patients with autosomal dominant hypercholesterolemia identified in Italy.

2013

Abstract Objective To determine the spectrum of gene mutations and the genotype–phenotype correlations in patients with Autosomal Dominant Hypercholesterolemia (ADH) identified in Italy. Methods The resequencing of LDLR , PCSK9 genes and a selected region of APOB gene were conducted in 1018 index subjects clinically heterozygous ADH and in 52 patients clinically homozygous ADH. The analysis was also extended to 1008 family members of mutation positive subjects. Results Mutations were detected in 832 individuals: 97.4% with LDLR mutations, 2.2% with APOB mutations and 0.36% with PCSK9 mutations. Among the patients with homozygous ADH, 51 were carriers of LDLR mutations and one was an LDLR / …

Adultmedicine.medical_specialtyHeterozygoteSettore MED/09 - Medicina InternaApolipoprotein BCoronary DiseaseBiologyGene mutationmedicine.disease_causeHyperlipoproteinemia Type IITendonschemistry.chemical_compoundReference ValuesInternal medicinemedicineXanthomatosisHumansGeneAllelesGenetic Association StudiesAgedGeneticsMutationCholesterolPCSK9Cholesterol HDLSerine EndopeptidasesSmokingAlcohol Dehydrogenasenutritional and metabolic diseasesCholesterol LDLMiddle AgedEndocrinologyPhenotypechemistryItalyLDL receptorMutationbiology.proteinAutosomal dominanthypercholesterolemia LDL receptor Apolipoprotein B PCSK9 Mutationslipids (amino acids peptides and proteins)Allelic heterogeneityFemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicineAtherosclerosis
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New records of corticioid fungi from Sicily

2016

This paper is the result of an on-going study on distribution and ecology of corticioid wood-inhabiting fungi in Sicily. Twenty-five species not previously recorded in Sicily are here listed. For each taxon, ecological and distributional data are provided. Subulicystidium perlongisporum was recorded in Italy for the first time in two localities occurring on Quercus ilex L. wood. Description, distributional and ecological data of this rare taxon are also provided. Dendrophora versiformis and Kavinia alboviridis, considered rare species in Italy and Europe, are included in this report.

Aphyllophorale0106 biological sciencesAphyllophoralesQH301-705.5Rare species010607 zoologyEcological data010603 evolutionary biology01 natural sciencesMediterranean areaAphyllophorales; cystidia; Mediterranean area; Subulicystidium perlongisporum; wood-inhabiting fungiSubulicystidium perlongisporumBiology (General)Ecology Evolution Behavior and SystematicsDendrophoraEcologybiologyEcologySubulicystidium perlongisporumbiology.organism_classificationKavinia alboviridisCorticioid fungiTaxonwood-inhabiting fungiAphyllophoralescystidia
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