Search results for "MUTATION"

showing 10 items of 2830 documents

I vincoli della trasformazione: riflessioni sulla metamorfosi tra letteratura, filosofia e biologia

2019

Per sopravvivere gli esseri viventi sono costretto a modificarsi di continuo, adattandosi all’ambiente e al variare delle circostanze. In questa costante alterazione formale come si conciliano identità e mutamento? Come può l’individuo preservarsi dal totale dissolvimento in qualcos’altro? Questi sono solo alcuni dei quesiti che nei secoli hanno spinto studiosi di Morfologia, Estetica e Biologia a indagare le trasformazioni organiche. Nella presente trattazione cercheremo di chiarire le somiglianze e le differenze fra alcuni concetti chiave del vocabolario della metamorfosi (trasformazione, permutazione, vincolo, libertà di cambiamento, modularità organica) adottando un approccio multidisci…

Settore M-FIL/04 - Esteticametamorphosis transformation permutation constraints modularity
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Prognostic significance of p16INK4a alterations and 9p21 loss of heterozigosity in locally advanced laryngeal squamous cell carcinoma

2002

The p16INK4a gene, localized within chromosome 9p21, has been identified as a cyclin-dependent kinase inhibitor and may negatively regulate the cell cycle acting as a tumor suppressor. Genetic alterations involving the 9p21 region are common in human cancers. A consecutive series of 64 untreated patients (median of follow up 53 months) undergoing surgical resection for locally advanced laryngeal squamous-cell carcinomas (LSCCs) has been studied prospectively. Our purpose was to investigate p16 alterations (9p21 allelic loss, hypermethylation and point mutations) and their possible association with clinico-pathological data and flow cytometric variables (DNA-ploidy and S-phase fraction (SPF)…

Settore MED/06 - Oncologia MedicaPhysiologyClinical BiochemistryLoss of HeterozygosityBiologyBioinformaticsS PhaseLoss of heterozygosityp16INK4aHumansPoint MutationProspective StudiesLaryngeal NeoplasmsGeneProportional Hazards ModelsUnivariate analysisPloidiesBase SequenceProportional hazards modelGenes p16Point mutationSingle-strand conformation polymorphismDNA NeoplasmCell BiologyDNA MethylationCell cyclePrognosisMultivariate AnalysisDNA methylationCarcinoma Squamous CellCancer researchChromosomes Human Pair 9Journal of Cellular Physiology
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Identification and Characterization of BRCA1 and BRCA2 Founder Mutations

2012

A large number of cancer predisposing BRCA1/BRCA2 mutations have been reported, with a wide variety among populations. In some restricted groups, specific germline mutations in these tumor suppressor genes have been found with high predominance, due to a founder effect. We focused our review on the Italian founder mutations. The first Italian BRCA1 founder mutation, 5083del19, was found in Calabria: the presence of common allele in all carriers of this mutation (also in families with Calabrian origin living in other parts of Italy) confirmed its founder effect. The same BRCA1 mutation was identified in the Sicilian population, but only the haplotype analysis can reveal the common ancestor o…

Settore MED/06 - Oncologia Medicabusiness.industryObstetrics and GynecologyMedicineIdentification (biology)Computational biologyBRCA1; BRCA2; Founder mutationBRCA1Founder mutationbusinessBRCA2Current Women's Health Reviews
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Analysis of early strains of the norovirus pandemic variant GII.4 Sydney 2012 identifies mutations in adaptive sites of the capsid protein.

2014

AbstractGlobal surveillance for norovirus identified in 2012 the emergence of a novel pandemic GII.4 variant, termed Sydney 2012. In Italy, the novel pandemic variant was identified as early as November 2011 but became predominant only in the winter season 2012–2013. Upon sequencing and comparison with strains of global origin, the early Sydney 2012 strains were found to differ from those spreading in 2012–2013 in the capsid (ORF2) putative epitopes B, C and D, segregating into a distinct phylogenetic clade. At least three residues (333, 340 and 393, in epitopes B, C and D, respectively) of the VP1 varied among Sydney 2012 strains of different clades. These findings suggest that the spread …

Settore MED/07 - Microbiologia E Microbiologia ClinicaEvolutionMolecular Sequence DataCapsid protein VP1 epitopes Evolution GII.4 Italy Norovirus Sydney 2012 variantBiologymedicine.disease_causeEpitopeSydney 2012 variantVirologyPandemicmedicineHumansAmino Acid SequenceCladePandemicsPhylogenyPhylogenetic treeNorovirusCapsid protein VP1 epitopesVirologyGastroenteritisCapsidItalyMutationNorovirusCapsid ProteinsSeasonsWinter seasonGII.4Virology
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Identification of a novel ANGPTL3 mutation splicing associeted to severe hypobetalipoproteinemia

2012

Introduction. Primary hypobetalipoproteinemia (pHBL) is a monogenic heterogeneous condition inherited as a dominant or recessive trait characterized by total cholesterol (TC) and/or LDL cholesterol (LDL-C) and/or apolipoprotein B (APOB) levels below the 5th percentile of the reference population. Heterozygous APOB gene mutations are responsible for the majority of the dominant pHBL causing the familial hypobetalipoproteinemia (FHBL). Loss-of-function mutations in the PCSK9 gene also cause FHBL. Familial combined hypolipidemia is a recently discovered dyslipidemic phenotype characterized by low levels of TC, triglycerides (TG), LDL-C, and high-density lipoprotein cholesterol (HDL-C). The gen…

Settore MED/09 - Medicina InternaANGPTL3mutationHypobetalipoproteinemia
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Lipid and apoprotein composition of HDL in partial or complete CETP deficiency

2012

Hyperalphalipoproteinemia, as observed in patients who are either homozygous or heterozygous for cholesteryl ester transfer protein (CETP) deficiency, has been shown to be associated with striking changes in apolipoprotein size distribution, namely, of high-density lipoprotein (HDL) and HDL-like particles. We compared the effect of varying degrees of CETP activity on the HDL apolipoprotein profile in Caucasian CETP-deficient subjects and following pharmacological decrease in CETP activity, using Size Exclusion Chromatography followed by Reverse Phase Protein Array (SEC RPA). The main HDL-associated apolipoproteins (Apo), i.e. ApoA-I, ApoA-II, ApoC-I, and ApoC-III, co-eluted with the HDL pea…

Settore MED/09 - Medicina InternaApolipoprotein BCholesterol Ester Transfer Proteinmedicine.disease_causereverse phase protein arraychemistry.chemical_compoundExonMutationbiologyHomozygotescavenger receptor class B1size exclusion chromatographyLipidCholesteryl ester transfer proteinLipidstorcetrapibApolipoproteinBiochemistryELISAlipids (amino acids peptides and proteins)hyperalphalipoproteinemiaCardiology and Cardiovascular MedicineLipoproteins HDLHumandalcetrapibmedicine.medical_specialtyHeterozygoteDalcetrapibHypercholesterolemiaapolipoproteinhigh-density lipoproteinInternal medicineCholesterylester transfer proteinmedicineAnimalsHumansCholesteryl ester transfer protein; dalcetrapib; high-density lipoprotein; reverse phase protein array; scavenger receptor class B1; size exclusion chromatography; torcetrapib; apolipoprotein; hyperalphalipoproteinemia; ELISAPharmacologybusiness.industryAnimalPoint mutationCholesterol HDLTorcetrapibnutritional and metabolic diseasesLipid MetabolismCholesterol Ester Transfer Proteinscarbohydrates (lipids)Disease Models AnimalEndocrinologyApolipoproteinschemistrybiology.proteinbusinessLipoprotein
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eNOS Activation by HDL Is Impaired in Genetic CETP Deficiency.

2014

Mutations in the CETP gene resulting in defective CETP activity have been shown to cause remarkable elevations of plasma HDL-C levels, with the accumulation in plasma of large, buoyant HDL particles enriched in apolipoprotein E. Genetic CETP deficiency thus represents a unique tool to evaluate how structural alterations of HDL impact on HDL atheroprotective functions. Aim of the present study was to assess the ability of HDL obtained from CETP-deficient subjects to protect endothelial cells from the development of endothelial dysfunction. HDL isolated from one homozygous and seven heterozygous carriers of CETP null mutations were evaluated for their ability to down-regulate cytokine-induced…

Settore MED/09 - Medicina InternaCHOLESTEROL EFFLUXApolipoprotein BEpidemiologylcsh:MedicineANTIINFLAMMATORY PROPERTIESmedicine.disease_causeBiochemistryVascular Medicinechemistry.chemical_compoundHigh-density lipoproteinEnosMedicine and Health SciencesEndothelial dysfunctionlcsh:ScienceMutationMultidisciplinarybiologyHomozygoteCETP; eNOS; HDL;NeurochemistryLipidsGenetic EpidemiologyeNOSlipids (amino acids peptides and proteins)AnatomyNeurochemicalsLipoproteins HDLResearch Articlemedicine.medical_specialtyDrug Research and DevelopmentHDLNitric Oxide Synthase Type IIILipoproteinsENDOTHELIAL FUNCTIONINHIBITIONCardiologyDown-RegulationVascular Cell Adhesion Molecule-1Nitric OxideCELL-ADHESION MOLECULE-1Lipid Metabolism Inborn ErrorsESTER TRANSFER PROTEINInternal medicineCETPCholesterylester transfer proteinHuman Umbilical Vein Endothelial CellsmedicineHumansNITRIC-OXIDE SYNTHASEInflammationClinical GeneticsPharmacologyCholesterollcsh:RTorcetrapibEndothelial CellsBiology and Life SciencesProteinsnutritional and metabolic diseasesLipid MetabolismAtherosclerosismedicine.diseasebiology.organism_classificationCholesterol Ester Transfer Proteinscarbohydrates (lipids)MetabolismEndocrinologychemistryOther Clinical MedicineMutationImmunologyCardiovascular Anatomybiology.proteinlcsh:QTORCETRAPIBClinical MedicineHIGH-DENSITY-LIPOPROTEINSCAVENGER RECEPTOR BI
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New Frontiers in the Treatment of Homozygous Familial Hypercholesterolemia.

2021

: Homozygous familial hypercholesterolemia (HoFH) is a rare genetic disorder. The most common cause is a mutation in both alleles of the gene encoding for the low-density lipoprotein (LDL) receptor, although other causative mutations have been identified. Complications of atherosclerotic cardiovascular disease are common in these patients; therefore, reducing the elevated LDL-cholesterol burden is critical in their management. Conventionally, this is achieved by patients initiating lipid-lowering therapy, but this can present challenges in clinical practice. Fortunately, novel therapeutic strategies have enabled promising innovations in HoFH treatment. This review highlights recent and ongo…

Settore MED/09 - Medicina InternaGenetic enhancementHomozygous familial hypercholesterolemiaFamilial hypercholesterolemiaInclisiranBioinformaticsmedicine.disease_causeBenzimidazolePCSK9Hyperlipoproteinemia Type IIchemistry.chemical_compoundGene therapyAnticholesteremic AgentmedicineAngiopoietin-like 3HumansLow-density lipoprotein cholesterolAlleleAngiopoietin-like 3; Gene therapy; Gene-editing; Homozygous familial hypercholesterolemia; Inclisiran; Lomitapide; Low-density lipoprotein cholesterol; PCSK9MutationGene-editingAtherosclerotic cardiovascular diseasebusiness.industryPCSK9Anticholesteremic AgentsHomozygoteGenetic disorderGeneral MedicineCholesterol LDLmedicine.diseaseLomitapideLomitapidechemistrylipids (amino acids peptides and proteins)BenzimidazolesCardiology and Cardiovascular MedicinebusinessHumanHeart failure clinics
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Identification and molecular characterization of a novel mutation in MSH2 gene in a lynch syndrome family

2017

Background and aim of the work: The Lynch Syndrome (LS) is associated with germline mutations in one of the MisMatch Repair (MMR) genes, including MLH1, MSH2, MSH6, PMS2, MLH3 and MSH3. The molecular characterization of mutations in these MMR genes facilitates the pre-symptomatic diagnosis of subjects at risk to develop a colon cancer or a cancer LS-related. Methods: DHPLC and direct sequencing were performed for the mutation detection analysis. Results: In this study, we identified a novel frame shift mutation, the named is c.170delT in MSH2 gene that determined a premature stop codon and consequently, the formation of a truncated protein (p. Val56Glyfs*7). This is a novel mutation, as it …

Settore MED/18 - Chirurgia GeneraleLynch syndromeNovel variant MSH2 geneHNPCCFrame-shift mutationMSH2 gene
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Melanoma nei BRCA mutation carriers

2016

Settore MED/19 - Chirurgia PlasticaMELANOMA FAMILIAL MELANOMA brca MUTATION
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