Search results for "ELS"

showing 10 items of 12690 documents

Reconstructing the deep population history of Central and South America

2018

We report genome-wide ancient DNA from 49 individuals forming four parallel time transects in Belize, Brazil, the Central Andes, and the Southern Cone, each dating to at least ∼9,000 years ago. The common ancestral population radiated rapidly from just one of the two early branches that contributed to Native Americans today. We document two previously unappreciated streams of gene flow between North and South America. One affected the Central Andes by ∼4,200 years ago, while the other explains an affinity between the oldest North American genome associated with the Clovis culture and the oldest Central and South Americans from Chile, Brazil, and Belize. However, this was not the primary sou…

0301 basic medicineGene Flow010506 paleontologyHistoryPopulationPopulationPopulation ReplacementBiology01 natural sciencesGenomeMedical and Health SciencesDNA MitochondrialGeneral Biochemistry Genetics and Molecular BiologyGene flowAncient03 medical and health sciencesTheoreticalModelsGeneticsHumansGENÉTICA DE POPULAÇÕESanthropologyIndis de l'Amèrica CentralDNA AncientTransecteducationHistory Ancient0105 earth and related environmental scienceseducation.field_of_studypopulation geneticGenomeGenome HumanHuman Genomepopulation geneticsarchaeologyCentral AmericaDNABiological SciencesSouth AmericaModels TheoreticalArchaeologyMitochondrial030104 developmental biologyAncient DNAGenetics PopulationDevelopmental BiologyHuman
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Genetics and Gene Therapy of Anderson-Fabry Disease.

2018

Fabry's disease is a genetic disorder of X-linked inheritance caused by mutations in the alpha galactosidase A gene resulting in deficiency of this lysosomal enzyme. The progressive accumulation of glycosphingolipids, caused by the inadequate enzymatic activity, is responsible of organ dysfunction and thus of clinical manifestations. In the presence of a high clinical suspicion, a careful physical examination and specific laboratory tests are required, finally diagnosis of Fabry's disease is confirmed by the demonstration of absence or reduced alpha-galactosidase A enzyme activity in hemizygous men and gene typing in heterozygous females; in fact the performance of enzymatic activity assay …

0301 basic medicineGenetic enhancementChaperone therapyDisease030204 cardiovascular system & hematologyBioinformaticsMice0302 clinical medicineAlpha galactosidase ADrug DiscoveryGenetics (clinical)KidneybiologyTrihexosylceramidesGenetic disorderEnzyme replacement therapyDependovirusRecombinant ProteinsAlpha galactosidase A; Chaperone therapy; Enzyme replacement therapy; Fabry disease; Gene therapy; Viral vectors; Molecular Medicine; Molecular Biology; Genetics; Drug Discovery3003 Pharmaceutical Science; Genetics (clinical)Isoenzymesmedicine.anatomical_structureMolecular Medicinemedicine.symptomGenetic Vectors03 medical and health sciencesGene therapyViral vectorRare DiseasesGeneticGeneticsmedicineAnimalsHumansEnzyme Replacement TherapyMolecular BiologyAlpha-galactosidasebusiness.industryDrug Discovery3003 Pharmaceutical ScienceOrgan dysfunctionGenetic Therapymedicine.diseaseFabry diseaseDisease Models Animal030104 developmental biologyalpha-GalactosidaseMutationbiology.proteinFabry DiseasebusinessBiomarkersCurrent gene therapy
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Molecular disturbance underlies to arrhythmogenic cardiomyopathy induced by transgene content, age and exercise in a truncated PKP2 mouse model

2016

13 páginas, 9 tablas, 2 figuras. Contiene material suplementario.

0301 basic medicineGenetically modified mouseAgingmedicine.medical_specialtyTransgeneCardiomyopathyPlakoglobinConnexin030204 cardiovascular system & hematologyBiologyMice03 medical and health sciences0302 clinical medicineFibrosisInternal medicineGeneticsmedicineAnimalsHumansTransgenesMolecular BiologyArrhythmogenic Right Ventricular DysplasiaGenetics (clinical)General Medicinemedicine.diseasePhenotypeDisease Models Animal030104 developmental biologyEndocrinologyMutationDisease ProgressionPhysical EnduranceDesminPlakophilins
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Inducible knockdown of procollagen I protects mice from liver fibrosis and leads to dysregulated matrix genes and attenuated inflammation.

2017

Organ fibrosis is characterized by a chronic wound-healing response, with excess deposition of extracellular matrix components. Here, collagen type I represents the most abundant scar component and a primary target for antifibrotic therapies. Liver fibrosis can progress to cirrhosis and primary liver cancer, which are the major causes of liver related morbidity and mortality. However, a (pro-)collagen type I specific therapy remains difficult and its therapeutic abrogation may incur unwanted side effects. We therefore designed tetracycline-regulated procollagen alpha1(I) short hairpin (sh)RNA expressing mice that permit a highly efficient inducible knockdown of the procollagen alpha1(I) gen…

0301 basic medicineGenetically modified mouseLiver CirrhosisPathologymedicine.medical_specialtyCirrhosisInflammationMice TransgenicCollagen Type ISmall hairpin RNAExtracellular matrix03 medical and health sciencesMiceFibrosismedicineAnimalsRNA Small InterferingMolecular BiologyCells CulturedGene knockdownExtracellular Matrix ProteinsChemistryMouse Embryonic Stem CellsFibroblastsmedicine.diseaseProcollagen peptidaseDisease Models Animal030104 developmental biologyGene Expression RegulationGene Knockdown TechniquesCancer researchmedicine.symptomProcollagenMatrix biology : journal of the International Society for Matrix Biology
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Shifts in gut microbiota composition in an APP/PSS1 transgenic mouse model of Alzheimer's disease during lifespan.

2017

Alzheimer's disease (AD) is the most common form of dementia and one of the major causes of disability and dependency in older people. Accumulating evidences link gut microbiota with different diseases and its relationship with neurodegenerative diseases is becoming most intriguing. This study was aimed to compare the gut microbiota of transgenic APP/PS1 (TG) mice, a well‐established deterministic mouse model of AD, with their C57BL/6 wild‐type (WT) littermates. Faecal samples were collected from 3‐, 6‐ and 24‐month‐old mice and analysed by pyrosequencing of the V1–V3 region of the bacterial 16S rRNA genes. Bacterial profiles were similar in all young mice (3 months old), and started to div…

0301 basic medicineGenetically modified mouseMaleAgingRikenellaceaeTransgeneFirmicutesMice TransgenicDiseaseGut floraApplied Microbiology and Biotechnology03 medical and health sciencesMiceAlzheimer DiseaseRNA Ribosomal 16SProteobacteriamedicineDementiaIndicatorsAnimalsHumansNeuroinflammationMarkersbiologyIntestinal microbiologyBacteroidetesbiology.organism_classificationmedicine.diseaseGastrointestinal MicrobiomeMice Inbred C57BLDisease Models Animal030104 developmental biologyAgeingImmunologyMicrobial structureDisease processesLetters in applied microbiology
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Behavioral fragmentation in the D1CT-7 mouse model of Tourette's syndrome.

2017

Aim The transgenic D1CT-7 mouse is one of the best-characterized animal models of Tourette's syndrome (TS), exhibiting spontaneous tic-like Head-Body Twitches (HBT) and deficits in sensorimotor gating. This study is aimed at evaluating the behavioral dynamics of these mutants and their potential relevance to TS. Methods The behavior of D1CT-7 and Wild Type littermates was firstly assessed by considering frequencies and durations. To detect recurrent real-time behavioral sequences, the multivariate T-pattern analysis was employed. Analyses of transition probabilities among behaviors further provided an overall picture of the behavioral dynamics. Results T-patterns and transition matrices rev…

0301 basic medicineGenetically modified mouseMaleCholera ToxinTransgeneTourette's syndromeMice Transgenictransition matriceBiologyMotor ActivityTourette syndromeOpen fieldStatistics Nonparametric03 medical and health sciencesMice0302 clinical medicineSniffingPhysiology (medical)medicineAnimalsPharmacology (medical)tic disorderGait Disorders NeurologicPharmacologyMice Inbred BALB CD1CT-7Behavior AnimalReceptors Dopamine D1Wild typeBehavioral patternT-pattern analysiOriginal Articlesmedicine.diseasePhenotypeDisease Models Animal030104 developmental biologyPsychiatry and Mental HealthMotor SkillsExploratory BehaviorNeuroscience030217 neurology & neurosurgeryTourette SyndromeCNS neurosciencetherapeutics
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Gradual development of psoriatic skin lesions by constitutive low-level expression of IL-17A

2016

Psoriasis is a common chronic inflammatory skin disease restricted to humans. The understanding of its pathogenesis has long been hampered by the lack of suitable chronic mouse models. The cytokine IL-17A has emerged as a key player in epithelial immune responses and the defense against extracellular pathogens. Moreover, enhanced expression of IL-17A can turn pathologic and is closely associated with psoriasis. In this study, we generated a novel transgenic mouse model that recapitulates many characteristics of psoriasis. DC-1L-17A(ind) mice with constitutive low-level expression of IL-17A by CD11c(+) cells gradually develop skin lesions during adult life. The lesions preferentially occur a…

0301 basic medicineGenetically modified mousemedicine.medical_treatmentImmunologyCD11cInflammationAnimals Genetically ModifiedPathogenesisMice03 medical and health sciences0302 clinical medicineImmune systemSDG 3 - Good Health and Well-beingPsoriasismedicineAnimalsHumansPsoriasisCells CulturedSkinbusiness.industryInterleukin-17Dendritic Cellsmedicine.diseaseCD11c AntigenDisease Models Animal030104 developmental biologyCytokineImmunologyCytokinesInterleukin 17medicine.symptombusiness030215 immunologyCellular Immunology
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Model-based design of RNA hybridization networks implemented in living cells

2017

[EN] Synthetic gene circuits allow the behavior of living cells to be reprogrammed, and non-coding small RNAs (sRNAs) are increasingly being used as programmable regulators of gene expression. However, sRNAs (natural or synthetic) are generally used to regulate single target genes, while complex dynamic behaviors would require networks of sRNAs regulating each other. Here, we report a strategy for implementing such networks that exploits hybridization reactions carried out exclusively by multifaceted sRNAs that are both targets of and triggers for other sRNAs. These networks are ultimately coupled to the control of gene expression. We relied on a thermo-dynamic model of the different stable…

0301 basic medicineGeneticsNetwork architectureModels GeneticQHGene regulatory networkRNAGene ExpressionNucleic Acid HybridizationBiology03 medical and health sciencesNucleic acid thermodynamics030104 developmental biologyGene expressionModel-based designGeneticsEscherichia coliRNAThermodynamicsGene Regulatory NetworksSingle-Cell AnalysisSynthetic Biology and BioengineeringGeneQH426Function (biology)
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The dark side of centromeres: types, causes and consequences of structural abnormalities implicating centromeric DNA

2018

Centromeres are the chromosomal domains required to ensure faithful transmission of the genome during cell division. They have a central role in preventing aneuploidy, by orchestrating the assembly of several components required for chromosome separation. However, centromeres also adopt a complex structure that makes them susceptible to being sites of chromosome rearrangements. Therefore, preservation of centromere integrity is a difficult, but important task for the cell. In this review, we discuss how centromeres could potentially be a source of genome instability and how centromere aberrations and rearrangements are linked with human diseases such as cancer.

0301 basic medicineGenome instabilityCell division[SDV]Life Sciences [q-bio]ScienceCentromereGeneral Physics and AstronomyAneuploidy[SDV.BC]Life Sciences [q-bio]/Cellular BiologyReview ArticleBiologyChromosomeModels BiologicalGenomeChromosomesGenomic InstabilityGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compoundCentromeremedicineHumansDiseaselcsh:ScienceChromosome separationComputingMilieux_MISCELLANEOUSGeneticsMultidisciplinaryQChromosomeDNAGeneral Chemistrymedicine.diseaseSettore BIO/18 - Genetica030104 developmental biologychemistrylcsh:QDNANature Communications
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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