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showing 10 items of 10618 documents

FastaHerder2: Four Ways to Research Protein Function and Evolution with Clustering and Clustered Databases.

2016

The accelerated growth of protein databases offers great possibilities for the study of protein function using sequence similarity and conservation. However, the huge number of sequences deposited in these databases requires new ways of analyzing and organizing the data. It is necessary to group the many very similar sequences, creating clusters with automated derived annotations useful to understand their function, evolution, and level of experimental evidence. We developed an algorithm called FastaHerder2, which can cluster any protein database, putting together very similar protein sequences based on near-full-length similarity and/or high threshold of sequence identity. We compressed 50…

0301 basic medicineProtein structure databaseProteomicsProteomeSequence analysisComputer sciencecomputer.software_genreSensitivity and SpecificitySet (abstract data type)Evolution Molecular03 medical and health sciences0302 clinical medicineSimilarity (network science)Sequence Analysis ProteinGeneticsCluster (physics)AnimalsCluster AnalysisHumansCluster analysisDatabases ProteinMolecular BiologySequenceDatabaseFunction (mathematics)Computational Mathematics030104 developmental biologyComputational Theory and MathematicsModeling and SimulationData miningcomputer030217 neurology & neurosurgerySoftwareJournal of computational biology : a journal of computational molecular cell biology
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Quantitative analysis of the impact of a human pathogenic mutation on the CCT5 chaperonin subunit using a proxy archaeal ortholog

2017

The human chaperonin complex is a ~ 1 MDa nanomachine composed of two octameric rings formed from eight similar but non-identical subunits called CCT. Here, we are elucidating the mechanism of a heritable CCT5 subunit mutation that causes profound neuropathy in humans. In previous work, we introduced an equivalent mutation in an archaeal chaperonin that assembles into two octameric rings like in humans but in which all subunits are identical. We reported that the hexadecamer formed by the mutant subunit is unstable with impaired chaperoning functions. This study quantifies the loss of structural stability in the hexadecamer due to the pathogenic mutation, using differential scanning calorim…

0301 basic medicineProtein subunitMutantBiophysicsHeterologousBiochemistryChaperoninChaperoninlcsh:Biochemistry03 medical and health sciencesDSC differential scanning calorimetryCCT% chaperoninPf Pyrococcus furiosusDenaturation (biochemistry)lcsh:QD415-436Molecular Biologylcsh:QH301-705.5DLS dynamic light scatteringbiologyITC isothermal titration calorimetryWild typeIsothermal titration calorimetryCell BiologyChaperonopathiesbiology.organism_classificationProtein calorimetryNeuropathyPyrococcus furiosus030104 developmental biologyBiochemistryBiophysiclcsh:Biology (General)Pyrococcus furiosusChaperonopathieCCT5; Chaperonin; Chaperonopathies; Neuropathy; Protein calorimetry; Pyrococcus furiosus; Biophysics; Biochemistry; Molecular Biology; Cell BiologyCCT5Pyrococcus furiosuResearch ArticlePf-CD1 Pyrococcus furiosus chaperonin subunit with the last 22 amino acids deletedBiochemistry and Biophysics Reports
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Multi-level integration of environmentally perturbed internal phenotypes reveals key points of connectivity between them

2017

The genotype and external phenotype of organisms are linked by so-called internal phenotypes which are influenced by environmental conditions. In this study, we used five existing -omics datasets representing five different layers of internal phenotypes, which were simultaneously measured in dietarily perturbed mice. We performed 10 pair-wise correlation analyses verified with a null model built from randomized data. Subsequently, the inferred networks were merged and literature mined for co-occurrences of identified linked nodes. Densely connected internal phenotypes emerged. Forty-five nodes have links with all other data-types and we denote them "connectivity hubs." In literature, we fou…

0301 basic medicineProteomicsPhysiologySystems biologyComputational biologyBiologyProteomicslcsh:PhysiologyCorrelation03 medical and health sciences0302 clinical medicineGenotype-phenotype distinctionGastrointestinal tractPhysiology (medical)GenotypeMetabolomicsSystems and Synthetic BiologyHost-Microbe InteractomicsFokkerij & GenomicaTranscriptomicsOriginal ResearchVLAGHost Pathogen Interaction & DiagnosticsGeneticsSysteem en Synthetische BiologieInternal phenotypelcsh:QP1-981Null modelMicrobiotaBacteriologieBacteriologyBacteriology Host Pathogen Interaction & DiagnosticsPhenotypeHost Pathogen Interactie & Diagnostiek030104 developmental biologyBacteriologie Host Pathogen Interactie & DiagnostiekKey (cryptography)Data integrationSystems biology030217 neurology & neurosurgeryAnimal Breeding & Genomics
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Influenza virus damages the alveolar barrier by disrupting epithelial cell tight junctions

2016

A major cause of respiratory failure during influenza A virus (IAV) infection is damage to the epithelial–endothelial barrier of the pulmonary alveolus. Damage to this barrier results in flooding of the alveolar lumen with proteinaceous oedema fluid, erythrocytes and inflammatory cells. To date, the exact roles of pulmonary epithelial and endothelial cells in this process remain unclear.Here, we used an in vitro co-culture model to understand how IAV damages the pulmonary epithelial–endothelial barrier. Human epithelial cells were seeded on the upper half of a transwell membrane while human endothelial cells were seeded on the lower half. These cells were then grown in co-culture and IAV wa…

0301 basic medicinePulmonary and Respiratory Medicine030106 microbiologyBiologymedicine.disease_causeVirusCell LineTight Junctions03 medical and health sciencesInfluenza A Virus H1N1 SubtypemedicineInfluenza A virusHumansTight junctionInfluenza A Virus H5N1 SubtypeEpithelial CellsVirologyIn vitroEpitheliumCoculture TechniquesCell biologyPulmonary Alveoli030104 developmental biologymedicine.anatomical_structureCell cultureCytokinesPulmonary alveolusLumen (unit)European Respiratory Journal
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Eight novel variants in the SLC34A2 gene in pulmonary alveolar microlithiasis

2020

BackgroundPulmonary alveolar microlithiasis (PAM) is caused by genetic variants in the SLC34A2 gene, which encodes the sodium-dependent phosphate transport protein 2B (NaPi-2b). PAM is characterised by deposition of calcium phosphate concretions (microliths) in the alveoli leading to pulmonary dysfunction. The variant spectrum of SLC34A2 has not been well investigated and it is not yet known whether a genotype–phenotype correlation exists.MethodsWe collected DNA from 14 patients with PAM and four relatives, and analysed the coding regions of SLC34A2 by direct DNA sequencing. To determine the phenotype characteristics, clinical data were collected and a severity score was created for each va…

0301 basic medicinePulmonary and Respiratory MedicineGeneticsbusiness.industrymedicine.diseasePhenotypeAsymptomaticDNA sequencing03 medical and health sciences030104 developmental biology0302 clinical medicine030228 respiratory systemPulmonary alveolar microlithiasismedicineCoding regionMissense mutationAllelemedicine.symptombusinessGene
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A Tuft Cell-Like Signature Is Highly Prevalent in Thymic Squamous Cell Carcinoma and Delineates New Molecular Subsets Among the Major Lung Cancer His…

2020

Abstract Introduction In-depth genomic characterization of thymic epithelial tumors (TETs), comprising thymomas and thymic carcinomas (TCs), failed to identify targetable mutations and suggested unique biology of TETs, including KIT expression in most TCs. Recently, tuft cell–like medullary thymic epithelial cells were identified in the murine thymus, and our reanalysis of the published gene expression data revealed that these cells express KIT. In addition, recently, a minor subset of SCLCs with tuft cell–like features was described. Methods We interrogated mRNA expression data from our tumor cohorts (N = 60) and publicly available, independent data sets from TETs and NSCLC (N = 1199) for …

0301 basic medicinePulmonary and Respiratory MedicineLung NeoplasmsThymomaurologic and male genital diseasesmedicine.disease_cause03 medical and health sciencesMice0302 clinical medicinemedicineAnimalsHumansLung cancerThymic carcinomaThymic Squamous Cell Carcinomaurogenital systembusiness.industryCancerThymus Neoplasmsmedicine.diseasePhenotypeSmall Cell Lung Carcinomafemale genital diseases and pregnancy complications3. Good health030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchCarcinoma Squamous CellImmunohistochemistryTuft cellbusinessCarcinogenesisJournal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer
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Accelerated telomere attrition in children and teenagers with α1-antitrypsin deficiency.

2016

Numerous studies have shown that oxidative stress accelerates telomere shortening in several lung pathologies. Since oxidative stress is involved in the pathophysiology of α1-antitrypsin deficiency (AATD), we hypothesised that telomere shortening would be accelerated in AATD patients. This study aimed to assess telomere length in AATD patients and to study its association with α1-antitrypsin phenotypes.Telomere length, telomerase activity, telomerase reverse transcriptase (hTERT) expression and biomarkers of oxidative stress were measured in 62 children and teenagers (aged 2–18 years) diagnosed with AATD and 18 controls (aged 3–16 years).Our results show that intermediate-risk (MZ; SZ) and …

0301 basic medicinePulmonary and Respiratory MedicineOncologyMalemedicine.medical_specialtyTelomeraseAdolescentmedicine.disease_causeBody Mass Index03 medical and health sciencesInternal medicinealpha 1-Antitrypsin DeficiencymedicineHumansTelomerase reverse transcriptaseChildLungTelomeraseTelomere ShorteningAlpha 1-antitrypsin deficiencybusiness.industryCase-control studyTelomeremedicine.diseaseMolecular biologyPathophysiologyTelomereOxidative Stress030104 developmental biologyPhenotypeSpirometryCase-Control StudiesChild PreschoolBiomarker (medicine)FemalebusinessOxidative stress
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Bacterial-viral load and the immune response in stable and exacerbated COPD: significance and therapeutic prospects.

2016

Silvestro Ennio D’Anna,1 Bruno Balbi,2 Francesco Cappello,3,4 Mauro Carone,2 Antonino Di Stefano21Department of Rehabilitation, Cardiorespiratory Unit, Fondazione Istituto G. Giglio di Cefalù, 2Pneumology Unit and Laboratory of Cytoimmunopathology of Heart and Lung, Fondazione Salvatore Maugeri, IRCCS, Veruno (NO) and Cassano delle Murge (BA), 3Human Anatomy Section, Department of Experimental Biomedicine and Clinical Neuroscience, University of Palermo, Palermo, Italy; 4Euro-Mediterranean Institute of Science and Technology, Palermo, ItalyAbstract: Chronic obstructive pulmonary disease (COPD) is characterized by persistent airflow limitation and an abnormal inflammatory respon…

0301 basic medicinePulmonary and Respiratory MedicinePulmonary diseasemicrobiomeReview03 medical and health sciencesPulmonary Disease Chronic Obstructive0302 clinical medicineImmune systemexacerbationsmedicineHumansMicrobiomeRespiratory systemlcsh:RC705-779COPDImmunity CellularLungseverity of COPDbusiness.industryBiomarkers; COPD phenotype; Exacerbations; Microbiome; Severity of COPD; Pulmonary and Respiratory Medicine; Public Health Environmental and Occupational Health; Health PolicyHealth PolicyPublic Health Environmental and Occupational HealthbiomarkersExacerbationlcsh:Diseases of the respiratory systemBiomarkerGeneral MedicineViral Loadmedicine.diseaseBacterial Loadrespiratory tract diseases030104 developmental biologymedicine.anatomical_structure030228 respiratory systemImmunologyDisease ProgressionCOPD phenotypebusinessViral loadRespiratory tractInternational journal of chronic obstructive pulmonary disease
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JAK2 mediates lung fibrosis, pulmonary vascular remodelling and hypertension in idiopathic pulmonary fibrosis: an experimental study

2018

BackgroundPulmonary hypertension (PH) is a common disorder in patients with idiopathic pulmonary fibrosis (IPF) and portends a poor prognosis. Recent studies using vasodilators approved for PH have failed in improving IPF mainly due to ventilation (V)/perfusion (Q) mismatching and oxygen desaturation. Janus kinase type 2 (JAK2) is a non-receptor tyrosine kinase activated by a broad spectrum of profibrotic and vasoactive mediators, but its role in PH associated to PH is unknown.ObjectiveThe study of JAK2 as potential target to treat PH in IPF.Methods and resultsJAK2 expression was increased in pulmonary arteries (PAs) from IPF (n=10; 1.93-fold; P=0.0011) and IPF+PH (n=9; 2.65-fold; P<0.00…

0301 basic medicinePulmonary and Respiratory Medicinemedicine.medical_specialtyHypertension PulmonaryBlotting WesternMyocytes Smooth MuscleFluorescent Antibody TechniqueVasodilationVascular RemodelingReal-Time Polymerase Chain ReactionVascular remodelling in the embryo03 medical and health sciencesIdiopathic pulmonary fibrosisTransforming Growth Factor betaRight ventricular hypertrophyInternal medicinepulmonary hypertensionAnimalsHumansMedicineRNA Small InterferingRats WistarCells CulturedCell ProliferationBKCaJanus kinase 2biologybusiness.industryEndothelial CellsJanus Kinase 2idiopathic pulmonary fibrosismedicine.diseaseImmunohistochemistryPulmonary hypertensionIdiopathic Pulmonary FibrosisTriterpenesRatsPhenotype030104 developmental biologyJAK2biology.proteinCardiologyAnimal studiesJanus kinasebusinessSignal TransductionPulmonary artery smooth muscle cells Pulmonary artery endothelial cells.Thorax
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Metabolites related to purine catabolism and risk of type 2 diabetes incidence; modifying effects of the TCF7L2-rs7903146 polymorphism

2019

Studies examining associations between purine metabolites and type 2 diabetes (T2D) are limited. We prospectively examined associations between plasma levels of purine metabolites with T2D risk and the modifying effects of transcription factor-7-like-2 (TCF7L2) rs7903146 polymorphism on these associations. This is a case-cohort design study within the PREDIMED study, with 251 incident T2D cases and a random sample of 694 participants (641 non-cases and 53 overlapping cases) without T2D at baseline (median follow-up: 3.8 years). Metabolites were semi-quantitatively profiled with LC-MS/MS. Cox regression analysis revealed that high plasma allantoin levels, including allantoin-to-uric acid rat…

0301 basic medicinePurineMalePolymorphism (Crystallography)endocrine system diseaseslcsh:MedicineType 2 diabetesDiabetis no-insulinodependentchemistry.chemical_compound0302 clinical medicineBlood plasmaMetabolitesNon-insulin-dependent diabetesProspective Studieslcsh:ScienceMultidisciplinaryDiabetisIncidencePrognosisMetabòlits3. Good healthMetabolomeFemaleTranscription Factor 7-Like 2 Proteinmedicine.drugmedicine.medical_specialtyendocrine systemPolymorphism Single NucleotideArticle03 medical and health sciencesAllantoin:Ciencias de la Salud::Medicina preventiva [Materias Investigacion]Diabetes mellitusInternal medicinemedicineHumansGenetic Predisposition to DiseaseInosineAgedbusiness.industrylcsh:Rnutritional and metabolic diseasesPolimorfisme (Cristal·lografia)Xanthinemedicine.disease030104 developmental biologyEndocrinologychemistryDiabetes Mellitus Type 2PurinesSpainCase-Control Studieslcsh:QbusinessTCF7L2030217 neurology & neurosurgeryBiomarkersFollow-Up Studies
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