Search results for "brief"

showing 10 items of 347 documents

Risk of Classic Kaposi Sarcoma With Combinations of Killer Immunoglobulin-Like Receptor and Human Leukocyte Antigen Loci: A Population-Based Case-con…

2015

BACKGROUND Kaposi sarcoma (KS) is a complication of KS-associated herpesvirus (KSHV) infection. Other oncogenic viral infections and malignancies are associated with certain HLA alleles and their natural killer (NK) cell immunoglobulin-like receptor (KIR) ligands. We tested whether HLA-KIR influences the risk of KSHV infection or KS. METHODS In population-based case-control studies, we compared HLA class I and KIR gene frequencies in 250 classic (non-AIDS) KS cases, 280 KSHV-seropositive controls, and 576 KSHV-seronegative controls composing discovery and validation cohorts. Logistic regression was used to calculate sex- and age-adjusted odds ratios (ORs) and 95% confidence intervals. RESUL…

0301 basic medicineGenotypevirusescase-control studyPopulationchemical and pharmacologic phenomenaHuman leukocyte antigenBiologyLymphocyte ActivationSettore MED/42 - Igiene Generale E ApplicataMajor Articles and Brief Reports03 medical and health sciencesReceptors KIRnatural killer–cell immunoglobulin-like receptorsHLA AntigensRisk FactorsSeroepidemiologic Studieshuman leukocyte antigenGenotypeotorhinolaryngologic diseasesHLA-B AntigensHumansImmunology and AllergySeroprevalenceGenetic Predisposition to Diseasehuman geneticeducationSarcoma Kaposieducation.field_of_studyClassic Kaposi SarcomaCase-control studyvirus diseasesKaposi sarcomaOdds ratiomajor histocompatibility complex030104 developmental biologyInfectious DiseasesGene Expression RegulationItalyCase-Control StudiesItaly; Kaposi sarcoma; case-control study; human genetics; human leukocyte antigens; major histocompatibility complex; natural killer–cell immunoglobulin-like receptorsHerpesvirus 8 HumanImmunologyJournal of Infectious Diseases
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Mitochondrial Function in Hereditary Spastic Paraplegia: Deficits in SPG7 but Not SPAST Patient-Derived Stem Cells

2020

Mutations in SPG7 and SPAST are common causes of hereditary spastic paraplegia (HSP). While some SPG7 mutations cause paraplegin deficiency, other SPG7 mutations cause increased paraplegin expression. Mitochondrial function has been studied in models that are paraplegin-deficient (human, mouse, and Drosophila models with large exonic deletions, null mutations, or knockout models) but not in models of mutations that express paraplegin. Here, we evaluated mitochondrial function in olfactory neurosphere-derived cells, derived from patients with a variety of SPG7 mutations that express paraplegin and compared them to cells derived from healthy controls and HSP patients with SPAST mutations, as …

0301 basic medicineHereditary spastic paraplegiaoxidative phosphorylationOxidative phosphorylationMitochondrionmedicine.disease_causeSpastinSPG7lcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASThereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMutationparapleginParapleginGeneral NeuroscienceBrief Research Reportspastinmedicine.diseasePhenotypeCell biologymitochondria030104 developmental biology030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in Neuroscience
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The Commensal Microbiota Enhances ADP-Triggered Integrin αIIbβ3 Activation and von Willebrand Factor-Mediated Platelet Deposition to Type I Collagen

2020

The commensal microbiota is a recognized enhancer of arterial thrombus growth. While several studies have demonstrated the prothrombotic role of the gut microbiota, the molecular mechanisms promoting arterial thrombus growth are still under debate. Here, we demonstrate that germ-free (GF) mice, which from birth lack colonization with a gut microbiota, show diminished static deposition of washed platelets to type I collagen compared with their conventionally raised (CONV-R) counterparts. Flow cytometry experiments revealed that platelets from GF mice show diminished activation of the integrin αIIbβ3 (glycoprotein IIbIIIa) when activated by the platelet agonist adenosine diphosphate (ADP). Fu…

0301 basic medicineMaleGene Expression030204 cardiovascular system & hematologyvon Willebrand factorlcsh:Chemistrychemistry.chemical_compoundMice0302 clinical medicinePlateletToll-like receptor-2lcsh:QH301-705.5SpectroscopyMice KnockoutbiologyChemistryBrief ReportαIIbβ3General MedicineArteriesComputer Science ApplicationsCell biologyAdenosine DiphosphatePlatelet Glycoprotein GPIb-IX Complexgerm-freeplateletsFemaleType I collagenBlood PlateletsIntegrinPrimary Cell CulturePlatelet Glycoprotein GPIIb-IIIa ComplexCatalysisCollagen Type IInorganic Chemistry03 medical and health sciencesVon Willebrand factormedicineCell AdhesionmicrobiotaAnimalsGerm-Free LifeHumansPhysical and Theoretical ChemistryThrombusSymbiosisMolecular Biologyα<sub>IIb</sub>β<sub>3</sub>Innate immune systemOrganic ChemistryThrombosismedicine.diseaseImmunity InnateToll-Like Receptor 2Gastrointestinal MicrobiomeMice Inbred C57BLAdenosine diphosphateTLR2030104 developmental biologylcsh:Biology (General)lcsh:QD1-999biology.proteinInternational Journal of Molecular Sciences
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Proper assignation of reactivation in a COVID-19 recurrence initially interpreted as a reinfection

2021

A 77-year-old-male (Case R) who had had a previous diagnosis of mild COVID-19 episode, was hospitalized 35 days later. On Day 23 post-admission, he developed a second COVID-19 episode, now severe, and finally died. Initially, Case R COVID-19 recurrence was interpreted as a reinfection due to the exposure to a SARS-CoV-2 RT-PCR-positive room-mate. However, whole-genome-sequencing indicated that case R recurrence corresponded to a reactivation of the strain involved in his first episode. Case R reactivation had major consequences, leading to a more severe episode, and causing a subsequent transmission to another two hospitalized patients, one of them with fatal outcome.

0301 basic medicineMalePediatricsmedicine.medical_specialty2019-20 coronavirus outbreakFatal outcomeCoronavirus disease 2019 (COVID-19)Hospitalized patientsSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2)Antibodies Viral03 medical and health sciences0302 clinical medicineNosocomial transmissionRecurrencemedicineImmunology and AllergyHumans030212 general & internal medicineAgedFirst episodeWhole Genome Sequencingbusiness.industrySARS-CoV-2Nosocomial transmissionBrief ReportCOVID-19Reactivation030104 developmental biologyInfectious DiseasesAcademicSubjects/MED00290ReinfectionbusinessWGS
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Facial cutaneo-mucosal venous malformations can develop independently of mutation of TEK gene but may be associated with excessive expression of Src…

2017

International audience; We aimed to search for mutations in the germline and somatic DNA of the TEK gene and to analyze the expression level of Src and phospho- Src (p-Src) in tumor and healthy tissues from patients with facial cutaneo-mucosal venous malformations (VMCM). Eligible patients from twelve families and thirty healthy controls were recruited respectively at the Departments of Stomatology and Oral Surgery, and Transfusion Medicine of Tlemcen University Medical Centre. Immunoblot analyses of Src and p-Src were performed after direct DNA sequencing. No somatic or germline mutations were found in all the 23 exons and their 5' and 3' intronic flanking regions, except for one case in w…

0301 basic medicineMaleSomatic cellVascular MalformationsCutaneo-mucosal venous malformationsTyrosine Kinase Tie2Bioinformaticsmedicine.disease_causeGermlineMetastasisp-SrcExonPharmacology Toxicology and Pharmaceutics(all)General Pharmacology Toxicology and PharmaceuticsPhosphorylationCancerMedicine(all)MutationBrief ReportGeneral MedicineReceptor TIE-2[SDV.BDD.MOR] Life Sciences [q-bio]/Development Biology/Morphogenesis3. Good healthsrc-Family Kinases[SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN]FemaleProto-oncogene tyrosine-protein kinase SrcReceptorSrc[SDV.MHEP.AHA] Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]AdolescentDirect sequencingContext (language use)BiologyVegfGeneral Biochemistry Genetics and Molecular BiologyPermeability03 medical and health sciencesGermline mutationTEK gene[SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry Molecular Biology/Genomics [q-bio.GN][ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologymedicine[SDV.MHEP.AHA]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumansAmino Acid SequenceGeneMucous MembraneCell-Lines[ SDV ] Life Sciences [q-bio]Base SequenceBiochemistry Genetics and Molecular Biology(all)[SDV.BDD.MOR]Life Sciences [q-bio]/Development Biology/MorphogenesisGermline and somatic DNA030104 developmental biologyFaceMutationCancer researchSkin AbnormalitiesAngiogenesisPathwayJournal of negative results in biomedicine
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Positive Role of the MHC Class-I Antigen Presentation Regulator m04/gp34 of Murine Cytomegalovirus in Antiviral Protection by CD8 T Cells

2020

Murine cytomegalovirus (mCMV) codes for MHC class-I trafficking modulators m04/gp34, m06/gp48, and m152/gp40. By interacting with the MHC class-Iα chain, these proteins disconnect peptide-loaded MHC class-I (pMHC-I) complexes from the constitutive vesicular flow to the cell surface. Based on the assumption that all three inhibit antigen presentation, and thus the recognition of infected cells by CD8 T cells, they were referred to as “immunoevasins.” Improved antigen presentation mediated by m04 in the presence of m152 after infection with deletion mutant mCMV-Δm06W, compared to mCMV-Δm04m06 expressing only m152, led us to propose renaming these molecules “viral regulators of antigen present…

0301 basic medicineMicrobiology (medical)BAC mutagenesisMuromegalovirusAdoptive cell transfer030106 microbiologyImmunologyAntigen presentationMutantlcsh:QR1-502CD8 T cellsPeptide bindingCD8-Positive T-LymphocytesMajor histocompatibility complexAntiviral AgentsMicrobiologylcsh:MicrobiologyMiceViral Proteins03 medical and health sciencesCellular and Infection MicrobiologyMHC class IAnimalsCytotoxic T cellnext-generation sequencing (NGS)adoptive cell transferimmune evasionAntigen PresentationMembrane GlycoproteinsbiologyMHC class I antigenHistocompatibility Antigens Class IimmunoevasinBrief Research ReportCell biology030104 developmental biologyInfectious Diseasesbiology.proteinrecombinant virusFrontiers in Cellular and Infection Microbiology
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The Anti-apoptotic Murine Cytomegalovirus Protein vMIA-m38.5 Induces Mast Cell Degranulation.

2020

Mast cells (MC) represent "inbetweeners" of the immune system in that they are part of innate immunity by acting as first-line sentinels for environmental antigens but also provide a link to adaptive immunity by secretion of chemokines that recruit CD8 T cells to organ sites of infection. An interrelationship between MC and cytomegalovirus (CMV) has been a blank area in science until recently when the murine model revealed a role for MC in the resolution of pulmonary infection by murine CMV (mCMV). As to the mechanism, MC were identified as a target cell type of mCMV. Infected MC degranulate and synthesize the CC-chemokine ligand-5 (CCL-5), which is released to attract protective virus-spec…

0301 basic medicineMicrobiology (medical)Chemokinebone marrow-derived mast cells (BMMC)Muromegalovirusmurine cytomegalovirus030106 microbiologyImmunologygene m38.5lcsh:QR1-502CytomegalovirusApoptosisInhibitor of apoptosisMicrobiologylcsh:MicrobiologyCell Degranulation03 medical and health sciencesMiceImmune systemCellular and Infection MicrobiologyCytotoxic T cellAnimalsperitoneal exudate-derived mast cells (PEMC)Mast CellsdegranulationInnate immune systembiologyDegranulationvirus diseasesTransfectionBrief Research ReportAcquired immune systemCell biologyvMIA030104 developmental biologyInfectious Diseasesbiology.proteinmast cell-specific Cre recombinationApoptosis Regulatory ProteinsFrontiers in cellular and infection microbiology
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Enhancement of Antigen Presentation by Deletion of Viral Immune Evasion Genes Prevents Lethal Cytomegalovirus Disease in Minor Histocompatibility Ant…

2020

Hematoablative treatment followed by hematopoietic cell transplantation (HCT) for reconstituting the co-ablated immune system is a therapeutic option to cure aggressive forms of hematopoietic malignancies. In cases of family donors or unrelated donors, immunogenetic mismatches in major histocompatibility complex (MHC) and/or minor histocompatibility (minor-H) loci are unavoidable and bear a risk of graft-vs.-host reaction and disease (GvHR/D). Transient immunodeficiency inherent to the HCT protocol favors a productive reactivation of latent cytomegalovirus (CMV) that can result in multiple-organ CMV disease. In addition, there exists evidence from a mouse model of MHC class-I-mismatched GvH…

0301 basic medicineMicrobiology (medical)nodular inflammatory focus (NIF)murine cytomegalovirusbone marrow transplantation030106 microbiologyImmunologyAntigen presentationlcsh:QR1-502Cytomegaloviruschemical and pharmacologic phenomenaCD8 T cellsBiologyCD8-Positive T-LymphocytesMajor histocompatibility complexMicrobiologylcsh:MicrobiologyMinor Histocompatibility Antigens03 medical and health sciencestransplantation toleranceMiceImmune systemCellular and Infection MicrobiologyAntigenMinor histocompatibility antigenAnimalsgraft-vs.-host disease (GvHD)Immune EvasionAntigen PresentationHematopoietic Stem Cell Transplantationhematopoietic reconstitutionBrief Research ReportHistocompatibilityTransplantationMice Inbred C57BL030104 developmental biologyInfectious DiseasesImmunologyCytomegalovirus Infectionsbiology.proteinCD8Frontiers in Cellular and Infection Microbiology
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Aurora Kinase A expression predicts platinum-resistance and adverse outcome in high-grade serous ovarian carcinoma patients

2016

High-Grade Serous Ovarian Carcinoma (HGSOC) is the predominant histotype of epithelial ovarian cancer (EOC), characterized by advanced stage at diagnosis, frequent TP53 mutation, rapid progression, and high responsiveness to platinum-based-chemotherapy. To date, standard first-line-chemotherapy in advanced EOC includes platinum salts and paclitaxel with or without bevacizumab. The major prognostic factor is the response duration from the end of the platinum-based treatment (platinum-free interval) and about 10–0 % of EOC patients bear a platinum-refractory disease or develop early resistance (platinum-free interval shorter than 6 months). On these bases, a careful selection of patients who …

0301 basic medicineOncologyAdultmedicine.medical_specialtyBevacizumabendocrine system diseasesPrognosimedicine.medical_treatmentHigh-grade serous ovarian carcinoma (HGSOC)Gene ExpressionAntineoplastic AgentsKaplan-Meier EstimateBrief Communication03 medical and health sciences0302 clinical medicineOvarian carcinomaInternal medicineObstetrics and GynaecologyMedicineHumansPlatinumAgedAurora Kinase ANeoplasm StagingGynecologyAged 80 and overOvarian NeoplasmsChemotherapyAURKAbusiness.industryObstetrics and GynecologyRetrospective cohort studyMiddle AgedPrognosisImmunohistochemistryfemale genital diseases and pregnancy complicationsCystadenocarcinoma SerousClinical trialSerous fluid030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisFemaleAurora Kinase APersonalized medicineTherapybusinessmedicine.drugJournal of Ovarian Research
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Parvovirus B19V Nonstructural Protein NS1 Induces Double-Stranded Deoxyribonucleic Acid Autoantibodies and End-Organ Damage in Nonautoimmune Mice

2018

Abstract Background Viral infection is implicated in development of autoimmunity. Parvovirus B19 (B19V) nonstructural protein, NS1, a helicase, covalently modifies self double-stranded deoxyribonucleic acid (dsDNA) and induces apoptosis. This study tested whether resulting apoptotic bodies (ApoBods) containing virally modified dsDNA could induce autoimmunity in an animal model. Methods BALB/c mice were inoculated with (1) pristane-induced, (2) B19V NS1-induced, or (3) staurosporine-induced ApoBods. Serum was tested for dsDNA autoantibodies by Crithidia luciliae staining and enzyme-linked immunosorbent assay. Brain, heart, liver, and kidney pathology was examined. Deposition of self-antigens…

0301 basic medicinePathogenesis and Host ResponseviruksetvirusesB19VKidney GlomerulusSLEApoptosisAutoimmunityanti-dsDNA antibodyViral Nonstructural Proteinsmedicine.disease_causeAutoimmunityautoimmuniteettiMice0302 clinical medicineGlomerulonephritisParvovirus B19 HumanImmunology and Allergy030212 general & internal medicineEnzyme InhibitorstolerancebiologyChemistryapoptosisBrainInfectious DiseasesLivervirustauditAntibodies AntinuclearmaksatulehdusFemaleAntibodyImmunosuppressive Agentsta3111infektiot03 medical and health sciencesohjelmoitunut solukuolemaMajor Articles and Brief ReportsExtracellular VesiclesAntigenmedicineCrithidia luciliaeAnimalsapoptotic bodiesparvoviruksetParvovirusTerpenesAnti-dsDNA antibodiesMyocardiumta1183parvovirusAutoantibodyta1182DNAbiology.organism_classificationStaurosporineMolecular biology030104 developmental biologyApoptosisbiology.proteinautovasta-aineetglomerulonephritisThe Journal of Infectious Diseases
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