Search results for "pathogen"

showing 10 items of 1657 documents

HCV genotype 5: an orphan virus

2013

HCV genotype 5 (HCV-5) is the least known HCV genotype. It is found mainly in South Africa and in restricted areas of Belgium, Spain, France, Syria and Greece. Sporadic cases are reported worldwide. The main modes of transmission are blood transfusion and iatrogenic causes. Little is known about its origin, but various studies have elucidated its spread worldwide. In endemic areas, patients infected with HCV-5 are on average older and have a higher viral load and more advanced fibrosis than those infected with non-HCV-5 genotypes. The current standard of care for HCV-5 chronic infection is 48 weeks of dual therapy with pegylated interferon plus ribavirin. ‘Favourable’ Il28B polymorphisms a…

Blood transfusionGenotypemedicine.medical_treatmentHepacivirusAntiviral Agentschemistry.chemical_compoundPegylated interferonGenotypemedicinePrevalenceHumansPharmacology (medical)PharmacologyTransmission (medicine)business.industryRibavirinvirus diseasesHepatitis Cmedicine.diseaseHepatitis Cdigestive system diseasesChronic infectionInfectious DiseasesTreatment OutcomechemistryImmunologyHost-Pathogen InteractionsbusinessViral loadmedicine.drug
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Buerger`s Disease and Hyperhomocysteinemia: Is there a Relationship?

2009

Thromboangiitis obliterans, also known as Buerger's disease, is a cause of juvenile lower limb ischaemia. Buerger's disease is idiopathic and one of diagnostic criteria is the absence of atherosclerotic risk factors other than smok- ing. A possible involvement of thrombophilia has been investigated and the role of hyperhomocysteinemia is still matter of discussion. We describe 9 patients with Buerger's disease followed-up for the past 3 years. We found a significant in- crease in circulating homocysteine levels (mean: 31.6 in patients vs 8.2 μmol/L in control subjects). We also analyzed the C677T mutation of MTHFR; 5/9 Buerger's patients were heterozygotes and 4/9 homozygotes for the mutati…

Buerger's diseasemedicine.medical_specialtyHyperhomocysteinemiaPathologyHomocysteinebiologybusiness.industryDiseasemedicine.diseaseThrombophiliaGastroenterologyPathogenesischemistry.chemical_compoundchemistrythrombophilia hyperhomocysteinemia MTHFR Buerger's diseaseInternal medicineMethylenetetrahydrofolate reductasemedicinebiology.proteinEndothelial dysfunctionbusinessThe Open Atherosclerosis & Thrombosis Journal
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Structural and functional changes in the gut microbiota associated to Clostridium difficile infection

2014

Antibiotic therapy is a causative agent of severe disturbances in microbial communities. In healthy individuals, the gut microbiota prevents infection by harmful microorganisms through direct inhibition (releasing antimicrobial compounds), competition, or stimulation of the host’s immune defenses. However, widespread antibiotic use has resulted in short- and long-term shifts in the gut microbiota structure, leading to a loss in colonization resistance in some cases. Consequently, some patients develop Clostridium difficile infection (CDI) after taking an antibiotic (AB) and, at present, this opportunistic pathogen is one of the main causes of antibiotic-associated diarrhea in hospitalized p…

C. difficile infectionMicrobiology (medical)biologymetabolic functionsmedicine.drug_classFirmicutesAntibioticslcsh:QR1-502Gut microbiotaColonisation resistanceClostridium difficileGut florabiology.organism_classificationMicrobiologylcsh:MicrobiologyMicrobiologyClostridiumcolonization resistancemedicinebacterial compositionOriginal Research ArticleBacteroidaceaePathogenFrontiers in Microbiology
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Correction to: Atypical pathogens in hospitalized patients with community-acquired pneumonia: a worldwide perspective (BMC Infectious Diseases, (2018…

2020

Following publication of the original article [1], the authors identified that they have been incorrectly tagged under the name of their related consortium GLIMP Study Group.

CAP Atypical pathogens EpidemiologySettore MED/10 - Malattie Dell'Apparato Respiratorio
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Biofonctionnements des sols tropicaux et mode de gestion des terres

2000

L'effet de deux peuplements de nématodes phytoparasites a été étudié en conditions contrôlées sur la croissance du mil (#Pennisetum glaucum$). Les plants de mil (cv. IKMV 8201) ont été cultivés en pots sur du col collecté au Sud du Sénégal dans un champ cultivé (sol cultivé) et dans une jachère de 17 ans (sol de jachère). La moitié du sol de chacun des prélèvements à été stérilisée. Pour compenser l'effet de la stérilisation, six cycles de cultures de mil de deux mois ont été faits avant l'expérimentation. A l'issu de cette période, trois espèces ont été observées sur le sol cultivé non stérilisé : #Scutellonema cavanessi$, #Tylenchorhynchus gladiolatus$ et #Ditylenchus myceliophagus$, dans…

CARACTERISTIQUE PHYSIQUEBIOMASSEMILSOL CULTIVEDIVERSITE SPECIFIQUE[SDV.SA.SDS]Life Sciences [q-bio]/Agricultural sciences/Soil studyJACHERENEMATODE PHYTOPARASITEPOUVOIR PATHOGENEMETHODE DE LUTTEETUDE COMPARATIVE[SDV.SA.SDS] Life Sciences [q-bio]/Agricultural sciences/Soil studyLUTTE BIOLOGIQUEComputingMilieux_MISCELLANEOUSCARACTERISTIQUE CHIMIQUE
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Timing of activation of CD4+ memory cells as a possible marker to establish the efficacy of vaccines against contagious agalactia in sheep

2013

Mycoplasma agalactiae is a major pathogen of sheep and goats in many areas of the world and particularly in Mediterranean countries. It causes contagious agalactia, an infectious disease primarily affecting mammary glands. Many vaccines against the pathogen are currently under development. The aim of the study was to investigate the involvement of T cell-mediated immunity during vaccination and challenge experiments against Mycoplasma agalactiae. A comparison of the antigen-specific expansion of interferon gamma positive T cell memory and naïve subsets was performed between vaccinated and non-vaccinated sheep to identify cellular subsets whose activation was different between protected and …

CD4-Positive T-LymphocytesCellular immunityTime FactorsT cellMycoplasma agalactiaeImmunologyved/biology.organism_classification_rank.speciesSheep DiseasesCD8-Positive T-LymphocytesBiologyLymphocyte ActivationMycoplasma agalactiaeInterferon-gammaT-Lymphocyte SubsetsImmunitymedicineAnimalsMycoplasma InfectionsInterferon gammaMycoplasma agalactiae Cellular immunity IFN-g + cellsPathogenSheep DomesticSheepGeneral Veterinaryved/biologyVaccine efficacyAntibodies BacterialVirologyVaccinationTreatment Outcomemedicine.anatomical_structureImmunoglobulin GBacterial VaccinesImmunologyFemaleImmunologic Memorymedicine.drugVeterinary Immunology and Immunopathology
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Reconstitution of CD8 T cells is essential for the prevention of multiple-organ cytomegalovirus histopathology after bone marrow transplantation.

1998

Cytomegalovirus (CMV) infection in the period of temporary immunodeficiency after haematoablative treatment and bone marrow transplantation (BMT) is associated with a risk of graft failure and multiple-organ CMV disease. The efficacy of immune system reconstitution is decisive for the prevention of CMV pathogenesis after BMT. Previous data in murine model systems have documented a redundancy in the immune effector mechanisms controlling CMV. CD8 T cells proved to be relevant but not irreplaceable as antiviral effectors. Specifically, in a state of long-term in vivo depletion of the CD8 T-cell subset, CD4 T cells were educed to become deputy effectors controlling CMV by a mechanism involving…

CD4-Positive T-LymphocytesCongenital cytomegalovirus infectionCytomegalovirusGraft vs Host DiseaseCD8-Positive T-LymphocytesBiologyVirus ReplicationLymphocyte DepletionPathogenesisMiceImmune systemRisk FactorsIn vivoVirologymedicineAnimalsHumansCytotoxic T cellImmunodeficiencyBone Marrow TransplantationMice Inbred BALB CEffectorvirus diseasesmedicine.diseaseVirologyDisease Models AnimalTransplantation IsogeneicCytomegalovirus InfectionsImmunologyCD8Journal of General Virology
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Perforin deficiency attenuates inflammation and tumor growth in colitis-associated cancer

2010

Background: Patients with inflammatory bowel disease (IBD) have a markedly increased risk to develop colon cancer, but there are only limited data about the host antitumor response in such colitis-associated cancer. In the present study we aimed at assessing the role of perforin-dependent effector mechanisms in the immune response in a murine model of colitis-associated colon cancer. Methods: Wildtype and perforin-deficient mice were analyzed in a mouse model of colitis-associated colon cancer using azoxymethane (AOM) and dextran sodium sulfate (DSS). Results: Tumors of wildtype mice showed infiltration of CD4+, CD8+ T cells, natural killer (NK) cells, high numbers of apoptotic cells, and e…

CD4-Positive T-LymphocytesCytotoxicity ImmunologicPore Forming Cytotoxic ProteinsT-LymphocytesMedizinInflammationCD8-Positive T-LymphocytesBiologymedicine.disease_causeInflammatory bowel diseaseMiceImmune systemmedicineAnimalsImmunology and AllergyCytotoxic T cellIntestinal MucosaColitisReverse Transcriptase Polymerase Chain ReactionPerforin DeficiencyDextran SulfateGastroenterologyColitismedicine.diseaseSpecific Pathogen-Free OrganismsKiller Cells NaturalMice Inbred C57BLDisease Models AnimalPerforinChronic DiseaseColonic NeoplasmsImmunologybiology.proteinmedicine.symptomCarcinogenesisInflammatory Bowel Diseases
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Stochastic Episodes of Latent Cytomegalovirus Transcription Drive CD8 T-Cell “Memory Inflation” and Avoid Immune Evasion

2021

Acute infection with murine cytomegalovirus (mCMV) is controlled by CD8+ T cells and develops into a state of latent infection, referred to as latency, which is defined by lifelong maintenance of viral genomes but absence of infectious virus in latently infected cell types. Latency is associated with an increase in numbers of viral epitope-specific CD8+ T cells over time, a phenomenon known as “memory inflation” (MI). The “inflationary” subset of CD8+ T cells has been phenotyped as KLRG1+CD62L- effector-memory T cells (iTEM). It is agreed upon that proliferation of iTEM requires repeated episodes of antigen presentation, which implies that antigen-encoding viral genes must be transcribed du…

CD4-Positive T-LymphocytesGene Expression Regulation Viral0301 basic medicineMuromegaloviruslatent infectionTime FactorsTranscription Geneticeffector memory CD8+ T cellsAntigen presentationImmunologyBiologyVirusImmediate-Early Proteins03 medical and health sciences0302 clinical medicineImmune systemImmunityAnimalsCytotoxic T cellImmunology and AllergyLatency (engineering)Antigens ViralLungGenememory inflationlatencyOriginal Researchimmune evasionMice Inbred BALB CStochastic ProcessesModels ImmunologicalHerpesviridae InfectionsRC581-607VirologyVirus LatencyDisease Models Animalvirus reactivationantigen presentationPhenotype030104 developmental biologyHost-Pathogen Interactionsgene expressionFemaleVirus ActivationImmunologic diseases. AllergyImmunologic MemoryCD8030215 immunologyFrontiers in Immunology
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Is TNF-α really involved in giant cell arteritis pathogenesis?

2013

Giant cell arteritis (GCA) is the most frequent vasculitis in people >50 years, and glucocorticoids (GC) remain the cornerstone of the treatment. However, this long-term treatment is responsible for numerous GC-related complications.1 Thus, reliable GC-sparing drugs need to be explored. Seror et al 2 have recently reported the inefficacy of adalimumab, a humanised anti-TNF-α therapy, as a GC-sparing drug in the treatment of GCA. These clinical results contrast with previous studies reporting a production of TNF-α by giant cells and macrophages in GCA lesions.3 However, recent advance in the knowledge of GCA pathogenesis have shown that macrophages and giant cells are not involved in the fir…

CD4-Positive T-LymphocytesMaleImmunologyGiant Cell ArteritisGeneral Biochemistry Genetics and Molecular BiologyPathogenesisRheumatologyimmune system diseasesAdalimumabImmunology and AllergyMedicineHumanscardiovascular diseasesskin and connective tissue diseasesAgedAged 80 and overbusiness.industryTumor Necrosis Factor-alphaMiddle Agedmedicine.diseaseGiant cell arteritisGiant cellImmunologycardiovascular systemTumor necrosis factor alphaFemalebusinessVasculitismedicine.drugAnnals of the rheumatic diseases
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