Search results for "eficiency"

showing 10 items of 1074 documents

A new model of chronic colitis in SCID mice induced by adoptive transfer of CD62L+ CD4+ T cells: insights into the regulatory role of interleukin-6 o…

2003

<i>Objective:</i> The proinflammatory cytokine interleukin (IL)-6 is involved in various chronic inflammatory processes. IL-6 is a predominant cytokine produced by lamina propria T cells in Crohn’s disease and experimental colitis. This study was designed to examine the effect of a neutralizing IL-6-receptor (IL-6R) antibody on the programmed cell death of mucosal T cells in the CD62L+ CD4+ SCID transfer model of chronic experimental colitis in mice and to gain more insight into the pathogenesis of this transfer colitis model. <i>Methods:</i> For adoptive transfer, we isolated CD62L+ CD4+ double-positive T cells from wild-type BALB/c mice followed by intraperitoneal …

CD4-Positive T-LymphocytesSTAT3 Transcription FactorAdoptive cell transferCell TransplantationColonApoptosisMice SCIDPathology and Forensic MedicineProinflammatory cytokineInterleukin 21MiceInterleukin 25In Situ Nick-End LabelingAnimalsIL-2 receptorIntestinal MucosaL-SelectinInterleukin 6Antibodies BlockingMolecular BiologyMice Inbred BALB CbiologyInterleukin-6InterleukinCell BiologyGeneral MedicineFlow CytometryAdoptive TransferReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalImmunologybiology.proteinTrans-ActivatorsInterleukin 18Colitis UlcerativeSevere Combined ImmunodeficiencySpleenPathobiology : journal of immunopathology, molecular and cellular biology
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Effect of female genital schistosomiasis and anti-schistosomal treatment on monocytes, CD4+ T-cells and CCR5 expression in the female genital tract

2014

Published version of an article from the journal: PLoS One. Also available from the publisher: http://dx.doi.org/10.1371/journal.pone.0098593 BACKGROUND: Schistosoma haematobium is a waterborne parasite that may cause female genital schistosomiasis (FGS), characterized by genital mucosal lesions. There is clinical and epidemiological evidence for a relationship between FGS and HIV. We investigated the impact of FGS on HIV target cell density and expression of the HIV co-receptor CCR5 in blood and cervical cytobrush samples. Furthermore we evaluated the effect of anti-schistosomal treatment on these cell populations. DESIGN: The study followed a case-control design with post treatment follow…

CD4-Positive T-LymphocytesViral DiseasesGynecologic InfectionsVDP::Medical disciplines: 700::Clinical medical disciplines: 750::Tropical medicine: 761Gene Expressionlcsh:MedicineGlobal HealthMonocytesPraziquantelWhite Blood CellsImmunodeficiency VirusesAnimal CellsMedicine and Health SciencesSchistosomiasisPublic and Occupational Healthlcsh:ScienceT CellsCoinfectionObstetrics and GynecologyGenitalia FemaleAIDSInfectious DiseasesPhenotypeMedical MicrobiologyHelminth InfectionsViral PathogensSchistosoma haematobiumFemaleCellular TypesResearch ArticleNeglected Tropical DiseasesAdultAdolescentReceptors CCR5Immune CellsUrologyImmunologySexually Transmitted DiseasesMicrobiologyImmunophenotypingYoung AdultParasitic DiseasesAnimalsHumansMicrobial PathogensBlood CellsGenitourinary Infectionslcsh:RBiology and Life SciencesHIVCell BiologyTropical DiseasesCase-Control StudiesWomen's HealthClinical Immunologylcsh:QGenital Diseases Female
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Homozygosity for a Mutation in the CYP11B2 Gene and GH Deficiency in a Child with Severe Growth Delay

2015

Background: Isolated hypoaldosteronism is an autosomal recessive inherited disorder of terminal aldosterone synthesis, leading to selective aldosterone deficiency. Two different biochemical forms of this disease have been described, called aldosterone synthase deficiency or corticosterone methyl oxydase, types 1 and 2. In type 1, there is no aldosterone synthase activity and the 18 hydroxycorticosterone (18 OHB) level is low, whereas in type 2, a residual activity of aldosterone synthase persists and 18 OHB is overproduced. Objective and hypotheses: Isolated aldosterone synthase deficiency should be considered in neonates and infants with failure to thrive and salt wasting. Normal levels of…

CYP11B2Settore MED/38 - Pediatria Generale E SpecialisticaSevere Growth DelayHomozygosityGH Deficiency
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Traducción y adaptación al castellano del cuestionario de salud para celíacos Canadian Celiac Health Survey

2014

Introducción: Adaptar y valorar el cuestionario de calidad de vida denominado Canadian Celiac Health Survey (CCHS). Objetivo: Traducir y adaptar en castellano el cuestionario CCHS para poder ser utilizado por la población de habla hispana puesto que se trata de un cuestionario específico para la celiaquía. Método: La adaptación del CCHS, que consta de 76 ítems distribuidos en 11 secciones diferentes, se realizó mediante el método de traducción-retrotraducción y tras ser revisado y consensuado se procedió a realizar una prueba piloto con 25 personas celíacas, de forma individual y por un miembro del grupo de investigación, para valorar la comprensión de los ítems y sus secciones. Las aportac…

Canadian Celiac Health Surveylcsh:Nutritional diseases. Deficiency diseasesQuestionnaireCalidad de vidaCeliacCelíacosCanadian celiac health surveyMétodo de traducción-retrotraducciónTranslation-back-translation Methodlcsh:RC620-627CuestionarioQuality Of LifeNutrición Hospitalaria
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The “unnatural” history of colorectal cancer in Lynch syndrome : lessons from colonoscopy surveillance

2021

Individuals with Lynch syndrome (LS), one of the most common inherited cancer syndromes, are at increased risk of developing malignancies, in particular colorectal cancer (CRC). Regular colonoscopy with polypectomy is recommended to reduce CRC risk in LS individuals. However, recent independent studies demonstrated that a substantial proportion of LS individuals develop CRC despite regular colonoscopy. The reasons for this surprising observation confirmed by large prospective studies are a matter of debate. In this review, we collect existing evidence from clinical, epidemiological and molecular studies and interpret them with regard to the origins and progression of LS-associated CRC. Alon…

Cancer ResearchColorectal cancermedicine.medical_treatmentColonoscopyDNA Mismatch RepairADENOMA DETECTION0302 clinical medicineRisk FactorsEpidemiologyMass ScreeningProspective cohort studyMUTATIONRISKmedicine.diagnostic_testincident cancer riskColonoscopyTUMORSLynch syndrome3. Good healthOncology030220 oncology & carcinogenesisPopulation SurveillancesyöpätauditColorectal Neoplasmskoloskopiamedicine.medical_specialtyLONG-TERM3122 Cancerscolorectal cancersuolistosyövätINTERVAL CANCERS03 medical and health sciencesINTESTINAL MICROBIOTACàncer colorectalCOLONmedicineMANAGEMENTHumansLynchin oireyhtymäIntensive care medicinepaksusuolisyöpäperinnölliset tauditseulontatutkimusbusiness.industrymismatch repair deficiencyMicrosatellite instabilityCancerColonoscòpiamedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisPolypectomydigestive system diseasesDNA Repair EnzymesLynch syndromemicrosatellite instabilitybusinesscolonoscopy surveillance
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In vivo targeting of human neutralizing antibodies against CD55 and CD59 to lymphoma cells increases the antitumor activity of rituximab.

2007

AbstractAn in vivo model of human CD20+ B-lymphoma was established in severe combined immunodeficiency mice to test the ability of human neutralizing miniantibodies to CD55 and CD59 (MB55 and MB59) to enhance the therapeutic effect of rituximab. The miniantibodies contained single-chain fragment variables and the hinge-CH2-CH3 domains of human IgG1. LCL2 cells were selected for the in vivo study among six B-lymphoma cell lines for their high susceptibility to rituximab-dependent complement-mediated killing enhanced by MB55 and MB59. The cells injected i.p. primarily colonized the liver and spleen, leading to the death of the animals within 30 to 40 days. Thirty percent of mice receiving bio…

Cancer ResearchLymphoma B-Cellmedicine.drug_classmedicine.medical_treatmentAntineoplastic AgentsCD59 AntigensAntigens CD59Mice SCIDPharmacologyMonoclonal antibodyAntigens CD55Antineoplastic AgentAntibodies Monoclonal Murine-DerivedMicerituximabIn vivomedicineAnimalsHumansantibodies against CD55 and CD59CD20Severe combined immunodeficiencyMice Inbred BALB CbiologyCD55 AntigensAnimalAntibody-Dependent Cell CytotoxicityAntibodies MonoclonalImmunotherapyrituximab; antibodies against CD55 and CD59medicine.diseaseDisease Models AnimalOncologyAnimals; Antibodies Monoclonal; Antibodies Monoclonal Murine-Derived; Antibody-Dependent Cell Cytotoxicity; Antigens CD55; Antigens CD59; Antineoplastic Agents; Disease Models Animal; Female; Humans; Lymphoma B-Cell; Mice; Mice Inbred BALB C; Mice SCID; Rituximab; Cancer Research; OncologyMonoclonalImmunologybiology.proteinRituximabFemaleAntibodymedicine.drugHuman
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Epidemiological, clinical and molecular characterization of Lynch‐like syndrome: A population‐based study

2019

Colorectal carcinomas that are mismatch repair (MMR)‐deficient in the absence of MLH1 promoter methylation or germline mutations represent Lynch‐like syndrome (LLS). Double somatic events inactivating MMR genes are involved in the etiology of LLS tumors. Our purpose was to define the clinical and broader molecular hallmarks of LLS tumors and the population incidence of LLS, which remain poorly characterized. We investigated 762 consecutive colorectal carcinomas operated in Central Finland in 2000–2010. LLS cases were identified by a stepwise protocol based on MMR protein expression, MLH1 methylation and MMR gene mutation status. LLS tumors were profiled for CpG Island Methylator Phenotype (…

Cancer ResearchMICROSATELLITE INSTABILITYDNA mismatch repairMISMATCH-REPAIR DEFICIENCYGene mutationmedicine.disease_cause0302 clinical medicinelynch syndromeFinlandMolecular Epidemiologyeducation.field_of_studyMutationISLAND METHYLATOR PHENOTYPENONPOLYPOSIS COLORECTAL-CANCERlynch-like syndromeTUMORSLynch syndrome3. Good healthOncology030220 oncology & carcinogenesissyöpätauditColorectal NeoplasmsMutL Protein Homolog 1Lynch-like syndromeAdult3122 CancersPopulationsuolistosyövätCpG island methylator phenotypeBiologyta3111FREQUENCYMLH103 medical and health sciencesGermline mutationcolorectal carcinomaBRAF MUTATIONCOLONmedicineHumansLynchin oireyhtymäeducationneoplasmsMSIAgedRetrospective StudiesCpG Island Methylator PhenotypeMicrosatellite instabilityDNASOMATIC MUTATIONSta3122CpG Island Methylator phenotypemedicine.diseaseColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasesCOPY NUMBERMutationCancer researchInternational Journal of Cancer
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Inhibition of human immunodeficiency virus-1 infection by human conglutinin-like protein: in vitro studies.

1992

The lectin-like protein analogous to bovine conglutinin was purified from human serum. The carbohydrate-binding ability of conglutinin-like protein was inhibited by D-mannose, N-acetylglucosamine and L-fucose as well as by mannan-containing oligosaccharides. By applying a lectin-based ELISA system it was demonstrated that conglutinin-like protein binds to human immunodeficiency virus-1 (HIV-1) glycoprotein 120 (gp120) via its carbohydrate binding site. In vitro experiments with T-lymphoblastoid CEM cells revealed that conglutinin-like protein abolishes infection by HIV-1; a 50% cytoprotective concentration of 23.9 micrograms/ml was measured. These findings demonstrate that human conglutinin…

Cancer ResearchMolecular Sequence DataCarbohydratesImmunoglobulinsEnzyme-Linked Immunosorbent AssayHIV Envelope Protein gp120Mannose-Binding LectinVirusChromatography AffinityArticleViral ProteinsConglutininProtein A/GHumansImmunoconglutininsBinding siteKey wordsConglutinin‐like proteinchemistry.chemical_classificationAcquired Immunodeficiency SyndromebiologyHIV‐1Immunization PassiveLectinMolecular biologyMannanIn vitrogp120OncologychemistryCarbohydrate Sequencebiology.proteinHIV-1Protein GGlycoproteinCarrier ProteinsLectinJapanese journal of cancer research : Gann
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The diagnostic plot: a concept for identifying different states of iron deficiency and monitoring the response to epoetin therapy.

2005

Iron balance is regulated by the rate of erythropoiesis and the size of the iron stores. Anemia that accompanies infection, inflammation, and cancer (anemia of chronic disease) features normal or increased iron stores, although patients may have functional iron deficiency, namely, an imbalance between iron requirements of the erythroid marrow and the actual supply. The proportion of hypochromic red cells and the hemoglobin content of reticulocytes are direct indicators of functional iron deficiency. Biochemical markers, especially the soluble transferrin receptor/log ferritin ratio (ferritin index), are useful indicators of the iron supply to erythropoiesis. The relationship between functio…

Cancer Researchmedicine.medical_specialtyAnemiaIronInternal medicinemedicineHumansErythropoiesisErythropoietinSoluble transferrin receptorbiologyAnemia Iron-Deficiencybusiness.industryEpoetin alfaHematologyGeneral MedicineIron deficiencyIron Deficienciesmedicine.diseaseRecombinant ProteinsFerritinEpoetin AlfaEndocrinologyOncologyImmunologybiology.proteinErythropoiesisHemoglobinbusinessBiomarkersAnemia of chronic diseasemedicine.drugMedical oncology (Northwood, London, England)
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Impact of Different Selection Approaches for Identifying Lynch Syndrome-Related Colorectal Cancer Patients: Unity Is Strength

2022

Lynch syndrome (LS) is an inherited genetic condition associated with increased predisposition to colorectal cancer (CRC) and other tumors and is caused by germline mutations in Mismatch Repair (MMR) or EPCAM genes. The identification of LS carriers is currently based on germline testing of subjects with MMR-deficient (dMMR) tumors or fulfilling clinical criteria, but the most efficient strategies to select patients who should be offered genetic testing are yet not well defined. In order to assess the most suitable selection mode to identify LS-related CRC patients, we retrospectively collected and analyzed all clinical and molecular information of 854 CRC patients, recruited from 2013 to 2…

Cancer Researchmismatch repair genesSettore MED/06 - Oncologia MedicaMMR-deficiency[SDV]Life Sciences [q-bio]MLH1Neoplasms. Tumors. Oncology. Including cancer and carcinogenscolorectal cancerdigestive system diseasesMSH2Lynch syndromeOncologygermline mutationsmicrosatellite instabilityRC254-282Frontiers in Oncology
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