Search results for "Progression"

showing 10 items of 1251 documents

Macrophage Migration Inhibitory Factor Induces Inflammation and Predicts Spinal Progression in Ankylosing Spondylitis

2017

Objective: To investigate the role of macrophage migration inhibitory factor (MIF) in the pathogenesis of ankylosing spondylitis (AS). Methods: Patients who met the modified New York criteria for AS were recruited for the study. Healthy volunteers, rheumatoid arthritis patients, and osteoarthritis patients were included as controls. Based on the annual rate of increase in modified Stoke AS Spine Score (mSASSS), AS patients were classified as progressors or nonprogressors. MIF levels in serum and synovial fluid were quantitated by enzyme-linked immunosorbent assay. Predictors of AS progression were evaluated using logistic regression analysis. Immunohistochemical analysis of ileal tissue was…

AnkylosingAdultMaleLogistic ModelMacrophageImmunologyEnzyme-Linked Immunosorbent AssayIntramolecular OxidoreductasePredictive Value of TestMonocyteSeverity of Illness IndexCalcificationCalcification PhysiologicPaneth CellRheumatologySynovial Fluidotorhinolaryngologic diseasesImmunology and AllergySpondylitis AnkylosingPhysiologicSpondylitiMacrophage Migration-Inhibitory FactorTumor Necrosis Factor-alphaOsteoblastB-LymphocyteHistocompatibility Antigens Class IIMiddle AgedSpineAntigens Differentiation B-LymphocyteSettore MED/16 - ReumatologiaAntigenDifferentiationDisease ProgressionFemaleCase-Control StudieHuman
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Deficiency of glutathione peroxidase-1 accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice.

2007

Background— We have recently demonstrated that activity of red blood cell glutathione peroxidase-1 is inversely associated with the risk of cardiovascular events in patients with coronary artery disease. The present study analyzed the effect of glutathione peroxidase-1 deficiency on atherogenesis in the apolipoprotein E-deficient mouse. Methods and Results— Female apolipoprotein E-deficient mice with and without glutathione peroxidase-1 deficiency were placed on a Western-type diet for another 6, 12, or 24 weeks. After 24 weeks on Western-type diet, double-knockout mice (GPx-1 −/− ApoE −/− ) developed significantly more atherosclerosis than control apolipoprotein E-deficient mice. Moreover…

Apolipoprotein Emedicine.medical_specialtyGPX1AntioxidantApolipoprotein Bmedicine.medical_treatmentLipoproteinsApoptosisBlood Pressuremedicine.disease_causeNitric OxideMitochondria HeartMonocyteschemistry.chemical_compoundMiceApolipoproteins EGlutathione Peroxidase GPX1SuperoxidesInternal medicinePeroxynitrous AcidmedicineAnimalsAortaCell Proliferationchemistry.chemical_classificationMice KnockoutReactive oxygen speciesGlutathione PeroxidaseMembranesbiologyGlutathione peroxidaseGlutathioneAtherosclerosisEndocrinologyPhenotypechemistryImmunologybiology.proteinDisease ProgressionFemaleCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidation-ReductionOxidative stressArteriosclerosis, thrombosis, and vascular biology
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Immunopathogenesis of atherosclerosis: endotoxin accelerates atherosclerosis in rabbits on hypercholesterolemic diet.

2001

Background—On the basis of our concept that atherosclerosis has an immunopathological background, we tested whether activation of the innate immune system influences its progression.Methods and Results—Hypercholesterolemic (0.5% wt/wt diet) rabbits received either repeated intravenous injections of endotoxin (Escherichia colilipopolysaccharide 1.25 to 2.5 μg, once per week) or a self-limiting cutaneousStaphylococcus aureusinfection with or without a quinolone antibiotic. Measured laboratory parameters, including LDL and HDL cholesterols, were similar in the different groups of hypercholesterolemic animals. All endotoxin-treated animals developed transient episodes of fever after endotoxin a…

ArteriosclerosisInnate immunologyHypercholesterolemiaTriglycerides bloodPathogenesisCholesterol Dietarychemistry.chemical_compoundImmunityPhysiology (medical)MedicineAnimalsAortaTriglyceridesInnate immune systemCholesterolbusiness.industryDisease progressionCholesterol HDLCholesterol LDLImmunity InnateCholesterol bloodEndotoxinsDisease Models AnimalCholesterolchemistryImmunologyDisease ProgressionDiet AtherogenicFemaleStaphylococcal Skin InfectionsRabbitsCardiology and Cardiovascular MedicinebusinessCirculation
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The matricellular protein SPARC supports follicular dendritic cell networking toward Th17 responses.

2011

Abstract Lymphnode swelling during immune responses is a transient, finely regulated tissue rearrangement, accomplished with the participation of the extracellular matrix. Here we show that murine and human reactive lymph nodes express SPARC in the germinal centres. Defective follicular dendritic cell networking in SPARC-deficient mice is accompanied by a severe delay in the arrangement of germinal centres and development of humoral autoimmunity, events that are linked to Th17 development. SPARC is required for the optimal and rapid differentiation of Th17 cells, accordingly we show delayed development of experimental autoimmune encephalomyelitis whose pathogenesis involves Th17. Not only h…

Autoimmune diseases; Extracellular matrix; Germinal centre reaction; Th17 cellsEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisImmunologyCell CommunicationBiologyfollicular dendritic cellExtracellular matrixAnimals Genetically ModifiedMiceImmune systemSPARC; follicular dendritic cell; Th17Autoimmune diseasemedicinegerminal centre reactionImmunology and AllergyAnimalsHumansautoimmune diseasesOsteonectinMice KnockoutB-LymphocytesCD40Follicular dendritic cellsExperimental autoimmune encephalomyelitisMatricellular proteinGerminal centerSPARCCell Differentiationmedicine.diseaseCell biologyExtracellular MatrixImmunity HumoralMice Inbred C57BLCrosstalk (biology)Disease Models AnimalImmunologybiology.proteinDisease ProgressionTh17 CellsImmunizationMyelin-Oligodendrocyte GlycoproteinTh17autoimmune diseases; extracellular matrix; germinal centre reaction; th17 cellsDendritic Cells FollicularMyelin ProteinsJournal of autoimmunity
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High Anti-Lymphoma Activity of Bendamustine/Mitoxantrone/Rituximab (BMR) in Rituximab Pretreated Relapsed or Refractory Indolent Lymphomas. A Multice…

2006

Abstract Purpose: Bendamustine is a new anti-lymphoma agent with promising activity. Based on a preceeding phase I study the current trial explored Bendamustine in combination with Mitoxantrone and Rituximab (BMR) in patients with relapsed or refractory indolent lymphomas. Patients and Methods: Patients with relapsed or refractory symptomatic stage III/IV indolent lymphomas with or without prior treatment with Rituximab were eligible. Therapy consisted of Bendamustine 90 mg/m2 days 1+2, Mitoxantrone 10 mg/m2 day 1, Rituximab 375 mg/m2 day 8. Treatment was repeated on day 29 for a total of 4 cycles. Results: Between 04/03 and 07/04 62 patients were recruited from 24 participating institution…

BendamustineMitoxantronemedicine.medical_specialtybusiness.industryImmunologyPhases of clinical researchCell BiologyHematologymedicine.diseaseBiochemistryGastroenterologyLymphomaSurgeryLeukocytopeniaInternal medicinemedicineHairy cell leukemiaRituximabProgression-free survivalbusinessmedicine.drugBlood
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Polatuzumab vedotin as a salvage and bridging treatment in relapsed or refractory large B-cell lymphomas

2021

The antibody-drug conjugate polatuzumab vedotin (pola) has recently been approved in combination with bendamustine and rituximab (pola-BR) for patients with refractory or relapsed (r/r) large B-cell lymphoma (LBCL). To investigate the efficacy of pola-BR in a real-world setting, we retrospectively analyzed 105 patients with LBCL who were treated in 26 German centers under the national compassionate use program. Fifty-four patients received pola as a salvage treatment and 51 patients were treated with pola with the intention to bridge to chimeric antigen receptor (CAR) T-cell therapy (n = 41) or allogeneic hematopoietic cell transplantation (n = 10). Notably, patients in the salvage and brid…

BendamustineOncologymedicine.medical_specialtyCancer ResearchImmunoconjugatesMedizinSalvage therapyInternal medicineAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansProgression-free survivalRetrospective StudiesSalvage TherapyLymphoid Neoplasiabusiness.industryAntibodies MonoclonalHematologyChemotherapy regimenPolatuzumab vedotinTransplantationRegimenbacteriaRituximabbusinessmedicine.drug
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Splenic marginal zone lymphoma.

2002

Splenic marginal zone lymphoma (SMZL) is a specific low-grade small B-cell lymphoma that is incorporated in the World Health Organization classification. Characteristic features are splenomegaly, moderate lymphocytosis with villous morphology, intrasinusoidal pattern of involvement of various organs, especially bone marrow, and relative indolent course. Tumor progression with increase of blastic forms and aggressive behavior are observed in a minority of patients. Molecular and cytogenetic studies have shown heterogeneous results probably because of the lack of standardized diagnostic criteria. To date, no definitive therapy has been established. Therapeutic options include treatment absten…

BendamustinePathologymedicine.medical_specialtyLymphoma B-CellLymphocytosismedicine.medical_treatmentImmunologySplenectomyBiochemistryImmunophenotypingDiagnosis DifferentialImmunophenotypingMedicineAnimalsHumansSplenic marginal zone lymphomabusiness.industryLymphoma Non-HodgkinSplenic NeoplasmsCell BiologyHematologymedicine.diseaseLymphomaTumor progressionCytogenetic AnalysisRituximabmedicine.symptombusinessmedicine.drugBlood
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GSK-3? Can Regulate the Sensitivity of MIA-PaCa-2 Pancreatic and MCF-7 Breast Cancer Cells to Chemotherapeutic Drugs, Targeted Therapeutics and Nutra…

2021

Glycogen synthase kinase-3 (GSK-3) is a regulator of signaling pathways. KRas is frequently mutated in pancreatic cancers. The growth of certain pancreatic cancers is KRas-dependent and can be suppressed by GSK-3 inhibitors, documenting a link between KRas and GSK-3. To further elucidate the roles of GSK-3β in drug-resistance, we transfected KRas-dependent MIA-PaCa-2 pancreatic cells with wild-type (WT) and kinase-dead (KD) forms of GSK-3β. Transfection of MIA-PaCa-2 cells with WT-GSK-3β increased their resistance to various chemotherapeutic drugs and certain small molecule inhibitors. Transfection of cells with KD-GSK-3β often increased therapeutic sensitivity. An exception was observed wi…

Berberineendocrine system diseasesmedicine.medical_treatmentRegulatormedicine.disease_causeDeoxycytidinePiperazinesTargeted therapychemotherapeutic drugsTargeted therapyNitrophenolsBreast cancerGSK-3BGlycolysisMolecular Targeted TherapyNeoplasm Metastasistargeted therapy;lcsh:QH301-705.5Tumor Stem Cell AssaySulfonamidesTumorbiologyChemistryGeneral MedicineTransfectionMetforminDisease ProgressionMCF-7 CellsFemaleKRASNutraceuticalsFluorouracilSignal transductionGlycolysisSignal TransductionBCL2bcl-X ProteinAntineoplastic AgentsBreast Neoplasmsmacromolecular substancesAdenocarcinomaArticleCell LineInhibitory Concentration 50Cell Line TumorThiadiazolesmedicineDiabetes MellitusKRasHumansGlycogen synthaseProtein Kinase InhibitorsCell ProliferationChemotherapeu-tic drugsGlycogen Synthase Kinase 3 betaGSK-3βAdenylate KinaseBiphenyl Compoundsnutraceuticals;PDACβ-cateninGemcitabine?-cateninMalariaPancreatic Neoplasmslcsh:Biology (General)MCF-7DoxorubicinDietary SupplementsCancer researchbiology.protein
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The potential use of biomarkers as an adjunctive tool for staging bipolar disorder

2009

Recent data show that biomarkers differ in early and late-stage bipolar disorder (BD). Here we propose a model of staging for bipolar disorder that emphasizes the potential use of biomarkers for differentiating early and late-stage BD patients in the inter-episodic period. The proposed model includes a Latent phase: patients at "ultra-high-risk" for developing BD, characterized by a family history of BD, temperament traits, mood, and anxiety symptoms as well as genetic vulnerability for developing the disorder; Stage I: patients who return to their baseline level of functioning when mood episodes resolve; Stage II: biomarkers and functioning impairment are related to comorbidities or rapid-…

Bipolar Disordermedia_common.quotation_subjectAnxietyModels BiologicalRisk FactorsmedicineHumansNerve Growth FactorsBipolar disorderFamily historyTemperamentBiological Psychiatrymedia_commonPharmacologyCognitive disorderCognitionmedicine.diseaseAffectMoodDisease ProgressionCytokinesAnxietyTemperamentmedicine.symptomCognition DisordersPsychologyManiaBiomarkersClinical psychologyProgress in Neuro-Psychopharmacology and Biological Psychiatry
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Persistence of the effect of birth size on dysglycaemia and type 2 diabetes in old age: AGES-Reykjavik Study

2012

We studied the effect of birth size on glucose and insulin metabolism among old non-diabetic individuals. We also explored the combined effect of birth size and midlife body mass index (BMI) on type 2 diabetes in old age. Our study comprised 1,682 Icelanders whose birth records included anthropometrical data. The same individuals had participated in the prospective population-based Reykjavik Study, where BMI was assessed at a mean age of 47 years, and in the AGES-Reykjavik Study during 2002 to 2006, where fasting glucose, insulin and HbA₁c were measured and homeostasis model assessment for the degree of insulin resistance (HOMA-IR) calculated at a mean age of 75.5 years. Type 2 diabetes was…

Blood GlucoseMaleAgingmedicine.medical_specialtyPediatricsBirth weightPopulationIcelandType 2 diabetesWeight GainArticleBody Mass IndexInsulin resistanceDiabetes mellitusInternal medicinemedicineBirth WeightHumansInsulinsyntymäpainoProspective StudieseducationAgedAged 80 and overGlucose tolerance testeducation.field_of_studydiabetesmedicine.diagnostic_testbusiness.industryIncidenceagingGeneral MedicineGlucose Tolerance TestMiddle Agedmedicine.diseaseLow birth weightikääntyminenEndocrinologyDiabetes Mellitus Type 2Population SurveillanceDisease ProgressionFemaleInsulin ResistanceGeriatrics and Gerontologymedicine.symptombusinessBody mass indexbirth sizeFollow-Up StudiesAGE
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