Search results for "PATHOGEN"

showing 10 items of 1657 documents

Chemical heterogeneity of amyloid in the carpal tunnel syndrome

1987

140 biopsies from 108 patients afflicted with the carpal tunnel syndrome were studied, 27 of whom showed deposition of amyloid, in 6 of them to such an extent that the amyloid was considered significant in the pathogenesis of the carpal tunnel syndrome. Morphologically, vessels and ligaments were affected and especially the peritendinous structures. As it was always part of generalized amyloidosis, the amyloid in the carpal tunnel consisted immunohistologically of amyloid A in three cases (including one case with simultaneous amyloid deposition of the AA- and the AB-type), of amyloid A kappa in one case, of amyloid of prealbumin origin in seventeen cases and of AB-amyloid in eight cases. We…

musculoskeletal diseasesAmyloidPathologymedicine.medical_specialtyAmyloidBiopsyPathology and Forensic MedicinePathogenesismental disordersHumansMedicineCarpal tunnelSerum amyloid ACarpal tunnel syndromeMolecular BiologyRetrospective StudiesSerum Amyloid A ProteinImmunoperoxidasebiologyHistocytochemistrybusiness.industryAmyloidosisAmyloidosisCell BiologyGeneral Medicinemusculoskeletal systemmedicine.diseaseCarpal Tunnel SyndromeImmunohistochemistrybody regionsTransthyretinmedicine.anatomical_structurebiology.proteinbusinessVirchows Archiv A Pathological Anatomy and Histopathology
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Tumour necrosis factor   in rheumatoid arthritis and osteoarthritis patients in blood serum and synovial fluid

2010

Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown cause which affects the ability of elderly people to work. There is strong evidence to suggest that inflammatory mediators such as tumour necrosis factor α (TNFα) and interleukin 1 (IL1) have a critical role in the pathogenesis of RA. Biological treatment blocks pathological pathways in the actions of these proinflammatory cytokines. The aim of this study was …

musculoskeletal diseasesAutoimmune diseasebusiness.industryImmunologyInterleukinmedicine.diseaseGeneral Biochemistry Genetics and Molecular BiologyProinflammatory cytokinePathogenesisBlood serumRheumatologyRheumatoid arthritisImmunologymedicineImmunology and AllergySynovial fluidTumor necrosis factor alphabusinessAnnals of the Rheumatic Diseases
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Targeting of the transcription factor STAT4 by antisense phosphorothioate oligonucleotides suppresses collagen-induced arthritis

2007

Abstract The transcription factor STAT4 mediates signals of various proinflammatory cytokines, such as IL-12, IL-15, and IL-23, that initiate and stabilize Th1 cytokine production. Although Th1 cytokine production has been suggested to play a major pathogenic role in rheumatoid arthritis, the role of STAT4 in this disease is poorly understood. In this study, we demonstrate a key functional role of STAT4 in murine collagen-induced arthritis (CIA). In initial studies we found that STAT4 expression is strongly induced in CD4+ T cells and to a lesser extent in CD11b+ APCs during CIA. To analyze the role of STAT4 for arthritis manifestation, we next investigated the outcome of interfering with S…

musculoskeletal diseasesImmunologyAntigen-Presenting CellsCodon InitiatorArthritisBiologyProinflammatory cytokineArthritis RheumatoidPathogenesisMiceimmune system diseasesmedicineAnimalsImmunology and Allergyskin and connective tissue diseasesSTAT4Cells CulturedMice KnockoutMice Inbred BALB CCD11b Antigenhemic and immune systemsOligonucleotides AntisenseSTAT4 Transcription FactorTh1 CellsThionucleotidesmedicine.diseaseArthritis ExperimentalIntegrin alpha MRheumatoid arthritisImmunologybiology.proteinExperimental pathologyTumor necrosis factor alpha
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The craniovertebral junction in rheumatoid arthritis: State of the art

2019

Rheumatoid arthritis (RA) is a chronic inflammatory disorder, characterized by polyarticular inflammation causing progressive joint damage and disability. The mechanisms underlying its pathogenesis involve activation of innate and adaptive immunity, microvascular endothelial cell activation, and inflammatory infiltration of lymphocytes and monocytes into the synovium. Spinal involvement in RA is not typical; when it occurs, the main radiological features are (1) atlantoaxial subluxation (AAS), which is the most typical form of cervical spine involvement; (2) cranial settling—also known as basilar impression, atlantoaxial impaction or superior migration of the odontoid—which is the most seve…

musculoskeletal diseasesJoint InstabilityPathologymedicine.medical_specialtyBasilar invaginationTransoral decompressionInflammation030218 nuclear medicine & medical imagingPathogenesisArthritis Rheumatoid03 medical and health sciences0302 clinical medicineImmune systemSynovitisCervical spinemedicineRheumatoid arthritiTransnasal decompressionAtlantoaxial instabilitySubluxationInflammationSkull Basebusiness.industrySettore MED/27 - NeurochirurgiaInstrumentation and fusion procedureCraniovertebral junctionmedicine.diseaseAcquired immune systemAtlantoaxial dislocationAtlanto-Axial JointAtlantoaxial instabilityRheumatoid arthritisCervical Vertebraemedicine.symptombusinessAtlantoaxial synoviti030217 neurology & neurosurgeryHuman
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Intestinal dysbiosis and hormonal neuroendocrine secretion in the fibromyalgic patient

2018

Fibromyalgia is a rheumatic syndrome and its pathogenesis is controversial. The recent literature has placed considerable attention on the link between alteration of the intestinal microbiota and fibromyalgia, emphasizing the close connection between the neuroenteric system and the CNS. This study aims to evaluate the probable relationship between intestinal dysbiosis and altered secretion of hormones and vitamins such as cortisol, serotonin, Vitamin D and thyroid hormones in a patient with fibromyalgia.

musculoskeletal diseasesPhysiologylcsh:MedicineIntestinal dysbiosiscortisolGeneral Biochemistry Genetics and Molecular BiologyPathogenesis03 medical and health sciences0302 clinical medicineFibromyalgiaVitamin D and neurologymicrobiotaMedicineSecretion030203 arthritis & rheumatologyhormonesbusiness.industrylcsh:Rvitamin ddysbiosismedicine.diseasehumanitiesserotoninfibromyalgiaSerotoninbusinessDysbiosis030217 neurology & neurosurgeryHormoneBiomedical Papers
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Interleukin 1 Gene Polymorphisms Presumably Participate in the Pathogenesis of Chronic Spontaneous Autocreative Urticaria

2020

Recent studies underline a potential role of autoimmune and genetic disturbances in this disorder pathogenesis. Variants in genes related to inflammatory processes may possibly predispose to chronic spontaneous urticaria (CSU) occurrence. The objective of this study was to search for an association of Il1 genes polymorphisms with the pathogenesis of CSU. The examined group consisted of 153 unrelated chronic spontaneous autoreactive urticaria patients. The control group consisted of 104 unrelated healthy volunteers. In all studied subjects, IL1 rs1304037 and rs180058 polymorphisms were examined. The Urticaria Activity Score was used to assess disease intensity. The age of disease onset was a…

musculoskeletal diseasesbusiness.industryImmunologyHaplotypeInterleukinCell BiologyDiseaseinterleukin 1chronic urticariapolymorphismPathogenesis030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicineVirologyImmunologyGenotypeMedicineAllelebusinessGeneChronic urticaria030215 immunologyJournal of Interferon and Cytokine Research
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Pathogenesis of polymyalgia rheumatica

2018

Polymyalgia rheumatica (PMR) is a chronic, inflammatory disorder of unknown cause, almost exclusively occurring in people aged over 50 and often associated with giant cell arteritis. The evidence that PMR occurs almost exclusively in individuals aged over 50 may indicate that age-related immune alterations in genetically predisposed subjects contribute to development of the disease. Several infectious agents have been investigated as possible triggers of PMR even though the results are inconclusive. Activation of the innate and adaptive immune systems has been proved in PMR patients as demonstrated by the activation of dendritic cells and monocytes/macrophages and the altered balance betwee…

musculoskeletal diseaseslcsh:Internal medicineGiant Cell ArteritisAdaptive immunityeducationlcsh:MedicineDiseaseT-Lymphocytes RegulatoryPathogenesisPolymyalgia rheumatica03 medical and health sciences0302 clinical medicineImmune systemRheumatologyPathogenesiHumansMedicinelcsh:RC31-1245Giant Cell ArteritiB cellAgedInnate immunity030203 arthritis & rheumatologyB-LymphocytesEvidence-Based MedicineInnate immune systembusiness.industrylcsh:RPolymyalgia rheumaticaB-LymphocyteCell DifferentiationBiomarkerPathogenesis.medicine.diseaseAcquired immune systemImmunity InnateSettore MED/16 - ReumatologiaGiant cell arteritismedicine.anatomical_structure030220 oncology & carcinogenesisImmunologyTh17 CellsbusinessBiomarkersHumanReumatismo
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Treatment with a CO-releasing molecule (CORM-3) reduces joint inflammation and erosion in murine collagen-induced arthritis.

2008

Contains fulltext : 70589.pdf (Publisher’s version ) (Closed access) OBJECTIVE: CO-releasing molecules (CO-RMs) are a novel class of anti-inflammatory agents. We have examined the possible therapeutic effects of CORM-3 in collagen-induced arthritis (CIA). METHODS: Arthritis was induced in DBA-1/J mice by type II collagen. Animals were treated with CORM-3 (5 and 10 mg/kg/day, intraperitoneally) or the inactive compound iCORM-3 (10 mg/kg/day, intraperitoneally) unable to release CO, from days 22 to 31. Production of anti-type II collagen antibodies, cytokines and cartilage olimeric matrix protein (COMP) was evaluated by enzyme-linked immunosorbent assay, and prostaglandin E(2) (PGE(2)) by rad…

musculoskeletal diseasesmedicine.medical_treatmentImmunologyAnti-Inflammatory AgentsDrug Evaluation PreclinicalType II collagenArthritisInflammationPharmacologyAuto-immunity transplantation and immunotherapy [N4i 4]DinoprostoneGeneral Biochemistry Genetics and Molecular BiologyMiceRheumatologyOrganometallic CompoundsPerception and Action [DCN 1]medicineAnimalsImmunology and AllergyChronic inflammation and autoimmunity [UMCN 4.2]Dose-Response Relationship Drugbiologybusiness.industryRANK LigandInterleukinIntercellular Adhesion Molecule-1medicine.diseaseArthritis ExperimentalPathogenesis and modulation of inflammation [N4i 1]Cellular infiltrationCyclooxygenase 2Mice Inbred DBARANKLImmunologybiology.proteinCytokinesTumor necrosis factor alphaMicrobial pathogenesis and host defense [UMCN 4.1]Inflammation Mediatorsmedicine.symptombusinessInfection and autoimmunity [NCMLS 1]Heme Oxygenase-1Immunity infection and tissue repair [NCMLS 1]Prostaglandin E
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Methylprednisolone-induced hepatotoxicity in a 16-year-old girl with multiple sclerosis.

2018

Multiple sclerosis (MS) is a chronic inflammatory disease with demyelination of the central nervous system. High-dosage corticosteroids are the first-line therapy in the acute relapsing of MS. We report a case of severe high-dose methylprednisolone-induced acute hepatitis in a patient with a new diagnosis of MS. A 16-year-old girl was admitted for urticaria, angioedema, nausea and vomiting a month later she had been diagnosed with MS and treated with high-dosage methylprednisolone. Laboratory investigations showed hepatic insufficiency with grossly elevated liver enzymes. A liver biopsy showed focal centrilobular hepatocyte necrosis with interface hepatitis. Methylprednisolone-induced hepat…

paediatrics (drugs And Medicines)safetymedicine.medical_specialtyMultiple SclerosisAdolescentNauseaAnti-Inflammatory AgentsGastroenterologyMethylprednisoloneDiagnosis Differential03 medical and health sciencesLiver disease0302 clinical medicineInternal medicinemedicineHumansunwanted effects/adverse reactionsGlucocorticoidsmedicine.diagnostic_testAngioedemabusiness.industryMultiple sclerosisGeneral Medicinemedicine.diseaseMethylprednisolonePulse Therapy DrugLiver biopsyVomitingSettore MED/26 - Neurologia030211 gastroenterology & hepatologyFemaleDifferential diagnosismedicine.symptomChemical and Drug Induced Liver Injuryliver diseasebusiness030217 neurology & neurosurgerymedicine.drugFindings That Shed New Light on the Possible Pathogenesis of a Disease or an Adverse EffectBMJ case reports
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Evolutionary Dynamics of Pathoadaptation Revealed by Three Independent Acquisitions of the VirB/D4 Type IV Secretion System in Bartonella

2017

The α-proteobacterial genus Bartonella comprises a group of ubiquitous mammalian pathogens that are studied as a model for the evolution of bacterial pathogenesis. Vast abundance of two particular phylogenetic lineages of Bartonella had been linked to enhanced host adaptability enabled by lineage-specific acquisition of a VirB/D4 type IV secretion system (T4SS) and parallel evolution of complex effector repertoires. However, the limited availability of genome sequences from one of those lineages as well as other, remote branches of Bartonella has so far hampered comprehensive understanding of how the VirB/D4 T4SS and its effectors called Beps have shaped Bartonella evolution. Here, we repor…

parallel evolution0301 basic medicineBartonellaAMPylation; bacterial effector; filamentation induced by cAMP; parallel evolutionVirulence FactorsIn silico030106 microbiologyBiologyfilamentation induced by cAMPGenomeEvolution MolecularType IV Secretion Systems03 medical and health sciencesBacterial ProteinsBartonella InfectionsGeneticsAMPylationHumansEvolutionary dynamicsBacterial Secretion SystemsPhylogenyEcology Evolution Behavior and SystematicsPhylogenetic treeEffectorbiology.organism_classificationbacterial effectorVirology030104 developmental biologyEvolutionary biologyFilamentation induced by cAMP; AMPylation; Parallel evolution; Bacterial effectorHost-Pathogen InteractionsParallel evolutionAdaptationBartonellaResearch Article
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