Search results for "PATHOGENESIS"

showing 10 items of 761 documents

Oxidative and nitrosative stress in acute pancreatitis. Modulation by pentoxifylline and oxypurinol

2011

Item does not contain fulltext Reactive oxygen species are considered mediators of the inflammatory response and tissue damage in acute pancreatitis. We previously found that the combined treatment with oxypurinol - as inhibitor of xanthine oxidase- and pentoxifylline - as inhibitor of TNF-alpha production-restrained local and systemic inflammatory response and decreased mortality in experimental acute pancreatitis. Our aims were (1) to determine the time-course of glutathione depletion and oxidation in necrotizing pancreatitis in rats and its modulation by oxypurinol and pentoxifylline; (2) to determine whether TNF-alpha is responsible for glutathione depletion in acute pancreatitis; and (…

MaleNitrosationOxypurinolPharmacologymedicine.disease_causeBiochemistryPentoxifyllineMicechemistry.chemical_compoundCell Line TumorAnimalsMedicinePentoxifyllineRats WistarXanthine oxidasePharmacologychemistry.chemical_classificationReactive oxygen speciesPancreatitis Acute Necrotizingbusiness.industryPathogenesis and modulation of inflammation Infection and autoimmunity [N4i 1]GlutathioneNitro Compoundsmedicine.diseaseRatsOxidative StresschemistryBiochemistryAcute pancreatitisPancreatitisDrug Therapy CombinationTumor necrosis factor alphabusinessOxidative stressmedicine.drugBiochemical Pharmacology
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Th1 and Th17 lymphocytes expressing CD161 are implicated in giant cell arteritis and polymyalgia rheumatica pathogenesis.

2012

International audience; OBJECTIVE: Giant cell arteritis (GCA) is the most frequently occurring vasculitis in elderly individuals, and its pathogenesis is not fully understood. The objective of this study was to decipher the role of the major CD4+ T cell subsets in GCA and its rheumatologic form, polymyalgia rheumatica (PMR). METHODS: A prospective study of the phenotype and the function of major CD4+ T cell subsets (Th1, Th17, and Treg cells) was performed in 34 untreated patients with GCA or PMR, in comparison with 31 healthy control subjects and with the 27 treated patients who remained after the 7 others withdrew. RESULTS: Compared with control subjects, patients with GCA and patients wi…

MalePathologyMESH: Th17 CellsCellMESH : AgedMESH : Prospective StudiesMESH: Flow CytometryT-Lymphocytes RegulatoryPathogenesisMESH : T-Lymphocytes Regulatory0302 clinical medicineimmune system diseasesMESH : Th1 CellsImmunology and Allergy[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyPharmacology (medical)MESH : FemaleProspective Studiesskin and connective tissue diseasesCells CulturedMESH: Aged0303 health sciencesMESH: Middle Agedmedicine.diagnostic_testMESH: Giant Cell ArteritisCell DifferentiationMESH : AdultMiddle AgedFlow CytometryMESH : NK Cell Lectin-Like Receptor Subfamily B3. Good healthMESH: NK Cell Lectin-Like Receptor Subfamily Bmedicine.anatomical_structure[SDV.IMM]Life Sciences [q-bio]/ImmunologyFemaleVasculitisMESH : Cell DifferentiationGlucocorticoidmedicine.drugNK Cell Lectin-Like Receptor Subfamily BMESH: Cells CulturedAdultMESH: Cell Differentiationmedicine.medical_specialty[SDV.IMM] Life Sciences [q-bio]/ImmunologyMESH : Flow CytometryT cellMESH : MaleImmunologyGiant Cell ArteritisBiologyPolymyalgia rheumatica03 medical and health sciencesRheumatologyBiopsyMESH : Cells CulturedmedicineMESH : Th17 CellsHumansMESH : Middle Aged030304 developmental biologyAged030203 arthritis & rheumatologyMESH: HumansMESH: T-Lymphocytes RegulatoryMESH : HumansMESH: AdultTh1 Cellsmedicine.diseaseMESH : Giant Cell ArteritisMESH: Prospective StudiesMESH: MaleGiant cell arteritisMESH: Th1 CellsPolymyalgia RheumaticaMESH: Polymyalgia RheumaticaImmunologyTh17 CellsMESH : Polymyalgia RheumaticaMESH: Female
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Lymphocytic Mitochondrial Aconitase Activity is Reduced in Alzheimer's Disease and Mild Cognitive Impairment

2015

Background: Specific mechanisms behind the role of oxidative/nitrosative stress and mitochondrial dysfunction in Alzheimer's disease (AD) pathogenesis remain elusive. Mitochondrial aconitase (ACO2) is a Krebs cycle enzyme sensitive to free radicalmediated damage. Objective: We assessed activity and expression of ACO2 extracted from blood lymphocytes of subjects with AD, mild cognitive impairment (MCI), older adults with normal cognition (OCN, age >= 65 years), and younger adults with normal cognition (YCN, age < 65 years). Plasma levels and activities of antioxidants were also measured. Methods: Blood samples were collected from 28 subjects with AD, 22 with MCI, 21 OCN, and 19 YCN. ACO2 act…

MalePathologyantioxidantAntioxidantmedicine.medical_treatmentLymphocyteMitochondrionmedicine.disease_causePolymerase Chain ReactionPathogenesisVitamin Eoxidative stressLymphocytesaconitase (aconitate hydratase)Aconitate Hydratasereactive oxygen speciesGeneral NeuroscienceACO2General MedicineAlzheimer's diseasemitochondriaPsychiatry and Mental healthClinical Psychologyantioxidantsmedicine.anatomical_structureDisease ProgressionSettore MED/26 - NeurologiaFemaleAlzheimer diseaseAlzheimer's diseaseAzheimer diseasereactive nitrogen speciemedicine.medical_specialtyaconitase (aconitate hydratase); Alzheimer disease; antioxidants; free radicals; lymphocyte; mild cognitive impairment; mitochondria; oxidative stress; reactive nitrogen species; reactive oxygen speciesBlotting Westernfree radicalslymphocytemild cognitive impairmentInternal medicinemedicineHumansCognitive DysfunctionRNA MessengerAgedfree radicaloxidative strebusiness.industryVitamin EAconitasimedicine.diseasereactive nitrogen speciesEndocrinologyGeriatrics and GerontologyAlzheimer's disease; Aconitasi; oxidative stress; Aconitase (aconitate hydratase) Azheimer disease antioxidants free radicals lymphocyte mild cognitive impairment mitochondria oxidative stress reactive nitrogen species reactive oxygen speciesMental Status SchedulebusinessBiomarkersOxidative stressJournal of Alzheimer's Disease
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Vascular damage and lack of angiogenesis in systemic sclerosis skin

2003

The aim of this study was to analyse microvascular damage and compensatory angiogenesis in skin from patients with systemic sclerosis (SSc) compared with systemic lupus erythematosus (SLE), Raynaud's phenomenon (RP) and healthy controls. Immunohistochemistry was used for skin biopsies (9 SSc, 10 SLE, 9 RP and 12 healthy controls) using von Willebrand factor and beta3 integrin subunit specific antibodies, TechMate immunostaining robot and biotin-streptavidin protocol. In the early stages of SSc, vWF was found in the perivascular space and interstitial matrix in papillary but not in the reticular dermis, in particular around small oedematous blood vessels infiltrated by mononuclear cells. The…

MalePathologymedicine.medical_specialtyAngiogenesisNeovascularization PhysiologicConnective tissueRisk AssessmentSeverity of Illness IndexPathogenesis03 medical and health sciences0302 clinical medicineRheumatologyInterstitial matrixVon Willebrand factorReference ValuesFibrosisvon Willebrand FactormedicineHumansLupus Erythematosus SystemicPerivascular spaceskin and connective tissue diseases030304 developmental biology030203 arthritis & rheumatology0303 health sciencesScleroderma Systemicintegumentary systembiologybusiness.industryBiopsy NeedleRaynaud DiseaseGeneral MedicinePrognosismedicine.diseaseImmunohistochemistry3. Good healthDermal papillaemedicine.anatomical_structureCase-Control Studiesbiology.proteinFemaleEndothelium VascularbusinessClinical Rheumatology
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Autoantibodies in experimental autoimmune hepatitis

1992

Experimental autoimmune hepatitis (EAH) can be induced in mice by immunization with syngeneic soluble liver antigens in complete Freund's adjuvant. It has previously been shown that autoreactive T cells play an important role in this animal model of autoimmune hepatitis. We have studied the occurrence of liver autoantibodies in EAH. Characteristic autoantibodies appeared several weeks after disease induction and antibody titres continued to rise when histological and biochemical signs of disease activity had already regressed. Autoantibodies in EAH seemed to recognize autoantigens other than those present in autoimmune chronic active hepatitis patients. We conclude that autoantibodies arise…

MalePathologymedicine.medical_specialtyBlotting WesternFluorescent Antibody TechniqueAutoimmune hepatitisHepatitis Animalmedicine.disease_causeAutoimmune DiseasesAutoimmunityPathogenesisMiceAntigenAnimalsMedicineAutoantibodiesHepatitisHepatologybiologybusiness.industryAutoantibodymedicine.diseaseMice Inbred C57BLImmunizationImmunologybiology.proteinAntibodybusinessJournal of Hepatology
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Portal Vein Thrombosis in a Preterm Newborn with Mutation of the MTHFR and PAI-1 Genes and Sepsis by Candida parapsilosis

2016

Objective This report discusses the role of both congenital and acquired risk factors in the pathogenesis of portal vein thrombosis (PVT). Study Design We describe the clinical management and treatment of PVT in a preterm newborn with a homozygous mutation of the methylenetetrahydrofolate reductase (MTHFR) and plasminogen activator inhibitor-1 (PAI-1) genes and sepsis by Candida parapsilosis. Results Although literature data suggest a minor role of genetic factors in thrombophilia in the case of only one mutation, we hypothesize that combined thrombophilic genetic defects may have a cumulative effect and significantly increase the thrombotic risk. Conclusion It could be appropriate to incl…

MalePathologymedicine.medical_specialtyCandida parapsilosis030204 cardiovascular system & hematologyBioinformaticsCandida parapsilosisThrombophiliaSepsisPathogenesis03 medical and health sciences0302 clinical medicineSepsis030225 pediatricsPlasminogen Activator Inhibitor 1medicineHumansMethylenetetrahydrofolate Reductase (NADPH2)Venous ThrombosisPolymorphism GeneticbiologyPortal Veinbusiness.industryCandidiasisInfant NewbornAnticoagulantsFactor VObstetrics and Gynecologyportal thrombosis fungal infection gene polymorphismmedicine.diseasebiology.organism_classificationPortal vein thrombosisSurgical Procedures OperativeMethylenetetrahydrofolate reductaseMutationPediatrics Perinatology and Child Healthbiology.proteinGene polymorphismbusinessPlasminogen activatorAmerican Journal of Perinatology
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NCAM (CD56) Expression in keratin-producing odontogenic cysts: aberrant expression in KCOT

2015

Background: Keratin-producing odontogenic cysts (KPOCs) are a group of cystic lesions that are often aggressive, with high rates of recurrence and multifocality. KPOCs included orthokeratinised odontogenic cyst (OOC) and parakeratotic odontogenic cysts, which are now considered true tumours denominated keratocystic odontogenic tumours (KCOTs). GLUT1 is a protein transporter that is involved in the active uptake of glucose across cell membranes and that is overexpressed in tumours in close correlation with the proliferation rate and positron emission tomography (PET) imaging results. Methods: A series of 58 keratin-producing odontogenic cysts was evaluated histologically and immunohistochemi…

MalePathologymedicine.medical_specialtyClinical NeurologyOdontogenic TumorsKeratocystsCohort StudiesPathogenesisBasal (phylogenetics)KeratinmedicineHumansCàncerNCAMReceptorNeural Cell Adhesion MoleculesGeneral DentistryRetrospective Studieschemistry.chemical_classificationRegulation of gene expressionOrthokeratinized odontogenic cystDentistry(all)business.industryResearchBiopsy NeedlePrognosisPatologiaImmunohistochemistryGene Expression Regulation NeoplasticKeratocystic odontogenic tumorLogistic Modelsnervous systemOtorhinolaryngologychemistryOdontogenic CystsKeratinsImmunohistochemistryFemaleNeural cell adhesion moleculeKeratocystic Odontogenic TumorNeurology (clinical)Neoplasm Recurrence LocalbusinessSignal TransductionHead &amp; Face Medicine
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Sporadic Parkinson disease and amyotrophic lateral sclerosis complex (Brait-Fahn-Schwartz disease).

2012

Clinical evidence for parkinsonism may accompany Amyotrophic Lateral Sclerosis with a frequency ranging from 5% to 17%. The concurrence of Amyotrophic Lateral Sclerosis and Parkinson's disease, outside the known Guam and Kii Peninsula foci, is instead rare, but this raises the possibility of a common pathogenesis. Clinically this complex presents with a levodopa-responsive parkinsonism and Amyotrophic Lateral Sclerosis and has been termed Brait-Fahn-Schwartz disease. Here we describe two patients with this uncommon neurodegenerative complex. Both presented with Parkinson disease and progressed to a full blown Amyotrophic Lateral Sclerosis. We further suggest that the association of Parkinso…

MalePathologymedicine.medical_specialtyExtrapyramidal signsbusiness.industryParkinsonismAmyotrophic Lateral SclerosisParkinson DiseaseDiseaseMiddle Agedmedicine.diseasenervous system diseasesPathogenesisNeurologyKii peninsulaClinical evidencemedicineHumansFemaleNeurology (clinical)Sporadic Parkinson diseaseAmyotrophic lateral sclerosisbusinessAgedJournal of the neurological sciences
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Pathogenesis of Paraneoplastic Follicular Hyperkeratotic Spicules in Multiple Myeloma

1990

• We describe a 62-year-old man with multiple myeloma who developed horny spicules on his face, particularly on his nose. IgG-λ monoclonal gammopathy was detected, and the serum dysprotein was shown to be a cryoglobulin, which forms a cryogel at low temperatures. Light and electron microscopic and immunohistochemical examinations showed an intercellular precipitation and massive accumulation of the IgG dysprotein and cryoglobulin between the keratinocytes of the upper epidermis and the infundibular epithelium. The follicles were dilated and filled with parakeratotic cells, the protein deposits between them and a rudimentary hair thus resulting in the clinically visible symptoms of horny spi…

MalePathologymedicine.medical_specialtyFluorescent Antibody TechniqueDermatologyBiologyPathogenesisCryoglobulinImmunoglobulin lambda-ChainsHypergammaglobulinemiamedicineHumansMultiple myelomaEpidermis (botany)KeratosisGeneral MedicineMiddle Agedmedicine.diseaseImmunohistochemistryCryoglobulinemiaEpitheliumMicroscopy Electronmedicine.anatomical_structureCryoglobulinemiaImmunoglobulin GImmunohistochemistryBody regionMultiple MyelomaFacial DermatosesHairArchives of Dermatology
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Heterozygous nonsense SCN5A mutation W822X explains a simultaneous sudden infant death syndrome.

2008

The sudden, unexpected, and unexplained death of both members of a set of healthy twins (simultaneous sudden infant death syndrome (SSIDS)) is defined as a case in which both infants meet the definition of sudden infant death syndrome individually. A search of the world medical literature resulted in only 42 reported cases of SSIDS. We report the case of a pair of identical, male, monozygotic twins, 138 days old, who suddenly died, meeting the full criteria of SSIDS and where a genetic screen was performed, resulting in a heterozygous nonsense SCN5A mutation (W822X) in both twins. Immunohistochemistry was performed on cardiac tissue samples utilizing polyclonal antibodies anti-Na+ CP type V…

MalePathologymedicine.medical_specialtyNav1.5 protein functionv1.5 protein functionmedia_common.quotation_subject2734Nonsense mutationNonsenseNa+ channel functionMuscle ProteinsSocio-culturaleBiology+Nav1.5 protein function; Na+ channel function; SCN5A gene mutation; Simultaneous sudden infant death syndrome; W822X mutation; Codon Nonsense; Diseases in Twins; Humans; Infant; Male; Muscle Proteins; NAV1.5 Voltage-Gated Sodium Channel; Sodium Channels; Sudden Infant Death; 2734Sudden deathSodium ChannelsNAV1.5 Voltage-Gated Sodium ChannelPathology and Forensic MedicinePathogenesisSCN5A gene mutationDiseases in TwinsmedicineHumansSimultaneous sudden infant death syndromeSCN5A gene mutationW822X mutationNa+ channel functionNav1.5 protein functionNaSimultaneous sudden infant death syndrome SCN5A gene mutation W822X mutation Na+ channel function Nav1.5 protein function CodonMolecular BiologyCellular localizationmedia_commonSimultaneous sudden infant death syndromeSettore BIO/16 - Anatomia UmanaSimultaneous sudden infant death syndrome SCN5A gene mutation W822X mutation Na+ channel function Nav1.5 protein functionW822X mutationInfantCell BiologyGeneral MedicineSudden infant death syndromeNonsenseTerminal deoxynucleotidyl transferaseCodon NonsenseImmunohistochemistryNa; v; 1.5 protein function; Na; +; channel function; SCN5A gene mutation; Simultaneous sudden infant death syndrome; W822X mutationchannel functionSudden Infant Death
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