Search results for "type 1"

showing 10 items of 540 documents

Hypertrophic agonists induce the binding of c-Fos to an AP-1 site in cardiac myocytes: implications for the expression of GLUT1

2003

Objectives: Serum is among the agents known to induce hypertrophy of cardiac myocytes, which occurs concomitant with an increase in AP-1-mediated transcription. We have examined if this effect correlates with changes in the relative abundance of particular AP-1 heterodimers, as their exact composition under these conditions is unknown. Furthermore, we obtained insight on the specific role of c-Fos from studying the induction of the glucose transporter GLUT1 by serum in fibroblasts. Methods: We characterised the AP-1 heterodimers expressed in neonatal cardiac myocytes by supershift electrophoretic mobility shift assay (EMSA) analysis. Quantitative changes in transcription were measured using…

Monosaccharide Transport ProteinsTranscription GeneticMAP Kinase Signaling SystemPyridinesPhysiologyJUNBBlotting WesternElectrophoretic Mobility Shift Assayc-FosCell LineMicePhysiology (medical)Gene expressionAnimalsMyocyteMyocytes CardiacElectrophoretic mobility shift assayCells CulturedFlavonoidsGlucose Transporter Type 1biologyImidazolesGlucose transporterFibroblastsMolecular biologyRatsEnzyme ActivationTranscription Factor AP-1Animals Newbornbiology.proteinGLUT1Mitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-fosGene DeletionProtein BindingFOSBCardiovascular Research
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Role of apoptosis in autoimmunity.

2004

Autoimmune diseases are characterized by the activity of autoreactive lymphocytes that produce antibodies targeting self tissue or organ for destruction. Although the pathogenesis of these diseases is poorly understood, during the past two decades basic research has indicated apoptosis as the pivotal molecular mechanism leading to autoimmunity. Recently cytokines have been invoked in the regulation of the apoptosis-related factors and death receptors in autoimmune target destruction. These research advances have contributed to the identification of mechanisms controlling autoimmunity for defining novel therapeutic strategies.

Multiple SclerosisbiologyImmunologyThyroiditis AutoimmuneApoptosisAutoimmunitymedicine.disease_causeapoptosiGraves DiseaseAutoimmunityAutoimmune DiseasesPathogenesisDiabetes Mellitus Type 1Basic researchApoptosisImmunologybiology.proteinMolecular mechanismmedicineImmunology and AllergyDeath ReceptorsAnimalsHumansAntibodyJournal of clinical immunology
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Vascular complications following bladder drained, simultaneous pancreas-kidney transplantation: the University of Miami experience

2000

Vascular complications remain a significant nonimmunologic source of pancreas allograft loss. From February 1993 through January 1998, we performed 98 simultaneous pancreas-kidney transplantations (SPK) using pancreatic exocrine bladder drainage in patients with type 1 insulin-dependent diabetes mellitus and end-stage renal disease. They originally received quadruple immunosuppression, and since May 1997 triple immunosuppression protocol (tacrolimus, mycophenolate mofetil, and steroids). The patients' mean age was 37 years (range 24-53 years), including 50 women and 48 men with a mean follow-up of 42 months. The overall rate of vascular complications was 6% (5 patients). The vascular compli…

NephrologyAdultMalemedicine.medical_specialtyTime FactorsUrinary BladderArteriovenous fistulaHospitals UniversityPseudoaneurysmMesenteric VeinsPostoperative ComplicationsMesenteric Artery Superiormedicine.arteryInternal medicinemedicineHumansDiabetic NephropathiesSuperior mesenteric arteryVascular DiseasesSuperior mesenteric veinRetrospective StudiesVenous ThrombosisTransplantationbusiness.industryAnticoagulantsMiddle Agedmedicine.diseaseThrombosisKidney TransplantationSurgerymedicine.anatomical_structureDiabetes Mellitus Type 1Splenic veinFloridaKidney Failure ChronicDrug Therapy CombinationFemalePancreas TransplantationPancreasbusinessAneurysm FalseImmunosuppressive AgentsSpleenTransplant International
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Tubular markers do not predict the decline in glomerular filtration rate in type 1 diabetic patients with overt nephropathy.

2011

Recent studies have shown that both glomerular and tubulointerstitial damage are important factors in the pathophysiology and progression of diabetic nephropathy. To examine whether markers of tubular damage are useful in monitoring the progression of disease, we measured urinary levels of neutrophil gelatinase-associated lipocalin (NGAL), liver-fatty acid-binding protein (LFABP), and kidney injury molecule-1 (KIM-1) in a 3-year intervention study of 63 type 1 diabetic patients with kidney disease. The baseline mean glomerular filtration rate (GFR) was 87 ml/min per 1.73 m(2) and urinary albumin excretion 1141 mg/24 h. Patients with the highest compared with the lowest quartile of urinary N…

NephrologyAdultMalemedicine.medical_specialtyUrinary systemUrologyRenal functiontubule cellsFatty Acid-Binding ProteinsLosartanDiabetic nephropathyLipocalin-2Internal medicineDiabetes mellitusProto-Oncogene ProteinsMedicineHumansDiabetic NephropathiesHepatitis A Virus Cellular Receptor 1Type 1 diabetesKidneyMembrane Glycoproteinsbusiness.industrydiabetic nephropathyMiddle Agedmedicine.diseaseLipocalinsEndocrinologymedicine.anatomical_structureDiabetes Mellitus Type 1Nephrologydiabetes mellitusReceptors VirusFemalebusinessBiomarkersKidney diseaseAcute-Phase ProteinsGlomerular Filtration RateKidney international
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Type A competitiveness traits correlate with downregulation of c-Fos expression in patients with type 1 diabetes.

2019

International audience; AimType A personality has been associated with increased survival in people with type 1 diabetes (T1D). Systemic low-grade inflammation may play a critical role, as suggested in recent reports, although the links between the inflammatory circulating transcriptome and Type A remain unknown. This prompted our exploration of the potential associations between Type A personality and c-Fos gene expression, a candidate gene closely linked to inflammatory processes, in T1D.MethodsType A personality was assessed by Bortner questionnaire in patients with T1D, and two subscales – ‘speed’ and ‘competitiveness’ – were used to measure these specific dimensions of Type A. Expressi…

OncologyAdultMalemedicine.medical_specialtyCandidate geneInverse AssociationCompetitive BehaviorEndocrinology Diabetes and MetabolismDown-RegulationGene Expression030209 endocrinology & metabolismPilot Projects030204 cardiovascular system & hematologyType ATranscriptomeCohort Studies03 medical and health sciencesddc:616.890302 clinical medicineEndocrinologyInternal medicineGene expressionInternal MedicinemedicineHumansGene[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismInflammationType 1 diabetesc-FosBlood Cellsbusiness.industryGene Expression ProfilingDiabetesType A and Type B personality theoryType A PersonalityGeneral Medicine[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismMiddle Agedmedicine.diseaseCompetitivenessDiabetes Mellitus Type 1businessBody mass indexProto-Oncogene Proteins c-fosDiabetic AngiopathiesPersonalityDiabetesmetabolism
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Breast-cancer predisposition in multiple endocrine neoplasia type 1

2014

Women with multiple endocrine neoplasia type 1 related to mutations in the gene encoding menin (MEN1) have approximately twice the risk of breast cancer as do women in the general population.

OncologyAdultRiskcongenital hereditary and neonatal diseases and abnormalitiesendocrine systemmedicine.medical_specialtyendocrine system diseasesGenotypePopulationVascular damage Radboud Institute for Health Sciences [Radboudumc 16]Breast Neoplasmsmedicine.disease_causeArticleBreast cancerSDG 3 - Good Health and Well-beingInternal medicineProto-Oncogene ProteinsGenotypemedicineCarcinomaMultiple Endocrine Neoplasia Type 1HumansMEN1Genetic Predisposition to DiseaseLongitudinal StudiesMultiple endocrine neoplasiaeducationGeneralLiterature_REFERENCE(e.g.dictionariesencyclopediasglossaries)GeneNetherlandsMutationeducation.field_of_studybusiness.industryCarcinoma Ductal BreastGeneral MedicineMiddle Agedmedicine.diseaseCarcinoma PapillaryImmunologyMutationFemalebusiness
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Microregional expression of glucose transporter-1 and oxygenation status: lack of correlation in locally advanced cervical cancers.

2005

Abstract Purpose: Glucose transporter-1 (GLUT-1), a target gene of hypoxia-inducible factor-1, has been considered a candidate endogenous marker of tumor hypoxia. Expression of GLUT-1 may also serve as an indicator for the induction of the transcriptional response to hypoxia, which has been linked to enhanced proliferation, resistance to therapy, and metastatic propagation of cancer cells. Overexpression of GLUT-1 has been shown to correlate with poor prognosis in several tumor entities, among them cancers of the uterine cervix. The validity of these hypotheses is investigated. Experimental Design: The expression of GLUT-1 was assessed in 80 biopsies of Eppendorf oxygenation measurement tra…

OncologyCancer Researchmedicine.medical_specialtyPathologyMonosaccharide Transport ProteinsUterine Cervical NeoplasmsBiologyInternal medicinemedicineHumansSurvival analysisNeoplasm StagingProportional Hazards ModelsCervical cancerGlucose Transporter Type 1Tumor hypoxiaProportional hazards modelGlucose transporterHypoxia (medical)Middle Agedmedicine.diseaseImmunohistochemistrySurvival AnalysisOxygenOncologyCancer cellMultivariate AnalysisImmunohistochemistryFemalemedicine.symptomClinical cancer research : an official journal of the American Association for Cancer Research
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Higher risk of death among MEN1 patients with mutations in the JunD interacting domain: a Groupe d'etude des Tumeurs Endocrines (GTE) cohort study.

2013

International audience; Multiple endocrine neoplasia syndrome type 1 (MEN1), which is secondary to mutation of the MEN1 gene, is a rare autosomal-dominant disease that predisposes mutation carriers to endocrine tumors. Although genotype-phenotype studies have so far failed to identify any statistical correlations, some families harbor recurrent tumor patterns. The function of MENIN is unclear, but has been described through the discovery of its interacting partners. Mutations in the interacting domains of MENIN functional partners have been shown to directly alter its regulation abilities. We report on a cohort of MEN1 patients from the Groupe d'étude des Tumeurs Endocrines. Patients with a…

OncologyMaleendocrine system diseasesProto-Oncogene Proteins c-jun[SDV]Life Sciences [q-bio]Diseasemedicine.disease_causeMESH: Protein Structure Tertiary0302 clinical medicineRisk FactorsMESH: Risk FactorsMESH : FemaleGenetics (clinical)MutationGeneral MedicineMESH: Follow-Up StudiesMESH : Risk Factors3. Good health030220 oncology & carcinogenesisCohortMESH : Proto-Oncogene ProteinsFemaleMESH : MutationMESH : Protein Structure TertiaryMESH : Proto-Oncogene Proteins c-junMESH : Multiple Endocrine Neoplasia Type 1Cohort studymedicine.medical_specialtyendocrine systemMESH: MutationGenetic counselingMESH : MaleMESH: Multiple Endocrine Neoplasia Type 1030209 endocrinology & metabolismBiology03 medical and health sciencesInternal medicineProto-Oncogene ProteinsGeneticsmedicineMultiple Endocrine Neoplasia Type 1HumansMEN1FamilyMolecular BiologyMESH: FamilyMESH: HumansMESH: Proto-Oncogene Proteins c-jun[ SDV ] Life Sciences [q-bio]Proportional hazards modelMESH : HumansCancerMESH : Follow-Up Studiesmedicine.diseaseMESH: MaleProtein Structure TertiaryMESH: Proto-Oncogene ProteinsMutationCancer researchMESH : FamilyMESH: FemaleFollow-Up Studies
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Retinal detachment with spontaneous dialysis of the ora serrata in a 13-year-old child with neurofibromatosis type 1: a case report.

2020

A 13‑year‑old child diagnosed with neurofibromatosis type 1 who on a routine control presented with rhegmatogenous retinal detachment associated to dialysis of the ora serrata in the left eye (OS). There were no clinical signs or history of contuse ocular trauma. Neurofibromatosis produces alterations in fibroblasts of the cortex of the vitreous base. This results in deficient production of the collagen fibers that anchor the vitreous base to the pars plana and the peripheral neurosensory retina. Thus, suboptimal function of the fibroblasts explains spontaneous avulsion of the vitreous base. Such avulsion in turn is related to dialysis of the ora serrata.

Pars planamedicine.medical_specialtygenetic structuresmedicine.medical_treatmentCase Reportsneurofibromatosis type 1Avulsion03 medical and health sciences0302 clinical medicinelcsh:OphthalmologyOphthalmologyfibroblastsmedicineOra serrataNeurofibromatosisDialysisRetinabusiness.industryrhegmatogenous retinal detachmentRetinal detachmentdialysis of the ora serratamedicine.diseaseeye diseasesvitreous baseOphthalmologymedicine.anatomical_structurelcsh:RE1-994030221 ophthalmology & optometrysense organsbusinessVitreous baseUlls030217 neurology & neurosurgery
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