Search results for "Progress"

showing 10 items of 1620 documents

Impact of infectious burden on progression of carotid atherosclerosis.

2002

Background and Purpose— Recent findings suggest a causative role of infections in the pathogenesis of atherosclerosis. The extent of atherosclerosis and the prognosis of patients with atherosclerosis seem to be increased by the number of infections to which an individual has been exposed. In a prospective study, we evaluated the effect of 8 pathogens and the aggregate pathogen burden on the progression of carotid atherosclerosis. Methods— In 504 patients (74.9% men; age, 62.9±10 years), we measured intima-media thickness and prevalence of carotid artery stenosis. Follow-up measurements after a mean of 2.5 years were available in 427 patients (85%). Blood samples were taken, and IgG or IgA …

Carotid Artery DiseasesMalemedicine.medical_specialtyMycoplasma pneumoniaePathologyEpstein-Barr Virus InfectionsStatinHaemophilus Infectionsmedicine.drug_classComorbiditymedicine.disease_causeAntibodies ViralInfectionsGastroenterologyVirusHelicobacter InfectionsSeroepidemiologic StudiesInternal medicineGermanymedicineOdds RatioPrevalenceHumansMycoplasma InfectionsProspective StudiesProspective cohort studyChlamydophila InfectionsUltrasonographyAdvanced and Specialized NursingChlamydiaVascular diseasebusiness.industryHerpes SimplexOdds ratioMiddle Agedmedicine.diseaseAntibodies BacterialImmunoglobulin AHerpes simplex virusCarotid ArteriesImmunoglobulin GCytomegalovirus InfectionsDisease ProgressionFemaleNeurology (clinical)Cardiology and Cardiovascular MedicinebusinessTunica IntimaTunica MediaStroke
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Changes in ultrasound-assessed carotid intima-media thickness and plaque with a Mediterranean diet: a substudy of the PREDIMED trial.

2014

OBJECTIVE - : The Prevención con Dieta Mediterránea (PREDIMED) trial showed that a Mediterranean diet (MedDiet) supplemented with either extra virgin olive oil or 30 g/d of mixed nuts reduced incident cardiovascular events compared with a control (low fat) diet. The mechanisms of cardiovascular protection afforded by MedDiets remain to be uncovered. We assessed the effect of both supplemented MedDiets on internal carotid intima-media thickness (ICA-IMT) and plaque height, the ultrasound features that best predict future cardiovascular events, in subjects at high cardiovascular risk. APPROACH AND RESULTS - : In a PREDIMED subcohort (n=175), plaque height and carotid IMT of 3 prespecified seg…

Carotid Artery DiseasesMalemedicine.medical_specialtyTime FactorsMediterranean dietCarotid imtDiet MediterraneanCarotid Intima-Media ThicknessPredictive Value of TestsRisk FactorsInternal medicinemedicineCarotid stenosisHumansNutsPlant OilsCarotid intima-media thicknessUltrasonography Doppler ColorOlive OilDieta mediterraneaAgedAged 80 and overChi-Square Distributionbusiness.industryUltrasoundMiddle AgedPredimedConfidence intervalPlaque AtheroscleroticSurgeryLogistic ModelsTreatment OutcomeIntima-media thicknessSpainMultivariate AnalysisCardiologycardiovascular systemDisease ProgressionLinear ModelsFemaleCardiology and Cardiovascular MedicinebusinessOlive oilCarotid Artery InternalOlive oilArteriosclerosis, thrombosis, and vascular biology
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Nonalcoholic Fatty Liver Disease, Cardiovascular Risk, and Carotid Inflammation.

2015

Nonalcoholic fatty liver disease (NAFLD) is defined by excessive triglycerides (TGs) accumulation in the liver (>5% of hepatocytes histologically) in the absence of alcohol excess. The NAFLD ranges from simple steatosis to steatohepatitis and cirrhosis. The NAFLD and nonalcoholic steatohepatitis (NASH) are now the number one cause of liver disease in Western countries. The prevalence of NAFLD is increasing but is underreported, and the epidemiology and demographic characteristics vary worldwide. The prevalence is increasing because of the rising occurrence of obesity and type 2 diabetes (T2DM); in fact, NAFLD is considered as the hepatic manifestation of metabolic syndrome (MetS). Nonalcoho…

Carotid Artery Diseasesmedicine.medical_specialtyVery low-density lipoproteinLipoproteins//purl.org/becyt/ford/3.3 [https]Risk FactorsInternal medicineNonalcoholic fatty liver diseasemedicinePrevalenceHumansInflammationAdiponectinbusiness.industryFatty liverNon Alcoholic Fatty Liver Diseasenutritional and metabolic diseasesmedicine.diseasedigestive system diseasesFatty LiverOxidative StressEndocrinologyCardiovascular DiseasesDisease Progression//purl.org/becyt/ford/3 [https]Hepatic lipaseMetabolic syndromeSteatohepatitisInsulin ResistanceCardiology and Cardiovascular MedicinebusinessBiomarkersLipoproteinAngiology
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Influence of age on osteoarthritis progression after anterior cruciate ligament transection in rats.

2013

Abstract The anterior cruciate ligament transection (ACLT) model of osteoarthritis (OA) in young rats is widely used to study the pathogenesis of OA and possible treatment approaches. As aging is a key factor in the progression of this condition, it is hypothesized that animals may vary in their responses to ACLT according to their age. The histopathological features of young (2 month-old) and middle-aged (12 month-old) rats in the presence or absence of ACLT were compared. The results indicated that moderate degradative changes can be detected in the knee joints of sham-operated middle-aged rats compared with young animals. After ACLT, cartilage degradation was significantly higher in midd…

Cartilage ArticularMalemedicine.medical_specialtyAgingAnterior cruciate ligamentOsteoarthritisBiochemistryCartilage degradationPathogenesisEndocrinologyInternal medicineSynovitisOsteoarthritisGeneticsmedicineAnimalsRats WistarMolecular BiologyCollagen Type IISynovitisbusiness.industryExperimental modelAnterior Cruciate Ligament InjuriesInterleukinCell Biologymedicine.diseaseArthritis ExperimentalSurgeryRatsmedicine.anatomical_structureEndocrinologyDisease ProgressionCytokinesProteoglycansAnalysis of varianceInflammation MediatorsbusinessExperimental gerontology
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The Odyssey of Hsp60 from Tumor Cells to Other Destinations Includes Plasma Membrane-Associated Stages and Golgi and Exosomal Protein-Trafficking Mod…

2012

BACKGROUND: In a previous work we showed for the first time that human tumor cells secrete Hsp60 via exosomes, which are considered immunologically active microvesicles involved in tumor progression. This finding raised questions concerning the route followed by Hsp60 to reach the exosomes, its location in them, and whether Hsp60 can be secreted also via other mechanisms, e.g., by the Golgi. We addressed these issues in the work presented here. PRINCIPAL FINDINGS: We found that Hsp60 localizes in the tumor cell plasma membrane, is associated with lipid rafts, and ends up in the exosomal membrane. We also found evidence that Hsp60 localizes in the Golgi apparatus and its secretion is prevent…

Cell Physiologyanimal structuresAnatomy and PhysiologyHistologylcsh:MedicineGolgi ApparatusBiologyExosomesBiochemistrysymbols.namesakeCytosolMembrane MicrodomainsDiagnostic MedicineCell Line TumorOrganelleMolecular Cell BiologyPathologyHumansSecretionlcsh:ScienceLipid raftBiologyhsp60 exosomeOrganellesMultidisciplinarylcsh:RfungiChaperonin 60Golgi apparatusMicrovesiclesCellular StructuresTransport proteinCell biologyProtein TransportMembrane proteinSubcellular OrganellesTumor progressionsymbolsCytochemistryMedicinelcsh:QMembranes and SortingExtracellular SpaceBiomarkersResearch ArticleGeneral PathologyPLoS ONE
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Modulation of Cell Cycle Components by Epigenetic and Genetic Events

2005

Cell cycle progression is monitored by surveillance mechanisms, or cell cycle checkpoints, that ensure that initiation of a later event is coupled with the completion of an early cell cycle event. Deregulated proliferation is a characteristic feature of tumor cells. Moreover, defects in many of the molecules that regulate the cell cycle have been implicated in cancer formation and progression. Key among these are p53, the retinoblastoma protein (pRb) and its related proteins, p107 and pRb2/p130, and cdk inhibitors (p15, p16, p18, p19, p21, p27), all of which act to keep the cell cycle from progressing until all repairs to damaged DNA have been completed. The pRb (pRb/p16(INK4a)/cyclin D1) a…

Cell cycle checkpointCyclin ABiologymedicine.disease_causeModels BiologicalRetinoblastoma ProteinEpigenesis GeneticCyclin-dependent kinaseNeoplasmsmedicineAnimalsHumansEpigeneticsCell ProliferationCell growthCell CycleRetinoblastoma proteinHematologyCell cycleCell biologyOncologyDisease Progressionbiology.proteinTumor Suppressor Protein p53biological phenomena cell phenomena and immunityCarcinogenesisSignal TransductionSeminars in Oncology
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Multiple sclerosis patient-derived CSF induces transcriptional changes in proliferating oligodendrocyte progenitors.

2014

Background: Cerebrospinal fluid (CSF) is in contact with brain parenchyma and ventricles, and its composition might influence the cellular physiology of oligodendrocyte progenitor cells (OPCs) thereby contributing to multiple sclerosis (MS) disease pathogenesis. Objective: To identify the transcriptional changes that distinguish the transcriptional response induced in proliferating rat OPCs upon exposure to CSF from primary progressive multiple sclerosis (PPMS) or relapsing remitting multiple sclerosis (RRMS) patients and other neurological controls. Methods: We performed gene microarray analysis of OPCs exposed to CSF from neurological controls, or definitive RRMS or PPMS disease course. R…

Cell physiologyAdultPathologymedicine.medical_specialtyTranscription GeneticGalectin 3GalectinsImmunocytochemistryBiologyArticleCerebrospinal fluidMultiple Sclerosis Relapsing-RemittingNeural Stem CellsmedicineAnimalsHumansProgenitor cellCells CulturedCell ProliferationCerebrospinal FluidMultiple sclerosisBrainHuman brainBlood ProteinsMultiple Sclerosis Chronic Progressivemedicine.diseaseMicroarray AnalysisNeural stem cellOligodendrocyteRatsUp-RegulationOligodendrogliamedicine.anatomical_structureNeurologyNeurology (clinical)Multiple sclerosis (Houndmills, Basingstoke, England)
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High anti-JCPyV serum titers coincide with high CSF cell counts in RRMS patients

2020

Background: Progressive multifocal leukoencephalopathy (PML) can in rare cases occur in natalizumab-treated patients with high serum anti-JCPyV antibodies, hypothetically due to excessive blockade of immune cell migration. Objective: Immune cell recruitment to the central nervous system (CNS) was assessed in relapsing-remitting multiple sclerosis (RRMS) patients stratified by low versus high anti-JCPyV antibody titers as indicator for PML risk. Methods: Cerebrospinal fluid (CSF) cell counts of 145 RRMS patients were quantified by flow cytometry. Generalized linear models were employed to assess influence of age, sex, disease duration, Expanded Disability Status Scale (EDSS), clinical/radiol…

CellCell Countprogressive multifocal leukoencephalopathycerebrospinal fluidMultiple sclerosis03 medical and health sciencesMultiple Sclerosis Relapsing-Remitting0302 clinical medicineNatalizumabCerebrospinal fluidmedicineHumansJCV index030304 developmental biology0303 health sciencesbiologybusiness.industryNatalizumabMultiple sclerosisProgressive multifocal leukoencephalopathyLeukoencephalopathy Progressive MultifocalJCPyVmedicine.diseaseJC VirusCSF cell countstissue-resident memory cellsBlockadeclinical activityTitermedicine.anatomical_structureNeurologyImmunologybiology.proteinNeurology (clinical)AntibodybusinessOriginal Research Papers030217 neurology & neurosurgerymedicine.drugMultiple Sclerosis Journal
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The Relationship between Gray Matter Quantitative MRI and Disability in Secondary Progressive Multiple Sclerosis

2016

Purpose: In secondary progressive Multiple Sclerosis (SPMS), global neurodegeneration as a driver of disability gains importance in comparison to focal inflammatory processes. However, clinical MRI does not visualize changes of tissue composition outside MS lesions. This quantitative MRI (qMRI) study investigated cortical and deep gray matter (GM) proton density (PD) values and T1 relaxation times to explore their potential to assess neuronal damage and its relationship to clinical disability in SPMS. Materials and Methods: 11 SPMS patients underwent quantitative T1 and PD mapping. Parameter values across the cerebral cortex and deep GM structures were compared with 11 healthy controls, and…

Central Nervous SystemMalePathologyPhysiologylcsh:MedicinePathology and Laboratory MedicineNervous SystemBrain mappingDiagnostic Radiology030218 nuclear medicine & medical imaging0302 clinical medicineThalamusMedicine and Health SciencesRelaxation TimeMedicineGray Matterlcsh:ScienceCerebrospinal FluidCerebral CortexMultidisciplinarymedicine.diagnostic_testRadiology and ImagingPhysicsPutamenNeurodegenerationBrainNeurodegenerative DiseasesMultiple Sclerosis Chronic ProgressiveMagnetic Resonance ImagingBody Fluidsmedicine.anatomical_structureNeurologyCerebral cortexPhysical SciencesFemaleAnatomyResearch ArticleAdultmedicine.medical_specialtyMultiple SclerosisImaging TechniquesImmunologyCentral nervous systemThalamusResearch and Analysis MethodsAutoimmune Diseases03 medical and health sciencesSigns and SymptomsDiagnostic MedicineIntellectual DisabilityHumansddc:610Relaxation (Physics)business.industryMultiple sclerosislcsh:RBiology and Life SciencesMagnetic resonance imagingmedicine.diseaseDemyelinating DisordersCase-Control StudiesLesionslcsh:QClinical ImmunologyClinical Medicinebusiness030217 neurology & neurosurgeryPLOS ONE
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Molecular mechanisms linking neuroinflammation and neurodegeneration in MS.

2013

Multiple sclerosis (MS) is an inflammatory demyelinating autoimmune disorder of the central nervous system (CNS) and one of the leading causes of neurological deficits and disability in young adults in western countries. Current medical treatment mainly influences disease progression via immunomodulatory or immunosuppressive actions. Indeed, MS research has been foremost focused on inflammation in the CNS, but more recent evidence suggests that chronic disability in MS is caused by neurodegeneration. Imaging studies show an early involvement of neurodegeneration as brain atrophy and gray matter lesions can be observed at disease onset. Thus, neuroprotective treatment strategies and the eluc…

Central Nervous SystemMultiple SclerosisCentral nervous systemBiologyNeuroprotectionPathogenesisAtrophyDevelopmental NeurosciencemedicineAnimalsHumansImmunologic FactorsNeuroinflammationInflammationMultiple sclerosisExperimental autoimmune encephalomyelitisNeurodegenerationmedicine.diseaseDisease Models Animalmedicine.anatomical_structureNeurologyImmunologyNerve DegenerationDisease ProgressionCytokinesNeuroscienceExperimental neurology
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