Search results for "arteriosclerosi"

showing 10 items of 131 documents

Leukocyte flow properties, polymorphonuclear membrane fluidity, and cytosolic Ca2+ content in subjects with vascular atherosclerotic disease with and…

1996

The aim of this research was the evaluation of white blood cell (WBC) filtration, reflecting WBC flow properties, polymorphonuclear cell membrane fluidity, and cytosolic Ca 2+ content in subjects with vascular atherosclerotic disease (VAD) and in VAD subjects with noninsulin-dependent diabetes mellitus (NIDDM), in good hemodynamic balance. The authors examined WBC filtration (unfractionated, mononuclear [MN], polymorphonu clear [PMN] cells), using the St. George Filtrometer and considering, respectively, the initial relative flow rate (IRFR) and the clogging rate (CR); the PMN membrane fluidity, employing the fluorescent probe TMA-DPH and calculating the fluorescence polarization degree; a…

Malemedicine.medical_specialtyArteriosclerosisMembrane FluidityNeutrophilsHemodynamicschemistry.chemical_element030204 cardiovascular system & hematologyGranulocyteCalcium03 medical and health sciencesCytosol0302 clinical medicineWhite blood cellInternal medicineDiabetes mellitusLeukocytesmedicineMembrane fluidityHumans030212 general & internal medicineAgedbusiness.industryMiddle Agedmedicine.diseasePathophysiologyCytosolEndocrinologymedicine.anatomical_structureDiabetes Mellitus Type 2chemistryCalciumFemaleCardiology and Cardiovascular MedicinebusinessDiabetic Angiopathies
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Genetic and environmental influences on the fibrinolytic system: a twin study.

2004

SummaryThe determination of heritability is a key issue to assess the predictive power of polymorphisms for disease in clinical studies. The aim of this study was to determine the heritability of proteins and activation markers of the fibrinolytic system in a large cohort of healthy twins. Heritability was calculated as 0.76 for thrombin activatable fibrinolysis inhibitor (TAFI), 0.44 for plasminogen activator inhibitor-1 (PAI-1), and 0.43 for tissue plasminogen activator. No significant genetic influence was observed for α2-antiplasmin-plasmin-complex and D-dimer. Heritability explained by single gene polymorphisms was 25.2% for TAFI 505G>A, 31.5% for 1542C>G, and 50.0% for combinati…

Malemedicine.medical_specialtyCarboxypeptidase B2GenotypeArteriosclerosismedicine.medical_treatmentBiologyEnvironmentTissue plasminogen activatorCohort StudiesFibrin Fibrinogen Degradation ProductsInternal medicineFibrinolysisPlasminogen Activator Inhibitor 1medicineDiseases in TwinsHumansFibrinolysinGeneGeneticsalpha-2-AntiplasminPolymorphism GeneticActivator (genetics)FibrinolysisHematologyTwins MonozygoticHeritabilityTwin studyEndocrinologyPhenotypeHaplotypesHemostasisTwin Studies as TopicFemalePlasminogen activatormedicine.drugThrombosis and haemostasis
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The relationships between lipid ratios and arterial stiffness

2017

Although dyslipidemia is associated with cardiovascular disease, there are conflicting data about the role of serum lipids and their ratios in promoting arterial stiffness. The authors aimed to compare serum lipid profiles to predict arterial stiffness, which was assessed by brachial‐ankle pulse wave velocity in young Chinese men. A total of 1015 participants aged 18 to 44 years without serious comorbidities were recruited for conventional detection. Anthropometrics, brachial‐ankle pulse wave velocity, serum lipids, and other laboratory data were measured. Univariate analysis and multivariate logistic regression were performed to examine the relationship between serum lipid profiles and bra…

Malemedicine.medical_specialtySettore MED/09 - Medicina InternaLipoproteinsEndocrinology Diabetes and Metabolism030204 cardiovascular system & hematology03 medical and health sciencesVascular Stiffness0302 clinical medicineInternal medicineInternal MedicineHumansMedicine030212 general & internal medicineARTERIOSCLEROSIS - ARTERIAL STIFFNESS - LIPIDS - HYPERTENSIONSettore MED/14 - Nefrologiabusiness.industrynutritional and metabolic diseasesmedicine.diseaseLipidsSettore MED/11 - Malattie Dell'Apparato CardiovascolareSurgeryHypertensionArterial stiffnessCardiologyArterial Stiffnesslipids (amino acids peptides and proteins)Cardiology and Cardiovascular Medicinebusiness
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The organized subdural blood clot in forensic case work - a case report.

2000

The medico-legal assessment of a subdural haematoma (recent or organized) usually requires some information regarding its cause. Quite often, especially in the absence of a known history of trauma, minor head injuries, which are no longer verifiable, are simply assumed to be the most likely causes. Considering the fact that a subdural haematoma could also be non-traumatic, e.g. in haemorrhagic disorders, cardiac conditions with persistent passive hyperaemia, true inflammatory and degenerative processes of the dura, etc., the medico-legal implication of a possible head injury would require the exclusion of such non-traumatic conditions capable of causing subdural bleeding. In this respect, t…

Malemedicine.medical_specialtySubdural haematomaAutopsyPathology and Forensic MedicineHematomaFatal OutcomeCause of DeathmedicineCraniocerebral TraumaHumansCause of deathAgedAged 80 and overbusiness.industryVascular diseaseHead injuryMedical jurisprudencemedicine.diseaseIntracranial ArteriosclerosisSurgerySkullmedicine.anatomical_structureHematoma SubduralAccidental FallsAutopsybusinessLawForensic science international
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Enzymatically Degraded, Nonoxidized LDL Induces Human Vascular Smooth Muscle Cell Activation, Foam Cell Transformation, and Proliferation

2000

Background —Enzymatic, nonoxidative modification transforms LDL to an atherogenic molecule (E-LDL) that activates complement and macrophages and is present in early atherosclerotic lesions. Methods and Results —We report on the atherogenic effects of E-LDL on human vascular smooth muscle cells (SMC). E-LDL accumulated in these cells, and this was accompanied by selective induction of monocyte chemotactic protein-1 in the absence of effects on the expression of interleukin (IL)-8, RANTES, or monocyte inflammatory proteins-1α and -β). Furthermore, E-LDL stimulated the expression of gp130, the signal-transducing chain of the IL-6 receptor (IL-6R) family, and the secretion of IL-6. E-LDL invok…

Malemedicine.medical_specialtyVascular smooth muscleArteriosclerosismedicine.medical_treatmentBiologyFibroblast growth factorMuscle Smooth VascularStatistics NonparametricPhysiology (medical)Internal medicinemedicineHomeostasisHumansRNA MessengerAutocrine signallingAortaCells CulturedChemokine CCL2AgedFoam cellInterleukin-6Cell growthGrowth factorMonocyteCholesterol LDLReceptors Interleukin-6EnzymesCell biologymedicine.anatomical_structureEndocrinologyFemaleCardiology and Cardiovascular MedicineCell activationOxidation-ReductionCell DivisionFoam CellsCirculation
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Unfavourable interaction of microalbuminuria and mildly reduced creatinine clearance on aortic stiffness in essential hypertension

2010

The aim of our study was to assess the independent relationships of urinary albumin excretion rate (AER), of creatinine clearance (CrCl) and of their interaction with aortic stiffness in hypertensive patients without overt renal insufficiency. We studied 222 untreated nondiabetic essential hypertensives. In patients with reliable 24-h urine collections, AER and CrCl were determined. Microalbuminuria (MAU) was defined as an AER of 20 to 200microg/min. Aortic stiffness was assessed by measurement of carotid-femoral pulse wave velocity (c-f PWV). C-f PWV was higher in subjects with MAU than in those without it (p<0.001, even after adjustment for age, sex and mean arterial pressure) and in subj…

Mean arterial pressuremedicine.medical_specialtyRenal functionArteriosclerosiEssential hypertensionchemistry.chemical_compoundInternal medicinemedicineAlbuminuriaPulse wave velocityCreatininebusiness.industrymedicine.diseaseMild renal dysfunctionArterial stiffnePulse wave velocityEndocrinologychemistryHypertensioncardiovascular systemArterial stiffnessCardiologyMicroalbuminuriaAortic stiffnessCardiology and Cardiovascular Medicinebusiness
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Increased Arterial Augmentation and Augmentation Index as Surrogate Parameters for Arteriosclerosis in Subjects with Diabetes Mellitus and Nondiabeti…

2007

Background: Arterial augmentation (AP) and the augmentation index (Aix) are surrogate parameters of arterial stiffness and are commonly used as predictors for cardiovascular risk. The aim of this study is to compare these parameters in diabetic subjects and nondiabetic cardiovascular risk subjects with healthy control subjects. Methods: One hundred sixty-six nonsmoking subjects aged between 35 and 70 years were included in the study, which included 100 subjects with cardiovascular disease but not diabetes (mean age 62.73±8.75 years), 33 subjects with type 2 diabetes (66.58±2.69 years), and 33 healthy controls (51.89±8.91 years). In these subjects, arterial stiffness was measured by the diff…

Neurological and Microvascular Functionmedicine.medical_specialtybusiness.industryEndocrinology Diabetes and MetabolismBiomedical EngineeringCentral pressure030209 endocrinology & metabolismBioengineeringMean ageArteriosclerosisDiseaseType 2 diabetesmedicine.disease03 medical and health sciences0302 clinical medicineEndocrinologyDiabetes mellitusInternal medicineHealthy controlInternal MedicinemedicineArterial stiffnessCardiology030212 general & internal medicinebusinessJournal of Diabetes Science and Technology
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Enhanced susceptibility of cholesteryl sulfate-enriched low density lipoproteins to copper-mediated oxidation

1995

AbstractCholesteryl sulfate (CS) is a minor component of cell membranes, also present in lipoproteins, and its exact function is unknown. Since oxidation of low density lipoproteins (LDL) is thought to be an important determinant of atherogenesis, we investigated the influence of CS enrichment on copper-mediated oxidation of LDL. CS was found to act as a pro-oxidant, as measured by lipid oxidation parameters. The results also suggest that these effects were dependent on the sulfate group since pure cholesterol or cholesteryl acetate did not promote Cu2+-mediated oxidation. Our findings imply that CS may affect the oxidizability and hence the potential atherogenicity of LDL.

Oxidized LDLArteriosclerosisBiophysicschemistry.chemical_elementCholesteryl sulfateCholesteryl sulfateBiochemistryThiobarbituric Acid Reactive Substanceschemistry.chemical_compoundStructure-Activity RelationshipLipid oxidationStructural BiologyCholesterylester transfer proteinOxidationGeneticsHumansSulfateMolecular BiologyIntermediate-density lipoproteinbiologyCholesterolCell BiologyCopperLipoproteins LDLMembranechemistryBiochemistrybiology.proteinlipids (amino acids peptides and proteins)Cholesterol EstersLipid PeroxidationCopperFEBS Letters
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CD59 (homologous restriction factor 20), a plasma membrane protein that protects against complement C5b-9 attack, in human atherosclerotic lesions

1992

Blood cells express a cell membrane protein, termed homologous restriction factor 20 (HRF20) and identical to CD59, that can inhibit complement C5b-9 insertion into their membranes. In this report, we investigated by immunohistochemistry whether CD59 was present on cells in human atherosclerotic lesions since membranous C5b-9(m) has been found in lesions. Using a monoclonal anti-CD59 antibody, a cellular CD59 staining pattern was apparent in nearly all lesion specimens. CD59 stain co-localised with macrophage (CD14), T lymphocyte (CD7), endothelial cell (anti-factor VIII related antigen) and smooth muscle cell cytoskeletal-specific antigens (anti-alpha actin and muscle myosin). Endothelial …

Pathologymedicine.medical_specialtyCell typeArteriosclerosisCD59 Antigenschemical and pharmacologic phenomenaComplement Membrane Attack ComplexMyosinsBiologyAntigenAntigens CDMyosinmedicineHumansMacrophageSaphenous VeinActinComplement Inactivator ProteinsMembrane GlycoproteinsImmunohistochemistryActinsEndothelial stem cellCarotid ArteriesCD59 antigenEndothelium VascularCardiology and Cardiovascular MedicineComplement membrane attack complexAtherosclerosis
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Characteristic morphologic manifestation of CADASIL, cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy, in s…

1997

Pathologymedicine.medical_specialtyPhysiologyLeukoencephalopathyCellular and Molecular NeurosciencePhysiology (medical)medicineHumansCADASILMuscle SkeletalSkinbusiness.industryVascular diseaseLeukoencephalopathy Progressive MultifocalSkeletal muscleAnatomyCerebral InfarctionCADASIL SyndromeMiddle Agedmedicine.diseaseIntracranial ArteriosclerosisMicroscopy Electronmedicine.anatomical_structureFemaleNeurology (clinical)ComplicationbusinessMusclenerve
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