Search results for "aggregation."

showing 10 items of 544 documents

Chemistry of pheromonal and defensive secretions in the nymphs and the adults ofDysdercus cingulatus Fabr. (Heteroptera, Pyrrhocoridae)

1991

59 ref.; International audience; The exocrine secretions from the nymphs and the adults of both sexes in D. cingulatus were chemically investigated. Seven compounds were identified in the anterior glands, and eleven in the median dorsoabdominal glands of nymphs and adults of both sexes. Fifty-five compounds were identified in the defensive glands (34 in posterior dorsoabdominal glands ofnymphs and 21 in metathoracic glands of adults), and six in the sternal glandular epithelium of the males. The biological function of the glandular secretions and of their identified compounds were investigated and are discussed.

PYRRHOCORIDAE0106 biological sciencesExocrine gland[SDV]Life Sciences [q-bio]ZoologyAllomoneBiology010603 evolutionary biology01 natural sciencesBiochemistryDysdercus cingulatusBUGGlandular epitheliumstomatognathic systemHETEROPTEREPHEROMONESmedicineNymphEcology Evolution Behavior and SystematicsDEFENSIVE SECRETIONSDYSDERCUS CINGULATUSPyrrhocoridaeHeteropteraHETEROPTERACHIMIEGeneral MedicineAnatomyAGGREGATIONbiology.organism_classification010602 entomologymedicine.anatomical_structureALLOMONESSex pheromoneEXOCRINE GLANDSCOTTON STAINERJournal of Chemical Ecology
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Molecular mechanisms linking amyloid β toxicity and Tau hyperphosphorylation in Alzheimer׳s disease

2015

Neurofibrillary tangles (aggregates of cytoskeletal Tau protein) and senile plaques (aggregates mainly formed by amyloid β peptide) are two landmark lesions in Alzheimer׳s disease. Some researchers have proposed tangles, whereas others have proposed plaques, as primary lesions. For a long time, these were thought of as independent mechanisms. However, experimental evidence suggests that both lesions are intimately related. We review here some molecular pathways linking amyloid β and Tau toxicities involving, among others, glycogen synthase kinase 3β, p38, Pin1, cyclin-dependent kinase 5, and regulator of calcineurin 1. Understanding amyloid β and Tau toxicities as part of a common pathophys…

Pathologymedicine.medical_specialtyAmyloid beta-PeptidesbiologyChemistryKinaseNeurodegenerationTau proteinBACE1-AStau Proteinsmedicine.diseaseProtein Aggregation PathologicalBiochemistryBiochemistry of Alzheimer's diseaseAlzheimer DiseaseGSK-3Physiology (medical)mental disordersmedicinebiology.proteinCancer researchPIN1HumansSenile plaquesPhosphorylationFree Radical Biology and Medicine
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Microvascular in vivo assessment of reperfusion injury: significance of prostaglandin E1 and I2 in postischemic “no-reflow” and “reflow-paradox”

2004

Microvascular ischemia-reperfusion (I/R) injury is characterized by failure of capillary perfusion ("no-reflow") and reoxygenation-associated phenomena ("reflow-paradox"), including activation of leukocyte-endothelium interaction with cytotoxic mediator-induced loss of endothelial integrity. The objectives of this study were to elucidate the impact of both prostaglandins E(1) (PGE(1)) and I(2) (PGI(2)) in microvascular reperfusion injury, with special focus on the distinct pathophysiology of no-reflow- and reflow-paradox phenomena.By use of the hamster dorsal skinfold preparation and in vivo fluorescence microscopy, the microcirculation of a striated skin muscle was assessed before 4 h of p…

Pathologymedicine.medical_specialtyEndotheliummedicine.medical_treatmentIschemiaPharmacologyMicrocirculationCapillary Permeabilitychemistry.chemical_compoundIn vivoCricetinaemedicineAnimalsVascular Diseasescardiovascular diseasesAlprostadilMuscle SkeletalProstaglandin E1SkinMicroscopyMesocricetusbusiness.industryMicrocirculationmedicine.diseaseEpoprostenolPathophysiologyCapillariesChemotaxis Leukocytemedicine.anatomical_structurechemistryReperfusion InjuryModels Animalcardiovascular systemSurgeryEndothelium VascularbusinessReperfusion injuryPlatelet Aggregation InhibitorsProstaglandin EJournal of Surgical Research
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C-reactive protein and efficacy of antiplatelet therapy in (intracranial) atherosclerosis

2018

C-reactive protein (CRP) and other inflammatory biomarkers can indicate both the severity and extent of atherosclerosis, reflecting the inflammatory nature of the disease process.1 Atherogenesis begins with an inflammatory response to vascular injury with cells and mediators initiating the healing response and later inducing growth of atherosclerotic plaques. Inflammation then increases plaque instability, promoting rupture, fissuring, or erosion—the pathogenetic milieu of thrombosis in atherothrombotic ischemic strokes.

Pathologymedicine.medical_specialtyInflammationConstriction PathologicDisease030204 cardiovascular system & hematology03 medical and health sciences0302 clinical medicinemedicineHumansbiologyC-reactive protein intracranial atherosclerosisbusiness.industryIschemic strokesC-reactive proteinAtherosclerosismedicine.diseaseThrombosisInflammatory biomarkersC-Reactive Proteinbiology.proteinPlatelet aggregation inhibitorNeurology (clinical)Intracranial Atherosclerosismedicine.symptombusinessPlatelet Aggregation Inhibitors030217 neurology & neurosurgeryNeurology
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156th ENMC International Workshop: desmin and protein aggregate myopathies, 9-11 November 2007, Naarden, The Netherlands.

2008

Pathologymedicine.medical_specialtyProtein aggregationBiologyDesminNeurologyMuscular DiseasesPediatrics Perinatology and Child HealthmedicineMyotilinHumansDesminNeurology (clinical)Muscle SkeletalGenetics (clinical)Neuromuscular disorders : NMD
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121st ENMC International Workshop on Desmin and Protein Aggregate Myopathies. 7–9 November 2003, Naarden, The Netherlands

2004

The 121st European Neuromuscular Centre (ENMC)sponsored International Workshop on ‘DESMIN and Protein Aggregate Myopathies’, attended by 16 active participants from France, Germany, Poland, Spain, Sweden, the United Kingdom and the USA, was actually the fourth one in a row addressing the pathology of the muscle fibre intermediate filament desmin, its associated and similar diseases, all four [1–3] organized by Michel Fardeau and Hans H. Goebel. In his introduction, the chairman, Hans H. Goebel (Mainz), recorded the evolution of ‘Protein Aggregate Myopathies (PAM)’ which are marked by the accumulation of diverse proteins within muscle fibres as a morphologic hallmark in separate myopathies w…

Pathologymedicine.medical_specialtyProtein aggregationBiologymedicine.diseaseNemaline myopathyNeurologyPediatrics Perinatology and Child HealthmedicineCongenital muscular dystrophyMyotilinDesminNeurology (clinical)Muscle fibremedicine.symptomMyopathyIntermediate filamentGenetics (clinical)Neuromuscular Disorders
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Perineural pattern of aggregation of cellular blue nevus: probable histoarchitectural reminiscence of histogenesis.

2008

A striking feature of cellular blue nevus consists in the presence, in its histologic picture, of numerous hypertrophic nerves and nerve-like figures, positive for histochemical and immunohistochemical methods for nerve fibers and myelin sheaths. These findings, first described in Masson's original article and repeatedly highlighted in the past for their possible histogenetic significance, are currently considered as merely coincidental. However, the thin conventional histologic sections, catching only short tracts of the nerves, preclude a correct observation of their route and do not allow us to verify if there is an architectural relationship between them and the nevus as a whole. With t…

Pathologymedicine.medical_specialtySkin NeoplasmsDermatologyHistogenesisSettore MED/08 - Anatomia PatologicaPathology and Forensic MedicineNevus BluemedicineNevusHumansskin and connective tissue diseasesBlue nevusCell AggregationNeuronsbusiness.industryCellular Blue NevusCell DifferentiationEpithelial CellsGeneral MedicineAnatomyCellular blue nevus perineural aggregation histogenesismedicine.diseasemedicine.anatomical_structureNeural differentiationSchwann Cellsmedicine.symptomSilver impregnationPerineuriumbusinessNevus cellThe American Journal of dermatopathology
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Primary desminopathies.

2007

•  Introduction •  Desmin is an essential component of the extrasarcomeric cytoskeleton in striated muscle cells •  Distal myopathy,cardiac arrhythmias,cardiomyopathy:classical criteria of primary desminopathies •  Sub-sarcolemmal and cytoplasmic desmin-positive protein aggregates:the morphological hallmark of primary and secondary desminopathies •  The spectrum of pathogenic desmin gene mutations •  The molecular pathogenesis of primary desminopathies: some answers gained,but even more questions raised •  Diagnostic work-up to distinguish primary from secondary desminopathies •  Treatment and clinical management of primary desminopathy patients Abstract Mutations of the human desmin gene o…

Pathologymedicine.medical_specialtyintermediate filamentsCardiomyopathyReviewsgranulofilamentous materialdesmininclusion bodiesmacromolecular substancesBiologymyofibrillar myopathyprotein aggregationdesmin-related myopathySarcolemmaMuscular DiseasesmedicineMyocyteAnimalsHumansIntermediate filamentMyopathyMuscle SkeletalCytoskeletonGenetic heterogeneityCardiac muscleCell Biologymedicine.diseasemusculoskeletal systemmutationsmedicine.anatomical_structuredesminopathyMutationMolecular MedicineDesminmedicine.symptomMyofibrilJournal of cellular and molecular medicine
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Consensus document on intermittent claudication from the Central European Vascular Forum 1st edition - Abano Terme (Italy) - May 2005 2nd revision - …

2008

Peripheral Vascular DiseasesLegtrainingTiclopidineAspirinAcetylsalicylic acidanticoagulant agentantithrombocytic agentconsensus document; intermittent claudicatio; training; antiplatelets' therapyintermittent claudicatioIntermittent ClaudicationSettore MED/11 - Malattie Dell'Apparato CardiovascolareClopidogrelantiplatelets' therapyIschemiaDisease ProgressionExercise TestHumansCarotid StenosisUltrasonography Doppler Colorconsensus documentPlatelet Aggregation Inhibitors
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Hemorheologic profile of hyperlipidemic patients treated with gemfibrozil

1996

Abstract We measured the plasma lipid levels and the macrorheologic (whole-blood, plasma, and serum viscosity levels; fibrinogen; hematocrit; mean erythrocyte aggregation; and whole-blood filterability) and microrheologic (erythrocyte membrane fluidity and red cell membrane protein lateral mobility) determinants in a group of 19 hyperlipidemic patients (Fredrickson's classification phenotype IIa, 12 patients; phenotype IV, 4; phenotype IIb, 3) at baseline and after 45 and 90 days of treatment with gemfibrozil (900 mg orally once a day). At baseline we noted statistically significant increases in plasma viscosity level, fibrinogen, and mean erythrocyte aggregation, as well as a statistically…

PharmacologyChemotherapymedicine.medical_specialtymedicine.diagnostic_testbusiness.industrymedicine.medical_treatmentHealthy subjectsSerum viscosityHematocritFibrinogenErythrocyte aggregationEndocrinologyInternal medicinePlasma lipidsmedicineGemfibrozilPharmacology (medical)businessmedicine.drugCurrent Therapeutic Research
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