Search results for "Microfilament"

showing 10 items of 109 documents

Immunolocalization of integrins in the normal and neoplastic colonic epithelium.

1993

Cryosections of normal colon (NC), tubular and villous adenomas (TA, VA), and variably differentiated colon adenocarcinomas (CA) were immunostained with monoclonal antibodies to alpha 1-6 and alpha v, and beta 1-4 integrin subunits; select samples were stained for cytokeratin (Ck) 20 and villin. In NC, alpha 2 staining was strongest in crypt cells; alpha 1,3 and alpha v, and beta 1,3 and beta 4, and Ck 20 and villin predominated in superficial enterocytes. In TA and VA, monolayered glands showed integrin, Ck 20 and villin patterns that differed slightly from both crypt and superficial enterocytes. Complex glands in VA showed decreased integrin staining and basal polarization; Ck 20 and vill…

AdenomaPathologymedicine.medical_specialtyIntegrinsColonCryptIntegrinFluorescent Antibody TechniqueAdenocarcinomadigestive systemEpitheliumExtracellular matrixImmunoenzyme Techniques03 medical and health sciencesCytokeratin0302 clinical medicineKeratinmedicineHumansTissue Distribution030304 developmental biologychemistry.chemical_classification0303 health sciencesbiologyCarcinomaMicrofilament ProteinsAntibodies MonoclonalCell DifferentiationGeneral MedicineEpitheliummedicine.anatomical_structurechemistry030220 oncology & carcinogenesisColonic Neoplasmsbiology.proteinImmunohistochemistryKeratinsVillinCarrier ProteinsVirchows Archiv. B, Cell pathology including molecular pathology
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A mutation in myotilin causes spheroid body myopathy

2005

Background: Spheroid body myopathy (SBM) is a rare, autosomal dominant, neuromuscular disorder, which has only been previously reported in a single large kindred. Identification of the mutated gene in this disorder may provide insight regarding abnormal neuromuscular function. Methods: The authors completed a detailed clinical evaluation on an extensive kindred diagnosed with SBM. Genome-wide linkage analysis was performed to localize the disease gene to a specific chromosomal region. Further marker genotyping and screening of a positional, functional candidate gene were completed to detect the disease-causing mutation. Pathologic analysis of muscle biopsy was performed on three individuals…

AdultGenetic MarkersMaleCandidate genePathologymedicine.medical_specialtyDNA Mutational AnalysisMuscle ProteinsChromosome DisordersBiologyExonMuscular DiseasesmedicineHumansPoint MutationMyotilinConnectinGenetic Predisposition to DiseaseGenetic TestingMuscular dystrophyMuscle SkeletalMyopathyAgedGenes DominantAged 80 and overInclusion BodiesGeneticsMuscle biopsymedicine.diagnostic_testMicrofilament ProteinsChromosome MappingExonsMiddle Agedmedicine.diseasePedigreeCytoskeletal ProteinsMutationChromosomal regionbiology.proteinChromosomes Human Pair 5FemaleTitinNeurology (clinical)medicine.symptomNeurology
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Histological Features of Cerebellar Neuropathology in Patients With Alcoholic and Nonalcoholic Steatohepatitis

2018

Alcoholic steatohepatitis (ASH) and nonalcoholic steatohepatitis (NASH) affect 29 million people in the European Union. Patients with ASH and NASH may exhibit cognitive impairment, reducing their quality of life. Steatohepatitis induces cerebral alterations. It is not known if histological analysis could allow distinguishing ASH, NASH, and/or cirrhosis neuropathology and other entities. The aim of this work was to analyze a set of histopathological features characterizing the brain lesions due to ASH, NASH, and cirrhosis. We performed a histological study using hematoxylin and eosin staining and immunohistochemical techniques in cerebellum of 31 subjects who died with healthy liver (n = 6),…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyAlcoholic liver diseaseCerebellumCell CountNeuropathologyPathology and Forensic Medicine03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineNon-alcoholic Fatty Liver DiseaseCerebellumHumansMedicinemedia_common.cataloged_instanceEuropean unionAgedmedia_commonNeuronsAnalysis of Variancebusiness.industryCalcium-Binding ProteinsMicrofilament ProteinsFatty liverGeneral MedicineMiddle Agedmedicine.diseaseDNA-Binding Proteins030104 developmental biologymedicine.anatomical_structureNeurologyFemaleCerebellar atrophyAlcoholic fatty liverNeurology (clinical)AtrophySteatohepatitisbusinessNeuroglia030217 neurology & neurosurgeryFatty Liver AlcoholicJournal of Neuropathology & Experimental Neurology
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Recurrence of pleomorphic adenoma of the parotid gland-predictive value of cadherin-11 and fascin

2008

The predictive value of cadherin-11, tenascin, fascin, and mucin-1 as markers for the likelihood of recurrence in pleomorphic adenoma of the parotid gland was examined. In this retrospective study we analysed 20 tumours from16 patients by immunohistochemistry. Staining intensities were measured using a semiquantitative scoring approach; localisation (tumour centre vs border) as well as clinical data were analysed and correlated with follow-up. Cadherin-11 was increased in recurrent tumours. However, no changes of fascin, tenascin or mucin-1 were observed. Cadherin-11 and fascin were increased in primary tumours of patients with later recurrence, with fascin upregulation restricted to the tu…

AdultMaleMicrobiology (medical)Pathologymedicine.medical_specialtyAdolescentAdenoma PleomorphicTenascinmacromolecular substancesPathology and Forensic MedicinePleomorphic adenomaDownregulation and upregulationBiomarkers TumormedicineHumansParotid GlandImmunology and AllergyRetrospective StudiesFascinbiologyCadherinMicrofilament ProteinsMucin-1MucinTenascinGeneral MedicineMiddle AgedCadherinsPrognosismedicine.diseaseImmunohistochemistryParotid NeoplasmsParotid glandmedicine.anatomical_structurebiology.proteinImmunohistochemistryFemaleNeoplasm Recurrence LocalCarrier ProteinsAPMIS
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Apoptosis-related Proteins in Skeletal Muscle Fibers of Spinal Muscular Atrophy

1997

There is evidence that apoptosis in spinal muscular atrophies (SMA) is not restricted to motor neurons but also affects muscle fibers. Studying the expression of several apoptosis-associated proteins we found constant expression of bax in muscle fibers, which promoted cell death. The expression of bax correlated with defective innervation of muscle fibers was also indicated by upregulation of N-CAM. While in early-onset SMA atrophic as well as normo- and hypertrophic muscle fibers displayed expression of bax, muscle fibers in late-onset SMA and peripheral neuropathies showed bax-expression only in atrophic fibers. Other investigated apoptosis-associated factors comprised interleukin-1 beta …

AdultMaleProgrammed cell deathPathologymedicine.medical_specialtyMuscle Fibers Skeletalbcl-X ProteinMuscle ProteinsApoptosisBiologyMicrofilamentPathology and Forensic MedicineMuscular Atrophy SpinalCellular and Molecular NeuroscienceReference ValuesProto-Oncogene ProteinsmedicineHumansMyocyteMuscle SkeletalActinAgedbcl-2-Associated X ProteinCaspase 1InfantPeripheral Nervous System DiseasesGeneral MedicineSpinal muscular atrophyMiddle AgedSMA*Spinal muscular atrophiesmedicine.diseaseCell biologyCysteine EndopeptidasesProto-Oncogene Proteins c-bcl-2NeurologyFemaleNeural cell adhesion moleculeNeurology (clinical)Journal of Neuropathology and Experimental Neurology
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Studies on the subcellular pathophysiology of sublethal chronic cell injury.

1974

Summary This paper summarizes some of the important subcellular events occurring after chronic sublethal cell injury. Chronic cell injury is defined as the result of injurious stimuli which permit cell survival though in altered steady states for protracted periods of time. The importance of ultrastructural and biochemical studies of these phenomena is emphasized. Among the phenomena discussed are alterations in lysosomes, cellular hypertrophy, fatty metamorphosis, alterations in microfilaments and microtubules, alterations in mechanisms of transcription and replication, disturbances in the cell surface and transport across the cell membrane, and alterations in intracellular transport.

AdultMaleTime FactorsTranscription GeneticSurface PropertiesCellsCellGuinea PigsBronchiBiologyMicrofilamentMicrotubulesPathology and Forensic MedicineMuscle hypertrophyCell Physiological PhenomenaCell membraneMiceMicrotubuleTranscription (biology)medicineAnimalsHumansCerebral CortexMacrophagesMusclesCell MembraneBiological TransportGeneral MedicineHypertrophyMiddle AgedPathophysiologyCell biologyMicroscopy Electronmedicine.anatomical_structureLiverUltrastructureRabbitsLysosomesCell DivisionBeitrage zur Pathologie
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De novo 15q21.1q21.2 deletion identified through FBN1 MLPA and refined by 244K array-CGH in a female teenager with incomplete Marfan syndrome

2010

International audience; Interstitial deletions involving the 15q21.1 band are very rare. Only 4 of these cases have been studied using molecular cytogenetic techniques in order to confirm the deletion of the whole FBN1 gene. The presence of clinical features of the Marfan syndrome (MFS) spectrum associated with mental retardation has been described in only 2/4 patients. Here we report on a 16-year-old female referred for suspicion of MFS (positive thumb and wrist sign, scoliosis, joint hyperlaxity, high-arched palate with dental crowding, dysmorphism, mitral insufficiency with dystrophic valve, striae). She had therefore 3 minor criteria according to the Ghent nosology. She also had speech …

AdultMalemusculoskeletal diseasesProbandMarfan syndromecongenital hereditary and neonatal diseases and abnormalitiesAdolescent[SDV]Life Sciences [q-bio]Fibrillin-1BiologyFibrillinsBioinformaticsPolymerase Chain ReactionMarfan SyndromeLoss of heterozygosity03 medical and health sciencesTransforming Growth Factor betaIntellectual DisabilityGeneticsmedicineHumansMultiplex ligation-dependent probe amplificationAlleleChildGeneIn Situ Hybridization FluorescenceGenetics (clinical)Oligonucleotide Array Sequence AnalysisSequence Deletion030304 developmental biologyGeneticsChromosomes Human Pair 15Comparative Genomic Hybridization0303 health sciencesMicrofilament Proteins030305 genetics & heredityGeneral Medicinemedicine.diseasePedigree3. Good healthPhenotypeMutationMicrosatelliteFemaleDNA ProbesHaploinsufficiencyMicrosatellite RepeatsEuropean Journal of Medical Genetics
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Fetal akinesia caused by a novel actin filament aggregate myopathy skeletal muscle actin gene (ACTA1) mutation.

2010

We report a female newborn, diagnosed with fetal akinesia in utero, who died one hour after birth. Post-mortem muscle biopsy demonstrated actin-filament myopathy based on immunolabelling for sarcomeric actin, and large areas of filaments, without rod formation, ultrastructurally. Analysis of DNA extracted from the muscle disclosed a novel de novo heterozygous c.44G>A, GGC>GAC, 'p.Gly15Asp' mutation in the ACTA1 gene. Analysis of the location of the mutated amino-acid in the actin molecule suggests the mutation most likely causes abnormal nucleotide binding, and consequent pathological actin polymerization. This case emphasizes the association of fetal akinesia with actin-filament myopathy.

AdultSarcomeresmacromolecular substancesBiologymedicine.disease_causeSarcomereNemaline myopathyPregnancymedicineHumansMyopathyMuscle SkeletalGenetics (clinical)ActinMutationMuscle biopsymedicine.diagnostic_testMicrofilament ProteinsInfant NewbornSkeletal muscleDNANeuromuscular DiseasesActin cytoskeletonmedicine.diseaseMolecular biologyActin CytoskeletonFetal Diseasesmedicine.anatomical_structureNeurologyBiochemistryPediatrics Perinatology and Child HealthMutationFemaleNeurology (clinical)medicine.symptomNeuromuscular disorders : NMD
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Small GTP-binding proteins of the Rho- and Ras-subfamilies are not involved in the actin rearrangements induced by attaching and effacingEscherichia …

1998

Attaching and effacing Escherichia coli (AEEC) are extracellular pathogens that induce the formation of actin-rich structures at their sites of attachment to eukaryotic host cells. We analysed whether small GTP-binding proteins of the Rho- and Ras-subfamilies, which control the cellular actin system, are essential for these bacterial-induced microfilament reorganizations. For this purpose we specifically inactivated them using the Clostridium difficile toxins TcdB-10463 and TcdB-1470. Such treatment led to a dramatic breakdown of the normal actin cytoskeleton, but did not abrogate the bacterial-induced actin rearrangements. Our data therefore indicate that the microfilament reorganizations …

Bacterial ToxinsExotoxinsArp2/3 complexmacromolecular substancesShiga ToxinsMicrofilamentMicrobiologyGTP-Binding ProteinsEscherichia coliGeneticsAnimalsHumansActin-binding proteinCytoskeletonMolecular BiologyActinbiologyClostridioides difficileActin remodelingActin cytoskeletonActinsActin CytoskeletonMicroscopy ElectronBiochemistryMicroscopy Electron Scanningras Proteinsbiology.proteinCattleMDia1HeLa CellsFEMS Microbiology Letters
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Effects of oral niacin on endothelial dysfunction in patients with coronary artery disease: Results of the randomized, double-blind, placebo-controll…

2009

High-density-lipoproteins-cholesterol (HDL-C) is invertedly related to the incidence of cardiovascular events. Recent studies suggest that HDL-C directly improves endothelial function. Nicotinic acid (niacin) effectively raises serum HDL-C. We therefore hypothesized that treatment with niacin improves endothelial dysfunction in patients with coronary artery disease (CAD). One hundred seven patients with CAD were randomly assigned to double-blinded treatment for 12 weeks with extended-release (ER)-niacin 1000 mg/day (N) or placebo (C), respectively. Flow-mediated dilation (FMD) of the brachial artery, nitroglycerin-mediated endothelium-independent dilation (NMD) and serum lipid concentration…

Blood GlucoseMalemedicine.medical_specialtyBrachial ArteryVasodilator AgentsAdministration OralCoronary Artery DiseasePlaceboNiacinGastroenterologyCoronary artery diseaseNitroglycerinchemistry.chemical_compoundHigh-density lipoproteinDouble-Blind MethodInternal medicinemedicine.arterymedicineHumansProspective StudiesPhosphorylationEndothelial dysfunctionBrachial arteryTriglyceridesAgedUltrasonographyVascular diseasebusiness.industryCholesterol HDLMicrofilament Proteinsnutritional and metabolic diseasesCholesterol LDLMiddle AgedPhosphoproteinsmedicine.diseaseVasodilationB vitaminsTreatment OutcomeEndocrinologychemistryDelayed-Action PreparationsFemalelipids (amino acids peptides and proteins)Endothelium VascularCardiology and Cardiovascular MedicinebusinessCell Adhesion MoleculesBiomarkersNiacinAtherosclerosis
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