Search results for "mit"

showing 10 items of 11910 documents

DNA Damage Signaling Instructs Polyploid Macrophage Fate in Granulomas.

2018

Granulomas are immune cell aggregates formed in response to persistent inflammatory stimuli. Granuloma macrophage subsets are diverse and carry varying copy numbers of their genomic information. The molecular programs that control the differentiation of such macrophage populations in response to a chronic stimulus, though critical for disease outcome, have not been defined. Here, we delineate a macrophage differentiation pathway by which a persistent Toll-like receptor (TLR) 2 signal instructs polyploid macrophage fate by inducing replication stress and activating the DNA damage response. Polyploid granuloma-resident macrophages formed via modified cell divisions and mitotic defects and not…

0301 basic medicineGenome instabilityDNA damageLipoproteinsCellMitosisInflammationAtaxia Telangiectasia Mutated ProteinsBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyProto-Oncogene Proteins c-myc03 medical and health sciencesMicemedicineAnimalsHumansMacrophage Differentiation PathwayMitosisCell ProliferationInflammationGranulomaMacrophagesCell DifferentiationMycobacterium tuberculosisToll-Like Receptor 2Cell biologyMice Inbred C57BLTLR2030104 developmental biologymedicine.anatomical_structureImmunologymedicine.symptomCarcinogenesisDNA DamageCell
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
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Dicer prevents genome instability in response to replication stress

2019

Dicer, an endoribonuclease best-known for its role in microRNA biogenesis and RNA interference pathway, has been shown to play a role in the DNA damage response and repair of double-stranded DNA breaks (DSBs) in mammalian cells. However, it remains unknown whether Dicer is also important to preserve genome integrity upon replication stress. To address this question, we focused our study on common fragile sites (CFSs), which are susceptible to breakage after replication stress. We show that inhibition of the Dicer pathway leads to an increase in CFS expression upon induction of replication stress and to an accumulation of 53BP1 nuclear bodies, indicating transmission of replication-associate…

0301 basic medicineGenome instabilityreplication stressDNA damageChromosomal fragile siteBiologygenomic instabilitycommon fragile siteCell biologySettore BIO/18 - Genetica03 medical and health sciences030104 developmental biology0302 clinical medicineOncology030220 oncology & carcinogenesisFANCD2biology.proteinDicer PathwayMitosiscommon fragile sitesDroshaResearch PaperDicerDicerOncotarget
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Excessive daytime sleepiness is associated with an increased frequency of falls and sarcopenia.

2021

Background:\ud \ud This cross-sectional study aimed to examine associations between excessive daytime sleepiness (EDS) with falls and falls related conditions in older adults.\ud \ud Methods:\ud \ud To assess EDS, the Epworth Sleepiness Scale was used, with a score of ≥11/24 points indicating EDS. Number of falls and fall history (at least one) in the last year were recorded. Timed Up and Go test (TUG) was used to assess fall risk. Sarcopenia was defined by SARC-F tool. A grip strength score of the dominant hand, measured with a hand-grip dynamometer, less than 16 kg in females and 27 kg in males was accepted as dynapenia. Frailty status was defined by five dimensions including shrinking, e…

0301 basic medicineGerontologyMaleAgingSarcopeniaExcessive daytime sleepinessTimed Up and Go testDisorders of Excessive SomnolenceBiochemistry03 medical and health sciencesGrip strength0302 clinical medicineEndocrinologyGeneticsmedicineHumansMolecular BiologyGeriatric AssessmentPostural BalanceDepression (differential diagnoses)AgedPolypharmacyAged 80 and overbusiness.industryEpworth Sleepiness ScaleCell Biologymedicine.disease030104 developmental biologyCross-Sectional StudiesSarcopeniaDynapenia Excessive daytime sleepiness FallsFrailty SarcopeniaTime and Motion StudiesSoysal P. Smith L. Tan S. G. Capar E. Veronese N. Yang L. -Excessive daytime sleepiness is associated with an increased frequency of falls and sarcopenia.- Experimental gerontology ss.111364 2021Soysal P. Smith L. Tan S. G. Capar E. Veronese N. Yang L. -Excessive daytime sleepiness is associated with an increased frequency of falls and sarcopenia- 17 th EuGMS Athens Yunanistan 11 - 13 Ekim 2021 ss.3-4Marital statusAccidental FallsFemalemedicine.symptombusinesshuman activities030217 neurology & neurosurgeryExperimental gerontology
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A New Frailty Score for Experimental Animals Based on the Clinical Phenotype: Inactivity as a Model of Frailty.

2016

The development of animal models to study human frailty is important to test interventions to be translated to the clinical practice. The aim of this work was to develop a score for frailty in experimental animals based in the human frailty phenotype. We also tested the effect of physical inactivity in the development of frailty as determined by our score. Male C57Bl/6J mice, individually caged, were randomly assigned to one of two groups: sedentary (inactive) or spontaneous wheel-runners. We compared the sedentary versus the active lifestyle in terms of frailty by evaluating the clinical criteria used in humans: unintentional weight loss; poor endurance (running time); slowness (running sp…

0301 basic medicineGerontologymedicine.medical_specialtyWeaknessAgingFrail ElderlyPsychological interventionTranslational Research Biomedical03 medical and health sciencesGrip strengthMice0302 clinical medicinePhysical medicine and rehabilitationWeight lossPhysical Conditioning AnimalActivities of Daily LivingmedicineAnimalsHumansMobility LimitationClinical phenotypeAgedbusiness.industrymedicine.diseaseMotor coordinationRunning timeMice Inbred C57BL030104 developmental biologyResearch DesignSpainSarcopeniaModels AnimalGeriatrics and Gerontologymedicine.symptomSedentary Behaviorbusiness030217 neurology & neurosurgeryThe journals of gerontology. Series A, Biological sciences and medical sciences
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Prevalence of intestinal parasites, with emphasis on the molecular epidemiology of Giardia duodenalis and Blastocystis sp., in the Paranaguá Bay, Bra…

2018

BACKGROUND: Intestinal protozoan parasites are major contributors to the global burden of gastrointestinal disease causing significant socioeconomic consequences. Children living in resource-poor settings with restricted access to water and sanitary services are particularly at risk of these infections. METHODS: A prospective, community-based, cross-sectional survey was conducted in Paraná (southern Brazil) between May 2015 and May 2016. A total of 766 stool samples were individually collected from volunteers (male/female ratio: 0.99; age range: 0-76 years) and used for investigating the presence of intestinal helminth and protozoan species by routine microscopic procedures including the Ka…

0301 basic medicineGiardiasisMaleVeterinary medicineCommunityBlastocystis Infectionsmedicine.disease_causeFeces0302 clinical medicineResidence CharacteristicsSurveys and QuestionnairesPrevalenceProspective StudiesIntestinal Diseases ParasiticChildNematodeeducation.field_of_studyMicroscopySoil-transmitted helminthsMiddle AgedInfectious DiseasesChild PreschoolFemaleAscaris lumbricoidesBrazilHumanAdultGenotypingAdolescent030231 tropical medicinePopulationIntestinal parasiteBiologyDNA Ribosomallcsh:Infectious and parasitic diseases03 medical and health sciencesYoung Adultparasitic diseasesmedicineHelminthHelminthsHumanslcsh:RC109-216ProtozoaeducationAgedIntestinal parasitesBlastocystisMolecular epidemiologyEndolimax nanaResearchInfant NewbornGenetic VariationInfantbiology.organism_classification030104 developmental biologyCross-Sectional StudiesBlastocystisTrichuris trichiuraParasitologyGiardia lamblia
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Adipocytes as a Link Between Gut Microbiota-Derived Flagellin and Hepatocyte Fat Accumulation

2016

While the role of both elevated levels of circulating bacterial cell wall components and adipose tissue in hepatic fat accumulation has been recognized, it has not been considered that the bacterial components-recognizing adipose tissue receptors contribute to the hepatic fat content. In this study we found that the expression of adipose tissue bacterial flagellin (FLG)-recognizing Toll-like receptor (TLR) 5 associated with liver fat content (r = 0.699, p = 0.003) and insulin sensitivity (r = -0.529, p = 0.016) in humans (n = 23). No such associations were found for lipopolysaccharides (LPS)-recognizing TLR4. To study the underlying molecular mechanisms of these associations, human HepG2 he…

0301 basic medicineGlycerollcsh:MedicineAdipose tissueWhite adipose tissueflagellinBiochemistryImmune ReceptorsFatsEndocrinologyAnimal CellsAdipocytesMedicine and Health SciencesInsulinlcsh:ScienceToll-like ReceptorsConnective Tissue CellsMultidisciplinaryImmune System ProteinsbiologyLiver DiseasesFatty liverin kaltaiset reseptorit [toll]Lipidsadipose tissuePhysical sciencesChemistryMitochondrial respiratory chainAdipose TissueConnective Tissuebacterial componentsCellular TypesAnatomyinsuline sensitivityResearch ArticleSignal Transductionmedicine.medical_specialtyadipocytesImmunologyMonomers (Chemistry)Gastroenterology and Hepatologyta311103 medical and health sciencesInsulin resistanceInternal medicinemedicinePolymer chemistryDiabetic Endocrinologylcsh:Rta1183ta1182Biology and Life SciencesProteinsCell Biologyliver fatmedicine.diseasehepatic fatfat accumulationHormonesIRS1Fatty LiverInsulin receptor030104 developmental biologyEndocrinologyBiological TissueTLR5biology.proteinlcsh:QPLoS ONE
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Role of the DNA repair glycosylase OGG1 in the activation of murine splenocytes

2017

OGG1 (8-oxoguanine-DNA glycosylase) is the major DNA repair glycosylase removing the premutagenic DNA base modification 8-oxo-7,8-dihydroguanine (8-oxoG) from the genome of mammalian cells. In addition, there is accumulating evidence that OGG1 and its substrate 8-oxoG might function in the regulation of certain genes, which could account for an attenuated immune response observed in Ogg1-/- mice in several settings. Indications for at least two different mechanisms have been obtained. Thus, OGG1 could either act as an ancillary transcription factor cooperating with the lysine-specific demethylase LSD1 or as an activator of small GTPases. Here, we analysed the activation by lipopolysaccaride…

0301 basic medicineGuanineDNA RepairDNA repairp38 mitogen-activated protein kinasesBiologyBiochemistryDNA GlycosylasesMice03 medical and health sciencesAnimalsMolecular BiologyTranscription factorTumor Necrosis Factor-alphaKinaseActivator (genetics)MacrophagesDNACell BiologyBase excision repairMolecular biology030104 developmental biologyGene Expression RegulationDNA glycosylaseTumor necrosis factor alphaSpleenDNA DamageTranscription FactorsDNA Repair
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Mitochondrial Function in Hereditary Spastic Paraplegia: Deficits in SPG7 but Not SPAST Patient-Derived Stem Cells

2020

Mutations in SPG7 and SPAST are common causes of hereditary spastic paraplegia (HSP). While some SPG7 mutations cause paraplegin deficiency, other SPG7 mutations cause increased paraplegin expression. Mitochondrial function has been studied in models that are paraplegin-deficient (human, mouse, and Drosophila models with large exonic deletions, null mutations, or knockout models) but not in models of mutations that express paraplegin. Here, we evaluated mitochondrial function in olfactory neurosphere-derived cells, derived from patients with a variety of SPG7 mutations that express paraplegin and compared them to cells derived from healthy controls and HSP patients with SPAST mutations, as …

0301 basic medicineHereditary spastic paraplegiaoxidative phosphorylationOxidative phosphorylationMitochondrionmedicine.disease_causeSpastinSPG7lcsh:RC321-57103 medical and health sciences0302 clinical medicinemedicineSPASThereditary spastic paraplegialcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMutationparapleginParapleginGeneral NeuroscienceBrief Research Reportspastinmedicine.diseasePhenotypeCell biologymitochondria030104 developmental biology030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in Neuroscience
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