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showing 10 items of 3828 documents

The Use and Abuse of LexA by Mobile Genetic Elements

2016

The SOS response is an essential process for responding to DNA damage in bacteria. The expression of SOS genes is under the control of LexA, a global transcription factor that undergoes self-cleavage during stress to allow the expression of DNA repair functions and delay cell division until the damage is rectified. LexA also regulates genes that are not part of this cell rescue program, and the induction of bacteriophages, the movement of pathogenicity islands, and the expression of virulence factors and bacteriocins are all controlled by this important transcription factor. Recently it has emerged that when regulating the expression of genes from mobile genetic elements (MGEs), LexA often …

0301 basic medicineMicrobiology (medical)Transcription GeneticDNA repair030106 microbiologyRegulatorBiologyRegulonMicrobiology03 medical and health sciencesBacterial ProteinsVirologyGene expressionBacteriophagesSOS responseSOS Response GeneticsTranscription factorGeneGeneticsSerine Endopeptidasesbiochemical phenomena metabolism and nutritionInterspersed Repetitive Sequencesenzymes and coenzymes (carbohydrates)Infectious DiseasesbacteriaRepressor lexACorepressorDNA DamageTrends in Microbiology
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Cellular Responses in Human Dental Pulp Stem Cells Treated with Three Endodontic Materials

2017

Human dental pulp stem cells (HDPSCs) are of special relevance in future regenerative dental therapies. Characterizing cytotoxicity and genotoxicity produced by endodontic materials is required to evaluate the potential for regeneration of injured tissues in future strategies combining regenerative and root canal therapies. This study explores the cytotoxicity and genotoxicity mediated by oxidative stress of three endodontic materials that are widely used on HDPSCs: a mineral trioxide aggregate (MTA-Angelus white), an epoxy resin sealant (AH-Plus cement), and an MTA-based cement sealer (MTA-Fillapex). Cell viability and cell death rate were assessed by flow cytometry. Oxidative stress was m…

0301 basic medicineMineral trioxide aggregatelcsh:Internal medicineArticle SubjectDNA damageDentistrymedicine.disease_cause03 medical and health sciences0302 clinical medicineDental pulp stem cellsmedicineViability assaylcsh:RC31-1245Molecular Biologybusiness.industryChemistryRegeneration (biology)030206 dentistryCell Biology030104 developmental biologyCell cultureCancer researchbusinessGenotoxicityOxidative stressResearch ArticleStem Cells International
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The Role of NF-κB Triggered Inflammation in Cerebral Ischemia

2021

Cerebral ischemia is a devastating disease that affects many people worldwide every year. The neurodegenerative damage as a consequence of oxygen and energy deprivation, to date, has no known effective treatment. The ischemic insult is followed by an inflammatory response that involves a complex interaction between inflammatory cells and molecules which play a role in the progression towards cell death. However, there is presently a matter of controversy over whether inflammation could either be involved in brain damage or be a necessary part of brain repair. The inflammatory response is triggered by inflammasomes, key multiprotein complexes that promote secretion of pro-inflammatory cytoki…

0301 basic medicineMini ReviewIschemiaNeurosciences. Biological psychiatry. NeuropsychiatryContext (language use)InflammationBrain damageCervell Ferides i lesionsNeuroprotectionNF-κBcerebral ischemia03 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicinemedicinebusiness.industryNeurodegenerationneurodegenerationNF-κBInflammasomemedicine.disease030104 developmental biologychemistryinflammationCellular Neuroscienceneuroprotectionmedicine.symptombusinessOxigen Efectes fisiològicsNeuroscience030217 neurology & neurosurgeryRC321-571medicine.drugFrontiers in Cellular Neuroscience
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High Fidelity Deep Sequencing Reveals No Effect of ATM, ATR, and DNA-PK Cellular DNA Damage Response Pathways on Adenovirus Mutation Rate

2019

This article belongs to the Section Animal Viruses.

0301 basic medicineMutation ratemutation rateDNA RepairDNA damageMutation rateviruseslcsh:QR1-502Eukaryotic DNA replicationAtaxia Telangiectasia Mutated ProteinsDNA-Activated Protein KinaseHuman Adenovirus Type 5BiologyDNA damage responsemedicine.disease_causelcsh:MicrobiologyArticleDeep sequencingCell Line03 medical and health scienceschemistry.chemical_compoundVirologymedicineHumansexperimental evolutionPolymeraseMutation030102 biochemistry & molecular biologyAdenoviruses HumanHigh-Throughput Nucleotide SequencingDNA virus3. Good healthCell biologyHuman adenovirus type 5body regions030104 developmental biologyInfectious DiseasesExperimental evolutionchemistrybiology.proteinHuman Adenovirus Type 5.DNADNA DamageSignal TransductionViruses
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B-MIND: MOR208 plus bendamustine (BEN) versus rituximab (RTX) plus BEN in patients with relapsed or refractory (R-R) diffuse large B-cell lymphoma (D…

2017

TPS7571 Background: Patients ineligible for stem cell transplantation (SCT) or who relapse after SCT, and those who fail to respond to second-line or salvage chemotherapy, represent an unmet medical need for which new therapeutic strategies are required. MOR208 is a novel Fc-enhanced, humanized, monoclonal antibody directed against CD19. Significant single-agent activity of MOR208 in patients with R-R DLBCL (Jurczak et al., J Clin Oncol 34, 2016 [suppl; abstr 7545]) and enhancement of MOR208-mediated cytotoxicity by BEN in preclinical studies, provide a strong rationale to study MOR208 + BEN in patients with R-R DLBCL. Methods: B-MIND is a randomized (1:1), two-arm, multicenter, open-label…

0301 basic medicinePHASE II/III TRIALOncologyBendamustineCancer Researchmedicine.medical_specialtybusiness.industrymedicine.diseaseSurgeryTransplantation03 medical and health sciences030104 developmental biology0302 clinical medicineOncologyRefractory030220 oncology & carcinogenesisInternal medicinemedicineRituximabIn patientStem cellbusinessDiffuse large B-cell lymphomamedicine.drugJournal of Clinical Oncology
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Intracellular fluoride influences TASK mediated currents in human T cells.

2019

The expression of Kv1.3 and KCa channels in human T cells is essential for maintaining cell activation, proliferation and migration during an inflammatory response. Recently, an additional residual current, sensitive to anandamide and A293, compounds specifically inhibiting currents mediated by TASK channels, was observed after complete pharmacological blockade of Kv1.3 and KCa channels. This finding was not consistently observed throughout different studies and, an in-depth review of the different recording conditions used for the electrophysiological analysis of K+ currents in T cells revealed fluoride as major anionic component of the pipette intracellular solutions in the initial studie…

0301 basic medicinePatch-Clamp TechniquesTime FactorsPotassium CompoundsT-LymphocytesImmunologyMagnesium ChlorideMembrane Potentials03 medical and health scienceschemistry.chemical_compoundFluorides0302 clinical medicinePotassium Channels Tandem Pore DomainPotassium Channel BlockersImmunology and AllergyHumansCells CulturedKv1.3 Potassium ChannelActivator (genetics)ChemistryPipetteAnandamideElectrophysiology030104 developmental biologyMembraneBiophysicsCell activationFluorideIntracellular030215 immunologyJournal of immunological methods
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Mice are not Men: ADAM30 Findings Emphasize a Broader Look Towards Murine Alzheimer's Disease Models

2016

Due to the growing population of people at advanced age, the number of patients affected by Alzheimer's disease (AD) is increasing tremendously. In 2015 about 46.8 million people suffered from AD worldwide which is estimated to increase to 131.5 million by 2050. Brains of AD patients all show a common histopathology; they are marked by an atrophy and degeneration that is caused by a severe loss of neurons and synapses (Braak and Del Tredici, 2012). Moreover, so-called extracellular senile plaques that consist of predominantly amyloid β (Aβ) peptides can be detected in the grey matter where they surround neurons. Since generation of Aβ peptides is hypothesized to play a major role in AD path…

0301 basic medicinePathologymedicine.medical_specialtyADAM10Populationlcsh:MedicineMice TransgenicGrey matterBiologyGeneral Biochemistry Genetics and Molecular BiologyPathogenesisMice03 medical and health sciences0302 clinical medicineAtrophyAlzheimer DiseasemedicineAmyloid precursor proteinAnimalsHumansSenile plaqueseducationlcsh:R5-920education.field_of_studylcsh:RP3 peptideGeneral Medicinemedicine.diseaseADAM ProteinsDisease Models Animal030104 developmental biologymedicine.anatomical_structureDisease ProgressionCommentarybiology.proteinlcsh:Medicine (General)Neuroscience030217 neurology & neurosurgeryEBioMedicine
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Lack of NG2 exacerbates neurological outcome and modulates glial responses after traumatic brain injury

2015

Traumatic brain injury (TBI) is a major cause of death and disability. The underlying pathophysiology is characterized by secondary processes including neuronal death and gliosis. To elucidate the role of the NG2 proteoglycan we investigated the response of NG2-knockout mice (NG2-KO) to TBI. Seven days after TBI behavioral analysis, brain damage volumetry and assessment of blood brain barrier integrity demonstrated an exacerbated response of NG2-KO compared to wild-type (WT) mice. Reactive astrocytes and expression of the reactive astrocyte and neurotoxicity marker Lcn2 (Lipocalin-2) were increased in the perilesional brain tissue of NG2-KO mice. In addition, microglia/macrophages with acti…

0301 basic medicinePathologymedicine.medical_specialtyMicrogliaTraumatic brain injurybusiness.industryNeurotoxicityPoison controlBrain damagemedicine.diseaseBlood–brain barrier03 medical and health sciencesCellular and Molecular Neuroscience030104 developmental biologymedicine.anatomical_structurenervous systemNeurologyGliosisImmunologymedicineNeurogliamedicine.symptombusinessGlia
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Progranulin protects against exaggerated axonal injury and astrogliosis following traumatic brain injury

2016

In response to traumatic brain injury (TBI) microglia/macrophages and astrocytes release inflammatory mediators with dual effects on secondary brain damage progression. The neurotrophic and anti-inflammatory glycoprotein progranulin (PGRN) attenuates neuronal damage and microglia/macrophage activation in brain injury but mechanisms are still elusive. Here, we studied histopathology, neurology and gene expression of inflammatory markers in PGRN-deficient mice (Grn-/- ) 24 h and 5 days after experimental TBI. Grn-/- mice displayed increased perilesional axonal injury even though the overall brain tissue loss and neurological consequences were similar to wild-type mice. Brain inflammation was …

0301 basic medicinePathologymedicine.medical_specialtyTraumatic brain injuryInflammationBrain damageBlood–brain barrier03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicinemedicineNeuroinflammationMicrogliabiologybusiness.industrymedicine.diseaseAstrogliosis030104 developmental biologymedicine.anatomical_structurenervous systemNeurologybiology.proteinmedicine.symptombusiness030217 neurology & neurosurgeryNeurotrophinGlia
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Depletion of regulatory T cells increases T cell brain infiltration, reactive astrogliosis, and interferon-γ gene expression in acute experimental tr…

2019

Abstract Background Traumatic brain injury (TBI) is a major cause of death and disability. T cells were shown to infiltrate the brain during the first days after injury and to exacerbate tissue damage. The objective of this study was to investigate the hitherto unresolved role of immunosuppressive, regulatory T cells (Tregs) in experimental TBI. Methods “Depletion of regulatory T cell” (DEREG) and wild type (WT) C57Bl/6 mice, treated with diphtheria toxin (DTx) to deplete Tregs or to serve as control, were subjected to the controlled cortical impact (CCI) model of TBI. Neurological and motor deficits were examined until 5 days post-injury (dpi). At the 5 dpi endpoint, (immuno-) histological…

0301 basic medicinePathologymedicine.medical_specialtyTraumatic brain injuryRegulatory T cellT cellImmunologyT cellsExcitotoxicityBrain damagemedicine.disease_causelcsh:RC346-42903 medical and health sciencesCellular and Molecular NeuroscienceTraumatic brain injury0302 clinical medicinemedicineImmune responselcsh:Neurology. Diseases of the nervous systemInflammationGlial fibrillary acidic proteinbiologybusiness.industryResearchGeneral Neurosciencemedicine.diseaseAstrogliosisCD8A030104 developmental biologymedicine.anatomical_structureNeurologyAstrocytesbiology.proteinCytokinesMicrogliamedicine.symptombusiness030217 neurology & neurosurgeryJournal of Neuroinflammation
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