Search results for "DAMAGE"

showing 10 items of 1289 documents

SHORT-TERM VARIABILITY OF 24-H SYSTOLIC BLOOD PRESSURE IS ASSOCIATED WITH MICROALBUMINURIA IN PATIENTS WITH PRIMARY HYPERTENSION

2015

Introduction: Limited and conflicting data are available about the association between short-term blood pressure (BP) variability and urinary albumin excretion rate (uAER). Aim: To analyse the relationships between microalbuminuria, defined as an uAER between 20 and 200 lg/min, and short-term BP variability, assessed as average real variability (ARV), weighted standard deviation (SD) of 24-h BP, and as SD of daytime and nighttime BP. Methods: The study population consisted of 316 untreated essential hypertensive patients with normal estimated glomerular filtration rate ([60 ml/min/1.73m2), which underwent 24-h ambulatory BP monitoring and 24-h uAER determination. Results: Microalbuminuria w…

MICROALBUMINURIAAMBULATORY BLOOD PRESSURE.EARLY RENAL DAMAGEBLOOD PRESSURE VARIABILITY
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Metabolic Inflammation-Associated IL-17A Causes Non-alcoholic Steatohepatitis and Hepatocellular Carcinoma

2016

Obesity increases hepatocellular carcinoma (HCC) risks via unknown mediators. We report that hepatic unconventional prefoldin RPB5 interactor (URI) couples nutrient surpluses to inflammation and non-alcoholic steatohepatitis (NASH), a common cause of HCC. URI-induced DNA damage in hepatocytes triggers inflammation via T helper 17 (Th17) lymphocytes and interleukin 17A (IL-17A). This induces white adipose tissue neutrophil infiltration mediating insulin resistance (IR) and fatty acid release, stored in liver as triglycerides, causing NASH. NASH and subsequently HCC are prevented by pharmacological suppression of Th17 cell differentiation, IL-17A blocking antibodies, and genetic ablation of t…

Male0301 basic medicineCancer ResearchCarcinoma HepatocellularInflammationWhite adipose tissueDiet High-FatMice03 medical and health sciencesNon-alcoholic Fatty Liver DiseasemedicineAnimalsHumansUnconventional prefoldin RPB5 interactorbiologyInterleukin-17Liver NeoplasmsFatty liverIntracellular Signaling Peptides and ProteinsCell Biologymedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticRepressor Proteins030104 developmental biologyNeutrophil InfiltrationOncologyHepatocellular carcinomaImmunologybiology.proteinTh17 CellsInterleukin 17SteatosisSteatohepatitismedicine.symptomDNA DamageCancer Cell
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The nucleotide excision repair protein XPC is essential for bulky DNA adducts to promote interleukin-6 expression via the activation of p38-SAPK

2016

Polycyclic aromatic hydrocarbons (PAHs) are environmental pollutants, and many are potent carcinogens. Benzo[a]pyrene (B[a]P), one of the best-studied PAHs, is metabolized ultimately to the genotoxin anti-B[a]P-7,8-dihydrodiol-9,10-epoxide (BPDE). BPDE triggers stress responses linked to gene expression, cell death and survival. So far, the underlying mechanisms that initiate these signal transduction cascades are unknown. Here we show that BPDE-induced DNA damage is recognized by DNA damage sensor proteins to induce activation of the stress-activated protein kinase (SAPK) p38. Surprisingly, the classical DNA damage response, which involves the kinases ATM and ATR, is not involved in p38-SA…

Male0301 basic medicineCancer ResearchDNA RepairCarcinogenesisDNA damagep38 mitogen-activated protein kinases78-Dihydro-78-dihydroxybenzo(a)pyrene 910-oxideBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyReal-Time Polymerase Chain ReactionTransfectionp38 Mitogen-Activated Protein KinasesDNA AdductsMice03 medical and health scienceschemistry.chemical_compoundGeneticsmedicinepolycyclic compoundsAnimalsHumansRNA Small InterferingMolecular BiologyCarcinogenMice KnockoutCisplatinInterleukin-6KinaseFibroblastsCell biologyDNA-Binding ProteinsMice Inbred C57BL030104 developmental biologychemistryCarcinogensNIH 3T3 CellsCancer researchComet AssaySignal transductionDNADNA DamageHeLa CellsMutagensSignal Transductionmedicine.drugNucleotide excision repairOncogene
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Abilities of berberine and chemically modified berberines to inhibit proliferation of pancreatic cancer cells.

2018

Berberine (BBR) is a common nutraceutical consumed by millions worldwide. BBR has many different effects on human health, e.g., diabetes, diarrhea, inflammation and now more recently it has been proposed to have potent anti-cancer effects. BBR has been shown to suppress the growth of cancer cells more than normal cells. BBR has been proposed to exert its growth-inhibitory effects by many different biochemical mechanisms including: suppression of cell cycle progression, induction of reactive oxygen species, induction of apoptosis and autophagy and interactions with DNA potentially leading to DNA damage, and altered gene expression. Pancreatic cancer is a leading cancer worldwide associated w…

Male0301 basic medicineCancer ResearchSettore MED/09 - Medicina InternaBerberineDNA damagePopulationSignal transduction inhibitorsApoptosisInflammation03 medical and health sciences0302 clinical medicineCell Line TumorPancreatic cancerGeneticsmedicineHumanseducationChemotherapeutic drugMolecular BiologySignal transduction inhibitorAgededucation.field_of_studybusiness.industryCell CycleAutophagyCancerPDACDNA Neoplasmmedicine.diseaseGene Expression Regulation NeoplasticPancreatic Neoplasms030104 developmental biologyApoptosis030220 oncology & carcinogenesisCancer cellCancer researchMolecular MedicineChemotherapeutic drugsmedicine.symptombusinessDNA DamageSignal Transduction
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Modifications of expression of genes and proteins involved in DNA repair and nitric oxide metabolism by carbatonides [disodium-2,6-dimethyl-1,4-dihyd…

2017

Abstract Studies on the pathogenesis of diabetes mellitus complications indicate that the compounds reducing free radicals and enhancing DNA repair could be prospective as possible remedies. Carbatonides, the disodium-2,6-dimethyl-1,4- dihydropyridine-3,5-bis(carbonyloxyacetate) derivatives, were tested for these properties. EPR spectroscopy showed that metcarbatone was an effective scavenger of hydroxyl radicals produced in the Fenton reaction, etcarbatone, and propcarbatone were less effective, styrylcarbatone was ineffective. UV/VIS spectroscopy revealed that styrylcarbatone manifested a hyperchromic effect when interacting with DNA, while all other carbatonides showeda hypochromic effec…

Male0301 basic medicineDihydropyridinesDNA RepairDNA damageDNA repairGene ExpressionPharmacologyNitric OxideToxicologyDiabetes Mellitus ExperimentalDiabetes Complications03 medical and health sciences0302 clinical medicineEnosDiabetes mellitusGene expressionmedicineAnimalsProspective StudiesbiologyChemistryPublic Health Environmental and Occupational HealthDihydropyridinemedicine.diseasebiology.organism_classificationStreptozotocinRatsComet assay030104 developmental biology030220 oncology & carcinogenesismedicine.drugArchives of Industrial Hygiene and Toxicology
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Analysis of the Possible Persistent Genotoxic Damage in Workers Linked to the Ardystil Syndrome

2016

[EN] Background: A combination of several factors including a change in the paint application system; a lack of proper hygiene; and inadequate safety measures caused a severe health impact in the workers of some textile painting factories. This outbreak, mainly characterized by respiratory disorders, caused the death of six people and it has been classified as Ardystil syndrome. Materials and Methods: Fifty-two workers involved in the outbreak and 48 healthy subjects not known to have exposed to the potentially mutagenic agents participated in the study. The program evaluated possible genotoxic damage through the sister chromatid exchange (SCE) cytogenetic biomarker assay. We determined the…

Male0301 basic medicineHealth impactPhysiologySister chromatid exchangeINGENIERIA NUCLEARToxicology03 medical and health sciencesOccupational ExposureHumansMedicineGenetics (clinical)business.industrySignificant differenceHealthy subjectsOutbreakSyndromeGeneral MedicineRespiration Disorders030104 developmental biologyTextile IndustryDistribution patternBiomarker (medicine)FemalebusinessSister Chromatid ExchangeDNA DamageGenetic Testing and Molecular Biomarkers
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Inferring heterozygosity from ancient and low coverage genomes

2016

Abstract While genetic diversity can be quantified accurately from high coverage sequencing data, it is often desirable to obtain such estimates from data with low coverage, either to save costs or because of low DNA quality, as is observed for ancient samples. Here, we introduce a method to accurately infer heterozygosity probabilistically from sequences with average coverage <1× of a single individual. The method relaxes the infinite sites assumption of previous methods, does not require a reference sequence, except for the initial alignment of the sequencing data, and takes into account both variable sequencing errors and potential postmortem damage. It is thus also applicable to …

Male0301 basic medicineHeterozygotePopulationGenomicsInvestigationsBiologyGenome03 medical and health sciences0302 clinical medicineGeneticsheterozygosityHumanslow coverageDNA AncienteducationPopulation and Evolutionary Geneticsancient DNA030304 developmental biologyGeneticsWhole genome sequencing0303 health scienceseducation.field_of_studyGenetic diversityBase SequenceGenome HumanGenetic Carrier ScreeningChromosome MappingGenetic VariationContrast (statistics)Coverage dataSequence Analysis DNApostmortem damageVariable (computer science)Genetics Population030104 developmental biologyAncient DNAEvolutionary biologybase recalibrationSoftware030217 neurology & neurosurgeryReference genome
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Neurotensin up-regulation is associated with advanced fibrosis and hepatocellular carcinoma in patients with MAFLD

2020

Background & aims: Neurotensin (NTS), a 13-aminoacid peptide localized in central nervous system and gastrointestinal tract, is involved in lipid metabolism and promotes various cancers onset mainly by binding to neurotensin receptor 1 (NTSR1). Increased plasma levels of pro-NTS, the stable NTS precursor, have been associated with type 2 diabetes (T2D), cardiovascular diseases and metabolic associated fatty liver disease (MAFLD). We aimed to evaluate 1) the impact of NTS rs1800832 and NTSR1 rs6090453 genetic variants on liver damage in 1166 MAFLD European individuals, 2) the relation between NTS variant and circulating pro-NTS and 3) the hepatic NTS expression by RNAseq transcriptomic a…

Male0301 basic medicineLiver damagemedicine.medical_specialtyGenetic variantsCarcinoma HepatocellularNeurotensin receptor 1CirrhosisTherapeutic targetSettore MED/12 - GASTROENTEROLOGIAType 2 diabetesGastroenterology03 medical and health sciencesLiver disease0302 clinical medicineFibrosisInternal medicinemedicineHumansReceptors NeurotensinBiomarker; Genetic variants; Lipid metabolism; Liver damage; Therapeutic targetMolecular BiologyNeurotensinAgedCell Proliferationbusiness.industryLiver NeoplasmsFatty liverBiomarker Genetic variants Lipid metabolism Liver damage Therapeutic targetCell BiologyBiomarkerMiddle Agedrespiratory systemmedicine.diseaseFibrosisFatty Liver030104 developmental biologyLipid metabolismDiabetes Mellitus Type 2Gene Expression Regulationnervous systemHepatocellular carcinomaMutationFemale030211 gastroenterology & hepatologybusinessHepatic fibrosiscirculatory and respiratory physiology
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Plasminogen activator inhibitor‐1 augments damage by impairing fibrinolysis after traumatic brain injury

2019

Objective Plasminogen activator inhibitor-1 (PAI-1) is the key endogenous inhibitor of fibrinolysis, and enhances clot formation after injury. In traumatic brain injury, dysregulation of fibrinolysis may lead to sustained microthrombosis and accelerated lesion expansion. In the present study, we hypothesized that PAI-1 mediates post-traumatic malfunction of coagulation, with inhibition or genetic depletion of PAI-1 attenuating clot formation and lesion expansion after brain trauma. Methods We evaluated PAI-1 as a possible new target in a mouse controlled cortical impact (CCI) model of traumatic brain injury. We performed the pharmacological inhibition of PAI-1 with PAI-039 and stimulation b…

Male0301 basic medicineTraumatic brain injurymedicine.medical_treatmentBrain damagePharmacologyLesionMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineBrain Injuries TraumaticSerpin E2FibrinolysisAnimalsMedicineThrombusResearch ArticlesIndoleacetic Acidsbusiness.industryFibrinolysisBrainmedicine.diseaseMice Inbred C57BL030104 developmental biologyNeurologychemistryPlasminogen activator inhibitor-1Neurology (clinical)medicine.symptombusinessPlasminogen activator030217 neurology & neurosurgeryIntravital microscopyResearch ArticleAnnals of Neurology
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RS1 (Rsc1A1) deficiency limits cerebral SGLT1 expression and delays brain damage after experimental traumatic brain injury

2018

Acute cerebral lesions are associated with dysregulation of brain glucose homeostasis. Previous studies showed that knockdown of Na+ -D-glucose cotransporter SGLT1 impaired outcome after middle cerebral artery occlusion and that widely expressed intracellular RS1 (RSC1A1) is involved in transcriptional and post-translational down-regulation of SGLT1. In the present study, we investigated whether SGLT1 is up-regulated during traumatic brain injury (TBI) and whether removal of RS1 in mice (RS1-KO) influences SGLT1 expression and outcome. Unexpectedly, brain SGLT1 mRNA in RS1-KO was similar to wild-type whereas it was increased in small intestine and decreased in kidney. One day after TBI, SGL…

Male0301 basic medicinemedicine.medical_specialtyTraumatic brain injuryGene ExpressionBrain EdemaBrain damageBiochemistryProinflammatory cytokineMice03 medical and health sciencesCellular and Molecular NeuroscienceSodium-Glucose Transporter 10302 clinical medicineInternal medicineCortex (anatomy)Brain Injuries TraumaticmedicineAnimalsGlucose homeostasisEye ProteinsBrain ChemistryCerebral CortexMice KnockoutGene knockdownKidneyMovement DisordersMicrogliabusiness.industrydigestive oral and skin physiologyBrainmedicine.diseaseUp-RegulationMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEndocrinologyCytokinesMicrogliamedicine.symptombusinessCell Adhesion Molecules030217 neurology & neurosurgeryJournal of Neurochemistry
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