Search results for "fibrosi"

showing 10 items of 936 documents

Fasting inhibits hepatic stellate cells activation and potentiates anti-cancer activity of Sorafenib in hepatocellular cancer cells

2017

BACKGROUND: Hepatocellular carcinoma (HCC) has a poor outcome. Most HCCs develop in the context of liver fibrosis and cirrhosis caused by chronic inflammation. Short-term fasting approaches enhance the activity of chemotherapy in preclinical cancer models, other than HCC. Multi-tyrosine kinase inhibitor Sorafenib is the mainstay of treatment in HCC. However, its benefit is frequently short-lived. Whether fasting can alleviate liver fibrosis and whether combining fasting with Sorafenib is beneficial remains unknown. METHODS: 24 hour fasting (2% serum, 0.1% glucose)-induced changes on human hepatic stellate cells (HSC) LX-2 proliferation/viability/cell cycle were assessed by MTT and flow cyto…

0301 basic medicineSorafenibLipopolysaccharidesNiacinamidemedicine.medical_specialtyCirrhosisCarcinoma HepatocellularTime FactorsPhysiologyGlucose uptakeClinical BiochemistryAntineoplastic AgentsLiver Cirrhosis Experimental03 medical and health sciencesFibrosisNon-alcoholic Fatty Liver DiseaseInternal medicineSorafenib fastingmedicineHepatic Stellate CellsAnimalsHumansneoplasmsCell Proliferationhepatic stellate cellDose-Response Relationship Drugbusiness.industryMedicine (all)Phenylurea CompoundsLiver NeoplasmsCancerCell BiologyFastingHep G2 Cellshepatocellular carcinomaSorafenibmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyEndocrinologyGlucoseHepatocellular carcinomaHepatic stellate cellCancer researchSteatohepatitisbusinessmedicine.drug
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Insulin resistance and hyperandrogenism drive steatosis and fibrosis risk in young females with PCOS

2017

Background and aims Nonalcoholic fatty liver disease (NAFLD) and polycystic ovary syndrome (PCOS) recognize obesity and insulin resistance (IR) as common pathogenic background. We assessed 1) whether PCOS is a risk factor for steatosis, and 2) the impact, in PCOS patients, of IR and hyperandrogenism on steatosis and fibrosis. Methods We considered 202 consecutive Italian PCOS nondiabetic patients and 101 age-matched controls. PCOS was diagnosed applying the Rotterdam diagnostic criteria. Steatosis was diagnosed if hepatic steatosis index (HSI) >36, while fibrosis by using the FIB-4 score. As surrogate estimate of insulin sensitivity we considered the insulin sensitivity index (ISI). Free an…

0301 basic medicineSteatosisendocrine system diseasesPhysiologylcsh:MedicinePathology and Laboratory MedicineBiochemistryBody Mass IndexCytopathology0302 clinical medicineEndocrinologyNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseMedicine and Health SciencesInsulinlcsh:ScienceMultidisciplinaryLiver DiseasesFatty liverMiddle AgedPolycystic ovaryLipidsCholesterolOncologyPhysiological Parameters030211 gastroenterology & hepatologyFemalePolycystic Ovary SyndromeResearch ArticleAdultmedicine.medical_specialtyGastroenterology and Hepatology03 medical and health sciencesInsulin resistanceInternal medicinemedicineHumansObesityRisk factorTriglyceridesDiabetic Endocrinologybusiness.industryFree androgen indexHyperandrogenismCholesterol HDLBody Weightlcsh:RCancers and NeoplasmsBiology and Life Sciencesmedicine.diseaseFibrosisHormonesFatty Liver030104 developmental biologyEndocrinologyAnatomical Pathologylcsh:QSteatosisInsulin ResistancebusinessHyperandrogenismGynecological TumorsDevelopmental Biologyinsulin resistance PCOS
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GSE4-loaded nanoparticles a potential therapy for lung fibrosis that enhances pneumocyte growth, reduces apoptosis and DNA damage.

2021

© 2021 The Authors.

0301 basic medicineTelomeraseDNA damageApoptosismacromolecular substancesBleomycintelomeraseBiochemistryPulmonary fibrosisAlveolar cellsAlveolar cells03 medical and health scienceschemistry.chemical_compoundIdiopathic pulmonary fibrosisBleomycin0302 clinical medicineFibrosisPulmonary fibrosisGeneticsmedicineHumansMolecular BiologyTelomeraseLungLungNanopartículespulmonary fibrosisChemistrytechnology industry and agricultureFibrosi pulmonaralveolar cellsrespiratory systemmedicine.diseaseOxidative Stress030104 developmental biologymedicine.anatomical_structureAlveolar Epithelial CellsCancer researchGSE4NanoparticlesCollagenPeptides030217 neurology & neurosurgeryBiotechnologyDNA DamageFASEB journal : official publication of the Federation of American Societies for Experimental BiologyREFERENCES
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Multicenter validation study for the certification of a CFTR gene scanning method using next generation sequencing technology.

2018

AbstractBackground:Many European laboratories offer molecular genetic analysis of theCFTRgene using a wide range of methods to identify mutations causative of cystic fibrosis (CF) and CFTR-related disorders (CFTR-RDs). Next-generation sequencing (NGS) strategies are widely used in diagnostic practice, and CE marking is now required for most in vitro diagnostic (IVD) tests in Europe. The aim of this multicenter study, which involved three European laboratories specialized in CF molecular analysis, was to evaluate the performance of Multiplicom’s CFTR MASTR Dx kit to obtain CE-IVD certification.Methods:A total of 164 samples, previously analyzed with well-established “reference” methods for t…

0301 basic medicineValidation studycongenital hereditary and neonatal diseases and abnormalitiesCertification[SDV]Life Sciences [q-bio]Clinical BiochemistrySequencing dataCFTR molecular diagnosiCystic Fibrosis Transmembrane Conductance RegulatorComputational biology030105 genetics & heredityBiologyCFTR molecular diagnosisDNA sequencingIn vitro diagnosticCftr genecystic fibrosis03 medical and health sciencesHumanscystic fibrosiCE-IVD certificationBiochemistry (medical)Reproducibility of ResultsIllumina miseqSequence Analysis DNAGeneral MedicineMolecular analysisEurope030104 developmental biologyMulticenter studycomparative sequencing analysicomparative sequencing analysisMutationnext-generation sequencingMultiplex Polymerase Chain Reaction
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Calcifediol-loaded liposomes for local treatment of pulmonary bacterial infections.

2017

The influence of vitamin D3 and its metabolites calcifediol (25(OH)D) and calcitriol on immune regulation and inflammation is well described, and raises the question of potential benefit against bacterial infections. In the current study, 25(OH)D was encapsulated in liposomes to enable aerosolisation, and tested for the ability to prevent pulmonary infection by Pseudomonas aeruginosa. Prepared 25(OH)D-loaded liposomes were nanosized and monodisperse, with a negative surface charge and a 25(OH)D entrapment efficiency of approximately 23%. Jet nebulisation of liposomes was seen to yield an aerosol suitable for tracheo-bronchial deposition. Interestingly, 25(OH)D in either liposomes or ethanol…

0301 basic medicineVitaminRMCalcitriolCystic FibrosisPharmaceutical ScienceInflammationBronchiBiologyPharmacologymedicine.disease_causeMicrobiologyProinflammatory cytokineCell Line03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinePseudomonas infectionAdministration InhalationmedicineAnimalsHumansImmunologic FactorsPseudomonas InfectionsRespiratory Tract InfectionsCalcifediolLiposomePseudomonas aeruginosaEpithelial CellsGeneral Medicinemedicine.disease030104 developmental biology030228 respiratory systemchemistryLiposomesPseudomonas aeruginosaCytokinesNanoparticlesCalcifediolmedicine.symptomBiotechnologymedicine.drug
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Targeting Nonsense: Optimization of 1,2,4-Oxadiazole TRIDs to Rescue CFTR Expression and Functionality in Cystic Fibrosis Cell Model Systems

2020

Cystic fibrosis (CF) patients develop a severe form of the disease when the cystic fibrosis transmembrane conductance regulator (CFTR) gene is affected by nonsense mutations. Nonsense mutations are responsible for the presence of a premature termination codon (PTC) in the mRNA, creating a lack of functional protein. In this context, translational readthrough-inducing drugs (TRIDs) represent a promising approach to correct the basic defect caused by PTCs. By using computational optimization and biological screening, we identified three new small molecules showing high readthrough activity. The activity of these compounds has been verified by evaluating CFTR expression and functionality after…

0301 basic medicineYellow fluorescent proteinCystic Fibrosisnonsense mutationCystic Fibrosis Transmembrane Conductance RegulatorCystic fibrosislcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5SpectroscopyCells CulturedbiologyChemistryGeneral MedicineSmall moleculeCystic fibrosis transmembrane conductance regulatorComputer Science ApplicationsCell biologyCodon Nonsense030220 oncology & carcinogenesisNonsense mutationContext (language use)Settore BIO/11 - Biologia MolecolareCatalysisArticleInorganic Chemistry03 medical and health sciencesmedicineHumansRNA MessengerPhysical and Theoretical ChemistryMolecular BiologyGeneMessenger RNAOrganic ChemistryoxadiazolesSettore CHIM/06 - Chimica Organicapremature termination codonmedicine.diseaseSettore CHIM/08 - Chimica FarmaceuticaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulationlcsh:Biology (General)lcsh:QD1-999translational readthrough inducing drugsProtein BiosynthesisMutationbiology.proteingenetic disorderInternational Journal of Molecular Sciences
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Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice

2018

Fibrosis remains a serious health concern in patients with chronic liver disease. We recently reported that chemically induced chronic murine liver injury triggers increased expression of junctional adhesion molecules (JAMs) JAM-B and JAM-C by endothelial cells and de novo synthesis of JAM-C by hepatic stellate cells (HSCs). Here, we demonstrate that biopsies of patients suffering from primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) or autoimmune hepatitis (AIH) display elevated levels of JAM-C on portal fibroblasts (PFs), HSCs, endothelial cells and cholangiocytes, whereas smooth muscle cells expressed JAM-C constitutively. Therefore, localization and function of JA…

0301 basic medicine[SDV]Life Sciences [q-bio]Cholangitis SclerosingMyocytes Smooth MuscleeducationImmunologyImmunoglobulinsAutoimmune hepatitisVascular RemodelingChronic liver diseaseMural cellPrimary sclerosing cholangitisFatty Acids MonounsaturatedMice03 medical and health sciencesFibrosisCell AdhesionmedicineAnimalsHumansImmunology and AllergyMyofibroblastsCells CulturedInflammationMice KnockoutFibrous capsule of GlissonLiver Cirrhosis Biliarybusiness.industryfungiEndothelial Cellsmedicine.diseaseFibrosishumanities3. Good healthMice Inbred C57BLDisease Models AnimalHepatitis Autoimmune030104 developmental biologyLiverVasoconstrictioncardiovascular systemCancer researchHepatic stellate cellFemaleHepatic fibrosisbusinessCell Adhesion MoleculesJournal of Autoimmunity
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Autophagy Stimulation as a Potential Strategy Against Intestinal Fibrosis

2019

We recently observed reduced autophagy in Crohn’s disease patients and an anti-inflammatory effect of autophagy stimulation in murine colitis, but both anti- and pro-fibrotic effects are associated with autophagy stimulation in different tissues, and fibrosis is a frequent complication of Crohn’s disease. Thus, we analyzed the effects of pharmacological modulation of autophagy in a murine model of intestinal fibrosis and detected that autophagy inhibition aggravates, while autophagy stimulation prevents, fibrosis. These effects are associated with changes in inflammation and in collagen degradation in primary fibroblasts. Thus, pharmacological stimulation of autophagy may be useful against …

0301 basic medicineautophagyStimulationInflammationDiseaseIntestinal fibrosis03 medical and health sciencesMice0302 clinical medicineCrohn DiseaseFibrosismedicineintestinal fibrosisMurine colitisAnimalslcsh:QH301-705.5Sirolimusbusiness.industryBrief ReportAutophagyGeneral MedicineFibroblastsmedicine.diseaseFibrosisIntestinesMice Inbred C57BLDisease Models Animal030104 developmental biologylcsh:Biology (General)inflammationCancer research030211 gastroenterology & hepatologyCollagenmedicine.symptomComplicationbusinessImmunosuppressive AgentsCells
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Induction of Autophagy by Pterostilbene Contributes to the Prevention of Renal Fibrosis via Attenuating NLRP3 Inflammasome Activation and Epithelial-…

2020

Chronic kidney disease (CKD) is recognized as a global public health problem. NLRP3 inflammasome activation has been characterized to mediate diverse aspect mechanisms of CKD through regulation of proinflammatory cytokines, tubulointerstitial injury, glomerular diseases, renal inflammation, and fibrosis pathways. Autophagy is a characterized negative regulation mechanism in the regulation of the NLRP3 inflammasome, which is now recognized as the key regulator in the pathogenesis of inflammation and fibrosis in CKD. Thus, autophagy is undoubtedly an attractive target for developing new renal protective treatments of kidney disease via its potential effects in regulation of inflammasome. Howe…

0301 basic medicineautophagypterostilbeneATG5epithelial-mesenchymal transitionInflammationProinflammatory cytokine03 medical and health sciencesCell and Developmental Biology0302 clinical medicineFibrosismedicineRenal fibrosisEpithelial–mesenchymal transitionlcsh:QH301-705.5Original Researchbusiness.industryAutophagyInflammasomeCell Biologymedicine.diseaserenal fibrosisNLRP3 inflammasome030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisCancer researchmedicine.symptombusinessDevelopmental Biologymedicine.drugFrontiers in Cell and Developmental Biology
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Polyphosphate Reverses the Toxicity of the Quasi-Enzyme Bleomycin on Alveolar Endothelial Lung Cells In Vitro

2021

Simple Summary Bleomycin (BLM) is a medication introduced used to treat various types of cancer, including testicular cancer, ovarian cancer, and Hodgkin’s disease. Its most serious side effect is pulmonary fibrosis and impaired lung function. Using A549 human lung cells it is shown that, in parallel to an increased cell toxicity and DNA damage, BLM causes a marked enlargement of the cell nucleus. This effect is abolished by inorganic polyphosphate (polyP), if this physiological polymer is administered together with BLM. The detoxification of BLM is–most likely–caused by the upregulation of the gene encoding the BLM hydrolase which inactivates BLM in vitro and in vivo. This study contribute…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA damageBleomycinlcsh:RC254-282Article03 medical and health scienceschemistry.chemical_compound0302 clinical medicineanti-SARS-CoV-2 activityDownregulation and upregulationprevention of fibrosischemistry.chemical_classificationbleomycinpulmonary fibrosisurogenital systemChemistryCell growthCOVID-19nutritional and metabolic diseasespolyphosphatelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologyIn vitroChromatin030104 developmental biologyEnzymeOncology030220 oncology & carcinogenesisToxicityCancers
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