Search results for "Lung"

showing 10 items of 2389 documents

In vivo studies of altered expression patterns of p53 and proliferative control genes in chronic vitamin A deficiency and hypervitaminosis

2003

Several clinical trials have revealed that individuals who were given beta-carotene and vitamin A did not have a reduced risk of cancer compared to those given placebo; rather, vitamin A could actually have caused an adverse effect in the lungs of smokers [Omenn, G.S., Goodman, G.E., Thornquist, M.D., Balmes, J., Cullen, M.R., Glass, A., Keogh, J.P., Meyskens, F.L., Valanis, B., Williams, J.H., Barnhart, S. & Hammar, S. N. Engl. J. Med (1996) 334, 1150-1155; Hennekens, C.H., Buring, J.E., Manson, J.E., Stampfer, M., Rosner, B., Cook, N.R., Belanger, C., LaMotte, F., Gaziano, J.M., Ridker, P.M., Willet, W. & Peto, R. (1996) N. Engl. J. Med. 334, 1145-1149]. Using differential display techniq…

Cyclin-Dependent Kinase Inhibitor p21VitaminRetinyl Estersmedicine.medical_specialtyMacromolecular SubstancesProto-Oncogene Proteins c-junReceptors Retinoic AcidBlotting WesternRetinoic acidBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundIn vivoCyclinsInternal medicinemedicineAnimalsHypervitaminosis ARNA MessengerRats WistarVitamin AReceptorLungDifferential displayReverse Transcriptase Polymerase Chain ReactionVitamin A DeficiencyGene Expression ProfilingDNAmedicine.diseaseHypervitaminosisPrecipitin TestsRatsVitamin A deficiencyEndocrinologyGene Expression RegulationLiverchemistryChronic DiseaseImmunologyDiterpenesTumor Suppressor Protein p53CarcinogenesisCell DivisionEuropean Journal of Biochemistry
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Roflumilast improves corticosteroid resistance COPD bronchial epithelial cells stimulated with toll like receptor 3 agonist

2015

Chronic obstructive pulmonary disease (COPD) is characterised by chronic pulmonary inflammation punctuated by periods of viral exacerbations. Recent evidence suggests that the combination of roflumilast with corticosteroids may improve the compromised anti-inflammatory properties of corticosteroids in COPD. We analyzed differential and combination anti-inflammatory effects of dexamethasone and roflumilast N-oxide in human bronchial epithelial cells (HBECs) stimulated with viral toll like receptor (TLR) agonists. Lung tissue and HBECs were isolated from healthy (n = 15), smokers (n = 12) and smokers with COPD (15). TLR3 expression was measured in lung tissue and in HBECs. IL-8 secretion was …

CyclopropanesMaleAnti-Inflammatory AgentsDrug ResistanceAminopyridinesDexamethasonePulmonary Disease Chronic ObstructiveRoflimilastAdrenal Cortex HormonesToll like receptorsCells CulturedCOPDSmokingMiddle Agedmedicine.anatomical_structureBenzamidesCorticosteroidViral exacerbationDrug Therapy CombinationFemalePulmones - Enfermedadesmedicine.drugSignal TransductionAgonistPulmonary and Respiratory Medicinemedicine.medical_specialtymedicine.drug_classCorticosteroid resistanceBronchiInternal medicinemedicineCOPDHumansInterleukin 8DexamethasoneRoflumilastAgedLungbusiness.industryResearchInterleukin-8Epithelial CellsAparato respiratoriomedicine.diseaserespiratory tract diseasesToll-Like Receptor 3EndocrinologyPoly I-CCase-Control StudiesTLR3businessRespiratory Research
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Roflumilast Prevents the Metabolic Effects of Bleomycin-Induced Fibrosis in a Murine Model

2015

Fibrotic remodeling is a process common to chronic lung diseases such as chronic obstructive pulmonary disease (COPD), pulmonary fibrosis, acute respiratory distress syndrome and asthma. Based on preclinical studies phosphodiesterase 4 (PDE4) inhibitors may exhibit beneficial anti-inflammatory and anti-remodeling properties for the treatment of these respiratory disorders. Effects of PDE4 inhibitors on changes in the lung metabolome in models of pulmonary fibrotic remodeling have not yet been explored. This work studies the effects of the PDE4 inhibitor roflumilast on changes in the lung metabolome in the common murine model of bleomycin-induced lung fibrosis by nuclear magnetic resonance (…

CyclopropanesMalePathologymedicine.medical_specialtyMagnetic Resonance SpectroscopyPulmonary Fibrosislcsh:MedicineAminopyridinesPharmacologyBiologyBleomycinBleomycinMicechemistry.chemical_compoundFibrosisPulmonary fibrosismedicineMetabolomeAnimalsRespiratory systemlcsh:ScienceLungRoflumilastCOPDMultidisciplinaryLunglcsh:Rmedicine.diseaserespiratory tract diseasesMice Inbred C57BLDisease Models Animalmedicine.anatomical_structurechemistryBenzamidesMetabolomelcsh:QResearch Articlemedicine.drugPLOS ONE
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Roflumilast, a phosphodiesterase 4 inhibitor, alleviates bleomycin-induced lung injury

2009

Mandarin translation of abstract Background and purpose:  The effects of a phosphodiesterase 4 (PDE4) inhibitor, roflumilast, on bleomycin-induced lung injury were explored in ‘preventive’ and ‘therapeutic’ protocols and compared with glucocorticoids. Experimental approach:  Roflumilast (1 and 5 mg·kg−1·d−1, p.o.) or dexamethasone (2.5 mg·kg−1·d−1, p.o.) was given to C57Bl/6J mice from day 1 to 14 (preventive) or day 7 to 21 (therapeutic) after intratracheal bleomycin (3.75 U·kg−1). In Wistar rats, roflumilast (1 mg·kg−1·d−1, p.o.) was compared with methylprednisolone (10 mg·kg−1·d−1, p.o.) from day 1 to 21 (preventive) or from day 10 to 21 (therapeutic), following intratracheal instillatio…

CyclopropanesMalemedicine.medical_specialtyPhosphodiesterase InhibitorsPulmonary FibrosisAminopyridinesLung injuryBiologyBleomycinBronchoalveolar Lavagechemistry.chemical_compoundBleomycinMiceFibrosisRight ventricular hypertrophyInternal medicinePulmonary fibrosismedicineAnimalsRats WistarLungDexamethasoneRoflumilastPharmacologymedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionLung Injuryrespiratory systemmedicine.diseaseResearch Papersrespiratory tract diseasesRatsMice Inbred C57BLDisease Models AnimalBronchoalveolar lavageEndocrinologychemistryBenzamidesPhosphodiesterase 4 InhibitorsBronchoalveolar Lavage Fluidmedicine.drug
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The preclinical pharmacology of roflumilast--a selective, oral phosphodiesterase 4 inhibitor in development for chronic obstructive pulmonary disease

2009

After more than two decades of research into phosphodiesterase 4 (PDE4) inhibitors, roflumilast (3-cyclopropylmethoxy-4-difluoromethoxy-N-[3,5-di-chloropyrid-4-yl]-benzamide) may become the first agent in this class to be approved for patient treatment worldwide. Within the PDE family of 11 known isoenzymes, roflumilast is selective for PDE4, showing balanced selectivity for subtypes A-D, and is of high subnanomolar potency. The active principle of roflumilast in man is its dichloropyridyl N-oxide metabolite, which has similar potency as a PDE4 inhibitor as the parent compound. The long half-life and high potency of this metabolite allows for once-daily, oral administration of a single, 500…

CyclopropanesPulmonary and Respiratory MedicinePhosphodiesterase Inhibitorsmedicine.drug_classDrug Evaluation PreclinicalAdministration OralAminopyridinesInflammationPharmacologyPulmonary Disease Chronic ObstructiveCOPD; Inflammation; Oral therapy; Phosphodiesterase 4; Preclinical pharmacology; RoflumilastBronchodilatormedicineAnimalsHumansCOPDPharmacology (medical)RoflumilastPhosphodiesterase 4InflammationCOPDLungOral therapybusiness.industryAnti-Inflammatory Agents Non-SteroidalBiochemistry (medical)medicine.diseasePulmonary hypertensionObstructive lung diseasemedicine.anatomical_structureTolerabilityBenzamidesImmunologyPhosphodiesterase 4 InhibitorsPreclinical pharmacologymedicine.symptombusinessRoflumilastmedicine.drug
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Myc Promoter-Binding Protein-1 (MBP-1) Is a Novel Potential Prognostic Marker in Invasive Ductal Breast Carcinoma

2010

BackgroundAlpha-enolase is a glycolytic enzyme that catalyses the formation of phosphoenolpyruvate in the cell cytoplasm. α-Enolase and the predominantly nuclear Myc promoter-binding protein-1 (MBP-1) originate from a single gene through the alternative use of translational starting sites. MBP-1 binds to the P2 c-myc promoter and competes with TATA-box binding protein (TBP) to suppress gene transcription. Although several studies have shown an antiproliferative effect of MBP-1 overexpression on several human cancer cells, to date detailed observations of α-enolase and MBP-1 relative expression in primary tumors versus normal tissues and their correlation with clinicopathological features ha…

CytoplasmAlpha-enolasePROGRESSIONAged 80 and overRegulation of gene expressionMultidisciplinaryQRGenetics and Genomics/Gene ExpressionMiddle AgedPrognosisPathology/Molecular PathologyNUDE-MICETransport proteinCarcinoma DuctalDNA-Binding ProteinsGene Expression Regulation NeoplasticProtein Transportmedicine.anatomical_structureGLYCOLYTIC ENZYMEOncology/Breast CancerMedicineCELL LUNG-CANCER; ALPHA-ENOLASE; PROTEOMIC ANALYSIS; GLYCOLYTIC ENZYME; NUDE-MICE; GENE; IDENTIFICATION; PROGRESSION; EXPRESSION; METASTASESFemalePROTEOMIC ANALYSISEnolase MBP-1 Breast cancer ImmunohistochemistryResearch ArticleAdultEXPRESSIONScienceCELL LUNG-CANCERBreast NeoplasmsBiologyDNA-binding proteinBiomarkers TumormedicineHumansNeoplasm InvasivenessGeneAgedCell NucleusIDENTIFICATIONBinding proteinALPHA-ENOLASEGENEMolecular biologySettore BIO/18 - GeneticaCell nucleusMETASTASESCytoplasmPhosphopyruvate Hydratasebiology.proteinPLoS ONE
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Immunosurveillance of lung melanoma metastasis in EBI-3-deficient mice mediated by CD8+ T cells.

2008

Abstract EBV-induced gene 3 (EBI-3) codes for a soluble type I receptor homologous to the p40 subunit of IL-12 that is expressed by APCs following activation. In this study, we assessed the role of EBI-3 in a model of lung melanoma metastasis. Intravenous injection of the B16-F10 cell line resulted in a significant reduction of lung tumor metastasis in EBI-3−/− recipient mice compared with wild-type mice. The immunological finding accompanying this effect was the expansion of a newly described cell subset called IFN-γ producing killer dendritic cells associated with CD8+ T cell responses in the lung of EBI-3−/− mice including IFN-γ release and TNF-α-induced programmed tumor cell death. Depl…

Cytotoxicity ImmunologicAdoptive cell transferLung NeoplasmsT cellImmunologyMelanoma ExperimentalBiologyCD8-Positive T-LymphocytesArticleMetastasisMinor Histocompatibility AntigensGene Knockout TechniquesMiceCell Line TumormedicineImmunology and AllergyCytotoxic T cellAnimalsLung MelanomaReceptors CytokineImmunologic SurveillanceCell Line TransformedMice KnockoutMelanomamedicine.diseaseImmunosurveillanceMice Inbred C57BLmedicine.anatomical_structureCell Transformation NeoplasticImmunologyInjections IntravenousAnimals; CD8-Positive T-Lymphocytes; Cell Line Transformed; Cell Line Tumor; Cell Transformation Neoplastic; Cytotoxicity Immunologic; Gene Knockout Techniques; Immunologic Surveillance; Injections Intravenous; Lung Neoplasms; Melanoma Experimental; Mice; Mice Inbred C57BL; Mice Knockout; Neoplasm Transplantation; Receptors Cytokine; T-Box Domain ProteinsCancer researchT-Box Domain ProteinsCD8Neoplasm Transplantation
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Gemcitabine sensitizes lung cancer cells to Fas/FasL system-mediated killing

2014

Gemcitabine is a chemotherapy agent commonly used in the treatment of non-small cell lung cancer (NSCLC) that has been demonstrated to induce apoptosis in NSCLC cells by increasing functionally active Fas expression. The aim of this study was to evaluate the Fas/Fas ligand (FasL) system involvement in gemcitabine-induced lung cancer cell killing. NSCLC H292 cells were cultured in the presence or absence of gemcitabine. FasL mRNA and protein were evaluated by real-time PCR, and by Western blot and flow cytometry, respectively. Apoptosis of FasL-expressing cells was evaluated by flow cytometry, and caspase-8 and caspase-3 activation by Western blot and a colorimetric assay. Cytotoxicity of ly…

Cytotoxicity ImmunologicAntimetabolites AntineoplasticFas Ligand ProteinLung NeoplasmsImmunologychemical and pharmacologic phenomenaApoptosisSettore MED/10 - Malattie Dell'Apparato RespiratorioDeoxycytidineFas ligandFlow cytometryCarcinoma Non-Small-Cell LungCell Line TumormedicineImmunology and AllergyCytotoxic T cellHumansfas ReceptorLung cancerAutocrine signallingKiller Cells Lymphokine-ActivatedCaspase 8Lymphokine-activated killer cellmedicine.diagnostic_testChemistryCaspase 3Original Articlesmedicine.diseaseMolecular biologyGemcitabineGemcitabineApoptosisapoptosis cytotoxic lymphocytes non-small cell lung cancermedicine.drug
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Effect of the protein kinase inhibitors, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine H-7 and N-(2-[methylamino]ethyl)-5-isoquinoline-sulfonamide H…

1998

The effects of 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine H-7 (a cAMP-dependent protein kinase and protein kinase C inhibitor), n-(2-[methylamino]ethyl)-5-isoquinoline-sulfonamide H-8 (a cAMP- and cGMP-dependent protein kinase inhibitor) and indomethacin (IND, a cyclooxygenase inhibitor) on both the spontaneous metastatic ability of 3LL (Lewis lung carcinoma) tumor cells and anti-tumor host response were studied. The study of tumor progression showed that H-7 and H-8 (2 mg kg(-1) day(-1) , i.p., for 8 days) significantly reduced the mean number of metastases (0.8 +/- 0.2 and 1.0 +/- 0.7, respectively, P0.05) with respect to the number of lung metastases (4.2 +/- 2.1) observed in the con…

Cytotoxicity ImmunologicMalemedicine.medical_specialtymedicine.drug_classIndomethacinCarcinoma Lewis LungMiceInternal medicine1-(5-Isoquinolinesulfonyl)-2-MethylpiperazinemedicineAnimalsCyclooxygenase InhibitorsLymphocytesEnzyme InhibitorsNeoplasm MetastasisCytotoxicityProtein kinase AProtein kinase CPharmacologybiologyLewis lung carcinomaProtein kinase inhibitorIsoquinolinesMice Inbred C57BLEndocrinologyEnzyme inhibitorTumor progressionbiology.proteinCancer researchDisease ProgressionLeukocytes MononuclearCyclooxygenaseCell DivisionNeoplasm TransplantationSpleenEuropean journal of pharmacology
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Metabolic and Functional Genomic Studies Identify Deoxythymidylate Kinase as a target in LKB1 Mutant Lung Cancer

2013

Abstract The LKB1/STK11 tumor suppressor encodes a serine/threonine kinase, which coordinates cell growth, polarity, motility, and metabolism. In non–small cell lung carcinoma, LKB1 is somatically inactivated in 25% to 30% of cases, often concurrently with activating KRAS mutations. Here, we used an integrative approach to define novel therapeutic targets in KRAS-driven LKB1-mutant lung cancers. High-throughput RNA interference screens in lung cancer cell lines from genetically engineered mouse models driven by activated KRAS with or without coincident Lkb1 deletion led to the identification of Dtymk, encoding deoxythymidylate kinase (DTYMK), which catalyzes dTTP biosynthesis, as synthetica…

DNA Replicationcongenital hereditary and neonatal diseases and abnormalitiesLung NeoplasmsMutantSTK11BiologyAMP-Activated Protein KinasesProtein Serine-Threonine Kinasesmedicine.disease_causeArticleProto-Oncogene Proteins p21(ras)MiceDeoxythymidylate kinaseAMP-Activated Protein Kinase KinasesRNA interferenceCell Line TumorCarcinoma Non-Small-Cell LungmedicineMetabolomicsThymine NucleotidesAnimalsHumansMolecular Targeted TherapyLung cancerskin and connective tissue diseasesCell DeathModels GeneticKinaseCell growthGenomicsmedicine.diseaseMolecular biologyHigh-Throughput Screening AssaysOncologyGene Knockdown TechniquesCancer researchRNA InterferenceKRASNucleoside-Phosphate KinaseDNA Damage
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