Search results for "Forming."

showing 10 items of 1704 documents

Progressive pulmonary fibrosis is mediated by TGF-β isoform 1 but not TGF-β3

2007

Tissue repair is a well-orchestrated biological process involving numerous soluble mediators, and an imbalance between these factors may result in impaired repair and fibrosis. Transforming growth factor (TGF)-beta is a key profibrotic element in this process and it is thought that its three isoforms act in a similar way. Here, we report that TGF-beta3 administered to rat lungs using transient overexpression initiates profibrotic effects similar to those elicited by TGF-beta1, but causes less severe and progressive changes. The data suggest that TGF-beta3 does not lead to inhibition of matrix degradation in the same way as TGF-beta1, resulting in non-fibrotic tissue repair. Further, TGF-bet…

medicine.medical_specialtyPulmonary FibrosisSMADBiologyBiochemistryArticleCell LineRats Sprague-DawleyTransforming Growth Factor beta1Extracellular matrixTransforming Growth Factor beta3Downregulation and upregulationFibrosisInternal medicinePulmonary fibrosismedicineAnimalsLungCell Biologymedicine.diseaseRatsCTGFEndocrinologyCancer researchFemaleWound healingReceptors Transforming Growth Factor betaTransforming growth factorThe International Journal of Biochemistry & Cell Biology
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Diastolic dysfunction and central obesity related hypertension: role of trasforming growth factor beta-1

2004

Abstract P-368 Key Words: Diastolic Dysfunction, Obesity Related Hypertension, Trasforming Growth Factor beta-1

medicine.medical_specialtySettore MED/09 - Medicina InternaMegalencephalic leukoencephalopathy with subcortical cystsmedicine.medical_treatmentDiastoleSettore MED/10 - Malattie Dell'Apparato RespiratorioOverweightLeft ventricular hypertrophyInternal medicineInternal MedicinemedicineSystolebiologybusiness.industryGrowth factorDiastolic Dysfunction Obesity Related Hypertension Trasforming Growth Factor beta-1Transforming growth factor betaDiastolic dysfunction HypertensionTrasforming factor beta 1medicine.diseaseSettore MED/11 - Malattie Dell'Apparato CardiovascolareObesityEndocrinologybiology.proteinCardiologymedicine.symptombusinessAmerican Journal of Hypertension
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Ultrasound as first line step in anaemia diagnostics

2019

This review covers the role of ultrasonography as an essential non-invasive diagnostic approach when facing patients with anemia, a common clinical problem. Abdomen ultrasound is well recognized as a first-line examination in the setting of blood loss, both acute and chronic. Less is clear about the additional opportunities, given by ultrasound in anemia, due to the many other possible causes.
 Here we provide information on the utility of ultrasound in different contexts and a practical guide for clinicians facing anemic patients

medicine.medical_specialtySettore MED/09 - Medicina Internalcsh:RC633-647.5business.industryFirst lineUltrasoundAnaemiaReview Articlelcsh:Diseases of the blood and blood-forming organsHematology030204 cardiovascular system & hematologyAbdomen ultrasound03 medical and health sciences0302 clinical medicineInfectious DiseasesBlood lossanaemia; ultrasoundUltrasoundmedicine030211 gastroenterology & hepatologyRadiologyUltrasonographybusiness
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Expression of differentiation antigens and growth-related genes in normal kidney, autosomal dominant polycystic kidney disease, and renal cell carcin…

1992

Cellular differentiation and mRNA levels of genes involved in kidney growth were investigated in normal kidney cells, cyst-lining epithelial cells of polycystic kidney disease, and renal carcinoma cells (RCC). All cells comparatively studied exhibited an antigenic phenotype of proximal tubular cells as shown by the expression of a panel of brush border membrane enzymes and kidney-associated cell surface antigens. The epithelial developmental antigen Exo-1 was expressed in 50% to 80% of cyst-lining epithelia in polycystic kidney tissue and in 20% to 30% of polycystic kidney cells cultured in vitro. Normal kidney cells and RCC were negative under identical culture conditions. The expression o…

medicine.medical_specialtyTGF alphaCellular differentiationAutosomal dominant polycystic kidney diseaseGene ExpressionBiologyKidneyEpitheliumProto-Oncogene Proteins c-mycGrowth factor receptorEpidermal growth factorInternal medicinemedicinePolycystic kidney diseaseHumansRNA MessengerGrowth SubstancesCarcinoma Renal CellCells CulturedKidneyurogenital systemAntibodies MonoclonalTransforming Growth Factor alphamedicine.diseasePolycystic Kidney Autosomal DominantAntigens DifferentiationImmunohistochemistryKidney NeoplasmsErbB ReceptorsEndocrinologymedicine.anatomical_structureGenesNephrologyAntigens SurfaceCancer researchTransforming growth factorAmerican journal of kidney diseases : the official journal of the National Kidney Foundation
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Glutathione S Transferase Polymorphisms Influence on Iron Overload in β-Thalassemia Patients

2013

In patients with β-thalassemia iron overload that leads to damage to vital organs is observed. Glutathione S transferase (GST) enzymes have an antioxidant role in detoxification processes of toxic substances. This role is determined genetically. In this study, we correlated GSTT1 and GSTM1 genotypes with iron overload measured with direct and indirect non-invasive methods; in particular, we used serum ferritin and signal intensity of the magnetic resonance image (MRI) in 42 patients with β-thalassemia, which were regularly subjected to chelation and transfusion therapy. Multiplex polymerase chain reaction was used to determine the genotype. The loss of both alleles leads to a decreased valu…

medicine.medical_specialtyThalassemiaglutathione S transferases; β-thalassemia; iron overloadBiologymedicine.diseaseglutathione S transferases β-thalassemia iron overload.EndocrinologyGlutathione S-transferaseBiochemistryInternal medicinemedicinebiology.proteinDiseases of the blood and blood-forming organsRC633-647.5Thalassemia Reports
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Bacterial inactivation/sterilization by argon plasma treatment on contaminated titanium implant surfaces: in vitro study

2015

Background: Surface treatment by argon plasma is widely used as the last step of the manufacturing process of ti- tanium implant fixtures before their sterilization by gamma rays. The possibility of using such a technology in the daily clinical practice is particularly fascinating. The aim of the present study was to assess the effects of the argon plasma treatment on different titanium implant surfaces previously exposed in vitro to bacterial contamination. Material and Methods: Sterile c.p. titanium implant discs with turned (T, Sa: 0.8μm), sandblasted/acid-etched (SAE, Sa: 1.3μm) and titanium plasma sprayed (TPS, Sa: 3.0μm) surface were used in this study. A strain of Ag- gregatibacter a…

medicine.medical_specialtyTitanium implantMaterials sciencePlasma GasesSurface Propertieschemistry.chemical_elementPlasma treatmentOdontología02 engineering and technologyAggregatibacter actinomycetemcomitans03 medical and health sciences0302 clinical medicineArgon plasma titanium implant surface Aggregatibacter actinomycetemcomitans.Aggregatibacter actinomycetemcomitanmedicineIn vitro studyArgonGeneral DentistryDecontaminationDental ImplantsTitaniumColony-forming unitArgonBacteriaResearchRadiochemistrySterilization030206 dentistrySterilization (microbiology)Contamination:CIENCIAS MÉDICAS [UNESCO]021001 nanoscience & nanotechnologyCiencias de la saludSurgeryArgon plasmaOtorhinolaryngologychemistryUNESCO::CIENCIAS MÉDICASEquipment ContaminationSurgeryOral SurgeryTitanium implant surface0210 nano-technologyTitanium
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Regulation of PTHrP and PTH/PTHrP receptor by extracellular Ca2+ concentration and hormones in the breast cancer cell line 8701-BC.

2000

AbstractIt was previously reported that 8701-BC breast tumour cells express the gene for parathyroid hormonerelated peptide (PTHrP) and PTH/PTHrP receptor (PTHrPR) and release immunoreactive PTHrP (iPTHrP) into the extracellular medium. Since the regulation of PTHrP and PTHrPR by breast cancer cells has been poorly investigated so far, we have chosen the 8701- BC cell line as a model system to investigate whether alterations in the extracellular Ca[2+] concentration ([Ca[2+]]) and treatment with some wellknown differentiation agents for breast cells, such as dimethyl sulfoxide, hydrocortisone, progesterone, prolactin, alltrans retinoic acid and transforming growth factorβ1 might (i) modulat…

medicine.medical_specialtyTranscription GeneticRNA SplicingClinical BiochemistryRetinoic acidCodon InitiatorBreast NeoplasmsTretinoinBiochemistrychemistry.chemical_compoundTranscription (biology)Transforming Growth Factor betaInternal medicinemedicineExtracellularTumor Cells CulturedHumansProtein IsoformsRNA MessengerPromoter Regions GeneticMolecular BiologyGeneChemistryParathyroid Hormone-Related ProteinProteinsProlactinHormonesNeoplasm ProteinsEndocrinologyGene Expression RegulationCell cultureRNA splicingReceptors Parathyroid HormoneCalciumExtracellular Spacehormones hormone substitutes and hormone antagonistsHormoneBiological chemistry
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Liver specific deletion of CYLDexon7/8 induces severe biliary damage, fibrosis and increases hepatocarcinogenesis in mice

2012

Background & Aims CYLD is a tumor suppressor gene that is mutated in familial cylindromatosis, an autosomal dominant predisposition to tumors of skin appendages. Reduced CYLD expression has been observed in other tumor entities, including hepatocellular carcinoma. In the present study, we analyzed the role of CYLD in liver homeostasis and hepatocarcinogenesis in vivo . Methods Mice with liver-specific deletion of CYLDexon7/8 ( CYLD FF xAlbCre ) were generated. Liver tissues were histologically analyzed and oval cell activation was investigated. Hepatocarcinogenesis was induced by diethylnitrosamine/phenobarbital (DEN/PB). Microarray expression profiling of livers was performed in untreated …

medicine.medical_specialtyTumor suppressor geneBiliary Tract DiseasesIn Vitro TechniquesBiologymedicine.disease_causeDimethylnitrosamineDeubiquitinating Enzyme CYLDMiceRisk FactorsFibrosisInternal medicinemedicineAnimalsHomeostasisGenetic Predisposition to DiseaseHepatologyLiver NeoplasmsExonsTransforming growth factor betamedicine.diseaseFibrosisMice Mutant StrainsDeubiquitinating Enzyme CYLDMice Inbred C57BLGene expression profilingCysteine EndopeptidasesDisease Models AnimalPhenotypeEndocrinologyLiverPhenobarbitalHepatocellular carcinomaCancer researchbiology.proteinCell activationCarcinogenesisGene DeletionJournal of Hepatology
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Estradiol Stimulates Vasodilatory and Metabolic Pathways in Cultured Human Endothelial Cells

2009

Vascular effects of estradiol are being investigated because there are controversies among clinical and experimental studies. DNA microarrays were used to investigate global gene expression patterns in cultured human umbilical vein endothelial cells (HUVEC) exposed to 1 nmol/L estradiol for 24 hours. When compared to control, 187 genes were identified as differentially expressed with 1.9-fold change threshold. Supervised principal component analysis and hierarchical cluster analysis revealed the differences between control and estradiol-treated samples. Physiological concentrations of estradiol are sufficient to elicit significant changes in HUVEC gene expression. Notch signaling, actin cyt…

medicine.medical_specialtyUmbilical Veinsmedicine.drug_classScienceEstrogen receptorBiologyAmidohydrolasesTransforming Growth Factor beta1chemistry.chemical_compoundInternal medicinemedicineCluster AnalysisEstrogen Receptor betaHumansEstrogen receptor betaCell Biology/Gene ExpressionCells CulturedOligonucleotide Array Sequence AnalysisRegulation of gene expressionPrincipal Component AnalysisMultidisciplinaryEstradiolPhysiology/EndocrinologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingQPhysiology/Cardiovascular Physiology and CirculationREstrogen Receptor alphaEndothelial CellsReproducibility of ResultsActin cytoskeletonVasodilationEndocrinologychemistryGene Expression RegulationEstrogenCyclooxygenase 1MedicineSignal transductionAsymmetric dimethylarginineEstrogen receptor alphahormones hormone substitutes and hormone antagonistsMetabolic Networks and PathwaysResearch ArticleSignal TransductionPLoS ONE
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Involvement of Different networks in mammary gland involution after the pregnancy/lactation cycle: Implications in breast cancer

2015

Early pregnancy is associated with a reduction in a woman's lifetime risk for breast cancer. However, different studies have demonstrated an increase in breast cancer risk in the years immediately following pregnancy. Early and long-term risk is even higher if the mother age is above 35 years at the time of first parity. The proinflammatory microenvironment within the mammary gland after pregnancy renders an "ideal niche" for oncogenic events. Signaling pathways involved in programmed cell death and tissue remodeling during involution are also activated in breast cancer. Herein, the major signaling pathways involved in mammary gland involution, signal transducer and activator of transcripti…

medicine.medical_specialtybiologyClinical BiochemistryMammary glandCell BiologyTransforming growth factor betamedicine.disease_causemedicine.diseaseBiochemistryChromatin remodelingmedicine.anatomical_structureEndocrinologyBreast cancerInternal medicineGeneticsmedicinebiology.proteinCancer researchInvolution (medicine)Signal transductionCarcinogenesisMolecular BiologyMammary gland involutionIUBMB Life
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