Search results for "medicine.disease_cause"

showing 10 items of 6035 documents

C 4 -Dicarboxylate Utilization in Aerobic and Anaerobic Growth

2016

C 4 -dicarboxylates and the C 4 -dicarboxylic amino acid l -aspartate support aerobic and anaerobic growth of Escherichia coli and related bacteria. In aerobic growth, succinate, fumarate, D - and L -malate, L -aspartate, and L -tartrate are metabolized by the citric acid cycle and associated reactions. Because of the interruption of the citric acid cycle under anaerobic conditions, anaerobic metabolism of C 4 -dicarboxylates depends on fumarate reduction to succinate (fumarate respiration). In some related bacteria (e.g., Klebsiella ), utilization of C 4 -dicarboxylates, such as tartrate, is independent of fumarate respiration and uses a Na + -dependent membrane-bound oxaloacetate decarbo…

0301 basic medicineCarboxy-LyasesCitric Acid Cycle030106 microbiologySuccinic AcidContext (language use)medicine.disease_causeMicrobiology03 medical and health sciencesFumaratesKlebsiellaEscherichia colimedicineHumansDicarboxylic AcidsAnaerobiosisEscherichia coliDicarboxylic Acid TransportersbiologyEscherichia coli ProteinsMembrane Transport ProteinsBiological TransportGene Expression Regulation BacterialMetabolismFumarate reductasebiology.organism_classificationAerobiosisCitric acid cycle030104 developmental biologyOxaloacetate decarboxylaseBiochemistryAnaerobic exerciseBacteriaEcoSal Plus
researchProduct

Ginkgo biloba induces different gene expression signatures and oncogenic pathways in malignant and non-malignant cells of the liver

2018

Ginkgo biloba (EGb761) is a widely used botanical drug. Several reports indicate that EGb761 confers preventive as well as anti-tumorigenic properties in a variety of tumors, including hepatocellular carcinoma (HCC). We here evaluate functional effects and molecular alterations induced by EGb761 in hepatoma cells and non-malignant hepatocytes. Hepatoma cell lines, primary human HCC cells and immortalized human hepatocytes (IH) were exposed to various concentrations (0-1000 μg/ml) of EGb761. Apoptosis and proliferation were evaluated after 72h of EGb761 exposure. Response to oxidative stress, tumorigenic properties and molecular changes were further investigated. While anti-oxidant effects w…

0301 basic medicineCarcinogenesisApoptosismedicine.disease_causeBiochemistryAntioxidantsTranscriptome0302 clinical medicineCell SignalingAnimal CellsMedicine and Health SciencesCellular Stress ResponsesCultured Tumor CellsMultidisciplinaryCell DeathbiologyGinkgo bilobaTOR Serine-Threonine KinasesLiver NeoplasmsQRLiverOncologyCell Processes030220 oncology & carcinogenesisHepatocellular carcinomaMedicineBiological CulturesCellular TypesAnatomyResearch ArticleSignal TransductionCarcinoma HepatocellularNF-E2-Related Factor 2ScienceResearch and Analysis MethodsCell Line03 medical and health sciencesmedicineHumansCell ProliferationOncogenic SignalingPlant ExtractsBiology and Life SciencesGinkgo bilobaCell BiologyCell Culturesbiology.organism_classificationmedicine.diseaseOxidative Stress030104 developmental biologyCell cultureApoptosisCancer cellHepatocytesCancer researchHepatoma CellsTranscriptomeCarcinogenesisOxidative stressPLOS ONE
researchProduct

Innate Sensing through Mesenchymal TLR4/MyD88 Signals Promotes Spontaneous Intestinal Tumorigenesis

2019

Summary MyD88, an adaptor molecule downstream of innate pathways, plays a significant tumor-promoting role in sporadic intestinal carcinogenesis of the Apcmin/+ model, which carries a mutation in the Apc gene. Here, we show that deletion of MyD88 in intestinal mesenchymal cells (IMCs) significantly reduces tumorigenesis in this model. This phenotype is associated with decreased epithelial cell proliferation, altered inflammatory and tumorigenic immune cell infiltration, and modified gene expression similar to complete MyD88 knockout mice. Genetic deletion of TLR4, but not interleukin-1 receptor (IL-1R), in IMCs led to altered molecular profiles and reduction of intestinal tumors similar to …

0301 basic medicineCarcinogenesisBiologymedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyExtracellular matrixMice03 medical and health sciences0302 clinical medicinemedicinetumor microenvironmentAnimalsHumansReceptorinnate immunityTumor microenvironmentInnate immune systemMesenchymal stem cellCell biologyIntestinesToll-Like Receptor 4030104 developmental biologyMyeloid Differentiation Factor 88Knockout mouseTLR4Carcinogenesiscancer-associated fibroblasts030217 neurology & neurosurgerySignal Transduction
researchProduct

Mcl-1 targeting could be an intriguing perspective to cure cancer

2018

The Bcl-2 family, which plays important roles in controlling cancer development, is divided into antiapoptotic and proapoptotic members. The change in the balance between these members governs the life and death of the cells. Mcl-1 is an antiapoptotic member of this family and its distribution in normal and cancerous tissues strongly differs from that of Bcl-2. In human cancers, where upregulation of antiapoptotic proteins is common, Mcl-1 expression is regulated independent of Bcl-2 and its inhibition promotes senescence, a major barrier to tumorigenesis. Cancer chemotherapy determines various kinds of responses, such as senescence and autophagy; however, the ideal response to chemotherapy…

0301 basic medicineCarcinogenesisPhysiologyClinical BiochemistryApoptosisBiologymedicine.disease_causecancer care03 medical and health sciencesMcl-1 in cancer0302 clinical medicineBcl-2 familyimmune system diseasesCancer stem cellhemic and lymphatic diseasesNeoplasmsmedicinecancer-stem-cellHumansPost-translational regulationMolecular Targeted TherapyneoplasmsCellular SenescenceOncogeneBcl-2 familyAutophagyCancerCell Biologymedicine.diseaseMcl-1 isoformGene Expression Regulation Neoplastic030104 developmental biologyUSP9XProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCancer researchtargeting Mcl-1Myeloid Cell Leukemia Sequence 1 ProteinCarcinogenesisProtein Processing Post-Translational
researchProduct

MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
researchProduct

Hepatitis C Virus Eradication by Direct Antiviral Agents Improves Carotid Atherosclerosis in patients with Severe Liver Fibrosis.

2018

Abstract BACKGROUND AND AIM: Recent studies suggest an association between HCV infection and cardiovascular damage, including carotid atherosclerosis, with a possible effect of HCV clearance on cardiovascular outcomes. We aimed to examine whether HCV eradication by direct antiviral agents (DAA) improves carotid atherosclerosis in HCV-infected patients with advanced fibrosis/compensated cirrhosis. MATERIALS AND METHODS: One hundred eighty-two consecutive HCV patients with advanced fibrosis or compensated cirrhosis were evaluated by virological, anthropometric and metabolic measurements. All patients underwent DAA-based antiviral therapy according to AISF/EASL guidelines. Intima-media thickne…

0301 basic medicineCarotid atherosclerosisCarotid Artery DiseasesMalemedicine.medical_specialtyCirrhosisSVRSustained Virologic ResponseHepatitis C virusHepacivirusmedicine.disease_causeGastroenterologyAntiviral AgentsCarotid Intima-Media Thickness03 medical and health sciencesLiver disease0302 clinical medicineRisk FactorsInternal medicineDiabetes mellitusmedicineGlucose homeostasisHumansIn patientProspective StudiesDAAHepatologybusiness.industryHepatitis C ChronicMiddle Agedmedicine.disease030104 developmental biologyTreatment OutcomeATHEROSCLEROSISHCVcardiovascular system030211 gastroenterology & hepatologyFemalebusinessDirect actingFollow-Up Studies
researchProduct

Staphylococcus aureus α-toxin: small pore, large consequences

2018

Abstract The small β-pore-forming α-toxin, also termed α-hemolysin or Hla is considered to be an important virulence factor of Staphylococcus aureus. Perforation of the plasma membrane (PM) by Hla leads to uncontrolled flux of ions and water. Already a small number of toxin pores seems to be sufficient to induce complex cellular responses, many of which depend on the efflux of potassium. In this article, we discuss the implications of secondary membrane lesions, for example, by endogenous channels, for Hla-mediated toxicity, for calcium-influx and membrane repair. Activation of purinergic receptors has been proposed to be a major contributor to the lytic effects of various pore forming prot…

0301 basic medicineCell Membrane PermeabilityStaphylococcal ToxoidBacterial ToxinsClinical BiochemistryPerforation (oil well)Endocytosismedicine.disease_causeBiochemistryVirulence factorHemolysin Proteins03 medical and health sciencesCytosol0302 clinical medicinemedicineHumansMolecular BiologyPore-forming toxinIon TransportChemistryToxinCell MembranePurinergic receptorCell biologyCytosol030104 developmental biologyCalciumEffluxProtein Kinases030217 neurology & neurosurgeryBiological Chemistry
researchProduct

Cytotoxic effects induced by patulin, deoxynivalenol and toxin T2 individually and in combination in hepatic cells (HepG2).

2018

Abstract Patulin (PAT), deoxynivalenol (DON) and toxin T-2 (T-2) are mycotoxins distributed worldwide in food and feed. Cytotoxicity of the three mycotoxins individually or in combination in human hepatocellular carcinoma (HepG2) cells was evaluated by MTT assay over 24, 48 and 72 h of exposure. The concentration ranges used were 0.625–15 μM for DON, 1.25–50 nM for T-2 and 0.45–7.5 μM for PAT. The IC 50 values obtained ranged from 9.30 to 2.53 μM, from 33.69 to 44.37 nM and from 2.66 to 1.17 μM for DON, T-2 and PAT, respectively. The most cytotoxic mycotoxin to HepG2 cells was T-2 followed by PAT and DON. The combination ratios used for the mixtures were 1:3 (DON: T-2), 1:5 (DON: PAT), 1:1.…

0301 basic medicineCell SurvivalComplex MixturesToxicologymedicine.disease_causePatulin03 medical and health scienceschemistry.chemical_compoundInhibitory Concentration 500404 agricultural biotechnologymedicineCytotoxic T cellHumansMTT assayDrug InteractionsCytotoxicityMycotoxinDose-Response Relationship DrugToxin04 agricultural and veterinary sciencesGeneral MedicineHep G2 CellsMycotoxinsmedicine.disease040401 food scienceMolecular biologyDrug CombinationsT-2 Toxin030104 developmental biologyPatulinchemistryLiverHepatocellular carcinomaHepatic stellate cellTrichothecenesFood ScienceFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
researchProduct

Transcytosis of Bacillus subtilis extracellular vesicles through an in vitro intestinal epithelial cell model

2020

Bacterial EVs have been related to inter-kingdom communication between probiotic/pathogenic bacteria and their hosts. Our aim was to investigate the transcytosis process of B. subtilis EVs using an in vitro intestinal epithelial cell model. In this study, using Confocal Laser Scanning Microscopy, we report that uptake and internalization of CFSE-labeled B. subtilis EVs (115 nm ± 27 nm) by Caco-2 cells are time-dependent. To study the transcytosis process we used a transwell system and EVs were quantified in the lower chamber by Fluorescence and Nanoparticle Tracking Analysis measurements. Intact EVs are transported across a polarized cell monolayer at 60–120 min and increased after 240 min …

0301 basic medicineCell Survivalmedia_common.quotation_subjectNanoparticle tracking analysislcsh:MedicineBacillus subtilisCellular imagingmedicine.disease_causeModels BiologicalGastrointestinal epitheliumArticleEpithelium//purl.org/becyt/ford/1 [https]Extracellular Vesicles03 medical and health sciences0302 clinical medicineFunctional FoodmedicineHumansCellular microbiology//purl.org/becyt/ford/1.6 [https]Internalizationlcsh:ScienceCell Proliferationmedia_commonMicroscopy ConfocalMultidisciplinarybiologyChemistryProbioticslcsh:RCell PolarityEpithelial CellsPathogenic bacteriaExtracellular vesiclesbiology.organism_classificationGITIn vitroEpitheliumCell biologyIntestines030104 developmental biologymedicine.anatomical_structureTranscytosis030220 oncology & carcinogenesislcsh:QCaco-2 CellsTranscytosisBacillus subtilisScientific Reports
researchProduct

Immunohistochemistry of Human Hsp60 in Health and Disease: From Autoimmunity to Cancer

2017

Hsp60 (also called Cpn60) is a chaperonin with essential functions for cell physiology and survival. Additionally, its involvement in the pathogenesis of a variety of diseases (e.g., some autoimmune disorders and cancer) is becoming evident with new research. For example, the distribution and levels of Hsp60 in cells and tissues have been found altered in many pathologic conditions, and the significance of these alterations is being investigated in a number of laboratories. The aim of this ongoing research is to determine the meaning of these Hsp60 alterations with regard to pathogenetic mechanisms, diagnosis, classification of lesions, and assessing prognosis and response to treatment. Hsp…

0301 basic medicineCell physiologyHsp60 in cancerDiseasemedicine.disease_causeHsp60 immunostainingAutoimmunityPathogenesis03 medical and health sciences0302 clinical medicineHsp60 and autoimmunityGeneticsmedicineMolecular BiologyHsp60 immunohistochemistrybusiness.industryCancerHsp60Hsp60 antibodiemedicine.diseaseChaperonin Hsp60Molecular mimicry030104 developmental biology030220 oncology & carcinogenesisImmunologyHsp60 locationImmunohistochemistryHSP60Hsp60 in tissuebusinessMolecular mimicry
researchProduct