Search results for "Mice"

showing 10 items of 6027 documents

Nuovi Catalizzatori Sol-Gel per la Chimica Fine e la Valorizzazione della Biomassa

2014

nanomaterialiemicellulosa.cross-couplingvalorizzazione della biomassamateriali e processi sol-gelchimica finecatalisi eterogenea
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Antitumor Cell-Complex Vaccines Employing Genetically Modified Tumor Cells and Fibroblasts

2014

The present study evaluates the immune response mediated by vaccination with cell complexes composed of irradiated B16 tumor cells and mouse fibroblasts genetically modified to produce GM-CSF. The animals were vaccinated with free B16 cells or cell complexes. We employed two gene plasmid constructions: one high producer (pMok) and a low producer (p2F). Tumor transplant was performed by injection of B16 tumor cells. Plasma levels of total IgG and its subtypes were measured by ELISA. Tumor volumes were measured and survival curves were obtained. The study resulted in a cell complex vaccine able to stimulate the immune system to produce specific anti-tumor membrane proteins (TMP) IgG. In the g…

non-viralHealth Toxicology and MutagenesisGenetic enhancementCellMelanoma Experimentallcsh:MedicineBiologyToxicologyArticleImmunoglobulin GMicePlasmidImmune systemCell Line TumormedicineAnimalsCells Culturedlcsh:RGranulocyte-Macrophage Colony-Stimulating FactorMembrane ProteinsTransfectionFibroblastsMolecular biologygene therapycell complexesTumor BurdenGenetically modified organismGranulocyte macrophage colony-stimulating factormedicine.anatomical_structureImmunoglobulin Gbiology.proteincancer vaccinesbystander cellsmedicine.drugToxins
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The corticotrophin-releasing factor/urocortin system regulates white fat browning in mice through paracrine mechanisms.

2015

Objectives:\ud The corticotrophin-releasing factor (CRF)/urocortin system is expressed in the adipose tissue of mammals, but its functional role in this tissue remains unknown.\ud \ud Methods:\ud Pharmacological manipulation of the activity of CRF receptors, CRF1 and CRF2, was performed in 3T3L1 white pre-adipocytes and T37i brown pre-adipocytes during in vitro differentiation. The expression of genes of the CRF/urocortin system and of markers of white and brown adipocytes was evaluated along with mitochondrial biogenesis and cellular oxygen consumption. Metabolic evaluation of corticosterone-deficient or supplemented Crhr1-null (Crhr1−/−) mice and their wild-type controls was performed alo…

obesitycrf1Corticotropin-Releasing Hormonecrf2Endocrinology Diabetes and MetabolismIMPAIRED STRESS-RESPONSE[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionAdipocytes WhiteMedicine (miscellaneous)urocortinWhite adipose tissueMOUSEMicebrown adiposte tissue0302 clinical medicineBrowningUrocortinsUrocortin0303 health sciencesNutrition and Dietetics[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismParacrine mechanisms[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismImmunohistochemistryADIPOCYTESAdipocytes BrownADIPOSE-TISSUESKELETAL-MUSCLEhormones hormone substitutes and hormone antagonistsSignal TransductionEXPRESSIONmedicine.medical_specialtyendocrine systemTHERMOGENESISBiologycrfReceptors Corticotropin-Releasing Hormone03 medical and health scienceswhite adipose tissueInternal medicine3T3-L1 CellsmedicineAnimalsRNA MessengerGLUCOCORTICOIDS030304 developmental biologyENERGY HOMEOSTASISCorticotrophin releasing factoradipose plasticityPigments BiologicalUROCORTIN-II GENEQPEndocrinologyGene Expression Regulation[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgery
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The effects of physical activity and diet change on intracellular lipids and metabolism in mice with diet-induced obesity

2014

obesitydiet changemicerasvatphysical activityylipainoliikuntafysiologiahiiretliikuntainsuliiniresistenssiruokavaliotlipidsaikuisiän diabetesinsulin resistancelihavuusmetabolismaineenvaihduntametabolinen oireyhtymäaikuistyypin diabetesfyysinen aktiivisuus
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Preventive Impact of Long-Term Ingestion of Chestnut Honey on Glucose Disorders and Neurodegeneration in Obese Mice

2022

The purpose of the present study was to evaluate the impact of long-term honey ingestion on metabolic disorders and neurodegeneration in mice fed a high-fat diet (HFD). Three groups of mice were fed with a standard diet (STD), HFD or HFD supplemented with honey (HFD-H) for 16 weeks. Biochemical, histological, Western blotting, RT-PCR and Profiler PCR array were performed to assess metabolic parameters, peripheral and central insulin resistance and neurodegeneration. Daily honey intake prevented the HFD-induced glucose dysmetabolism. In fact, it reduced plasma fasting glucose, insulin and leptin concentrations and increased adiponectin levels. It improved glucose tolerance, insulin sensitivi…

obesityinsulin resistanceneurodegenerationHFD micehoneySettore BIO/09 - Fisiologia
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Comparison of acute and chronic exercise effects in the lipid droplets topography skeletal muscle, following high and low-fat diet in mice

2015

In the modern world, diet patterns high on lipids, sedentary lifestyle and obesity contribute all in the development of metabolic syndrome, which in turn can lead to type 2 diabetes. All the excess fats, that the majority of the population consumes nowadays, are stored as ectopic fat, particularly in the skeletal muscle, a tissue beyond doubt insulin-sensitive. Physical activity has been proposed according to various studies to be the most drastic factor, which can induce changes in skeletal muscle lipid metabolism,as well as different diet models. We hypothesized that different exercise patterns and diet-changes can alter the spatial arrangement in lipid droplets (LDs) in different skeleta…

obesitymicerasvatlipid dropletsphysical activityhiiretruokavaliotinsuliiniresistenssiinsulin resistancefiber typinglipid metabolismlihavuusdietaineenvaihduntafyysinen aktiivisuus
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Functional analysis of broadly tuned odorant receptors expressed in the mouse septal organ through patch-clamp recordings in an intact preparation an…

2010

The septal organ (SO) is a small island of olfactory epithelium located at the ventral base of the nasal septum. SO neurons express identified odorant receptors, but its function remains unknown. Using perforated patch clamp recordings, we investigated the response properties of SO neurons in the intact epithelium of mice to a panel of 45 odorants or mixtures. Out of 328 neurons tested, approximately 70% responded to odor stimulation. Among the responsive neurons, 72.5 % responded to multiple odorants. Responding neurons were tested with increasing concentrations of 3 odorants (octanoic acid, (+) camphor, amylacetate) and a mixture (fox urine). Dose-response curves show nanomolar threshold …

odorant receptor[SDV.AEN] Life Sciences [q-bio]/Food and Nutrition[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutrition[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC][SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC][SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]transgenic miceelectrophysiology[SDV.AEN]Life Sciences [q-bio]/Food and NutritionComputingMilieux_MISCELLANEOUSolfaction
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Increased dosage of Ink4/Arf protects against glucose intolerance and insulin resistance associated with aging

2013

Recent genome-wide association studies have linked type-2 diabetes mellitus to a genomic region in chromosome 9p21 near the Ink4/Arf locus, which encodes tumor suppressors that are up-regulated in a variety of mammalian organs during aging. However, it is unclear whether the susceptibility to type-2 diabetes is associated with altered expression of the Ink4/Arf locus. In the present study, we investigated the role of Ink4/Arf in age-dependent alterations of insulin and glucose homeostasis using Super-Ink4/Arf mice which bear an extra copy of the entire Ink4/Arf locus. We find that, in contrast to age-matched wild-type controls, Super-Ink4/Arf mice do not develop glucose intolerance with agi…

p16ink4amedicine.medical_specialtyAgingGlucose uptakemedicine.medical_treatmentMice TransgenicCarbohydrate metabolismCDKN2BMiceCDKN2AInsulin resistanceInsulin receptor substrateInternal medicineDiabetes mellitusinsulin resistanceGlucose IntolerancemedicineGlucose homeostasisAnimalsInsulininsulin signalingCyclin-Dependent Kinase Inhibitor p16biologydiabetesADP-Ribosylation FactorsInsulin18F-fluorodeoxyglucose-PETARFCell Biologypancreatic isletmedicine.diseaseMice Inbred C57BLInsulin receptorEndocrinologyGlucosebiology.proteinInsulin Resistancep15ink4bGenome-Wide Association Study
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Activation of the p38MAPK cascade is associated with upregulation of TNF alpha receptors in the spinal motor neurons of mouse models of familial ALS.

2005

Phosphorylated p38 mitogen-activated protein kinase (p38MAPK), but not activated c-jun-N-terminal kinase (JNK), increases in the motor neurons of transgenic mice overexpressing ALS-linked SOD1 mutants at different stages of the disease. This effect is associated with a selective increase of phosphorylated MKK3-6, MKK4 and ASK1 and a concomitant upregulation of the TNFalpha receptors (TNFR1 and TNFR2), but not IL1beta and Fas receptors. Activation of both p38 MAPK and JNK occurs in the activated microglial cells of SOD1 mutant mice at the advanced stage of the disease; however, this effect is not accompanied by the concomitant activation of the upstream kinases ASK1 and MKK3,4,6, while both …

p38 mitogen-activated protein kinasesMAP Kinase Kinase 3Mice TransgenicMAP Kinase Kinase 6BiologyMAP Kinase Kinase Kinase 5p38 Mitogen-Activated Protein KinasesReceptors Tumor Necrosis FactorCellular and Molecular NeuroscienceMiceSuperoxide Dismutase-1Downregulation and upregulationAnimalsHumansASK1RNA Messengerfas ReceptorPhosphorylationReceptorProtein kinase AMolecular BiologyP38MAPK cascadeMotor NeuronsKinaseSuperoxide DismutaseTumor Necrosis Factor-alphaAmyotrophic Lateral SclerosisJNK Mitogen-Activated Protein KinasesReceptors Interleukin-1Cell BiologyCell biologyEnzyme ActivationMice Inbred C57BLDisease Models AnimalTumor Necrosis Factor Decoy ReceptorsSpinal CordReceptors Tumor Necrosis Factor Type IDisease ProgressionTumor necrosis factor alphaSignal TransductionMolecular and cellular neurosciences
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Influence of aryl hydrocarbon- (Ah) receptor and genotoxins on DNA repair gene expression and cell survival of mouse hepatoma cells

2009

The aryl hydrocarbon receptor (AhR) mediates toxicity of a variety of environmental pollutants such as polycyclic aromatic hydrocarbons (PAHs) and dioxins. However, the underlying mechanisms and genetic programmes regulated by AhR to cause adverse effects but also to counteract poisoning are still poorly understood. Here we analysed the effects of two AhR ligands, benzo[a]pyrene (B[a]P), a DNA damaging tumour initiator and promotor and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a pure tumour promoter, on cell survival and on nucleotide excision repair (NER) gene expression. NER deals with so called "bulky" DNA adducts including those generated by enzymatically activated B[a]P. Therefore, t…

p53Aryl hydrocarbon receptor nuclear translocatorDNA RepairTumor suppressor geneCell SurvivalDNA damageDNA repairBlotting WesternDNA-Directed DNA Polymerasecis-PlatinBiologyToxicologyMiceLiver Neoplasms ExperimentalCell Line TumorGene expressionAnimals2378-Tetrachlorodibenzo-p-dioxinGeneAryl hydrocarbon receptorGene Expression ProfilingAryl Hydrocarbon Receptor Nuclear TranslocatorGenes p53Aryl hydrocarbon receptorMolecular biologyNucleotide excision repairBenzo[a]pyreneGene Expression RegulationReceptors Aryl HydrocarbonBiochemistrybiology.proteinEnvironmental PollutantsMutagensNucleotide excision repairToxicology
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