Search results for "type II"

showing 10 items of 607 documents

Interleukin-33-Dependent Innate Lymphoid Cells Mediate Hepatic Fibrosis

2013

SummaryLiver fibrosis is a consequence of chronic liver diseases and thus a major cause of mortality and morbidity. Clinical evidence and animal studies suggest that local tissue homeostasis is disturbed due to immunological responses to chronic hepatocellular stress. Poorly defined stress-associated inflammatory networks are thought to mediate gradual accumulation of extracellular-matrix components, ultimately leading to fibrosis and liver failure. Here we have reported that hepatic expression of interleukin-33 (IL-33) was both required and sufficient for severe hepatic fibrosis in vivo. We have demonstrated that IL-33’s profibrotic effects related to activation and expansion of liver resi…

Liver CirrhosisLiver cytologyImmunologyBiologyLymphocyte ActivationArticle03 medical and health sciencesMice0302 clinical medicineFibrosismedicineHepatic Stellate CellsAnimalsImmunology and AllergyLymphocytesReceptors Interleukin-4 Type IIInterleukin 4Tissue homeostasisCells Cultured030304 developmental biologyCell ProliferationInflammationMice Knockout0303 health sciencesMice Inbred BALB CInterleukin-13InterleukinsInnate lymphoid cellmedicine.diseaseInterleukin-33Adoptive Transfer3. Good healthInterleukin 33Mice Inbred C57BLInfectious DiseasesLiverImmunologyHepatic stellate cellHepatic fibrosisSTAT6 Transcription Factor030215 immunologySignal TransductionImmunity
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Fibrogenesis assessed by serological type III collagen formation identifies patients with progressive liver fibrosis and responders to a potential an…

2016

There are no approved treatments for liver fibrosis. To aid development of antifibrotic therapies, noninvasive biomarkers that can identify patients with progressive fibrosis and that permit monitoring of the response to antifibrotic therapy are much needed. Samples from a phase II antifibrotic trial of the glitazone farglitazar in patients with advanced hepatitis C, with matched follow-up liver biopsies, and from a phase III study of balaglitazone in patients with late-stage Type 2 diabetes (BALLET study) were analyzed for serological Pro-C3 levels in conjunction with other disease parameters. In the farglitazar study, a predefined cutoff value for Pro-C3 as a selection criterion led to t…

Liver CirrhosisMale0301 basic medicineNonalcoholic steatohepatitisPathologymedicine.medical_specialtyPhysiologyLiver fibrosisType 2 diabetesSerology03 medical and health sciencesCollagen formation0302 clinical medicineFibrosisSerum biomarkersPhysiology (medical)Journal ArticlemedicineHumansOxazolesType III collagenHepatologybusiness.industryPatient SelectionGastroenterologyMiddle Agedmedicine.disease3. Good healthCollagen Type III030104 developmental biologyQuinazolinesTyrosineFemaleThiazolidinediones030211 gastroenterology & hepatologybusinessBiomarkersAmerican Journal of Physiology-Gastrointestinal and Liver Physiology
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On the absence of BPS preonic solutions in IIA and IIB supergravities

2006

We consider the present absence of 31 out of 32 supersymmetric solutions in supergravity i.e., of solutions describing BPS preons. A recent result indicates that (bosonic) BPS preonic solutions do not exist in type IIB supergravity. We reconsider this analysis by using the G-frame method, extend it to the IIA supergravity case, and show that there are no (bosonic) preonic solutions for type IIA either. For the classical D=11 supergravity no conclusion can be drawn yet, although the negative IIA results permit establishing the conditions that preonic solutions would have to satisfy. For supergravities with `stringy' corrections, the existence of BPS preonic solutions remains fully open.

M-theoryPhysicsHigh Energy Physics - TheoryNuclear and High Energy PhysicsType iibHigh Energy Physics - Theory (hep-th)SupergravityFOS: Physical sciencesType (model theory)Mathematical physics
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The Late Endosomal Adaptor Molecule p14 (LAMTOR2) Regulates TGFβ1-Mediated Homeostasis of Langerhans Cells

2014

Langerhans cells (LCs), a sub-population of dendritic cells (DCs) in the skin, participate in the regulation of immunity and peripheral tolerance. The adaptor molecule p14 is part of the late endosomal/lysosomal adaptor and mitogen-activated protein kinase and mammalian target of rapamycin (mTOR) activator/regulator (LAMTOR) complex, which mediates the activation of lysosome-associated extracellular signaling regulated kinase (ERK) and the mTOR cascade. In previous work, we demonstrated that CD11c-specific deficiency of p14 disrupts LC homeostasis by affecting the LAMTOR-mediated ERK and mTOR signaling. In this study, we extended our analysis on p14 deficiency specifically in LCs. Langerin-…

MAPK/ERK pathwayMaleMAP Kinase Signaling SystemReceptor Transforming Growth Factor-beta Type IDown-Regulationchemical and pharmacologic phenomenaEndosomesDermatologyBiologyProtein Serine-Threonine KinasesDermatitis ContactBiochemistryArticleImmune toleranceImmunophenotypingTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementImmune ToleranceAnimalsHomeostasisProtein kinase AMolecular BiologyPI3K/AKT/mTOR pathway030304 developmental biologySkin0303 health sciencesintegumentary systemKinaseReceptor Transforming Growth Factor-beta Type IIPeripheral toleranceProteinshemic and immune systemsCell BiologyMice Mutant StrainsCell biologyCD11c AntigenLangerhans CellsFemaleReceptors Transforming Growth Factor beta030215 immunologyTransforming growth factorJournal of Investigative Dermatology
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Exercise and hormesis: activation of cellular antioxidant signaling pathway.

2006

Contraction-induced production of reactive oxygen species (ROS) has been shown to cause oxidative stress to skeletal muscle. As an adaptive response, muscle antioxidant defense systems are upregulated after heavy exercise. Nuclear factor (NF) kappaB and mitogen-activated protein kinases (MAPKs) are the major oxidative stress-sensitive signal transduction pathways in mammalian tissues. Activation of NF-kappaB signaling cascade has been shown to enhance the gene expression of important enzymes, such as mitochondrial superoxide dismutase (MnSOD) and inducible nitric oxide synthase (iNOS). MAPK activations are involved in a variety of cellular functions including growth, proliferation, and adap…

MAPK/ERK pathwayNitric Oxide Synthase Type IIBiologymedicine.disease_causeModels BiologicalGeneral Biochemistry Genetics and Molecular BiologyAntioxidantsGene Expression Regulation EnzymologicHistory and Philosophy of ScienceDownregulation and upregulationPhysical Conditioning AnimalmedicineAnimalsMuscle Skeletalchemistry.chemical_classificationReactive oxygen speciesKinaseSuperoxide DismutaseGeneral NeuroscienceNF-kappa BSkeletal muscleCell biologyMitochondriaNitric oxide synthaseEnzyme ActivationKineticsmedicine.anatomical_structurechemistrybiology.proteinSignal transductionMitogen-Activated Protein KinasesReactive Oxygen SpeciesOxidative stressSignal TransductionAnnals of the New York Academy of Sciences
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TLR4 elimination prevents synaptic and myelin alterations and long-term cognitive dysfunctions in adolescent mice with intermittent ethanol treatment.

2015

The adolescent brain undergoes important dynamic and plastic cell changes, including overproduction of axons and synapses, followed by rapid pruning along with ongoing axon myelination. These developmental changes make the adolescent brain particularly vulnerable to neurotoxic and behavioral effects of alcohol. Although the mechanisms of these effects are largely unknown, we demonstrated that ethanol by activating innate immune receptors toll-like receptor 4 (TLR4), induces neuroinflammation and brain damage in adult mice. The present study aims to evaluate whether intermittent ethanol treatment in adolescence promotes TLR4-dependent pro-inflammatory processes, leading to myelin and synapti…

MAPK/ERK pathwaySynaptic dysfunctionImmunologyNitric Oxide Synthase Type IIBrain damageHMGB1Behavioral NeuroscienceMyelinMiceCognitionmedicineAnimalsTLR4AxonHMGB1 ProteinReceptorNeuroinflammationMyelin SheathMice KnockoutMitogen-Activated Protein Kinase KinasesbiologyBinge ethanol treatmentEthanolEndocrine and Autonomic SystemsNF-kappa BCentral Nervous System DepressantsMyelin alterationsAdolescenceToll-Like Receptor 4medicine.anatomical_structureCyclooxygenase 2SynapsesTLR4biology.proteinmedicine.symptomPsychologyCognition DisordersNeuroscienceCognitive behaviorAlcohol-Related DisordersMyelin ProteinsSignal TransductionBrain, behavior, and immunity
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Prevalence Of familial hypercholeSTerolaemia (FH) in Italian Patients with coronary artERy disease: The POSTER study

2020

Background and aims: Familial hypercholesterolaemia (FH) is a powerful risk factor for cardiovascular (CV) events. High levels of low-density lipoprotein cholesterol (LDL-C) since birth are linked to the early onset of atherosclerotic disease. A genetic mutation determining FH is present in about one subject out of 250; FH should be more represented among subjects with a documented diagnosis of coronary artery disease (CAD). The POSTER Study evaluated the prevalence of FH in Italian patients with a recent CAD event. Methods: Eighty-two cardiology centres enrolled patients with a documented CAD event; CV risk profile, drug therapy and biochemical parameters were collected. Dutch Lipid Clinic…

Male0301 basic medicineAcute coronary syndromemedicine.medical_specialtySettore MED/09 - Medicina InternaFamilial hypercholesterolemiaFamilial hypercholesterolemia030204 cardiovascular system & hematologyCoronary revascularizationCoronary artery diseaseHyperlipoproteinemia Type IICoronary artery disease03 medical and health sciences0302 clinical medicinePharmacotherapyRisk FactorsInternal medicinePrevalencemedicineHumansLow-density lipoprotein cholesterolMyocardial infarctionRisk factorAgedHigh prevalencebusiness.industryCholesterol LDLMiddle Agedmedicine.diseaseCoronary revascularizationMyocardial infarction030104 developmental biologyItalyDutch lipid clinic networkCardiology and Cardiovascular MedicinebusinessAtherosclerosis
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Systemic blockade of ACVR2B ligands attenuates muscle wasting in ischemic heart failure without compromising cardiac function

2020

Signaling through activin receptors regulates skeletal muscle mass and activin receptor 2B (ACVR2B) ligands are also suggested to participate in myocardial infarction (MI) pathology in the heart. In this study, we determined the effect of systemic blockade of ACVR2B ligands on cardiac function in experimental MI, and defined its efficacy to revert muscle wasting in ischemic heart failure (HF). Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) to study its effect on post-MI cardiac remodeling and on later HF. Cardiac function was determined with echocardiography, and myocardium analyzed with histological and biochemical methods for hypertrophy and fibrosis. Pharmacological blo…

Male0301 basic medicineCardiac function curvemedicine.medical_specialtyActivin Receptors Type IIMyocardial IschemiaMyostatinBiochemistryMuscle hypertrophyMice03 medical and health sciences0302 clinical medicineInternal medicineGeneticsmedicineAnimalsMyocyteMyocardial infarctionMolecular BiologyVentricular Remodelingbiologybusiness.industrySkeletal muscleHeartmedicine.disease3. Good healthBlockadeMice Inbred C57BLDisease Models AnimalMuscular Atrophy030104 developmental biologymedicine.anatomical_structureCardiologybiology.proteinbusiness030217 neurology & neurosurgeryACVR2BSignal TransductionTranscription FactorsBiotechnologyThe FASEB Journal
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Lipoprotein-associated phospholipase A₂ activity is increased in patients with definite familial hypercholesterolemia compared with other forms of hy…

2018

International audience; Background and Aim: Lipoprotein-associated phospholipase A2 (Lp-PLA2) plays a key role in atherosclerosis development. It is considered a marker of increased risk of cardiovascular disease (CVD) and plaque vulnerability. Familial hypercholesterolemia (FH) is a genetic disorder characterized by elevated plasma levels of low-density lipoprotein cholesterol and a higher prevalence of early CVD. Our aim was to evaluate the differences in Lp-PLA2 activity in a population of hypercholesterolemic patients with and without definite FH.Methods and Results: Hypercholesterolemic patients were consecutively recruited. Definite FH was defined according to Dutch Lipid Clinic Netwo…

Male0301 basic medicineEndocrinology Diabetes and MetabolismMedicine (miscellaneous)Low density lipoproteinDiseaseFamilial hypercholesterolemia030204 cardiovascular system & hematologyGastroenterologychemistry.chemical_compound0302 clinical medicineVascular inflammationeducation.field_of_studyNutrition and Dieteticsmedicine.diagnostic_testGenetic disorderMiddle Aged[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismCardiovascular diseaseLipidsUp-Regulation3. Good healthPhenotypeLow-density lipoproteinApolipoprotein B-100Femalelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAdultmedicine.medical_specialtyStatin treatmentHypercholesterolemiaFamilial hypercholesterolemiaPopulationPhysical examinationHyperlipoproteinemia Type II03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineHumansLipoprotein-associated phospholipase A2Plaque vulnerabilityeducationAgedApolipoprotein A-Ibusiness.industryCholesterol HDLCholesterol LDLStatin treatmentAtherosclerosisCardiovascular riskmedicine.diseaseCross-Sectional Studies030104 developmental biologychemistry1-Alkyl-2-acetylglycerophosphocholine EsteraseHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessBiomarkersLipoproteinNutrition, Metabolism and Cardiovascular Diseases
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Homozygous Familial Hypercholesterolemia in Spain Prevalence and Phenotype-Genotype Relationship

2016

Background— Homozygous familial hypercholesterolemia (HoFH) is a rare disease characterized by elevated plasma levels of low-density lipoprotein cholesterol (LDL-C) and extremely high risk of premature atherosclerotic cardiovascular disease. HoFH is caused by mutations in several genes, including LDL receptor ( LDLR ), apolipoprotein B ( APOB ), proprotein convertase subtilisin/kexin type 9 ( PCSK9 ), and LDL protein receptor adaptor 1 ( LDLRAP1 ). No epidemiological studies have assessed HoFH prevalence or the clinical and molecular characteristics of this condition. Here, we aimed to characterize HoFH in Spain. Methods and Results— Data were collected from the Spanish Dyslipidemia Regist…

Male0301 basic medicineOncologyLdl receptor geneApolipoprotein BLipid-lowering therapyFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosity0302 clinical medicineAutosomal-dominant hypercholesterolemiaRisk FactorsEpidemiologyPrevalenceDiseaseRegistriesGenetics (clinical)Molecular EpidemiologybiologyhypercholesterolemiaHomozygoteDouble-blindMiddle AgedPhenotypeCardiovascular DiseasesApolipoprotein B-100allelesFemalelipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineMutationsAdultGenetic MarkersHeterozygotemedicine.medical_specialtyInhibitorAdolescentPlacebo-controlled trialHyperlipoproteinemia Type IIlipidsYoung Adult03 medical and health sciencesInternal medicineGeneticsmedicineHumansGenetic Predisposition to DiseaseAlleleAdaptor Proteins Signal TransducingRecessive hypercholesterolemiaPCSK9registriesCholesterol LDLApolipoprotein-bmedicine.disease030104 developmental biologyEndocrinologyReceptors LDLSpainMutationLDL receptorbiology.proteinmutationDyslipidemia
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