Search results for "Inflammation."

showing 10 items of 2627 documents

Multiple Sclerosis: Focus on Extracellular and Artificial Vesicles, Nanoparticles as Potential Therapeutic Approaches

2021

Multiple sclerosis (MS) is an autoimmune disease of the Central Nervous System, characterized by an inflammatory process leading to the destruction of myelin with neuronal death and neurodegeneration. In MS, lymphocytes cross the blood-brain barrier, creating inflammatory demyelinated plaques located primarily in the white matter. MS potential treatments involve various mechanisms of action on immune cells, immunosuppression, inhibition of the passage through the blood-brain barrier, and immunotolerance. Bio-nanotechnology represents a promising approach to improve the treatment of autoimmune diseases by its ability to affect the immune responses. The use of nanotechnology has been actively…

Multiple SclerosisQH301-705.5medicine.medical_treatmentCentral nervous systemInflammationReviewCatalysisInorganic ChemistryMyelinExtracellular VesiclesImmune systemDrug Delivery SystemsMedicinedrug delivery systemAnimalsHumansBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopyAutoimmune diseasenanotechnologybusiness.industryMultiple sclerosisOrganic ChemistryNeurodegenerationImmunosuppressionGeneral Medicinemedicine.diseaseComputer Science ApplicationsChemistrymedicine.anatomical_structureinflammationBlood-Brain BarrierLiposomesNanoparticlesmedicine.symptombusinessNeuroscienceImmunosuppressive AgentsimmunotoleranceInternational Journal of Molecular Sciences
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Demyelination patterns in a mathematical model of multiple sclerosis.

2016

In this paper we derive a reaction-diffusion-chemotaxis model for the dynamics of multiple sclerosis. We focus on the early inflammatory phase of the disease characterized by activated local microglia, with the recruitment of a systemically activated immune response, and by oligodendrocyte apoptosis. The model consists of three equations describing the evolution of macrophages, cytokine and apoptotic oligodendrocytes. The main driving mechanism is the chemotactic motion of macrophages in response to a chemical gradient provided by the cytokines. Our model generalizes the system proposed by Calvez and Khonsari (Math Comput Model 47(7–8):726–742, 2008) and Khonsari and Calvez (PLos ONE 2(1):e…

Multiple Sclerosismedicine.medical_treatmentInflammationApoptosisBiology01 natural sciencesModels BiologicalConcentric ring03 medical and health sciences0302 clinical medicineTuring instabilitymedicineHumansMultiple sclerosi0101 mathematicsSettore MAT/07 - Fisica MatematicaInflammationMicrogliaOligodendrocyte apoptosisPatternMultiple sclerosisTuring instabilityApplied MathematicsChemotaxismedicine.diseaseAgricultural and Biological Sciences (miscellaneous)Magnetic Resonance Imaging010101 applied mathematicsChemotaxis PDE modelCytokinemedicine.anatomical_structureModeling and SimulationImmunologymedicine.symptomNeuroscience030217 neurology & neurosurgeryDemyelinating DiseasesJournal of mathematical biology
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Differentiation of Murine C2C12 Myoblasts Strongly Reduces the Effects of Myostatin on Intracellular Signaling

2020

Alongside in vivo models, a simpler and more mechanistic approach is required to study the effects of myostatin on skeletal muscle because myostatin is an important negative regulator of muscle size. In this study, myostatin was administered to murine (C2C12) and human (CHQ) myoblasts and myotubes. Canonical and noncanonical signaling downstream to myostatin, related ligands, and their receptor were analyzed. The effects of tumorkines were analyzed after coculture of C2C12 and colon cancer-C26 cells. The effects of myostatin on canonical and noncanonical signaling were strongly reduced in C2C12 cells after differentiation. This may be explained by increased follistatin, an endogenous blocke…

Muscle Fibers Skeletallcsh:QR1-502lihaksetlcsh:MicrobiologyArticleTGF-BETA SUPERFAMILYCell LineMyoblastsMicetumorkineCell Line TumorfollistatinAnimalsHumansCANCER CACHEXIAskeletal muscleMUSCLE ATROPHYlihassolutSmadsoluviestintäRECEPTORCell DifferentiationIN-VITROMyostatinmusculoskeletal systemMAPKActivinsLEUKEMIA INHIBITORY FACTORACTIVIN-AinflammationCulture Media ConditionedCELLSPROTEIN-SYNTHESISmyotubeGROWTH1182 Biochemistry cell and molecular biologyproteiinit3111 BiomedicinecocultureSignal Transduction
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P.20.3 Targeting fibrosis and inflammation in Duchenne Muscular Dystrophy

2013

Duchenne Muscular Dystrophy is the most frequent genetic muscle disease worldwide affecting ∼1:5000 male births. It is caused by a defective DMD gene, which leads to reduced and defective dystrophin protein expression. The constant breakdown of fibres leads to focal necrosis, myophagocytosis and a considerable influx of inflammatory cells into the muscle tissue, which is followed by increasing endomysial fibrosis. Both, inflammation and fibrosis as well as a putative relation are not yet understood immunologically. Fibrosis directly correlates with adverse outcome and early loss of ambulation. We have studied how inflammation is linked to fibrosis in DMD, with an emphasis on the communicati…

Muscle biopsymedicine.diagnostic_testbiologyDuchenne muscular dystrophyInflammationDiseasemedicine.diseasePhenotypeImmune systemNeurologyFibrosisPediatrics Perinatology and Child HealthImmunologymedicinebiology.proteinNeurology (clinical)medicine.symptomDystrophinGenetics (clinical)Neuromuscular Disorders
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Activated IL-22 pathway occurs in the muscle tissues of patients with polymyositis or dermatomyositis and is correlated with disease activity.

2014

OBJECTIVE: The aim of this study was to assess the expression of IL-22, IL-22 receptor 1 (IL-22R1), IL-22 binding protein (IL-22BP) and p-STAT3 in muscle tissue from patients with PM and DM. METHODS: Levels of IL-22, IL-22R1, IL-22BP and STAT3 mRNA were quantified by RT-PCR. The expression of IL-22, IL-22R1, IL-22BP and p-STAT3 was also analysed using immunohistochemistry. RESULTS: Significant modulation of the IL-22 pathway was observed in inflammatory myopathic tissues. In particular, a significant overexpression of IL-22 at the protein but not the mRNA level was observed in PM/DM tissues and was correlated with myositis activity. IL-22R1 aberrant expression was also observed among infilt…

Muscle tissueSTAT3 Transcription FactorPathologymedicine.medical_specialtyBiopsyPolymyositisSeverity of Illness IndexDermatomyositisInterleukin 22NecrosisRheumatologySettore BIO/13 - Biologia ApplicataMedicineMyocyteHumansPharmacology (medical)RNA MessengerReceptorMuscle SkeletalPolymyositiInflammationbusiness.industrySettore MED/27 - NeurochirurgiaInterleukinsReceptors InterleukinDermatomyositismedicine.diseasePolymyositisSettore MED/16 - Reumatologiamedicine.anatomical_structureInterleukin 22Case-Control StudiesImmunohistochemistryInterleukin 17businessSignal Transduction
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Protective Effects of Foam Rolling against Inflammation and Notexin Induced Muscle Damage in Rats

2019

It is known that high-intensity exercise can cause inflammation and damage in muscle tissue, and in recent years, physical therapists and fitness professionals have begun to use foam rolling as a recovery method to improve performance. Despite the lack of basic science studies to support or refute the efficacy of foam rolling, the technique is very widely used in the sports world. In this respect, we investigated whether foam rolling could attenuate muscle damage and inflammation. Female Wistar rats were assigned to control (C), foam rolling (FR), notexin without foam rolling (N) and notexin with foam rolling (NFR) groups. A 4.5 x 2 cm foam roller was used to massage their hind legs (two 60…

Muscle tissuemedicine.medical_specialtyN-group (finite group theory)InflammationHindlimbMuscle damage03 medical and health sciencesGrip strengthmuscle recovery0302 clinical medicinePhysical Conditioning AnimalInternal medicinefoam rollingmedicineAnimalsHumansMuscle StrengthRange of Motion ArticularRats WistarMuscle SkeletalPhysical Therapy ModalitiesBalance (ability)Elapid VenomsInflammationMassageTumor Necrosis Factor-alphaChemistryGeneral MedicineRatsPhysical TherapistsDisease Models Animalcell deathmedicine.anatomical_structureEndocrinology030211 gastroenterology & hepatologyFoam rollingmedicine.symptomperformanceInterleukin-1SportsResearch PaperInternational Journal of Medical Sciences
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What effect can manual therapy have on a patient's pain experience?

2015

Manual therapy (MT) is a passive, skilled movement applied by clinicians that directly or indirectly targets a variety of anatomical structures or systems, which is utilized with the intent to create beneficial changes in some aspect of the patient pain experience. Collectively, the process of MT is grounded on clinical reasoning to enhance patient management for musculoskeletal pain by influencing factors from a multidimensional perspective that have potential to positively impact clinical outcomes. The influence of biomechanical, neurophysiological, psychological and nonspecific patient factors as treatment mediators and/or moderators provides additional information related to the proces…

Musculoskeletal painMalemedicine.medical_specialtyCerebral Cortex/physiopathologyAnatomical structuresPhysical medicine and rehabilitationHealthcare deliveryMusculoskeletal PainSpinal Cord/physiopathologyMedicineAnimalsHumansPhysical Therapy ModalitiesCerebral CortexPain experienceClinical Trials as TopicPain Perception/physiologybusiness.industryMusculoskeletal Pain/metabolismPerspective (graphical)Clinical reasoningPain PerceptionGeneral MedicinePain managementVariety (cybernetics)Treatment OutcomeSpinal CordPerspectiveFemaleManual therapyInflammation Mediatorsbusiness
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Cutting Edge: IL-1α Is a Crucial Danger Signal Triggering Acute Myocardial Inflammation during Myocardial Infarction

2016

Abstract Myocardial infarction (MI) induces a sterile inflammatory response that contributes to adverse cardiac remodeling. The initiating mechanisms of this response remain incompletely defined. We found that necrotic cardiomyocytes released a heat-labile proinflammatory signal activating MAPKs and NF-κB in cardiac fibroblasts, with secondary production of cytokines. This response was abolished in Myd88−/− fibroblasts but was unaffected in nlrp3-deficient fibroblasts. Despite MyD88 dependency, the response was TLR independent, as explored in TLR reporter cells, pointing to a contribution of the IL-1 pathway. Indeed, necrotic cardiomyocytes released IL-1α, but not IL-1β, and the immune acti…

MyocarditisImmunologyInterleukin-1betaMyocardial InfarctionInflammation030204 cardiovascular system & hematologyArticleProinflammatory cytokine03 medical and health sciencesMice0302 clinical medicineImmune system[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemIn vivoInterleukin-1alphamedicineImmunology and AllergyAnimalsMyocytes CardiacMyocardial infarction030304 developmental biologyInflammationMice Knockout0303 health sciencesbusiness.industryToll-Like Receptorsmedicine.disease[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemMyocarditisIL1AImmunologyMyeloid Differentiation Factor 88Cancer researchmedicine.symptomSignal transductionbusinessSignal Transduction
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PCSK9 Confers Inflammatory Properties to Extracellular Vesicles Released by Vascular Smooth Muscle Cells

2022

Vascular smooth muscle cells (VSMCs) are key participants in both early- and late-stage atherosclerosis and influence neighbouring cells possibly by means of bioactive molecules, some of which are packed into extracellular vesicles (EVs). Proprotein convertase subtilisin/kexin type 9 (PCSK9) is expressed and secreted by VSMCs. This study aimed to unravel the role of PCSK9 on VSMCs-derived EVs in terms of content and functionality. EVs were isolated from human VSMCs overexpressing human PCSK9 (VSMCPCSK9-EVs) and tested on endothelial cells, monocytes, macrophages and in a model of zebrafish embryos. Compared to EVs released from wild-type VSMCs, VSMCPCSK9-EVs caused a rise in the expression …

Myocytes Smooth MusclePCSK9; atherosclerosis; extracellular vesicles; inflammation; vascular smooth muscle cellsPCSK9; atherosclerosis; extracellular vesicles; inflammation; vascular smooth muscle cells.Muscle Smooth VascularCatalysisPCSK9Inorganic ChemistryExtracellular VesiclesSettore BIO/13 - Biologia ApplicataSettore MED/44 - Medicina del Lavorovascular smooth muscle cellsAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyZebrafishSpectroscopySettore MED/04 - Patologia GeneraleOrganic ChemistryEndothelial CellsGeneral MedicineComputer Science Applicationsinflammationextracellular vesicles; PCSK9; atherosclerosis; inflammation; vascular smooth muscle cellsSettore BIO/14 - FarmacologiaatherosclerosisProprotein Convertase 9International Journal of Molecular Sciences
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CXCR3-ligand-mediated skin inflammation in cutaneous lichenoid graft-versus-host disease.

2007

Background Lichenoid graft-versus-host disease (liGVHD) histologically shares several common features with other lichenoid dermatoses, such as cutaneous lupus erythematosus and lichen planus (LP), which collectively show a junctional infiltrate of cytotoxic lymphocytes with liquefaction of the basal layer ("interface dermatitis"). Because recent studies have shown a role for type I interferon (IFN)–associated inflammation, including lymphocyte recruitment via CXCR3 ligand interaction in cutaneous lupus erythematosus and LP, we hypothesized that similar mechanisms might also be involved in liGVHD. Methods Ten representative lesional skin biopsies taken from patients with different subsets of…

Myxovirus Resistance ProteinsChemokinePathologymedicine.medical_specialtyLichenoid EruptionsReceptors CXCR3CD3T-LymphocytesGraft vs Host DiseaseInflammationDermatitisDermatologyIn situ hybridizationCXCR3LigandsChemokine CXCL9Skin DiseasesGTP-Binding ProteinsMedicineCXCL10HumansLymphocytesRNA MessengerIn Situ Hybridizationbiologybusiness.industryLichen PlanusInterferon-alphaChemokine CXCL10stomatognathic diseasesImmunologyChronic DiseaseInterferon Type Ibiology.proteinCXCL9Immunohistochemistrymedicine.symptomEpidermisbusinessJournal of the American Academy of Dermatology
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