Search results for "inflammation"

showing 10 items of 2662 documents

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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Regulation of cholesterol metabolism in the retina under experimental conditions associated with glaucoma

2019

Cholesterol is a lipid found in every animal cell and is necessary for its survival. Among its multiple roles in the body, it is a component of cell membranes that is crucial for the maintenance of their structure and fluidity and is thus implicated in the modulation of many signalling pathways. Neurons are especially dependant on cholesterol input since the proper composition of their plasma membrane is required for vesicular exocytosis of neurotransmitters and transduction of the post-synaptic signal. It has been shown that both an excess and a lack of cholesterol is neurotoxic. Moreover, many neurodegenerative diseases, such as Alzheimer’s or Huntington’s disease, have been associated wi…

Müller cellsInflammation24(S)-Hydroxycholesterol24(S)-HydroxycholestérolGlioseCellules de MüllerLaser photocoagulationGliosisHyperpression oculaireOcular hypertensionPhotocoagulation laser[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM][SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]
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Increased immunosuppressive function of CD4(+)CD25(+)Foxp3(+)GITR+ T regulatory cells from NFATc2((-/-)) mice controls allergen-induced experimental …

2012

The expansion of effector T cells is tightly controlled by transcription factors like nuclear factor of activated T cells (NFAT) family members that mediate early intracellular responses to T cell receptor-mediated signals. In this study we show that, after allergen challenge, NFATc2((-/-)) mice had augmented number of functionally intact CD4(+)CD25(++)GITR(++) T regulatory (T regs) cells in the lung. Anti-GITR antibody treatment inhibited T regulatory cell function and enhanced the number of activated lung CD4(+) T cells associated with increased IL-2 and pSTAT-5 in the airways of NFATc2((-/-)) mice in experimental allergic asthma. This agonistic treatment led to increased inflammation in …

NFATC2T cellImmunologyInflammationBiologyT-Lymphocytes RegulatoryInterleukin 21MiceTh2 CellsGlucocorticoid-Induced TNFR-Related ProteinmedicineImmunology and AllergyAnimalsIL-2 receptorLungImmunosuppression TherapyMice KnockoutNFATC Transcription FactorsInterleukin-2 Receptor alpha SubunitFOXP3NFATForkhead Transcription FactorsHematologyAllergensAsthmarespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureImmunologyCD4 Antigensbiology.proteinCytokinesTh17 CellsFemalemedicine.symptomAntibodySpleenImmunobiology
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Molecular Mechanisms of Inflammasome in Ischemic Stroke Pathogenesis.

2022

Ischemic stroke (also called cerebral ischemia) is one of the leading causes of death and severe disability worldwide. NLR inflammasomes play a crucial role in sensing cell damage in response to a harmful stimuli and modulating the inflammatory response, promoting the release of pro-inflammatory cytokines such as IL-18 and IL-1β following ischemic injury. Therefore, a neuroprotective effect is achieved by inhibiting the expression, assembly, and secretion of inflammasomes, thus limiting the extent of brain detriment and neurological sequelae. This review aims to illustrate the molecular characteristics, expression levels, and assembly of NLRP3 (nucleotide-binding oligomerization domain-like…

NLRC4Settore MED/09 - Medicina InternaNLRP2 inflammasomeDrug Discoveryischemic strokeNLRP1 inflammasomePharmaceutical ScienceMolecular Medicinetherapeutic strategiesNLRP3 inflammasomeneuroinflammationPharmaceuticals (Basel, Switzerland)
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Hypoxia induces proinflammatory cytokines production in alpha-1 antitrypsin deficiency patients

2021

Introduction: Alpha-1 antitrypsin deficiency (AATD) is a rare respiratory condition characterized by abnormal inflammation, where neutrophils play a key role. Excessive neutrophil activation leads to an increase in the oxygen (O2) intake, causing local hypoxia and increased tissue-injury capacity. Tissue hypoxia is part of the inflammatory process so neutrophils can function effectively under these conditions. However, the mechanisms by which neutrophils mediate tissue damage under hypoxia remain unclear. The study aimed to determine whether hypoxia modifies the cytokine profile in AATD patients. Methods: Neutrophils from 22 AATD patients (6 MZ; 9 SZ; 7 ZZ) and 7 controls (MM) were exposed …

NecrosisLungAlpha 1-antitrypsin deficiencybusiness.industrymedicine.medical_treatmentInflammationHypoxia (medical)medicine.diseaseProinflammatory cytokineCytokinemedicine.anatomical_structureImmunologyMedicineTumor necrosis factor alphamedicine.symptombusinessMolecular pathology and functional genomics
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