Search results for "CYTOKINE"

showing 10 items of 1787 documents

Investigational agents for Crohn's disease.

2010

IMPORTANCE OF THE FIELD: Increased understanding of the biological mechanisms of Crohn's disease has opened the door to a large number of new molecules; some of these are approved for clinical use, while others remain under evaluation. In this review, we examine the clinical efficacy of all the new drugs that have been evaluated in controlled trials in the last 12 years. AREAS COVERED IN THIS REVIEW: Anti-TNF therapy has been reviewed briefly, given the many comprehensive reviews on this topic; attention is focused mainly on the other biological therapies. In assessing the clinical efficacy of these molecules, we consider only the remission rate, as this is considered the most meaningful en…

medicine.medical_specialtybiological therapy. Crohn' s disease. Integrins.Probiotics.Small molecules.DiseaseAdaptive ImmunityReceptors Tumor Necrosis FactorCrohn DiseaseGastrointestinal AgentsmedicineHumansImmunologic FactorsPharmacology (medical)Clinical efficacyIntensive care medicineRandomized Controlled Trials as TopicPharmacologyMitogen-Activated Protein Kinase KinasesBiological therapiesCrohn's diseaseEverolimusEnd pointINVESTIGATIONAL AGENTSbusiness.industryRemission InductionAntibodies MonoclonalGeneral MedicineDrugs Investigationalmedicine.diseaseImmunity InnateImmunologyCytokinesRemission rateImmunotherapybusinessCell Adhesion Moleculesmedicine.drugExpert opinion on investigational drugs
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FRI0613 H-ferritin and pro-inflammatory cytokines are increased in the bone marrow of adult patients affected by macrophage activation syndrome

2017

Background During macrophage activation syndrome (MAS), an inflammatory life-threatening syndrome, extremely high levels of serum ferritin may be observed [1]. Ferritin is an intracellular iron storage protein comprising 24 subunits that may be divided in heavy (H) subunits and light (L) subunits, based on their molecular weight [2]. The H-/L-subunits ratio may change, depending on the specific tissue and the physiologic status of the cell. In the normal condition, ferritin enriched in L subunits (L-ferritin) has been found in the liver and in the spleen, whereas the ferritin enriched in H subunits (H-ferritin), may be mainly observed in the heart and kidneys [2]. Objectives We investigated…

medicine.medical_specialtybiologymedicine.diagnostic_testbusiness.industryCD68Spleen030204 cardiovascular system & hematologyProinflammatory cytokineFerritin03 medical and health sciences0302 clinical medicineEndocrinologymedicine.anatomical_structureWestern blotInternal medicineImmunologymedicinebiology.proteinMacrophageTumor necrosis factor alpha030212 general & internal medicineBone marrowbusinessPoster Presentations
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Peptidergic Innervation in Chronic Pancreatitis

1990

The reason for the generation and continuation of chronic pain in chronic pancreatitis is unclear [6, 10, 11, 13, 61, 117]. Current concepts of the neurobiology of pain point to the possible role of various neuropeptides in pain processing and inflammation [8, 29, 32, 33, 44, 60, 64, 65, 68, 79, 104, 112]. A key function has been ascribed to the proinflammatory and pronociceptive peptides of the tachykininin (TK) family (8, 44, 104, 109]. That the tachykinin substance P (SP) may be involved in chronic inflammatory and painful disease of the gastrointestinal system is evidenced by a selective increase in the density of tachykinin receptors in the bowels of patients suffering from Crohn’s dis…

medicine.medical_specialtybusiness.industryChronic painInflammationSubstance PDiseasemedicine.diseaseGastroenterologyUlcerative colitisProinflammatory cytokinechemistry.chemical_compoundchemistryInternal medicinemedicinePancreatitismedicine.symptombusinessTachykinin receptor
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Uncontrolled immune response in acute myocardial infarction

2008

Recently, the theory that hyperinflammation is the body's primary response to potent stimulus has been challenged. Indeed, a deregulation of the immune system could be the cause of multiple organ failure. So far, clinicians have focused on the last steps of the inflammatory cascade. However, little attention has been paid to lymphocytes, which play an important role as strategists of the inflammatory response. Experimental evidence suggests a crucial role of T lymphocytes in the pathophysiology of atherosclerosis and acute myocardial infarction (AMI). In summary, from the bottom of an imaginary inverted pyramid, a few regulatory T-cells control the upper parts represented by the wide spectr…

medicine.medical_specialtybusiness.industryStimulus (physiology)medicine.diseaseBioinformaticsPathophysiologySurgeryProinflammatory cytokineSystemic inflammatory response syndromeImmune systemCirculatory systemMedicineLeukocytosisMyocardial infarctionmedicine.symptomCardiology and Cardiovascular MedicinebusinessAmerican Heart Journal
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THU0045 IL-25/IL-17RB AXIS IS ACTIVATED AND ASSOCIATED WITH ILC2 EXPANSION IN GRANULOMATOSIS WITH POLYANGIITIS (GPA)

2019

Background: Pathogenesis of Granulomatosis with polyangiitis (GPA) is still unknown. However, it has been observed a skewing of circulating CD4+ T cells toward the Th17 and Th2 phenotype. The pro-inflammatory cytokine interleukin 25 (IL-25) is a member of IL-17 cytokine family associated to the Th2 immune phenotype. Through the receptor IL17RB, IL-25 further sustains the Th2-type immune response and elicits the expansion of the type 2 innate lymphoid cells (ILC2) and M2 macrophages. A pathogenic role of the innate lymphoid cells in GPA has been recently demonstrated; however, the relevance of IL-25 in this condition remains unexplored. Objectives: Aim of the study was to evaluate the expres…

medicine.medical_specialtybusiness.industrymedicine.medical_treatmentInnate lymphoid cellConsensus conferenceGATA3medicine.diseaseGastroenterologyPathogenesisImmune systemCytokineInternal medicineMedicineRituximabbusinessGranulomatosis with polyangiitismedicine.drugPoster Presentations
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Exploring Sodium Glucose Co-Transporter-2 (SGLT2) Inhibitors for Organ Protection in COVID-19

2020

Hospital admissions and mortality from the Coronavirus disease 2019 (COVID-19) pandemic are spreading throughout the world, and second and third waves are thought to be likely. Risk factors for severe COVID-19 include diabetes, chronic kidney disease and cardiovascular disease. Currently, there is no vaccine and no approved therapy. Therapeutic approaches are aimed at preventing viral replication and spread, limiting the impact of the inflammatory overdrive (cytokine storm), preventing thromboembolic complications and replacing or supporting organ function. However, despite organ support, mortality is currently 65% for those receiving advanced respiratory support and 78% for those requiring…

medicine.medical_specialtyempagliflozinEmpagliflozinlcsh:MedicineContext (language use)ReviewDisease030204 cardiovascular system & hematologyCardiovascularSGLT203 medical and health scienceschemistry.chemical_compound0302 clinical medicineChronic kidney diseaseDiabetes mellitusmedicine030212 general & internal medicineCanagliflozinDapagliflozincanagliflozinIntensive care medicinediabetesbusiness.industrycardiovascularDiabeteslcsh:RCOVID-19dapagliflozinGeneral MedicineDapagliflozinmedicine.diseaseVirusClinical trialRespiratory failurechemistryCytokine stormbusinesschronic kidney diseaseKidney diseaseJournal of Clinical Medicine
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Endothelial Bmx tyrosine kinase activity is essential for myocardial hypertrophy and remodeling

2015

Cardiac hypertrophy accompanies many forms of heart disease, including ischemic disease, hypertension, heart failure, and valvular disease, and it is a strong predictor of increased cardiovascular morbidity and mortality. Deletion of bone marrow kinase in chromosome X (Bmx), an arterial nonreceptor tyrosine kinase, has been shown to inhibit cardiac hypertrophy in mice. This finding raised the possibility of therapeutic use of Bmx tyrosine kinase inhibitors, which we have addressed here by analyzing cardiac hypertrophy in gene-targeted mice deficient in Bmx tyrosine kinase activity. We found that angiotensin II (Ang II)-induced cardiac hypertrophy is significantly reduced in mice deficient i…

medicine.medical_specialtyendotheliumEndotheliumAngiogenesiscardiomyocyteCardiomegalyheartmTORC1030204 cardiovascular system & hematologyMitochondria Heart03 medical and health sciencesMice0302 clinical medicineInternal medicinemedicineAnimalsMyocytes Cardiac030304 developmental biologyMice Knockout0303 health sciencesMultidisciplinaryKinasebusiness.industryta1184Angiotensin IIBiological SciencesProtein-Tyrosine KinasesAngiotensin IImedicine.anatomical_structureEndocrinologyEtkcardiovascular systemCancer researchPhosphorylationCytokinesEndothelium VascularSignal transductionInflammation MediatorssignalingbusinessTyrosine kinaseSignal Transduction
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Interleukin-32 in systemic sclerosis, a potential new biomarker for pulmonary arterial hypertension

2020

Abstract Background Pulmonary arterial hypertension (PAH) is a severe complication of systemic sclerosis (SSc), associated with a progressive elevation in pulmonary vascular resistance and subsequent right heart failure and death. Due to unspecific symptoms, the diagnosis of PAH is often delayed. On this basis, it is of great value to improve current diagnostic methods and develop new strategies for evaluating patients with suspected PAH. Interleukin-32 (IL-32) is a proinflammatory cytokine expressed in damaged vascular cells, and the present study aimed to assess if this cytokine could be a new biomarker of PAH during SSc. Methods The IL-32 expression was evaluated in the sera and skin sam…

medicine.medical_specialtylcsh:Diseases of the musculoskeletal systemHypertension Pulmonarymedicine.medical_treatment030204 cardiovascular system & hematologyPulmonary arterial hypertensionGastroenterologyProinflammatory cytokineSystemic sclerosi03 medical and health sciences0302 clinical medicineInternal medicinemedicine.arterysystemic sclerosis; pulmonary arterial hypertension; IL-32medicineHumansskin and connective tissue diseases030203 arthritis & rheumatologyScleroderma Systemicintegumentary systembusiness.industryInterleukinsRheumatologyInterleukin 32Cytokinemedicine.anatomical_structureIL-32; Pulmonary arterial hypertension; Systemic sclerosisIL-32Pulmonary arteryVascular resistanceSystemic sclerosisBiomarker (medicine)Immunohistochemistrylcsh:RC925-935businessBiomarkersResearch ArticleArthritis Research & Therapy
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Depression subtyping based on evolutionary psychiatry: Proximate mechanisms and ultimate functions

2018

Major depressive disorder constitutes one of the leading causes of disability worldwide. However, it is not a unitary disease-it is a heterogeneous syndrome, with patients differing remarkably in symptom profile, pathophysiology and treatment responsiveness. Previous attempts to subtype major depressive disorder have showed limited clinical applicability. We present a classification of major depressive disorder episodes based on the proximate mechanisms that led to the original mood change that caused the depressive episode. We identify discrete depression subtypes that are induced by: 1) infection, 2) long-term stress, 3) loneliness, 4) traumatic experience, 5) hierarchy conflict, 6) grief…

medicine.medical_specialtymedia_common.quotation_subjectImmunologyProinflammatory cytokine03 medical and health sciencesBehavioral Neuroscience0302 clinical medicinemedicineHumansChronic stressPsychiatryDepression (differential diagnoses)media_commonDepressive Disorder MajorEndocrine and Autonomic SystemsLonelinessmedicine.disease030227 psychiatryAffectMoodEndogenous depressionMajor depressive disorderGriefGriefmedicine.symptomPsychology030217 neurology & neurosurgeryClinical psychologyBrain, Behavior, and Immunity
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Human antiphospholipid antibodies induce TNFα in monocytes via Toll-like receptor 8

2009

The antiphospholipid syndrome (APS) is characterized by recurrent arterial and/or venous thromboses, pregnancy loss and the presence of antiphospholipid antibodies (aPL). One of the discussed mechanisms of this thrombotic activity in APS patients is attributed to TNFalpha secretion in monocytes after aPL stimulation. To investigate this mechanism in detail, we employed a monoclonal aPL and IgG fractions of APS patients for stimulation of human peripheral monocytes. Stimulation with this monoclonal aPL resulted in an increased expression and secretion of TNFalpha, caused by specific upregulation of TLR8 mRNA and protein expression levels. To confirm the specificity of this finding we could d…

medicine.medical_specialtymedicine.drug_classBlotting WesternImmunologyEnzyme-Linked Immunosorbent AssayStimulationCell SeparationBiologyMonoclonal antibodyPeripheral blood mononuclear cellMonocytesProinflammatory cytokineDownregulation and upregulationimmune system diseasesAntiphospholipid syndromeInternal medicinemedicineHumansImmunology and AllergyReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaAntibodies MonoclonalHematologyAntiphospholipid SyndromeFlow Cytometrymedicine.diseaseEndocrinologyToll-Like Receptor 8MonoclonalImmunologyAntibodies AntiphospholipidElectrophoresis Polyacrylamide GelTumor necrosis factor alphaImmunobiology
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