2019
Chapter 83 Adaptive Immunity and Critical Illness
Schulte W, Maerz L, Moeckel G, Bucala R. Chapter 83 Adaptive Immunity and Critical Illness. 2019, 483-487. DOI: 10.1016/b978-0-323-44942-7.00083-2.Peer-Reviewed Original ResearchAcute kidney injuryCritical illnessEnd-stage renal diseaseChronic kidney diseaseChallenging clinical conditionIschemia-reperfusion injuryComplex disease processAdaptive immune systemAKI pathophysiologyKidney injuryHospitalized patientsRenal diseaseKidney diseaseInflammatory processCommon causeClinical conditionsAdaptive immunityLong-term consequencesDisease processImmune systemSubsequent treatmentInjuryIllnessDiseaseCurrent knowledge
2000
Neurotoxicity of Advanced Glycation End-Products for Cultured Cortical Neurons
Takeuchi M, Bucala R, Suzuki T, Ohkubo T, Yamazaki M, Koike T, Kameda Y, Makita Z. Neurotoxicity of Advanced Glycation End-Products for Cultured Cortical Neurons. Journal Of Neuropathology & Experimental Neurology 2000, 59: 1094-1105. PMID: 11138929, DOI: 10.1093/jnen/59.12.1094.Peer-Reviewed Original ResearchConceptsCortical neuronsAge 2Alzheimer's diseaseEnd-stage renal diseaseNeuronal cellsAdvanced glycation end productsDM HD patientsGreater cytopathic effectsSpecific antibodiesAnti-AGE antibodyCultured cortical neuronsDose-dependent increaseGlycation end productsBlood of individualsCultured neuronal cellsDiabetes mellitusDiabetic patientsRenal diseaseNeurodegenerative processesNormal controlsAdvanced glycationCytopathic effectEpitope 1Cytotoxic effectsMTT assayInvolvement of Macrophage Migration Inhibitory Factor (MIF) in Experimental Uric Acid Nephropathy
Kim Y, Huang X, Suga S, Mazzali M, Tang D, Metz C, Bucala R, Kivlighn S, Johnson R, Lan H. Involvement of Macrophage Migration Inhibitory Factor (MIF) in Experimental Uric Acid Nephropathy. Molecular Medicine 2000, 6: 837-848. PMID: 11126199, PMCID: PMC1949919, DOI: 10.1007/bf03401822.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorUric acid crystal depositionMigration inhibitory factorUric acid nephropathyGranuloma formationMIF mRNAMIF proteinOxonic acidInhibitory factorCrystal depositionAcute uric acid nephropathyAreas of granulomasMIF mRNA expressionProgressive tubulointerstitial injuryRoutine light microscopyUrate nephropathyWestern blot analysisMIF expressionLocal cellular responseMIF secretionTubulointerstitial damageTubulointerstitial injuryInterleukin-2RRenal diseaseDTH reaction
1997
TNF-α Up-regulates Renal MIF Expression in Rat Crescentic Glomerulonephritis
Lan H, Yang N, Metz C, Mu W, Song Q, Nikolic-Paterson D, Bacher M, Bucala R, Atkins R. TNF-α Up-regulates Renal MIF Expression in Rat Crescentic Glomerulonephritis. Molecular Medicine 1997, 3: 136-144. PMID: 9085256, PMCID: PMC2230061, DOI: 10.1007/bf03401805.Peer-Reviewed Original ResearchConceptsRenal MIF expressionMigration inhibitory factorMIF expressionCrescentic glomerulonephritisRat crescentic glomerulonephritisMIF productionDay 1BackgroundMacrophage migration inhibitory factorSoluble TNF-α receptorTumor necrosis factor αResident kidney cellsSerum MIF levelsPotent proinflammatory mediatorPathogenesis of endotoxemiaNecrosis factor αInterstitial macrophage infiltrationTNF-α receptorExperimental crescentic glomerulonephritisMIF levelsMIF secretionRenal injuryRenal damageRenal diseaseProinflammatory mediatorsMacrophage accumulation
1996
The role of advanced glycosylation end-products in the pathogenesis of atherosclerosis
Makita Z, Yanagisawa K, Kuwajima S, Bucala R, Vlassara H, Koike T. The role of advanced glycosylation end-products in the pathogenesis of atherosclerosis. Nephrology Dialysis Transplantation 1996, 11: 31-33. PMID: 9044304, DOI: 10.1093/ndt/11.supp5.31.Peer-Reviewed Original ResearchConceptsEnd-stage renal diseaseLow-density lipoproteinDiabetic patientsDevelopment of atherosclerosisAGE-LDLAdvanced glycosylationAGE-modified formCoronary artery diseaseSerum total cholesterolPathogenesis of atherosclerosisArtery diseaseDiabetes mellitusRenal diseaseTotal cholesterolCerebrovascular diseaseMarked elevationRapid progressionTissue injuryVascular pathologyNormal controlsPatientsAGE-modified peptidesAtherogenic formAtherosclerosisAGE modification
1995
Advanced Glycosylation Endproducts in Diabetic Renal Disease: Clinical Measurement, Pathophysiological Significance, and Prospects for Pharmacological Inhibition
Bucala R, Vlassara H. Advanced Glycosylation Endproducts in Diabetic Renal Disease: Clinical Measurement, Pathophysiological Significance, and Prospects for Pharmacological Inhibition. Blood Purification 1995, 13: 160-170. PMID: 7619388, DOI: 10.1159/000170199.Peer-Reviewed Original ResearchConceptsAdvanced glycosylation endproductsDiabetic renal diseaseNormal renal functionInactivate nitric oxideSpecific therapeutic modalitiesTissue LDL receptorsForms of LDLRenal functionRenal diseaseLDL levelsTherapeutic modalitiesVascular permeabilityPathophysiological significanceAdvanced glycosylationLipoprotein depositionPharmacological inhibitionLDL receptorClinical measurementsNitric oxideEndothelial cellsMarked increaseMiddle moleculesLDLToxic effectsEndproducts
1992
Hemoglobin-AGE: A Circulating Marker of Advanced Glycosylation
Makita Z, Vlassara H, Rayfield E, Cartwright K, Friedman E, Rodby R, Cerami A, Bucala R. Hemoglobin-AGE: A Circulating Marker of Advanced Glycosylation. Science 1992, 258: 651-653. PMID: 1411574, DOI: 10.1126/science.1411574.Peer-Reviewed Original ResearchConceptsAdvanced glycosylation end productsAdvanced glycosylationAGE-modified formAGE-specific antibodiesComplications of agingDiabetes-induced hyperglycemiaAge-related complicationsGlycosylation end productsCirculating MarkersDiabetic patientsRenal diseaseGlucose-derived Amadori productsNormal individualsComplicationsPatientsTissue modificationsTissue proteinsHemoglobinAmadori productsEnd productsPercentDiabeticsHyperglycemiaAtherosclerosisDiabetes