2000
Expression of macrophage migration inhibitory factor in human glomerulonephritis
Lan H, Yang N, Nikolic-Paterson D, Yu X, Mu W, Isbel N, Metz C, Bucala R, Atkins R. Expression of macrophage migration inhibitory factor in human glomerulonephritis. Kidney International 2000, 57: 499-509. PMID: 10652026, DOI: 10.1046/j.1523-1755.2000.00869.x.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAgedAged, 80 and overBiopsyCohort StudiesEpithelial CellsFemaleGene ExpressionGlomerulonephritis, MembranoproliferativeGlomerulonephritis, MembranousHumansIn Situ HybridizationKidney GlomerulusMacrophage Migration-Inhibitory FactorsMacrophagesMaleMiddle AgedReference ValuesRNA, MessengerT-LymphocytesConceptsMacrophage migration inhibitory factorMIF expressionMigration inhibitory factorFocal segmental glomerulosclerosisHuman glomerulonephritisProliferative formsMIF mRNAPathogenic roleExperimental glomerulonephritisInhibitory factorProgressive formRenal MIF expressionRenal function impairmentT cell accumulationT-cell infiltratesEpithelial cellsMinimal change diseaseFocal segmental lesionsGlomerular endothelial cellsTubular epithelial cellsNormal human kidneyAttractive therapeutic targetCreatinine clearanceGlomerular epithelial cellsLupus nephritisProtection from septic shock by neutralization of macrophage migration inhibitory factor
Calandra T, Echtenacher B, Roy D, Pugin J, Metz C, Hültner L, Heumann D, Männel D, Bucala R, Glauser M. Protection from septic shock by neutralization of macrophage migration inhibitory factor. Nature Medicine 2000, 6: 164-170. PMID: 10655104, DOI: 10.1038/72262.Peer-Reviewed Original ResearchConceptsMacrophage migration inhibitory factorSeptic shockMigration inhibitory factorLethal peritonitisSevere sepsisMIF antibodyRecombinant macrophage migration inhibitory factorAnti-tumor necrosis factorInhibitory factorTNFα knockout micePathogenesis of sepsisPlasma of patientsNew therapeutic targetsBacterial peritonitisIll patientsInvestigational therapiesCecal ligationNecrosis factorNormal micePivotal cytokineSystemic circulationKnockout miceTherapeutic targetSepsisPeritonitis
1997
Orally absorbed reactive glycation products (glycotoxins): An environmental risk factor in diabetic nephropathy
Koschinsky T, He C, Mitsuhashi T, Bucala R, Liu C, Buenting C, Heitmann K, Vlassara H. Orally absorbed reactive glycation products (glycotoxins): An environmental risk factor in diabetic nephropathy. Proceedings Of The National Academy Of Sciences Of The United States Of America 1997, 94: 6474-6479. PMID: 9177242, PMCID: PMC21074, DOI: 10.1073/pnas.94.12.6474.Peer-Reviewed Original ResearchConceptsAdvanced glycation endproductsDietary advanced glycation endproductsEndogenous advanced glycation endproductsDiabetes mellitusKidney diseaseRenal excretionRenal vascular injuryDiabetic nephropathy patientsSerum AGE levelsDegree of albuminuriaNondiabetic kidney diseaseEnvironmental risk factorsAGE immunoreactivityRenal complicationsCreatinine clearanceDiabetic nephropathyNephropathy patientsRenal failureDiabetic patientsRisk factorsFood intakeHealthy subjectsGlycation endproductsDietary restrictionCL diet
1985
Increased Levels of 16α-Hydroxyestrone-Modified Proteins in Pregnancy and in Systemic Lupus Erythematosus*
BUCALA R, LAHITA R, FISHMAN J, CERAMI A. Increased Levels of 16α-Hydroxyestrone-Modified Proteins in Pregnancy and in Systemic Lupus Erythematosus*. The Journal Of Clinical Endocrinology & Metabolism 1985, 60: 841-847. PMID: 3920233, DOI: 10.1210/jcem-60-5-841.Peer-Reviewed Original ResearchConceptsSystemic lupus erythematosusLupus erythematosusPregnant womenHigher mean levelsNormal womenAlpha-hydroxyestroneFemale hormonesNormal subjectsErythematosusNormal levelsElevated levelsMean levelsWomenLatter groupRed cellsLymphocyte proteinSimilar elevationsPregnancyOHEBasement membrane proteinsUseful indicatorLevelsPatientsModification of proteinsLymphocytes