J
John Badalamenti
Researcher at University of Texas Medical Branch
Publications - 13
Citations - 686
John Badalamenti is an academic researcher from University of Texas Medical Branch. The author has contributed to research in topics: Biopsy & Phospholipase C. The author has an hindex of 8, co-authored 11 publications receiving 664 citations. Previous affiliations of John Badalamenti include Boston University.
Papers
More filters
Journal ArticleDOI
Cardiac troponin T and C-reactive protein for predicting prognosis, coronary atherosclerosis, and cardiomyopathy in patients undergoing long-term hemodialysis.
Christopher DeFilippi,Steven S. Wasserman,Salvatore Rosanio,Eric Tiblier,Heidi Sperger,Monica Tocchi,Robert H. Christenson,Barry F. Uretsky,Mathew M. Smiley,Judith H. Gold,Henry Muniz,John Badalamenti,Charles A. Herzog,William L. Henrich +13 more
TL;DR: Both cTnT and CRP remained independent predictors of death after adjusting for a number of potential confounders, and among stable patients with ESRD, increasing levels of cTNT andCRP are associated with increased risk of death.
Journal ArticleDOI
Reduced amino acid availability inhibits muscle protein synthesis and decreases activity of initiation factor eIF2B
Hisamine Kobayashi,Elisabet Børsheim,Tracy G. Anthony,Daniel L. Traber,John Badalamenti,Scot R. Kimball,Leonard S. Jefferson,Robert R. Wolfe +7 more
TL;DR: It is concluded that a reduction in plasma amino acid concentrations below the normal basal value signals an inhibition of muscle protein synthesis and that corresponding changes in eIF2B activity suggest a possible role in mediating the response.
Journal Article
Decay accelerating factor regulates complement activation on glomerular epithelial cells.
TL;DR: DAF is present on human GEC in culture and in human kidney glomeruli, and a DAF-like protein is present in rat GEC, and these proteins regulate C activation in vitro and may play a role in controlling C activation on G EC in vivo.
Journal ArticleDOI
Complement C5b-9 complex activates phospholipases in glomerular epithelial cells
TL;DR: It is demonstrated that in cultured rat GEC, antibody-directed formation of noncytolytic amounts of the MAC induced a rapid and sustained increase in [Ca2+]i that was partly inhibited by ethylene glycol-bis(beta-aminoethyl ether)-N, N,N,N',N'-tetraacetic acid (EGTA).
Journal Article
Studies with antibodies to cultured rat glomerular epithelial cells: subepithelial immune deposit formation after in vivo injection
Richard J. Quigg,D. R. Abrahamson,A. V. Cybulsky,John Badalamenti,Andrew W. Minto,David J. Salant +5 more
TL;DR: Injection into rats of antibodies raised against cultured GEC can produce subepithelial immune deposits, a disease process classically induced by antibodies to BB or its purified components.