Today's Hours: 8:00am - 8:00pm
Lane Medical Library

Search

Filter Results

Did You Mean:

Search Results

Sort by
relevance
  • Book
    Yasuhiko Tomino., editor
    Contents:
    Part I. Pathogenesis
    Chapter 1. Is IgA nephropathy the same disease/a homogenous disease?
    Chapter 2. Genetic variations of IgA nephropathy
    Chapter 3. Is IgA nephropathy a familial or sporadic disease?
    Chapter 4. Heterogeneity of GdIgA1
    Chapter 5. Differences of histological classification between the Japanese guideline and the Oxford classification
    Chapter 6. Podocyte injury and the role of megalin
    Chapter 7. Complement activation
    Part II. Treatment
    Chapter 8. How different are the current understandings of treatments for IgA nephropathy?
    Chapter 9. Differences in etiology and treatment in China
    Chapter 10. Differences in etiology and treatment in Korea
    Chapter 11. Differences in etiology and treatment in Japan
    Chapter 12. The VALIGA study: Differences in treatment approaches within the EU
    Chapter 13. Differences in etiology and treatment in Scandinavian countries
    Chapter14 The Implication of the KDIGO Clinical Practice Guidelines on management of IgA Nephropathy
    Chapter15 Japanese Clinical Practice Guidelines for IgA Nephropathy: Difference from KDIGO Guidelines
    Chapter16 Limitations of RAS blockade in IgA nephropathy
    Chapter17 What is the goal for proteinuria in IgA nephropathy?
    Chapter 18. Rationale of tonsillectomy and steroid pulse therapy (TSP): Is it race dependent?
    Chapter 19. Is tonsillectomy a possible treatment for IgA nephropathy from RCT?
    Chapter 20. Is tonsillectomy a possible treatment for IgA nephrology from a retrospective analysis?.
    Digital Access Springer 2016
  • Article
    Wolfe RR, Elahi D, Spitzer JJ.
    Am J Physiol. 1977 Feb;232(2):E180-5.
    We studied the effects of E. coli endotoxin on the glucose and lactate kinetics in dogs by means of the primed constant infusion of [6(-3)H] glucose and Na-L-(+)-[U-14C] lactate. The infusion of endotoxin induced a transient hyperglycemic level, followed by a steady fall in plasma glucose to hypoglycemic levels. The rate of appearance (Ra) and the rate of disappearance (Rd) of glucose were both significantly elevated (P less than .05) for 150 min after endotoxin, after which neither differed from the preinfusion value. The metabolic clearance rate of glucose was significantly elevated at all times 30 min postendotoxin. By 30 min postendotoxin, Ra and Rd of lactate, plasma lactate concentration, and the percent of glucose turnover originating from lactate were significantly elevated and remained so for the duration of the experiment. We concluded that after endotoxin hypoglycemia developed because of an enhanced peripheral uptake of glucose and a failure of the liver to maintain an increased Ra of glucose. We also concluded that lactate became an important precursor for gluconeogenesis and an important metabolic substrate.
    Digital Access Access Options