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Atherosclerosis IV

Proceedings of the Fourth International Symposium

  • Editors
  • G. Schettler
  • Y. Goto
  • Y. Hata
  • G. Klose

Table of contents

  1. Front Matter
    Pages I-XLVI
  2. Relation Between Arterial Wall and Risk Factors for Coronary Heart Disease Connective Tissue and Immunological Mechanism on Atherosclerosis

    1. Front Matter
      Pages XLVII-XLVII
    2. C. J. Schwartz, R. G. Gerrity, L. J. Lewis, G. M. Chisolm, K. N. Bretherton
      Pages 1-11
    3. J. C. F. Poole
      Pages 12-15
    4. W. A. Thomas, J. M. Reiner, R. A. Florentin, K. Janakidevi, K. J. Lee
      Pages 16-23
    5. Elspeth B. Smith
      Pages 24-29
    6. M. Daria Haust
      Pages 30-35
    7. J. L. Beaumont, V. Beaumont
      Pages 36-44
    8. Dynamics of Lipoproteins and Lipids in the Arterial Wall

      1. A. J. Day
        Pages 45-46
      2. J. Patelski, M. Piorunska-Stolzmann, A. Waliszewska
        Pages 48-51
      3. G. Schettler, Y. Goto, Y. Hata, G. Klose
        Pages 63-72
    9. Hypertension, Arteriolar Disease and Atherosclerosis

      1. Yukio Yamori, Ryohichi Horie, Michiya Ohtaka, Yasuo Nara, Masaichi Fukase
        Pages 79-83
      2. Y. Yoshida, H. Shinkai, T. Sekiguchi, G. Ooneda
        Pages 83-87
      3. G. Schettler, Y. Goto, Y. Hata, G. Klose
        Pages 88-91
    10. Epidemiology of Atherosclerosis and Geographic Differences in Risk Factors

      1. Lars A. Solberg, Ingvar Hjermann, Anders Helgeland, Ingar Holme, Paul A. Leren, Jack P. Strong
        Pages 98-102
      2. Nisl H. Sternby
        Pages 102-104
      3. M. Hanefeld, W. Leonhardt, H. Haller
        Pages 104-108
      4. Mario R. Garcia-Palmieri, Maria I. Castillo, Margaret C. Oalmann, Paul D. Sorlie, Raúl Costas Jr.
        Pages 108-113
      5. G. N. Stemmermann, G. G. Rhoads, W. C. Blackwelder
        Pages 113-116
      6. G. Schettler, Y. Goto, Y. Hata, G. Klose
        Pages 125-128
    11. Measurement of Triglyceride Turnover

      1. Georg Steiner, Dan Streja
        Pages 129-132
      2. Alan Chait, John J. Albers, John D. Brunzell
        Pages 132-137
      3. G. Schettler, Y. Goto, Y. Hata, G. Klose
        Pages 146-148
    12. Smoking and Atherosclerosis

      1. Poul Astrup
        Pages 156-161
      2. John L. Gainer
        Pages 165-166
      3. G. Schettler, Y. Goto, Y. Hata, G. Klose
        Pages 170-173
  3. Lipoproteins

    1. Front Matter
      Pages 175-175
    2. Antonio M. Gotto, Richard L. Jackson
      Pages 177-188
    3. O. Stein, V. Ebin, H. Bar-On, Y. Stein
      Pages 189-191
    4. Richard J. Havel, Robert L. Hamilton
      Pages 192-196
    5. Shlomo Eisenberg
      Pages 197-204
    6. Y. Stein, O. Stein
      Pages 205-208
    7. Antonio M. Gotto Jr.
      Pages 209-219
    8. Lipoproteins

      1. G. Graham Shipley, Richard J. Deckelbaum, David Atkinson, Donald M. Small
        Pages 222-227
      2. H. Peeters, M. Rosseneu
        Pages 233-237

About these proceedings

Introduction

The presence of monotypism in thick atherosclerotic lesions of black females with G-6-PD mosaicism first reported by the Benditts (1973) has been confirmed in two other laboratories. However, we believe that it is premature to conclude that the finding of monotypism necessarily indicates monoclonal origin of athero­ sclerotic lesions. We have suggested two alternative explanations for the obser­ vation of monotypism which we believe must be shown to be invalid before accept­ ing monoclonal origin as the only plausible way to account for the observed G-6-PD monotypism. One of these two alternatives relates to clonal heterogeneity of cell growth potential, i. e. , during the course of progressive growth of a le­ sion, progeny of one cell may overgrow all others in a portion of the lesion. The other alternative is that one of the G-6-PD alleles may be linked to genes that afford a preferential survival characteristic in the abnormal environment present in atheroscerotic lesions. Thus, cells with one allele may be able to grow better than cells with the other allele, and this characteristic may be unrelated to "A-ness" or "B-ness". We have studied initiation of lesions in He diet-fed swine and demonstrated that all active lesions that were studied were of multiple cell origin (not monoclo­ nal). We have studied cell growth patterns in developing atherosclerotic lesions in He diet-fed swine and found evidence consistent with clonal heterogeneity in growth potential of lesion cells.

Keywords

Arterienverkalkung Stent atherosclerosis cell growth

Bibliographic information

  • DOI https://doi.org/10.1007/978-3-642-95308-8
  • Copyright Information Springer-Verlag Berlin Heidelberg 1977
  • Publisher Name Springer, Berlin, Heidelberg
  • eBook Packages Springer Book Archive
  • Print ISBN 978-3-642-95310-1
  • Online ISBN 978-3-642-95308-8
  • Buy this book on publisher's site