Pauling Therapy References

  1. NLM CIT. ID:  91067711
    
    TITLE:  Immunological evidence for the accumulation of lipoprotein(a) in
          the atherosclerotic lesion of the hypoascorbemic guinea pig.
    AUTHOR:  Rath M; Pauling L
    ADDRESS:
          Linus Pauling Institute of Science and Medicine, Palo Alto, CA
          94306-2025.
    PUBLICATION TYPES:
         JOURNAL ARTICLE
    LANGUAGE:  Eng
    REGISTRY NUMBERS:
         0 (Antibodies)
         0 (Lipoprotein(a))
         0 (Lipoproteins)
    ABSTRACT:
          Lipoprotein(a) [Lp(a)] is an extremely atherogenic lipoprotein.
          Lp(a) has been found in the plasma of humans and other primates,
          but until now only in a few other species. The mechanism by which
          it exerts its atherogenicity is still poorly understood. We
          observed that Lp(a) has been found in the plasma of several
          species unable to synthesize ascorbate and not in other species.
          We have now detected apoprotein(a) in the plasma of the guinea
          pig. We induced atherosclerosis in this animal by dietary
          ascorbate depletion and, using SDS/PAGE and subsequent
          immunoblotting, we identified Lp(a) as accumulating in the
          atherosclerotic plaque. Most importantly, adequate amounts of
          ascorbate (40 mg per kg of body weight per day) prevent the
          development of atherosclerotic lesions in this animal model and
          the accumulation of Lp(a) in the arterial wall. We suggest an
          analogous mechanism in humans because of the similarity between
          guinea pigs and humans with respect to both the lack of
          endogenous ascorbate production and the role of Lp(a) in human
          atherosclerosis.
    MAIN MESH HEADINGS:
          Lipoproteins/ANALYSIS/*METABOLISM
          Atherosclerosis/COMPLICATIONS/*METABOLISM/PATHOLOGY
          Ascorbic Acid Deficiency/COMPLICATIONS/*METABOLISM
    ADDITIONAL MESH SUBJECTS:
          Support, Non-U.S. Gov't
          Muscle, Smooth, Vascular/METABOLISM/PATHOLOGY
          Guinea Pigs
          Female
          Electrophoresis, Polyacrylamide Gel
          Blotting, Western
          Aorta/METABOLISM/PATHOLOGY
          Antibodies
          Animal
    SOURCE:  Proc Natl Acad Sci U S A 1990 Dec;87(23):9388-90
    

  2. NLM CIT. ID:  91031571
    
    TITLE:  Lipoprotein(a) in the arterial wall.
    AUTHOR:  Beisiegel U; Rath M; Reblin T; Wolf K; Niendorf A
    ADDRESS:
          Medizinische Kernklinik und Poliklinik, Universitatskrankenhaus
          Eppendorf, Hamburg, F.R.G.
    PUBLICATION TYPES:
         JOURNAL ARTICLE
    LANGUAGE:  Eng
    REGISTRY NUMBERS:
         0 (Apoproteins)
         0 (Lipoprotein(a))
         0 (Lipoproteins)
         0 (Triglycerides)
         57-88-5 (Cholesterol)
    ABSTRACT:
          We compared CHD patients with healthy blood donors to confirm the
          role of Lp(a) as an independent risk factor. More important, we
          performed biochemical and immunohistochemical studies to evaluate
          the potential mechanism by which Lp(a) causes CHD. We measured
          the Lp(a) concentration in comparison with other lipoprotein
          parameters in fresh human arterial wall biopsies and, in autopsy
          tissue, we localized apo (a) and apo B, as well as fibrin, with
          immunohistochemical methods in different vessel areas. Density
          gradient ultracentrifugation was used to analyse lipoprotein
          fractions isolated from human arterial wall. Lp(a) accumulates in
          the intima, preferentially in plaque areas, dependent on the
          serum Lp(a) level. Most of the Lp(a) can be located
          extracellularly, but apo(a) can also be detected in foam cells. A
          strong co-localization has been observed for apo(a) and apo B;
          only a few areas containing only apo B were detected. Moreover, a
          striking co-localization for apo(a) and fibrin was found. The
          possibilities for the pathways by which Lp(a) enters the arterial
          wall and accumulates extracellularly are discussed on the basis
          of the present data and recent data published by other groups.
    MAIN MESH HEADINGS:
          Lipoproteins/*ANALYSIS
          Endothelium, Vascular/*CHEMISTRY
          Coronary Disease/*METABOLISM
          Aorta/*CHEMISTRY
    ADDITIONAL MESH SUBJECTS:
          Triglycerides/ANALYSIS
          Support, Non-U.S. Gov't
          Proteins/ANALYSIS
          Middle Age
          Lipids/ANALYSIS
          Immunohistochemistry
          Human
          Cholesterol/ANALYSIS
          Apoproteins/ANALYSIS
    SOURCE:  Eur Heart J 1990 Aug;11 Suppl E:174-83
    

  3. NLM CIT. ID:  90349583
    
    TITLE:  Hypothesis: lipoprotein(a) is a surrogate for ascorbate
          [published erratum appears in Proc Natl Acad Sci U S A 1991 Dec
          15;88(24):11588]
    AUTHOR:  Rath M; Pauling L
    ADDRESS:
          Linus Pauling Institute of Science and Medicine, Palo Alto, CA
          94306.
    PUBLICATION TYPES:
         JOURNAL ARTICLE
    LANGUAGE:  Eng
    REGISTRY NUMBERS:
         0 (Antioxidants)
         0 (Lipoprotein(a))
         0 (Lipoproteins)
         50-81-7 (Ascorbic Acid)
    ABSTRACT:
          The concept that lipoprotein(a) [Lp(a)] is a surrogate for
          ascorbate is suggested by the fact that this lipoprotein is found
          generally in the blood of primates and the guinea pig, which have
          lost the ability to synthesize ascorbate, but only rarely in the
          blood of other animals. Properties of Lp(a) that are shared with
          ascorbate, in accordance with this hypothesis, are the
          acceleration of wound healing and other cell-repair mechanisms,
          the strengthening of the extracellular matrix (e.g., in blood
          vessels), and the prevention of lipid peroxidation. High plasma
          Lp(a) is associated with coronary heart disease and other forms
          of atherosclerosis in humans, and the incidence of cardiovascular
          disease is decreased by elevated ascorbate. Similar observations
          have been made in cancer and diabetes. We have formulated the
          hypothesis that Lp(a) is a surrogate for ascorbate in humans and
          other species and have marshaled the evidence bearing on this
          hypothesis.
    MAIN MESH HEADINGS:
          Lipoproteins/*PHYSIOLOGY
          Cardiovascular Diseases/*PHYSIOPATHOLOGY
          Ascorbic Acid/*METABOLISM
    ADDITIONAL MESH SUBJECTS:
          Wound Healing
          Neoplasms/PHYSIOPATHOLOGY
          Human
          Evolution
          Disease Models, Animal
          Diabetes Mellitus/PHYSIOPATHOLOGY
          Atherosclerosis/PHYSIOPATHOLOGY
          Antioxidants/METABOLISM
          Animal
    SOURCE:  Proc Natl Acad Sci U S A 1990 Aug;87(16):6204-7
    

  4. NLM CIT. ID:  90312898
    
    TITLE:  Morphological detection and quantification of lipoprotein(a)
          deposition in atheromatous lesions of human aorta and coronary
          arteries [published erratum appears in Virchows Arch A Pathol
          Anat Histopathol 1991;418(1):86]
    AUTHOR:  Niendorf A; Dietel M; Beisiegel U; Arps H; Peters S
          Wolf K; Rath M
    ADDRESS:
          Institut fur Pathologie, Universitat Hamburg, Federal Republic
          of Germany.
    PUBLICATION TYPES:
         JOURNAL ARTICLE
    LANGUAGE:  Eng
    REGISTRY NUMBERS:
         0 (Apolipoproteins A)
         0 (Apolipoproteins B)
         0 (Lipoprotein(a))
         0 (Lipoproteins)
    ABSTRACT:
          Lipoprotein(a), as an atherogenic particle, represents an
          independent risk factor for coronary heart disease. In the
          present study the morphological distribution of apoprotein (a)
          and apoprotein B within the arterial wall is described.
          Apoprotein B, a constituent of very low-density lipoprotein,
          low-density lipoprotein and lipoprotein(a) has previously been
          demonstrated in atheromatous lesions. Lipoprotein(a) possesses an
          additional protein, designated apoprotein (a). Autopsy material
          (n = 74) from the left coronary artery and from the thoracic
          aorta has been examined by means of immunohistochemistry and both
          apoprotein (a) and apoprotein B were detected, primarily
          associated with the extracellular matrix and accumulating in
          lesions in the arterial wall. The staining pattern for both
          antigens was almost always found to be congruent, suggesting that
          the detection of (a)-antigen has to be attributed at least in
          part to the presence of lipoprotein(a). It is concluded that both
          low-density lipoprotein and lipoprotein(a) have an important role
          in the pathogenesis of atherosclerosis.
    MAIN MESH HEADINGS:
          Lipoproteins/*METABOLISM
          Coronary Disease/*METABOLISM/PATHOLOGY
          Atherosclerosis/*METABOLISM/PATHOLOGY
          Arteriosclerosis/*METABOLISM
          Aortic Diseases/*METABOLISM/PATHOLOGY
    ADDITIONAL MESH SUBJECTS:
          Tissue Distribution
          Middle Age
          Infant, Newborn
          Infant
          Immunohistochemistry
          Human
          Coronary Vessels/METABOLISM/PATHOLOGY
          Comparative Study
          Child, Preschool
          Child
          Apolipoproteins B/METABOLISM
          Apolipoproteins A/METABOLISM
          Aorta/METABOLISM/PATHOLOGY
          Aged, 80 and over
          Aged
          Adult
          Adolescence
    SOURCE:  Virchows Arch A Pathol Anat Histopathol 1990;417(2):105-11
    

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