Nippon Ronen Igakkai Zasshi. Japanese Journal of Geriatrics
Print ISSN : 0300-9173
Volume 20 , Issue 2
Showing 1-4 articles out of 4 articles from the selected issue
  • Y. Itokawa, Y. Saito, M. Inada, R. Suzue, K. Okano, T. Onishi, M. Kiba ...
    1983 Volume 20 Issue 2 Pages 89-137
    Published: March 30, 1983
    Released: November 24, 2009
    JOURNALS FREE ACCESS
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  • Takeshi Sakai, Akira Watanabe, Takanobu Wakasugi, Ryozo Tatami, Toshih ...
    1983 Volume 20 Issue 2 Pages 138-142
    Published: March 30, 1983
    Released: November 24, 2009
    JOURNALS FREE ACCESS
    Failial Hypercholesterolemia (FHC) is charactarized clinically by hypercholesterolemia greater than 250mg/dl with tendon xanthomas (especially Achilles tendon xanthoma determined by radiographic method).
    In this paper we reported six FHC patients with spontaneously ruptured Achilles tendon. The results were as follows: 1) their ages were between 41 and 68yrs (53±4, Means±SEM). 2) the radiographic Achilles tendon thickness were between 9 and 14mm (11.5±1) on the non-ruptured side and between 12 and 17mm (14.5±0.7) on the ruptured side. 3) the serum cholesterol levels were between 251 and 402mg/dl (313±27). They had no systemic or local diseases expect FHC. The rediographic Achilles tendon thickness of 228 FHC patients showed a positive correlation with the ages (r:0.231, p<0.001) and the serum cholesterol leverls (r:0.195, p<0.001).
    These observations suggest that the long-term hypercholesterolemic state would lead to the degenerative changes and the spontaneous rupture of Achilles tendon in FHC.
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  • Noriko Hirunagi
    1983 Volume 20 Issue 2 Pages 143-153
    Published: March 30, 1983
    Released: November 24, 2009
    JOURNALS FREE ACCESS
    The report describes a quantitative study of lipofuscin of the spinal cord related to changes with using the image analyzed and score method. Spinal cords used in the study were obtained from 123 autopsied cases (64 males, 59 females: 0-97 years of age). All of the case had no spinal cord signs clinically. Quantitative analysis of lipofuscin was made on different function of the sponal cord neurons such as anterior horn neurons, dorsal nuclei, intermediolateral cells and Onufrowicz nuclei, Betz giant cells, cervical and sacral anterior horn neurons were studied for motor neurons' analysis. As for the aging central nervous system the relationship between the lipofuscin and the corpora amylacea, senile plaque, Alzheimer neurofibrillary tangles were studied. Further the report was based on the comparison of the control group and the degenerative disease such as amyotrophic lateral sclerosis (ALS) olivopontocerebellar atrophy (OPCA), and progerssive muscular dystrophy of Duchenne type (PMD).
    Results: 1. The amout of lipofuscin incresed lineary with the aging. It increases in anterior horn neurons most, followed by Onufrowicz nuclei, and intermediolateral nuclei. There was no difference between both sexes.
    2. The amout of lipofuscin in motor neurons at different levels of the spinal cord increases in sacral anterior horn neurons most, followed by cervical anterior horn neurons, and Betz giant cells.
    3. There is no relationship between the amount of lipofuscin and the amount of corpora anylacea in sacral spinal cord.
    4. Senile plaques were not detected in the spinal cords examined, but those in the cerebral cortex were studied. Much lipofuscin was found in the Betz giant cells, which showed no relationship with the lipofuscin of the sacral anterior horn neurons.
    5. The Alzheimer neurofibrillary tangles were found in the 3 cases of the aged (89, 85, 81 year old females).
    6. The amout of lipofuscin of the sacral anterior horn neurons were difinitely larger in 9 cases of the 10 cases of ALS and 2 cases of OPCA than one in the control, whereas no difference was found in 5 cases of PMD.
    This study clearly demonstrates that the amount of lipofuscin increases linerly with the aging, and is not correlated with the amount of corpora amylacea and senile plaque. It suggested that the degenerative disease such as ALS and OPCA acelerates the aging processes of neurons.
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  • 1983 Volume 20 Issue 2 Pages 154-192
    Published: March 30, 1983
    Released: November 24, 2009
    JOURNALS FREE ACCESS
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