| Project/Area Number |
62570161
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | Kyoto University |
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Principal Investigator |
HOSOKAWA Masanori Chest Disease Research Institute ASSOCIATE PROFESSOR, 胸部疾患研究所, 助教授 (00127135)
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| Co-Investigator(Kenkyū-buntansha) |
HIGUCHI Keiichi Chest Disease Research Institute LECTURER, 胸部疾患研究所, 講師 (20173156)
TAKEDA Toshio Chest Disease Research Institute PROFESSOR, 胸部疾患研究所, 教授 (00027088)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Senescence Accelerated Mouse (SAM) / Ageing / Senescence / Late-appealing cataract / Lens / 老化 / 疾患モデル |
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| Research Abstract |
A new strain of mouse with late-appearing hereditary cataract was developed in the Senescence Accelerated Mouse (SAM-R/3).
1. At the beginning of selection of new strain, 5% of adult mice had cataract at least uni-laterally. During selection and brother-sister inbreeding, the incidence increased and reached 80% at generation 12. Inflammatory lesions of the cornea and eyelids began to occur later in life and theincidence was lower than that of cataract. This observation suggested to us that the cataract of this new strain was not congenital in origin but rather was age-related and did not occur consequently after the onset of inflammatory lesions around the lens tissues. The wet weight and water contents showed that the lens of this strain developed normally and that the untoward events were the result but not the cause of cataract. Urinary suger was nil in all mice examined. This cataract was not inherited in a dominant fashion with high penetrability.
2. Histologically, the mature cataract showed extreme protrusion of the lens at posterior pole and lens nucleus displaced posteriorly. The posterior lens capsule was ruptured. Degeneration of lens fiber cells and liquefaction of the cortex were also observed. Response of lens epithelial cells were not remarkable. These changes were free from inflammation of the tisses around lens. Structure of the retina was normal. The persistent hyaloid vascular system still observed in the eyes of grade 1 cataract after 5 weeks of age. This suggested to us that the persistent hyaloid vascular system may play a role in cataractogenesis but age dependency and late onset of this cataract were hardly explained by this structural anomally alone.
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