| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
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| Research Abstract |
Mice lenses were injured at the anterior, lateral and posterior sides by means of a transcorneal or transscleral needle puncture, and the response of the lens was examined morphologically.
The lens epithelium, which covers the anterior half of the lens, has a mechanism for repairing any perforating injury. However, deep injuries or large area injuries resulted in the rapid development of opacity. The development of such opacity occurred in two patterns according to the site of liquefaction ; posterior opacity and anterior opacity. To examine the mechanism of the posterior opacity, the tracer was injected into the anterior cortex. The tracer was seen moving toward the posterior side along the periphery of the nucleus.Moreover, it was found that in the rodent lens there was a specific zone called the "perinuclear zone", which is prone to develop opacity in response to an injury.
When the lens was injured at the lateral side, its repair function was incomplete and cataractous prognession was rather accelerated. When the lens was injured at the posterior side, the protruded fibers became atrophic after 7 months. However, the wounded cortex remained almost unrepaired, and the lens became opaque by unusual thickening of the anterior cortex and posterior deviation of the nucleus.
These findings indicate that the lens becomes cataractous when the anterior injury exceeds the limit of the epithelial repair function, or when the posterior injury disturbed formation of the posterior cortex.
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