作者自建立了小鼠遗传性眼裂早期形成与其继发角膜白斑模型品系后,由遗传实验证实了小鼠眼裂早期形成的病态基因位于常染色体,是一种隐性遗传疾病。当这种隐性基因纯合时,就能使小鼠在胚胎发育的中、后期眼裂逐渐形成(正常健康小鼠无此现象)。幼鼠出生后,因小鼠的眼裂早期形成(正常小鼠2周后才睁眼),上、下眼睑无法闭合,起不到保护眼球的作用,故外界环境中的异物接触角膜,致使角膜干燥、损伤或继发炎症,引起眼科疾病。经观察该品系小鼠的视力均减退,严重者双目失明。为了巩固发展和广泛利用该品系,就必须充分了解在发生角膜白斑病后,是否会影响患鼠自身的正常生长、发育及繁殖,进一步探讨该品系小鼠和正常健康小鼠的生长、发 The author established a mouse hereditary rupture of early formation and its secondary leukoplakia model strains, confirmed by genetic experiments in mouse eyelid early pathological genes located in autosomal, is a recessive genetic disease. When this recessive gene is homozygous, mice can gradually develop in the middle and late stages of embryonic development (normal healthy mice do not have this phenomenon). After the birth of a baby mouse, the mouse’s eyelid is formed at an early stage (normal eyes open only after 2 weeks), and the upper and lower eyelids can not close and can not protect the eyeball. Therefore, foreign bodies in the external environment contact the cornea, causing the cornea to dry , Damage or secondary inflammation, causing eye diseases. The observed visual acuity of the strain of mice are diminished, in severe cases, both eyes are blind. In order to consolidate the development and extensive use of the strain, we must fully understand in the occurrence of corneal vitiligo, will affect the normal growth of their own mice, development and reproduction, to further explore the strains of mice and healthy mice growth, hair