The @entity735 of @entity19 caused by the lgMl mutation was prevented by prenatal administration of @entity1955 (T4) to the pregnant mother. Treatment on days 10 to 11 of gestation was most effective in preventing @entity735 . A contrasting worsening of the defect was seen after treatment on day 14 of gestation. A dose-response relationship for prevention appeared to be present up to a dose of 0.1 mg/ @entity19 , after which 39% of fetuses had both eyes closed compared to 2% in controls. Higher doses appeared to give little or no further increase in beneficial effect. Scanning electron microscopy was used to compare @entity1955 -treated and untreated lgMl/lgMl and normal CBA/J day 16 or 17 fetal eyes. Mutant eye closure after @entity1955 differed from untreated mutant in the growth of both @entity735 and in increased numbers of rounded periderm cells on the advancing lid edges. The underlying epithelial tissue layer appeared to fuse closed. The induced eye closure in the mutant was not normal, however. The periderm cell layer had disorderly fusion at the outer canthus, premature flattening, and failure to fuse in the inner canthus.

Prevention of the eye closure defect in lgMl/lgMl fetal XXXX by @entity1955 .

@entity19 :: ('10090', 'Species') :: ['mice', 'mouse'] @entity735 :: ('MESH:D005124', 'Disease') :: ['upper and lower eyelids across the eye', 'open-eyes', 'open-eye birth defect'] @entity1955 :: ('MESH:D013974', 'Chemical') :: ['thyroxine']
@entity19 :: (10090,Species) :: ['mice']
