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At least 73 records · Page 4Linked to original sources
PubMed2002

Lack of collagen XVIII/endostatin results in eye abnormalities.

Mice lacking collagen XVIII and its proteolytically derived product endostatin show delayed regression of blood vessels in the vitreous along the surface of the retina after birth and lack of or abnormal outgrowth of retinal vessels. This suggests that collagen XVIII/endostatin is critical for normal blood vessel formation in the eye. All basement membranes in wild-type eyes, except Descemet's membrane, showed immunogold labeling with antibodies against collagen XVIII. Labeling at sites where collagen fibrils in the vitreous are connected with the inner limiting membrane and separation of the vitreal matrix from the inner limiting membrane in mutant mice indicate that collagen XVIII is important for anchoring vitreal collagen fibrils to the inner limiting membrane. The findings provide an explanation for high myopia, vitreoretinal degeneration and retinal detachment seen in patients with Knobloch syndrome caused by loss-of-function mutations in collagen XVIII.

Angiogenesis Inhibitors↗
PubMed1980

Unusual eye abnormalities associated with congenital cytomegalovirus infection.

Seven children with congenital cytomegalovirus infection demonstrated a higher than expected incidence of "rare" ophthalmological abnormalities, including anophthalmia and Peters' anomaly. These data suggest that appropriate investigation for evidence of cytomegalovirus infection should be instituted in any child with congenital ocular defects.

Anophthalmos↗
PubMed1998

[Single umbilical artery (SUA) and congenital eye abnormalities. 2 case reports].

Two cases of single umbilical artery (SUA) are reported, associated respectively with unilateral microphthalmia the first case, with bilateral congenital glaucoma (buphthalmos) the second one. While the association between single umbilical artery and microphthalmia is reported in international literature, the association between single umbilical artery and congenital glaucoma (buphthalmos) described for the first time.

Eye Abnormalities↗
PubMed1979

Translocation 46XY, t (17;18) (q25;q21) in a mentally retarded boy with progressive eye abnormalities.

A 10-year-old boy with reciprocal translocation between chromosomes 17 and 18- 46XY,t (17;18) (q25; q21), appeared cytogenetically balanced. The patient was a healthy, thriving boy whose main abnormal feature was moderate mental retardation. However, abnormal ocular signs were present, including macular "fibrosis", optic disc abnormalities with a traction retinal detachment, tapeto-retinal degeneration, and tilting of the disc to the nasal side. These changes are consistent with the ocular changes previously described in the 18q- syndrome, suggesting that there has been a minimal deletion of chromosome material at the 18q21 breakpoint. The case also demonstrates that the ocular changes of the 18- syndrome may be progressive.

Child↗
PubMed1990

Tumorigenesis and eye abnormalities in transgenic mice expressing MSV-SV40 large T-antigen.

Transgenic mice which expressed SV40 large T-antigen under the control of the MSV enhancer and the SV40 promoter were generated. In animals containing an intact MSV enhancer, total lens cataracts and neuroectodermal brain tumors, originating in the pineal organ were observed. In contrast, 5' deletion of the MSV enhancer to a residual 53 bp resulted in a different spectrum of pathologies. Whilst lens cataracts still occurred, no brain tumors could be detected. Instead, fibrosarcomas and adenocarcinomas of the kidneys were induced. In addition, tumors of the endocrine pancreas were observed with both transgene constructs. We conclude that the MSV enhancer element is sufficient to direct the expression of the viral reporter gene to the lens and the pineal organ in transgenic mice. Deletion of the MSV enhancer correlates with the loss of DNA elements responsible for the pineal cell specific expression of SV40 large T-antigen.

Animals↗