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Results for “MICROPHTHALMOS”

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At least 919 records · Page 51Linked to original sources
PubMed1994

In vitro development of lower first molars from the osteopetrotic microphthalmic (mi) mouse.

While the precise mechanism of tooth eruption remains unknown it has been established that for tooth eruption to occur a functioning dental follicle is essential and normal bone resorption is required. In the osteopetrotic microphthalmic (mi) mouse, teeth fail to erupt and development is affected. In the present study, an organ culture technique was established to culture successfully lower first molars from normal and affected mi mice so as to determine if developmental defects were intrinsic to the dental tissue or whether such defects were a result of local environmental factors. Tissue was cultured for up to 13 days and development assessed morphologically at varying time intervals using standard light microscopy. Teeth developed similarly in both animal groups studied. The only variation in the appearance of cultured tissue occurred in the cervical loop region with more curling evident in dental tissue from the affected animals. The results of this study therefore showed that dental tissue from both normal and affected mi mice can be cultured for up to 13 days and that there is no difference in their development. It would appear that these teeth have the same ability to develop and consequently erupt, however the local environment influences tooth development and alters the eruption potential.

Ameloblasts↗
PubMed1979

Eye malformations in rats: induction by prenatal exposure to nickel carbonyl.

Exposure of pregnant rats to inhalation of nickel carbonyl on days 7 or 8 of gestation frequently causes the progeny to develop ocular anomalies, including anophthalmia and microphthalmia. The incidence of extraocular anomalies is very low. The specificity of nickel carbonyl for induction of ocular anomalies in rats appears to be unique among known teratogenic agents.

Abnormalities, Drug-Induced↗
PubMed2002

Unique and redundant connexin contributions to lens development.

Connexin genes encode intercellular channels that help to coordinate development. In mice, the targeted deletion of different connexins produces disparate effects on ocular growth and differentiation in the lens, and the need for multiple channel subunits is poorly understood. Knockout of Cx46 causes a loss of homeostasis and cataracts. Deletion of Cx50 results in reduced ocular growth and cataracts. Targeted replacement of Cx50 with Cx46 by genetic knock-in corrected defects in cellular differentiation and prevented cataracts, but did not restore normal growth. These data show that intrinsic properties of Cx50 were required for cellular growth, whereas nonspecific restoration of communication by Cx46 maintained differentiation.

Animals↗
PubMed1987

Genetic ablation: targeted expression of a toxin gene causes microphthalmia in transgenic mice.

Lineage-specific regulatory elements can be used to direct expression of a variety of genes to specific tissues in transgenic mice. If the hybrid constructs contain a gene encoding a cytotoxic gene product, then genetic ablation of a specific cell lineage can be achieved. We have generated six transgenic mice by introducing into fertilized eggs the mouse gamma 2-crystallin promoter fused to the coding region of the diphtheria toxin A-chain gene. Three of these mice and all the transgenic offspring analyzed were microphthalmic. The lenses of these mice displayed considerable heterogeneity: some were almost normal morphologically but reduced in size, whereas others were grossly aberrant and deficient in nuclear fiber cells. These studies indicate that programmed ablation of specific cell types can be stably transmitted through the germ line.

Animals↗
PubMed2005

Gorlin syndrome: the PTCH gene links ocular developmental defects and tumour formation.

AIM: To identify a gene linking microphthalmia with cyst with early onset medulloblastoma. METHODS: Mutation analysis of the PTCH gene. RESULTS: A mutation in exon 10 of the PTCH gene was identified, confirming a diagnosis of Gorlin syndrome. CONCLUSIONS: This is the first genetically identified mutation giving rise to microphthalmia with cyst and provides a valuable link in the eye developmental gene pathway.

Basal Cell Nevus Syndrome↗