It has been recognized that bone trace element composition analysis provides clues when analyzing bone-related physiological conditions. Increasing numbers of bone-related genetic diseases have been identified recently. In this study, we have analyzed bone trace element composition in a genetic mutant animal model. Mutations in the mouse microphthalmia (mi) gene affect the development of a number of cell types, including melanocytes, mast cells, and osteoclasts. Previous studies have shown that different alleles of the mi locus show osteopetrosis. In order to gain insights into the effects of a particular genetic defect on bone trace element composition and bone structure, we performed bone trace element composition analysis using inductively coupled plasma atomic emissions spectrometry (ICP-AES). Marked changes in bone trace element levels were found in vertebrate bones of mi mutant mice. The implications and possible applications of bone trace element analysis will be discussed in this article.

Animals↗

PubMedDate not supplied

Epiretinal membrane formation in Terson syndrome.

Clinical features of epiretinal membranes were examined in 22 eyes of 13 patients with Terson syndrome who were treated with pars plana vitrectomy. The shape and localization of the epiretinal membranes were intraoperatively evaluated and correlated with the presence or absence of posterior vitreous detachment (PVD). Patients with complete PVD, but with no membrane found during surgery, were followed postoperatively. Membrane formation ultimately developed in 13 of the 22 eyes. In eight eyes, PVD was incomplete and the epiretinal membrane was found at the optic disc or along the temporal vascular arcades, displaying retinal folds and vascular tortuosity. Three eyes had massive tractional retinal detachment; five of those with complete PVD developed a thin epiretinal membrane around the posterior pole that became more apparent during long-term follow-up. From these observations, we can classify epiretinal membrane formation in Terson syndrome into two groups: with complete, or with incomplete, PVD. It also appears that multiple pathological processes involving the vitreoretinal interface were responsible for the formation of epiretinal membranes.

Adult↗