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Biomedical subjects

D M Albert

Publications and source records attributed to D M Albert.

526 records · Page 30Linked to original sources

[Proliferation of retinal glia and excitatory amino acids].

Kainic acid administered intravitreally induced mitogenic effects in the adult rat retina at doses ranging from 60 nm to 200 nm. Similar effects resulted from the injection of domoic acid at doses ranging from 20 nm to 400 nm, and ouabain. L-glutamate, N-methyl D-aspartate and quisqualate provoked similar cytotoxic effects, i.e., swelling and vasuolization of the outer plexiform, inner nuclear and inner plexiform layer, and cell pycnosis. The latter induced no mitoses. The use of Rompun ketamine as anesthetic blocked the mitogenic effects. The immunohistochemical labelling of both glial fibrillary acidic protein and S100 protein in the dividing cells and the location of dividing nuclei in the inner nuclear layer are arguments for their Müllerian nature. We suggest that the mitogenic effects could account for reactive gliosis observed in some clinical conditions.

Amino Acids↗

Vitreous substitute. Experimental studies and review.

We studied a synthetic hydrogel, PHEA [poly(2-hydroxyethyl acrylate)], experimentally. The material is transparent, autoclavable , highly viscous, nonabsorbable, easily injectable, cohesive, and does not fragment on passage through small-gauge needles. Results in animal studies revealed that injection of PHEA into the vitreous cavity promoted inflammatory changes such as vitreous haziness , membrane formation, and chorioretinal atrophy. Histopathologic studies showed extensive retinal disorganization, chorioretinal scarring, and vitritis . We reviewed the literature and concluded that an ideal vitreous substitute for long-term use in complex cases of retinal detachment is not available at this time.

Animals↗

Ocular malformations of Xenopus laevis exposed to nickel during embryogenesis.

The pathogenesis of eye anomalies induced by exposure to Ni2+ (as nickel chloride) during embryogenesis was studied in the frog, Xenopus laevis. Eyes of control and Ni(2+)-exposed tadpoles were examined without staining using a dissecting microscope, by light microscopy of histological sections, and by electron microscopy. The ocular abnormalities of Ni(2+)-exposed tadpoles included (a) microphthalmia, (b) hypopigmentation, (c) hernias and cysts of the choroid and retina, and (d) iris coloboma; cataracts were uncommon. The pathogenesis of the ocular lesions appears to involve diffuse or focal dysplasia and loss of the retinal pigment epithelium, with dystrophy of photoreceptor outer segments and protrusion of neuroretina through gaps in the pigment epithelium. This study confirms that Ni2+ is a potent ocular teratogen for Xenopus embryos and points to the retinal pigment epithelium as a primary cellular target for Ni(2+)-induced embryotoxicity.

Abnormalities, Drug-Induced↗