ABSTRACT
A patient with macular corneal dystrophy who had a successful 6-mm corneal transplant 23 years ago underwent a second keratoplasty for marked irregular astigmatism. The excised button, which contained the original graft and a rim of host cornea, was divided into several portions. One portion was examined histologically, another portion was incubated in organ culture with radioactive precursors and the biosynthetically labeled products characterized, and a third portion was used for cell culture and karotype analysis. The results indicated that host stromacytes had not invaded the graft and that graft stromacytes had synthesized normal proteoglycans. Furthermore, although there was excessive synthesis of abnormal proteoglycan by host stromacytes and accumulation of this material in the host cornea, minor amounts of this material actually accumulated in the graft cornea, possible contributing to the astigmatism. A large transpant that would leave a minimum of host corneal tissue may be conductive to a longer-term good result in patients with macular corneal dystrophy.
Subject(s)
Cornea/pathology , Macular Degeneration/pathology , Chromatography, Agarose , Cornea/ultrastructure , Corneal Transplantation , Glycoproteins/isolation & purification , HLA Antigens/isolation & purification , Humans , Male , Middle Aged , Organ Culture TechniquesABSTRACT
Fibroblast strains from 12 patients with xeroderma pigmentosum had lower than normal rates of DNA repair, as determined by autoradiographic studies of ultraviolet-induced unscheduled nuclear DNA synthesis. The nuclei in binuclear cells, obtained by fusing fibroblasts from certain pairs of these strains, had a greater rate of DNA repair than the nuclei of either strain's unfused mononuclear cells. These results indicate that complementary corrections of the strains' repair defects had occurred in the fused cells. Four complementation groups were found, indicating that at least four mutations caused decreased DNA repair among these 12 strains. The unfused mononuclear cells of each group had a characteristic rate of repair that differed from the rates of the other groups.
