1/2. Repair of the corneal epithelial adhesion structures following keratectomy wounds in diabetic rabbits.In corneal tissue from a diabetic patient 15 months after delayed epithelial healing following vitrectomy surgery, electron microscopy revealed a discontinuous basement membrane; immunohistochemically, fibronectin was present in the basement membrane zone. To determine whether alterations in repair of the basement membrane, anchoring fibrils and hemidesmosomes occur in wounds in diabetics, we studied the pattern of histochemical localization of bullous pemphigoid antigen (the intracellular hemidesmosome plaque component), laminin and type VII collagen (the anchoring fibril collagen) in alloxan-induced diabetic rabbits following superficial keratectomy. Ultrastructural studies of basal laminae and hemidesmosomes also were performed. Epithelial wound closure was complete by 66-72 h after 7-mm superficial keratectomies. Type VII collagen localized at the base of the epithelium at the wound periphery by 66 h, appearing as a beaded line underlying the epithelium; at 1 week, as in control rabbits, the localization zone extended across the wound bed. Polyclonal antibodies to laminin and bullous pemphigoid antigen showed similar localization. Small segments of basal laminae were noted by electron microscopy of the wound periphery as early as 66 h post-keratectomy. By 2 weeks, an increase in hemidesmonsomes associated with segments of discontinuous basal lamina was apparent. No obvious differences in the time or pattern of re-appearance of the adhesion complex in keratectomy wounds could be discerned between normoglycemic and hyperglycemic rabbits. Thus, healing defects in diabetics may be due to factors other than reassembly of adhesion structures.- - - - - - - - - - ranking = 1keywords = antigen (Clic here for more details about this article) |
2/2. The syndrome of caudal dysplasia: a review, including etiologic considerations and evidence of heterogeneity.The syndrome of caudal dysplasia (CDS) and the wide spectrum of associated skeletal and other anomalies are reviewed, and a further case of this disorder is presented. The syndrome of CDS should be distinguished from the familial forms of sacral dysgenesis, three forms of which are tentatively identified. Two of these usually involve some degree of "hemi-sacrum." The third is usually manifested as partial sacral agenesis with absent distal segments. All these familial types are probably genetic dominants, and none is associated with maternal diabetes. Usually CDS is not familial, but it often is associated with a tendency toward diabetes in the mother. The suggestion is advanced here that CDS is the result of a combination of two principal factors represented by (a) a maternal diabetic tendency and (b) separate nondiabetogenic genes. Determination of the human leucocyte antigen (HLA) haplotypes involved in CDS is suggested to investigate the possibility of genetically distinctive factors in this condition.- - - - - - - - - - ranking = 0.5keywords = antigen (Clic here for more details about this article) |