Trabecular meshwork alteration and intraocular pressure change following pulsed near-infrared laser trabeculoplasty in cats.

BACKGROUND AND OBJECTIVE: To comparatively assess the safety and variation in intraocular pressure (IOP) of two pulsed near-infrared lasers (titanium:sapphire and alexandrite) for laser trabeculoplasty versus conventional blue-green argon laser trabeculoplasty in an animal model. MATERIALS AND METHODS: The left eyes of 15 healthy cats received a 180 degree laser trabeculoplasty treatment: 5 with a titanium:sapphire laser, 5 with an alexandrite laser, and 5 with an argon laser. Preoperatively and postoperatively, all animals underwent tonometry, gonioscopy, and slit-lamp examination. The cats were observed up to 12 weeks. Scanning electron microscopy and histologic examination were performed to evaluate potential alterations in the trabecular meshwork structure. RESULTS: IOP at 1 hour, 1 day, and 1 week following treatment was remarkably lower, irrespective of the laser source used. Following treatment with both near-infrared lasers, gonioscopy showed depigmentation underneath the area of the treated trabecular meshwork and histologic evaluation showed a decrease in pigment density. On scanning electron microscopy, damage to the trabecular meshwork structure could not be detected after treatment with near-infrared lasers. CONCLUSIONS: Near-infrared laser trabeculoplasty was found to be effective to temporarily lower IOP in cats. The lasers selectively altered pigment-containing cells, avoiding structural damage of the trabecular meshwork anatomy.

Non-apoptotic desquamation of cells from corneal epithelium: putative role for Muc4/sialomucin complex in cell release and survival.

Muc4/sialomucin complex (SMC), a large heterodimeric mucin composed of an extracellular mucin subunit ASGP-1 and a transmembrane subunit ASGP-2, is present at the rat ocular surface localized mainly to the most superficial layers of the epithelia. To investigate corneal homeostasis and the functions of Muc4/SMC at the ocular surface, we developed a corneal epithelial cell culture system from corneal explants, from which migrating cells formed an epithelial sheet resembling the native epithelium with regard to microanatomy, expression of characteristic markers, cell migration, and Muc4/SMC expression. Cells migrating from the explants expressed smooth muscle actin. Proliferation was detected only on the edge of epithelial sheet in the immature epithelium and throughout the sheet in confluent cultures. Microscopy revealed that the epithelial sheet was formed from four to six layers of cells expressing keratin 3 and Muc4/SMC in forms identical to those expressed at ocular surface in vivo. Electron microscopy showed cells in various morphological states in the process of releasing from the surface of the multilayer (desquamating). Surprisingly, few of these cells showed evidence of apoptosis, either by morphological or DNA fragmentation analyses. These results suggest a new model for desquamation from stratified epithelia, in which desquamation and apoptosis are independent and sequential processes. Desquamating cells also exhibit a high level of Muc4/SMC. Since Muc4/SMC has been shown to be a potent anti-adhesive and a repressor of apoptosis, we propose that it plays a role in the non-apoptotic desquamation process.

Viral papillomatosis in Florida manatees (Trichechus manatus latirostris).

The Florida manatee (Trichechus manatus latirostris) is one of the most endangered marine mammals in American coastal waters. Naturally resistant to infectious disease, the manatee immune system appears highly developed to protect it against the harsh marine environment and the effects of human-related injury. In 1997, seven captive Florida manatees developed multiple, cutaneous, pedunculated papillomas over a period of 6 months. Approximately 3 years later, four of the seven manatees developed multiple, cutaneous, sessile papillomas topically and clinically distinct from the initial lesions, some of which are still present. Histologic, ultrastructural, and immunohistochemical features indicated that the two distinct phenotypic lesions were caused by papillomaviruses (PVs). Preliminary immunologic data correlated with daily clinical observations suggested that the manatees were immunologically suppressed and that the papillomas were caused by activation of latent PV infections and reinoculation from active infections. The emergence of PV-induced papillomas in captive manatees, the possibility of activation of latent infection or transmission of active infection to free-ranging manatees, and the underlying cause of immune suppression predisposing manatees to develop viral papillomatosis are serious concerns for the future management of this highly endangered species.