Intracameral injections of preservative-free lidocaine, ropivacaine, and levobupivacaine induced significantly more apoptotic endothelial cell loss than BSS Plus and led to morphologic changes in the corneal endothelial cells in the early period. This effect was temporary, with recovery by 7 days. Considering the limited proliferative capacity in human eyes, the induced apoptosis might result in the permanent cell loss and enlargement in human corneal endothelium.

Minocycline is neuroprotective and contributes to functional improvement after traumatic SCI by eliminating the destructive process of secondary injury. Having both satisfying anti-inflammatory and antiapoptotic effects in experimental models, it promises to be of therapeutic use in human SCI.

ABSTRACT.Purpose: To evaluate the effect of different bevacizumab concentrations on retinal endothelial cell proliferation, retinal structures and apoptotic activity after intravitreal injection in a retinopathy of prematurity (ROP) mouse model. Methods: A total of 35 of C57BL ⁄ J6 mice were exposed to 75 ± 2% oxygen from postnatal day 7 to postnatal day 12. On day 12, 10 mice (group C) were injected with 2.5 lg intravitreal bevacizumab (IVB), 11 mice (group D) were injected with 1.25 lg IVB, and 14 mice (group E) were injected with 0.625 lg IVB in one eye. The contralateral eyes were injected with isotonic saline (control group = group B). Four nonexposed mice served as negative controls (group A). Neovascularization was quantified by counting the endothelial cell proliferation on the vitreal side of the inner limiting membrane of the retina. Histological and ultrastructural changes were examined by light and electron microscopy. Terminal deoxynucleotidyl transferase deoxy-UTP-nick end labelling (TUNEL) was used to detect apoptosis. Results: The endothelial cell count per histological section was lower in groups C (p < 0.0001), D (p < 0.0001) and E (p < 0.0001) compared with the control group B. Histological evaluation showed no retinal toxicity in any group. Electron microscopy revealed hyperoxia-induced mitochondrial dysmorphology in group B. Mitochondrial dysmorphology displayed dose-dependent gradual increase in IVB-injected eyes. Intravitreal bevacizumab induced no significant increase in apoptotic cell death. Conclusion: Bevacizumab suppresses endothelial cell proliferation in a ROP mouse model. In addition to hyperoxia-induced mitochondrial dysmorphology of C57BL ⁄ J6 retina, morphological findings implicate further mitochondrial vulnerability because of bevacizumab without increase in apoptotic cell death.

BackgroundThis experiment was performed to compare the effects of Phenytoin (PHT) and Hypericin (HP) cream on healing of burn wounds in rats.Material/MethodsTwenty rats were divided into 3 groups and second-degree burn wounds were created. The burn wounds in the first, second, and third groups were covered twice daily with PHT cream, HP cream, and saline (control), respectively. At the end of days 3, 7, 14, and 21, full-thickness skin biopsies were done for histopathologic and immunohistochemical analyses.ResultsHistopathologic evaluations at the 14th day showed that re-epithelialization scores were greater in the HP group than the PHT group, but on day 21, re-epithelialization scores were higher in the PHT group than the HP group. Collagen content on days 3 and 14 in the PHT group was found to be higher than in the HP group. Well-vascularized granulation tissue on day 7 in the PHT group was higher than in other groups. HP and PHT groups had a significant increase in VEGF and TGF-β expression in burn wound healing area compared to the control group on all days.ConclusionsTopical application of HP can promote re-epithelialization in burn wounds to shorten the wound healing time for superficial burns. Phenytoin, on the other hand, contributes to healing by increasing vascularized granulation tissue and collagen synthesis through re-epithelialization. The increased VEGF and TGF-β expression following PHT and HP treatment strongly indicate that PHT and HP treatment promotes VEGF and TGF-β production and action in the burn wound area.

Study design: A rat model of spinal cord injury was used to test the hypothesis that Nogo-A monoclonal antibody (NEP1-40) promotes morphologic and functional recoveries of injured spinal cord. Objective: Nogo-A is a myelin-associated neurite outgrowth inhibitory protein, which blocks elongation nerve fibers and limits neuronal regeneration after central nervous system injury. Methods: Forty-four rats were utilized and allocated into control (vehicle) and NEP1-40-treated groups. In all animals, the spinal cord was hemi-transected at Th-10 and phosphatebuffered saline solution was immediately applied on the injured area in the control group. NEP1-40 solution was immediately applied on the hemi-transected area in the treatment group. Each group was subdivided into three subgroups according to the postsurgical day of killing (3, 8 and 21 days). The spinal cords were removed for analysis. Results: Motor scores in the NEP1-40-treated groups were significantly higher than those in the vehicle groups both at 8 and 21 days post injury. Immunohistochemical staining for pancadherin, a marker of neuronal cell adhesion and axonal sprouting, revealed a significant increase in staining in the NEP1-40 treatment group at 8 and 21 days post injury. Transmission electron microscopical evaluation revealed degeneration of the myelin and loss of cytoarchitectural organization in the axons of controls. Better preservation and normal histologic features were observed in the NEP1-40-treated groups. Conclusion: We have demonstrated improved preservation of injured axons and significant pan-cadherin expression after NEP1-40 treatment after the spinal cord injury. Inhibition of Nogo-A may improve the capacity for neuronal regeneration after spinal cord injury.