Jansen Huynh (castraft6)

3 ± 19.0 vs. 605.9 ± 18.6 µm; P 0.05). Conclusions The relative significant thinning of the anterior sclera along the inferior meridian with increasing degree of myopia compared with the other three meridians indicates the potential role of AST, especially in the inferior meridian, to act as a marker for myopia progression.Purpose We developed a combined biomechanical and hemodynamic model of the human eye to estimate blood flow and oxygen concentration within the lamina cribrosa (LC) and rank the factors that influence LC oxygen concentration. Methods We generated 5000 finite-element eye models with detailed microcapillary networks of the LC and computed the oxygen concentration of the lamina retinal ganglion cell axons. For each model, we varied the intraocular pressure (IOP) from 10 mm Hg to 55 mm Hg in 5-mm Hg increments, the cerebrospinal fluid pressure (13 ± 2 mm Hg), cup depth (0.2 ± 0.1 mm), scleral stiffness (±20% of the mean values), LC stiffness (0.41 ± 0.2 MPa), LC radius (1.2 ± 0.12 mm), average LC pore size (5400 ± 2400 µm2), the microcapillary arrangement (radial, isotropic, or circumferential), and perfusion pressure (50 ± 9 mm Hg). Blood flow was assumed to originate from the LC periphery and drain via the central retinal vein. Finally, we performed linear regressions to rank the influence of each factor on the LC tissue oxygen concentration. Results LC radius and perfusion pressure were the most important factors in influencing the oxygen concentration of the LC. IOP was another important parameter, and eyes with higher IOP had higher compressive strain and slightly lower oxygen concentration. In general, superior-inferior regions of the LC had significantly lower oxygen concentration than the nasal-temporal regions, resulting in an hourglass pattern of oxygen deficiency. Conclusions To the best of our knowledge, this study is the first to implement a comprehensive hemodynamical model of the eye that accounts for the biomechanical forces and morphological parameters of the LC. The results provide further insight into the possible relationship of biomechanical and vascular pathways leading to ischemia-induced optic neuropathy.Purpose Neurons carry electrical signals and communicate via electrical activities. The therapeutic potential of electrical stimulation (ES) for the nervous system, including the retina, through improvement of cell survival and function has been noted. Here we investigated the neuroprotective and regenerative potential of ES in a mouse model of inherited retinal degeneration. Methods Rhodopsin-deficient (Rho-/-) mice received one or two sessions of transpalpebral ES or sham treatments for 7 consecutive days. Intraperitoneal injection of 5-ethynyl-2'-deoxyuridine was used to label proliferating cells. Weekly electroretinograms were performed to monitor retinal function. Retinal morphology, photoreceptor survival, and regeneration were evaluated in vivo using immunohistochemistry and genetic fate-mapping techniques. Müller cell (MC) cultures were employed to further define the optimal conditions of ES application. Results Noninvasive transpalpebral ES in Rho-/- mice improved photoreceptor survival and electroretinography function in vivo. ES also triggered residential retinal progenitor-like cells such as MCs to reenter the cell cycle, possibly producing new photoreceptors, as shown by immunohistochemistry and genetic fate-mapping techniques. ES directly stimulated cell proliferation and the expression of progenitor cell markers in MC cultures, at least partially through bFGF signaling. Bcl-2 modulator Conclusions Our study showed that transpalpebral ES improved photoreceptor survival and retinal function and induced the proliferation, probably photoreceptor regeneration, of MCs; this occurs via stimulation of the bFGF pathways. These results suggest the exciting possibility of applying noninvasive ES as a versatile tool for preventing photoreceptor loss and mobilizing endogenous progen