These data support a novel and flexible model of modest ocular hypertension with axon loss. The maximal duration of IOP elevation will be further characterized in future studies.

Luminescent solar concentrators (LSCs) use down-converting luminophores embedded in a waveguide to absorb sunlight and deliver high irradiance, narrowband output light for driving photovoltaic and other solar energy conversion devices. Achieving a technologically useful level of optical gain requires bright, broadly absorbing, large-Stokes-shift luminophores incorporated into low-loss waveguides, a combination that has long posed a challenge to the development of practical LSCs. The recent introduction of giant effective Stokes shift semiconductor nanocrystal (NC) phosphors for LSC applications has led to significant performance improvements by increasing solar absorption while reducing escape cone and nonradiative losses compounded by reabsorption, placing increased emphasis on the importance of minimizing parasitic waveguide losses caused by scattering from NC aggregates and optical imperfections. Here, we report a detailed analysis of optical losses in polymer–NC composite waveguide LSCs based on CuInS2/CdS NC phosphors, which have been shown to provide best-in-class performance in large-area, semitransparent concentrators. A comprehensive analytical optical model is introduced enabling quantification of parasitic waveguide, scattering, escape cone, and nonradiative relaxation losses on the basis of distance-dependent edge-emission measurements. By examining the effect of NC loading, we show that NC clustering in polymer composite waveguides leads to light scattering losses that ultimately limit efficiency at large geometric gain. By optimizing NC concentration, optical power efficiencies up to 5.7% under AM1.5 illumination are demonstrated for devices having a geometric gain G = 6.7×, with limiting achievable efficiencies predicted to exceed 10%.

Glaucoma is a group of optic neuropathies associated with aging and sensitivity to intraocular pressure (IOP). The disease causes vision loss through the degeneration of retinal ganglion cell neurons and their axons in the optic nerve. Using an inducible model of glaucoma, we elevated IOP in the squirrel monkey ( Saimiri boliviensis ) using intracameral injection of 35 μm polystyrene microbeads and measured common pathogenic outcomes in the optic projection. A 42% elevation in IOP over 28 weeks reduced anterograde transport of fluorescently-labeled cholera toxin beta from retina to the lateral geniculate nucleus (60% decrease), and to the superior colliculus (49% decrease). Pressure also reduced survival of ganglion cellaxons in the optic nerve by 22%. The same elevation caused upregulation of proteins associated with glaucomatous neurodegeneration in the retina and optic nerve, including complement 1q, interleukin 6, and brain-derived neurotrophic factor. That axon degeneration in the nerve lagged deficits in anterograde transport is consistent with progression in rodent models, while the observed protein changes also occur in tissue from human glaucoma patients. Thus, microbead occlusion in a non-human primate with a visual system similar to our own represents an attractive model to investigate neurodegenerative mechanisms and therapeutic interventions for glaucoma.

Background and Objective Patient portal use has increased over the last two decades in response to consumer demand and government regulation. Despite growing adoption, few guidelines exist to direct successful implementation and governance. We describe the policies and procedures that have governed over a decade of continuous My Health at Vanderbilt (MHAV) patient portal use. Methods We examined MHAV usage data between May 2007 and November 2017. We classified patient portal activity into eight functional categories: Appointment, Billing, Document Access, Genetics, Health Result, Immunization, Medication, and Messaging. We describe our operating policies and measure portal uptake, patient account activity, and function use over time. Results By the end of the study period, there were 375 517 registered accounts. Policies made MHAV available to competent adults and adolescents 13 and over. Patients signed up for a limited access account online, which could be upgraded to a full-access account after identity verification. Patients could assign proxy accounts to family and caregivers, which permitted nonpatient access to select MHAV functions. Laboratory and radiology results were accessible via MHAV. Results were classified into three groups based on sensitivity, which govern the length of delay before results appeared in MHAV. Discussion and Conclusion Patient portals offer significant opportunity to engage patients in their healthcare. However, there remains a need to understand how policies can promote uptake and use. We anticipate that other institutions can apply concepts from our policies to support meaningful patient portal engagement.

Glaucoma is a group of optic neuropathies associated with aging and sensitivity to intraocular pressure (IOP). The disease is the leading cause of irreversible blindness worldwide. Early progression in glaucoma involves dysfunction of retinal ganglion cell (RGC) axons, which comprise the optic nerve. Deficits in anterograde transport along RGC axons to central visual structures precede outright degeneration, and preventing these deficits is efficacious at abating subsequent progression. HE3286 is a synthetic sterol derivative that has shown therapeutic promise in models of inflammatory disease and neurodegenerative disease. We examined the efficacy of HE3286 oral delivery in preventing loss of anterograde transport in an inducible model of glaucoma (microbead occlusion). Adult rats received HE3286 (20 or 100 mg/kg) or vehicle daily via oral gavage for 4 weeks. Microbead occlusion elevated IOP ~30% in all treatment groups, and elevation was not affected by HE3286 treatment. In the vehicle group, elevated IOP reduced anterograde axonal transport to the superior colliculus, the most distal site in the optic projection, by 43% (p = 0.003); HE3286 (100 mg/kg) prevented this reduction (p = 0.025). HE3286 increased brain-derived neurotrophic factor (BDNF) in the optic nerve head and retina, while decreasing inflammatory and pathogenic proteins associated with elevated IOP compared to vehicle treatment. Treatment with HE3286 also increased nuclear localization of the transcription factor NFκB in collicular and retinal neurons, but decreased NFκB in glial nuclei in the optic nerve head. Thus, HE3286 may have a neuroprotective influence in glaucoma, as well as other chronic neurodegenerations.