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Perimetry is a non-invasive clinical psychometric examination used for diagnosing ophthalmic and neurological conditions. At its core, perimetry relies on a subject pressing a button whenever they see a visual stimulus within their field of view. This sequential process then yields a 2D visual field image that is critical for clinical use. Perimetry is painfully slow however, with examinations lasting 7-8 minutes per eye. Maintaining high levels of concentration during that time is exhausting for the patient and negatively affects the acquired visual field. We introduce PASS, a novel perimetry testing strategy, based on reinforcement learning, that requires fewer locations in order to effectively estimate 2D visual fields. PASS uses a selection policy that determines what locations should be tested in order to reconstruct the complete visual field as accurately as possible, and then separately reconstructs the visual field from sparse observations. Furthermore, PASS is patient-specific and non-greedy. It adaptively selects what locations to query based on the patient's answers to previous queries, and the locations are jointly selected to maximize the quality of the final reconstruction. In our experiments, we show that PASS outperforms state-of-the-art methods, leading to more accurate reconstructions while reducing between 30% and 70% the duration of the patient examination., (Copyright © 2019 Elsevier B.V. All rights reserved.)

We report on two patients with type 1 diabetes (T1D) after solitary islet transplantation in 2001. They received steroid-sparing immunosuppression (daclizumab, sirolimus, and tacrolimus according to the Edmonton protocol). Both patients became insulin independent for 2 years: Patient A, a 42-year-old female with a 12-year history of T1D, received two islet infusions; patient B, a 53-year-old female with a 40-year T1D history, received one islet infusion. Pretransplant, both had undetectable C-peptide concentrations and frequent and severe hypoglycemia. Pretransplant, hemoglobin A1c (HbA1c) was 7.8% and 8.8% and insulin requirements were 0.47 and 0.33 units/kg/day, respectively. Posttransplant, C-peptide levels remained detectable while immunosuppression was continued, but decreased over time. Insulin was re-started 2 years posttransplant in both patients. Since patient A's glycemia and insulin requirements trended toward pretransplant levels, immunosuppression was discontinued after 13 years. This resulted in a sudden cessation of C-peptide secretion. Patient B continues on immunosuppression, has better HbA1c, and half the insulin requirement compared to pretransplant. Both patients no longer experience severe hypoglycemia. Herein, we document blood glucose concentrations over time (>30 000 measurements per patient) and β cell function based on C-peptide secretion. Despite renewed insulin dependence, both patients express satisfaction with having undergone the procedure., Competing Interests: The authors of this manuscript have no conflicts of interest to disclose as described by the American Journal of Transplantation., (© Copyright 2015 The American Society of Transplantation and the American Society of Transplant Surgeons.)

Purpose: To investigate retrograde axonal degeneration for its potential to cause microcystic macular edema (MME), a maculopathy that has been previously described in patients with demyelinating disease. To identify risk factors for MME and to expand the anatomic knowledge on MME., Design: Retrospective case series., Participants: We included 117 consecutive patients and 180 eyes with confirmed optic neuropathy of variable etiology. Patients with glaucoma were excluded., Methods: We determined age, sex, visual acuity, etiology of optic neuropathy, and the temporal and spatial characteristics of MME. Eyes with MME were compared with eyes with optic neuropathy alone and to healthy fellow eyes. With retinal layer segmentation we quantitatively measured the intraretinal anatomy., Main Outcome Measures: Demographic data, distribution of MME in the retina, and thickness of retinal layers were analyzed., Results: We found MME in 16 eyes (8.8%) from 9 patients, none of whom had multiple sclerosis or neuromyelitis optica. The MME was restricted to the inner nuclear layer (INL) and had a characteristic perifoveal circular distribution. Compared with healthy controls, MME was associated with significant thinning of the ganglion cell layer and nerve fiber layer, as well as a thickening of the INL and the deeper retinal layers. Youth is a significant risk factor for MME., Conclusions: Microcystic macular edema is not specific for demyelinating disease. It is a sign of optic neuropathy irrespective of its etiology. The distinctive intraretinal anatomy suggests that MME is caused by retrograde degeneration of the inner retinal layers, resulting in impaired fluid resorption in the macula., (Copyright © 2014 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.)