We report on the realization of all-polymer solar cells based on blends of poly(3-hexylthiophene-2,5-diyl) (P3HT) as a donor and poly{[N,N 0 -bis(2-octyldodecyl)-naphthalene-1,4,5,8-bis(dicarboximide)-as an acceptor. High fill factors are demonstrated for the first time in this class of devices suggesting high dissociation efficiency for the bounded electron-hole pairs and balanced electron and hole mobility along the thin films. The use of the high-mobility n-type P(NDI2OD-T2) polymer enables us to overcome one of the problems limiting the efficiency of all-polymer solar cells, resulting in fill factors comparable with those reported for fullerene-based devices.

PurposeStudies of Fuchs' dystrophy have largely focused on individuals of European origin. Characterization of disease among African Americans is required to ensure prognostic factors and therapeutic approaches are applicable across diverse patient populations.MethodsWe assessed all self-reported black and white patients aged older than 40 years at a tertiary care institution with a diagnosis of cataract over a 3-year period for concurrent diagnosis of Fuchs' dystrophy. Affected patients in a longitudinal cohort were invited to provide a blood sample from which we extracted genomic DNA. The CTG18.1 trinucleotide repeat length was determined using a two-step, triplet repeat primed PCR protocol. Expansion was defined as >40 CTG repeats. Demographic information, including race, was documented.ResultsOf 59,365 self-reported black and white adults who presented for cataract evaluation, the odds ratio of presenting with Fuchs' dystrophy among black compared to white patients was 0.6992 (95% confidence interval [CI], 0.6210–0.7872). A total of 60 black and 549 white patients with Fuchs' corneal dystrophy enrolled in the longitudinal study, of which 21 (35.0%) black and 343 (62.5%) white patients demonstrated trinucleotide repeat expansion, a significant difference (P = 7.7 × 10−5). In a multivariable linear regression model, repeat expansion but not race was significantly associated with mean clinical grading of severity.ConclusionsBlack patients with Fuchs' dystrophy were less likely than white patients to demonstrate CTG18.1 allele expansion. The data contribute to our understanding of population differences in clinical presentation, and highlight the need for considering diversity of patient populations in clinical research.

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PurposeAmantadine use has been temporally associated with bilateral corneal edema in a series of cases; however, its pathophysiological mechanisms have yet to be elucidated. We sought to rule out subclinical Fuchs dystrophy as a contributor, characterize its pattern of corneal edema, and describe the long-term outcome of concurrent topical steroids while resuming amantadine.Patient and methodsAfter a 44-year-old woman presented with new acute onset bilateral corneal edema, amantadine was discontinued, with clinical improvement. However, neurological decompensation required restarting amantadine, which she did concurrently with topical loteprednol. To determine whether subclinical Fuchs dystrophy might be present, triplet-primed polymerase chain reaction was conducted to measure copy number of the CTG18.1 trinucleotide repeat in TCF4. Specular microscopy and Scheimpflug imaging were conducted and followed for 32 months to assess for resolution and stability. Literature review was conducted to assess for consistency of the clinical phenotype.ResultsCorneal edema resolved clinically 4 weeks after discontinuation of amantadine. Serial Scheimpflug imaging demonstrated resolution of posterior and central corneal edema and specular microscopy revealed intracellular opacities with loss of endothelial cell density. Despite resuming amantadine, Scheimpflug imaging and specular microscopy measurements remained stable at 32 months. Triplet-primed PCR of CTG18.1 in TCF4 revealed no trinucleotide repeat expansion.ConclusionsAmantadine-associated corneal edema is characteristically posterior and central and appears unlikely to represent early or subclinical decompensation of Fuchs dystrophy. We describe the unique outcome of continued corneal clearance after restarting amantadine concurrently with steroids, a pattern that has persisted over 32 months to date.