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951). Reinterventions did not differ significantly among groups (Log-rank P = .598). Hospital deaths occurred in seven patients (3.4%). There was no difference in survival between groups (Log-rank P = .221). The median liver stiffness score was 18.65 kPa and the eight patients had advanced liver fibrosis (grade F3-4) in group A. CONCLUSION PTFE is the recommended conduit for TCPC with a lower risk of thrombosis compared to BJV and PET. BJV conduits in TCPC circuits may not protect against liver fibrosis. BJV should not be considered as an option for TCPC. © 2020 Wiley Periodicals, Inc.IMPORTANCE Long-term data of intravitreal injections of vascular endothelial growth factor (VEGF) inhibitors are lacking. BACKGROUND This study aims to assess visual and anatomic outcomes of eyes with neovascular age-related macular degeneration (nAMD) after 10 years of anti-VEGF therapy. DESIGN Retrospective analysis of data from a prospectively designed database. PARTICIPANTS One hundred and sixteen eyes with nAMD (94 participants) that started anti-VEGF therapy at least 10 years earlier. METHODS Eyes were tracked by the Fight Retinal Blindness! registry. MAIN OUTCOME MEASURES Mean change in visual acuity at 10 years vs baseline. Visual acuity was assessed by the number of letters read on a logarithm of the minimum angle of resolution chart. RESULTS Eyes received a median of 27.5 injections over 10 years. Mean visual acuity was 57.5 letters (SD 17.5) at baseline. It increased slightly at 1 year, then dropped steadily by 18 letters (95% CI 13.7; 22.3) at 10 years. Overall, 10% of eyes gained ≥10 letters, 64% lost ≥10 letters and 23% remained stable (±5 letters from baseline). Geographic atrophy and subretinal fibrosis were found in 93% and 71%, respectively, after 10 years, both mostly affecting the centre of the fovea. Pre-treated eyes (47.5%) had significantly worse visual acuity than treatment-naïve eyes at baseline and during follow-up and were significantly more likely to have atrophy and fibrosis. CONCLUSIONS AND RELEVANCE Despite short-term stabilization, long-term visual outcomes of nAMD eyes under anti-VEGF therapy may be poor. Development of atrophy and fibrosis, resulting from the natural progression of the disease, may partly explain this evolution. © 2020 Royal Australian and New Zealand College of Ophthalmologists.IMPORTANCE A framework for understanding the phenotypic features of CRX retinopathy was established. BACKGROUND To perform a phenotype-genotype correlation analysis in two groups of patients with heterozygous mutations in distinct locations of the CRX gene, encoding the cone-rod homeobox. DESIGN Multicentre retrospective study. selleck products PARTICIPANTS Twenty-one Japanese patients from 14 families with a heterozygous CRX mutation. METHODS Retrospective data analysis. MAIN OUTCOME MEASURES Clinical records on CRX mutation, symptoms, best-corrected visual acuity (BCVA), visual field, fundus photography, fundus auto-fluorescence, optical coherence tomography and electroretinograms (ERGs). RESULTS Six different CRX heterozygous mutations were identified in the subjects. Twelve patients from 9 families shared the p.R41W mutation and 1 patient had the p.R43C mutation, both of which affect the homeobox domain of CRX. These patients often displayed adult-onset retinal dystrophy with macular degeneration. In contrast, five patients with downstream mutations (p.S204fs, p.S213fs, p.G243X and p.L299F) displayed retinal degeneration or macular degeneration with bone-spicule pigmentation. Three asymptomatic carriers with different mutations (p.R41W, p.S213fs and p.G243X) were present in both groups. Nearly all patients and carriers had an electronegative ERG in response to a bright flash under dark adaptation. There was no cross-sectional association between patients' age and BCVA, despite progressive decline in BCVA. CONCLUSIONS AND RELEVANCE Heterozygous mutations within or downstream of the homeobox domain in CRX relate to the difference associated retinal phenotypes, which was confounded by variable expressivity and electronegative ERGs. CRX mutations should be considered in patients with an electronegative ERG with minimal or no macular changes. © 2020 Royal Australian and New Zealand College of Ophthalmologists.DNA nanotechnology holds substantial promise for future biomedical engineering and the development of novel therapies and diagnostic assays. The subnanometer-level addressability of DNA nanostructures allows for their precise and tailored modification with numerous chemical and biological entities, which makes them fit to serve as accurate diagnostic tools and multifunctional carriers for targeted drug delivery. The absolute control over shape, size, and function enables the fabrication of tailored and dynamic devices, such as DNA nanorobots that can execute programmed tasks and react to various external stimuli. Even though several studies have demonstrated the successful operation of various biomedical DNA nanostructures both in vitro and in vivo , major obstacles remain in the path to real-world applications of DNA-based nanomedicine. Here, we summarize the current status of the field and the main implementations of biomedical DNA nanostructures. We in particular focus on open challenges and untackled issues and discuss possible solutions. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.AIM To analyse the heterogeneity of fibroblasts isolated from the fibrous capsules of radicular cysts and explore the effects of fibroblast subsets on bone destruction. METHODOLOGY Radicular cysts were divided into groups according to varying perilesional sclerosis identified by radiograph. Colony forming units (CFUs) were isolated from the fibrous capsules of cysts, by which Trap+MNCs were induced, and the expression of osteoclastogenesis-related genes was compared among groups by real-time PCR. The variances in gene profiles of CFUs were identified by principal component analysis, and then CFUs were divided into subsets using cluster analysis. The induction of Trap+MNCs and related gene expression were compared among subsets, and osteoclastogenic induction was blocked by IST-9 or bevacizumab. The fibroblast subsets in cysts were investigated by retrospective immunostaining with IST-9, VEGF-A, and CD34. A fibroblast subset that underwent gene editing by CRISPR/Cas was injected into the site of bone defects in animal models, and the in vivo effects on osteoclastogenesis were investigated.