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Objectives To assess the quality of diabetic eye disease clinical practice guidelines. Study design and setting A systematic search of diabetic eye disease guidelines was conducted on six online databases and guideline repositories. Four reviewers independently rated quality using the Appraisal of Guidelines, Research, and Evaluation (AGREE II) instrument. Aggregate scores (%) for six domains and overall quality assessment were calculated. A “good quality” guideline was one with ≥60% score for “rigor of development” and in at least two other domains. Results Eighteen guidelines met the inclusion criteria, of which 13 were evidence-based guidelines (involved systematic search and grading of evidence). The median scores (interquartile range (IQR)) for “scope and purpose,” “stakeholder involvement,” “rigor of development,” “clarity of presentation,” “applicability” and “editorial independence” were 73.6% (54.2%–80.6%), 48.6% (29.2%–71.5%), 60.2% (30.9%–78.1%), 86.6% (76.7%–94.4%), 28.6% (18.0%–37.8%) and 60.2% (30.9%–78.1%), respectively. The median overall score (out of 7) of all guidelines was 5.1 (IQR: 3.7–5.8). Evidence-based guidelines scored significantly higher compared to expert-consensus guidelines. Half (n = 9) of the guidelines (all evidence-based) were of “good quality.” Conclusion A wide variation in methodological quality exists among diabetic eyecare guidelines, with nine demonstrating “good quality.” Future iterations of guidelines could improve by appropriately engaging stakeholders, following a rigorous development process, including support for application in clinical practice and ensuring editorial transparency.

Purpose To apply computational methods to model normal age-related changes in corneal parameters and to establish their association with demographic factors, thereby providing a framework for improved detection of subclinical corneal ectasia (SCE). Design Cross-sectional study. Methods One hundred seventeen healthy participants were enrolled from Centre for Eye Health (Sydney, Australia). Corneal thickness (CT), front surface sagittal curvature (FSSC), and back surface sagittal curvature (BSSC) measurements were extracted from 57 corneal locations from 1 eye per participant using the Pentacam HR. Cluster analyses were performed to identify locations demonstrating similar variations with age. Age-related changes were modeled using polynomial regression with sliding window methods, and model accuracy was verified with Bland–Altman comparisons. Pearson correlations were applied to examine the impacts of demographic factors. Results Concentric cluster patterns were observed for CT and FSSC but not for BSSC. Sliding window analyses were best fit with quartic and cubic regression models for CT and FSSC/BSSC, respectively. CT and FSSC sliding window models had narrower 95% limits of agreement compared with decade-based models (0.015 mm vs 0.017 mm and 0.14 mm vs 0.27 mm, respectively), but were wider for BSSC than decade-based models (0.73 mm vs 0.54 mm). Significant correlations were observed between CT and astigmatism (P = .02-.049) and FSSC and BSSC and gender (P = Conclusions The developed models robustly described aging variations in CT and FSSC; however, other mechanisms appear to contribute to variations in BSSC. These findings and the identified correlations provide a framework that can be applied to future model development and establishment of normal databases to facilitate SCE detection.

PURPOSE: To develop location specific models of normal, age-related changes in the macular ganglion cell layer (GCL) from optical coherence tomography (OCT). Using these OCT-derived models, we predicted visual field (VF) sensitivity and compared these results to actual VF sensitivities. DESIGN: Retrospective cohort study METHODS: Single eyes of 254 normal participants were retrospectively enrolled from the Centre for Eye Health (Sydney, Australia). Macular GCL measurements were obtained using Spectralis OCT. Cluster algorithms were performed to identify spatial patterns demonstrating similar age-related change. Quadratic and linear regression models were subsequently utilized to characterize age-related GCL decline. 40 participants underwent additional testing with Humphrey VFs, and 95% prediction intervals were calculated to measure the predictive ability of structure-function models incorporating cluster-based pooling, age-correction and consideration of spatial summation. RESULTS: Quadratic GCL regression models provided a superior fit (p =

The most effective measure to prevent or stop the spread of infectious diseases is the early identification and isolation of infected individuals through comprehensive screening. At present, in the COVID-19 pandemic, such screening is often limited to isolated regions as determined by local governments. Screening of potentially infectious individuals should be conducted through coordinated national or global unified actions. Our current research focuses on using resources to conduct comprehensive national and regional regular testing with a risk rate based, algorithmic guided, multiple-level, pooled testing strategy. Here, combining methodologies with mathematical logistic models, we present an analytic procedure of an overall plan for coordinating state, national, or global testing. The proposed plan includes three parts 1) organization, resource allocation, and distribution; 2) screening based on different risk levels and business types; and 3) algorithm guided, multiple level, continuously screening the entire population in a region. This strategy will overcome the false positive and negative results in the polymerase chain reaction (PCR) test and missing samples during initial tests. Based on our proposed protocol, the population screening of 300,000,000 in the US can be done weekly with between 15,000,000 and 6,000,000 test kits. The strategy can be used for population screening for current COVID-19 and any future severe infectious disease when drugs or vaccines are not available., Graphical abstract Unlabelled Image

Canine progressive rod–cone degeneration ( prcd ) is a retinal disease previously mapped to a broad, gene-rich centromeric region of canine chromosome 9. As allelic disorders are present in multiple breeds, we used linkage disequilibrium (LD) to narrow the ∼6.4-Mb interval candidate region. Multiple dog breeds, each representing genetically isolated populations, were typed for SNPs and other polymorphisms identified from BACs. The candidate region was initially localized to a 1.5-Mb zero recombination interval between growth factor receptor-bound protein 2 ( GRB2 ) and SEC14-like 1 ( SEC14L ). A fine-scale haplotype of the region was developed, which reduced the LD interval to 106 kb and identified a conserved haplotype of 98 polymorphisms present in all prcd -affected chromosomes from 14 different dog breeds. The findings strongly suggest that a common ancestor transmitted the prcd disease allele to many of the modern dog breeds and demonstrate the power of the LD approach in the canine model.

Progressive rod-cone degeneration (prcd) is an autosomal recessive retinal degeneration of dogs that maps to chromosome 9 (CFA9). Positional cloning and candidate gene approaches are presently used to identify the disease-causing gene. To complement these strategies and identify novel candidate genes, we have used a subtraction approach to detect modified gene expression caused by prcd that may be causally associated with the disease, or, alternatively, be involved in the molecular mechanisms leading to the disease phenotype. With this technique we characterized a 4503 nucleotide open reading frame (ORF) within a 5.6 kb cDNA that predicts a protein of 1500 amino acids. The gene shows about 90% homology to the human and rat glucocorticoid receptor DNA binding factor 1 (GRLF1) gene, also known as p190-A. The transcript was detected in several tissues, including retina, and the protein was localized to the photoreceptor cell layer. The canine GRLF1 maps near the telomere of CFA1 close to CRX, a region synteny to human chromosome 19q13 (HSA19q13). Based on its chromosomal location, GRLF1 has been excluded as a candidate gene for prcd. Northern blot analysis also failed to prove down-regulation of the gene in early stages of disease in six different non-allelic canine retinal degenerations. However, we were able to show that in advanced stages of prcd, GRLF1 is expressed in remaining photoreceptor cells, thus, providing a challenging task to uncover the gene's exact function in the retina and degenerative processes.