Background Optical coherence tomography angiography (OCTA) can image the retinal vasculature in vivo, without the need for contrast dye. This technology has been commercially available since 2014, however, much of its use has been limited to the research setting. Over time, more clinical practices have adopted OCTA imaging. While countless publications detail OCTA’s use for the study of retinal microvasculature, few studies outline OCTA’s clinical utility. Body This review provides an overview of OCTA imaging and details tips for successful interpretation. The review begins with a summary of OCTA technology and artifacts that arise from image acquisition. New methods and best practices to prevent image artifacts are discussed. OCTA has the unique ability among retinovascular imaging modalities to individually visualize each retinal plexus. Slabs offered in standard OCTA devices are reviewed, and clinical uses for each slab are outlined. Lastly, the use of OCTA for the clinical interpretation of retinal pathology, such as diabetic retinopathy and age-related macular degeneration, is discussed. Conclusion OCTA is evolving from a scientific tool to a clinical imaging device. This review provides a toolkit for successful image interpretation in a clinical setting.
The availability of nucleotides has a direct impact on transcription. Inhibition of dihydroorate dehydrogenase (DHODH) with leflunomide impacts nucleotide pools by reducing pyrimidine levels. Leflunomide abrogates effective transcription elongation of genes required for neural crest development and melanoma growth in vivo 1 . To define the mechanism of action, we undertook an in vivo chemical suppressor screen for restoration of neural crest after leflunomide treatment. Surprisingly, we found that alterations in progesterone and progesterone receptor (Pgr) signalling strongly suppressed leflunomide-mediated neural crest effects in zebrafish. Progesterone additionally bypasses the transcriptional elongation block resulting from Paf complex deficiency, rescuing neural crest defects in ctr9 morphant and paf1(aln z24 ) mutant embryos. Using proteomics, we found that Pgr binds the RNA helicase protein Ddx21. Ddx21 -deficient zebrafish show resistance to leflunomide-induced stress. On a molecular level, nucleotide depletion reduced the chromatin occupancy of DDX21 in human A375 melanoma cells. Nucleotide supplementation reversed the gene expression and DDX21 occupancy changes prompted by leflunomide. Together, our results show that DDX21 acts as a sensor and mediator of transcription during nucleotide stress.
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