From polyps to pixels: understanding coral reef resilience to local and global change across scales

Abstract Context Coral reef resilience is the product of multiple interacting processes that occur across various interacting scales. This complexity presents challenges for identifying solutions to the ongoing worldwide decline of coral reef ecosystems that are threatened by both local and global human stressors. Objectives We highlight how coral reef resilience is studied at spatial, temporal, and functional scales, and explore emerging technologies that are bringing new insights to our understanding of reef resilience. We then provide a framework for integrating insights across scales by using new and existing technological and analytical tools. We also discuss the implications of scale on both the ecological processes that lead to declines of reefs, and how we study those mechanisms. Methods To illustrate, we present a case study from Kāneʻohe Bay, Hawaiʻi, USA, linking remotely sensed hyperspectral imagery to within-colony symbiont communities that show differential responses to stress. Results In doing so, we transform the scale at which we can study coral resilience from a few individuals to entire ecosystems. Conclusions Together, these perspectives guide best practices for designing management solutions that scale from individuals to ecosystems by integrating multiple levels of biological organization from cellular processes to global patterns of coral degradation and resilience

Integrated genomic characterization of oesophageal carcinoma

Oesophageal cancers are prominent worldwide; however, there are few targeted therapies and survival rates for these cancers remain dismal. Here we performed a comprehensive molecular analysis of 164 carcinomas of the oesophagus derived from Western and Eastern populations. Beyond known histopathological and epidemiologic distinctions, molecular features differentiated oesophageal squamous cell carcinomas from oesophageal adenocarcinomas. Oesophageal squamous cell carcinomas resembled squamous carcinomas of other organs more than they did oesophageal adenocarcinomas. Our analyses identified three molecular subclasses of oesophageal squamous cell carcinomas, but none showed evidence for an aetiological role of human papillomavirus. Squamous cell carcinomas showed frequent genomic amplifications of CCND1 and SOX2 and/or TP63, whereas ERBB2, VEGFA and GATA4 and GATA6 were more commonly amplified in adenocarcinomas. Oesophageal adenocarcinomas strongly resembled the chromosomally unstable variant of gastric adenocarcinoma, suggesting that these cancers could be considered a single disease entity. However, some molecular features, including DNA hypermethylation, occurred disproportionally in oesophageal adenocarcinomas. These data provide a framework to facilitate more rational categorization of these tumours and a foundation for new therapies