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The detailed morphology of human development has intrigued scientists and the medical field alike. However, the scarcity of specimens hampers detailed mapping of tissue architecture. Furthermore, inaccuracies in the description of human development have crept into textbooks from observations of animal models that are extrapolated to humans. By mapping normal developmental processes and patterns, such as the growth and relative placement of organs, congenital anomalies can be better understood. de Bakker et al. generated interactive three-dimensional digital reconstructions based on the Carnegie collection of histologically sectioned human embryos spanning the first 2 months of gestation. These interactive models will serve as educational and scientific resources for normal and abnormal human development. Science , this issue p. 10.1126/science.aag0053 Interactive three-dimensional models unveil early human development. Current knowledge about human development is based on the description of a limited number of embryonic specimens published in original articles and textbooks, often more than 100 years ago. It is exceedingly difficult to verify this knowledge, given the restricted availability of human embryos. We created a three-dimensional digital atlas and database spanning the first 2 months of human development, based on analysis of nearly 15,000 histological sections of the renowned Carnegie Collection of human embryonic specimens. We identified and labeled up to 150 organs and structures per specimen and made three-dimensional models to quantify growth, establish changes in the position of organs, and clarify current ambiguities. The atlas provides an educational and reference resource for studies on early human development, growth, and congenital malformations.

Objective: Hyperglycemia and type 2 diabetes (T2D) are caused by failure of pancreatic beta cells. The role of the gut microbiota in T2D has been studied but causal links remain enigmatic. Design: Obese individuals with or without T2D were included from two independent Dutch cohorts. Human data was translated in vitro and in vivo by using pancreatic islets from C57BL6/J mice and by injecting flagellin into obese mice. Results: Flagellin is part of the bacterial locomotor appendage flagellum, present on gut bacteria including Enterobacteriaceae, which we show to be more abundant in the gut of individuals with T2D. Subsequently, flagellin induces a pro-inflammatory response in pancreatic islets mediated by the Toll-like receptor (TLR)-5 expressed on resident islet macrophages. This inflammatory response associated with beta-cell dysfunction, characterized by reduced insulin gene expression, impaired proinsulin processing and stress-induced insulin hypersecretion in vitro and in vivo in mice. Conclusion: We postulate that increased systemically disseminated flagellin in T2D is a contributing factor to beta cell failure in time and represents a novel therapeutic target. Competing Interest Statement The authors have declared no competing interest.