New data on the cranial anatomy of Pterogonaspis (Tridensaspidae, Galeaspida) from the lower Devonian of Yunnan, China and its evolutionary implications.

New material of the tridensaspid Pterogonaspis yuhaii is described from the Xujiachong Formation in Qujing City, Yunnan Province, revealing the morphology of the ventral side of the headshield for the first time. Most significantly, the cranial anatomy of Pterogonaspis provides the first fossil evidence for the position of the esophagus in galeaspids. The esophagus and dorsal aortae display a central placement in the postbranchial region and do not share a common canal as in osteostracans.

Establishment and Genetic Manipulation of Murine Hepatocyte Organoids.

The liver is the largest organ in mammals. It plays an important role in glucose storage, protein secretion, metabolism and detoxification. As the executor for most of the liver functions, primary hepatocytes have limited proliferating capacity.

Cullin 4b-RING ubiquitin ligase targets IRGM1 to regulate Wnt signaling and intestinal homeostasis.

Hierarchical organization of intestine relies on the self-renewal and tightly regulated differentiation of intestinal stem cells (ISCs). Although signals like Wnt are known to sustain the continued intestinal renewal by maintaining ISCs activity and lineage commitment, molecular mechanisms underlying ISCs 'stemness' and supportive niche have not been well understood. Here, we found that CUL4B-RING ubiquitin ligase (CRL4B) regulates intestinal homeostasis by targeting immunity-related GTPase family M member 1 (IRGM1) for proteasomal degradation.

Discovery of an insulin-induced gene binding compound that ameliorates nonalcoholic steatohepatitis by inhibiting sterol regulatory element-binding protein-mediated lipogenesis.

Background And Aims: NASH is associated with high levels of cholesterol and triglyceride (TG) in the liver; however, there is still no approved pharmacological therapy. Synthesis of cholesterol and TG is controlled by sterol regulatory element-binding protein (SREBP), which is found to be abnormally activated in NASH patients. We aim to discover small molecules for treating NASH by inhibiting the SREBP pathway.