• Journal for History of Mathematics
• /
• v.33 no.1
• /
• pp.21-32
• /
• 2020

Daniel Coit Gilman, the first president of Johns Hopkins University, aspired to build an ideal university focused on the competent faculty and their research. His plan was carried out through opening the first American graduate program, hiring professors with the highest-level research performances, assigning them less teaching burdens, and encouraging them to actively publish professional journals. He introduced Department of Mathematics as an initial model to put his plan into practice, and James Joseph Sylvester, a British mathematician invited as the first mathematics professor to Johns Hopkins University, made it possible in a short time. Their concerted efforts led to building the Department of Mathematics as a professional research institute for research, higher education, and expert training as well as to publishing American Journal of Mathematics.

• Journal of Life Science
• /
• v.31 no.9
• /
• pp.796-805
• /
• 2021

Hepatic endoplasmic reticulum (ER) stress contributes to the development of steatosis and insulin resistance. The components of unfolded protein response (UPR) regulate lipid metabolism. Recent studies have reported an association between ER stress and aberrant cellular lipid control; moreover, research has confirmed the involvement of sterol regulatory element-binding proteins (SREBPs)-the central regulators of lipid metabolism-in the process. However, the exact role of SREBPs in controlling lipid metabolism during ER stress and its contribution to fatty liver disease remain unknown. Here, we show that SREBP-1c deficiency protects against ER stress-induced hepatic steatosis in mice by regulating UPR, inflammation, and fatty acid oxidation. SREBP-1c directly regulated inositol-requiring kinase 1α (IRE1α) expression and mediated ER stress-induced tumor necrosis factor-α activation, leading to a reduction in expression of peroxisome proliferator-activated receptor γ coactivator 1-α and subsequent impairment of fatty acid oxidation. However, the genetic ablation of SREBP-1c prevented these events, alleviating hepatic inflammation and steatosis. Although the mechanism by which SREBP-1c deficiency prevents ER stress-induced inflammatory signaling remains to be elucidated, alteration of the IRE1α signal in SREBP-1c-depleted Kupffer cells might be involved in the signaling. Overall, the results suggest that SREBP-1c plays a crucial role in the regulation of UPR and inflammation in ER stress-induced hepatic steatosis.