A 46-kb upstream region of the mouse sequence containing evolutionarily-conserved regions has been confirmed as a mesoderm-specific enhancer element in a previous study of transgenic mice. To evaluate the gene expression of Bmp4, we constructed two novel reporter vectors utilizing the 7-kb enhancer/promoter region, together with 59noncoding exons and introns of the Bmp4 gene. It is noteworthy that this reporter is strongly expressed in pancreas islet cells and regulated by nutrient circumstance. Bmp4 expression in the pancreatic islets has been reported to occur especially in b cells. b cells constitute 90% of the islets, and the localization of luciferase expression in this study was therefore consistent with previous results. Bmp4 and Bmp Receptor 1A are expressed in pancreatic b cells, and autocrine Bmp4 through Smad signaling is involved in insulin gene expression, proinsulin processing, glucose sensing, secretionstimulus coupling, incretin signaling, and insulin exocytosis. On the other hand, a recent report showed that Bmp4 stimulation blocked the differentiation and promoted the expansion of endocrine progenitor cells, thereby revealing a novel paradigm of signaling explaining the balance between expansion and differentiation of 4-Demethylepipodophyllotoxin pancreatic duct epithelial progenitors. Autophagy induced by deprivation of nutrients is an evolutionarily-conserved lysosomal degradation pathway in which the cell self-digests its own proteins and organelles, and thus maintains macromolecular synthesis and ATP production. b-cell-specific autophagy-deficient mice show hypoinsulinemia and hyperglycemia. Autophagy is required to maintain the structure, mass and function of pancreatic b cells; accordingly, expression of LC3 -positive cells was increased in the pancreas of 24-h-fasted transgenic mice. Our observations suggest that fasting or starvation stress in pancreatic cells independently induces both an autophagy response and Bmp4 expression, or that autophagy signals induce Bmp4 expression. Further studies are needed to clarify this issue. Type 2 diabetes is characterized by abnormal regulation of nutrients and their metabolites, and develops as a consequence of combined insulin resistance and relative insulin deficiency. Insulin and its downstream signal molecules, such as mTOR, are well-known inhibitors of autophagy, whereas glucagon,Gambogic-acid a counter-regulatory hormone of insulin, induces autophagy. Type 2 diabetes models based on p7kb-Bmp4Luc transgenic mice may be suitable for evaluating disease onset, and these transgenic mice may provide a useful tool for future toxicological screening studies, and for further studies to reveal the functions of Bmp4 in the pancreas. Influenza virus can cause occasional pandemics and seasonal epidemics in humans. At the beginning of an influenza pandemic, preexisting immunity to the newly emerging virus is generally low in humans; thus, the virus can easily transfer from one person to another and rapidly spread across the globe. Later, on the one hand, immune antibodies to the virus are gradually induced in the host, decreasing the virulence and transmissibility of the virus. While on the other hand, the pandemic virus undergoes gradual changes in its antigenic structure so as to escape the immune pressure imposed by the host. Such pressure and drift lead to the transformation of the pandemic virus to a seasonal one as well as the subsequent evolution of the seasonal influenza virus. Protein glycosylation is believed to be involved in the evolution of influenza viruses. Variation in protein glycosylation is a more efficient mechanism than even the direct mutation of amino acids for the virus to escape the surveillance of the host immune system because the glycans themselves are host-derived and hence considered as ‘‘self’’ by the immune system