Sorting sex, controlling sex: Masui Kiyoshi's chicken research and experimental system, 1915-1950.

Masui Kiyoshi (1887-1981), a prominent Japanese geneticist, is best known for inventing the sex-sorting method of chicks and his contributions to experimental genetics in Japan. Masui drew inspiration from Goldschmidt's sex determination theory and used chickens, transplantation techniques, and his own "chick sexing" methods in his scientific work. This paper examines the intersection of genetics and industrial breeding by tracing the evolution of Masui's experimental systems. During the early 20th century, poultry farming emerged as a significant industry in Japan, resulting in the development of standardized organisms and techniques for chicken farming. Masui, a professor at Tokyo Imperial University, collaborated with the Imperial Zootechnical Experimental Station to use these organisms as models for sex determination theory while exploring their further industrial possibilities. First, the paper show how Masui viewed chickens as epistemological objects and transformed his anatomical discoveries into standardized industrial practices. Next, it describes how Masui's collaboration with German geneticist Richard Goldschmidt led to new academic questions about sex determination mechanisms and how he integrated his knowledge of chicken physiology into his research on "experimental gynandromorphs" to elaborate the theories. Lastly, the paper discusses the biotechnological ideals that Masui aimed to achieve and how they were co-constructed with his mass-production method of intersex chickens from the early 1930s. The trajectory of Masui's experimental systems highlights the dynamic relationship between agroindustry and genetics in the early twentieth century and demonstrates the 'biology of history' in which the biological processes of organisms intertwine with their epistemological history.

Hydrolyzed fumonisin B1 induces less inflammatory responses than fumonisin B1 in the co-culture model of porcine intestinal epithelial and immune cells.

Fumonisin B1 (FB1), mainly produced by Fusarium verticillioides and Fusarium proliferatum, can be converted to the less toxic metabolite hydrolyzed FB1 (HFB1) by enzymatic degradation. The application of an FB1degrading enzyme as a feed additive is a strategy to reduce fumonisin exposure of animals. However, the difference between the effect of FB1 and HFB1 on porcine intestinal immunity is poorly documented. We investigated the toxic effects of FB1 and HFB1 exposure on porcine gut barrier function and intestinal immunity by using a co-culture model of intestinal porcine epithelial cells (IPEC-J2) and porcine peripheral blood mononuclear cells (PBMCs). First, we confirmed that Fusarium mycotoxin (deoxynivalenol; DON), in the presence of an endotoxin (lipopolysaccharide: LPS), disrupted gut permeability of IPEC-J2 and induced inflammatory response in the co-culture system. FB1 induced additional damage to gut barrier function and promoted pro-inflammatory responses in the presence of LPS and DON compared to only LPS/DON treatment. In the co-culture system, FB1/LPS/DON induced increased cell death of PBMCs and pro-inflammatory cytokines than LPS/DON treatment. In contrast, the application of HFB1 resulted in reduced levels of chemokines and pro-inflammatory cytokines together with marginal immune cell death compared to FB1/LPS/DON in the IPEC-J2/PBMC co-culture system. These findings suggest that FB1 aggravates LPS/DON-induced intestinal inflammation, and HFB1 showed less toxicity to immune response. Therefore, enzymatic degradation of FB1 to HFB1 could be an effective strategy to reduce intestinal inflammation in pigs.