加圧・加熱処理豚肉ゲルの嚥下食としてのテクスチャー特性、官能評価および嚥下特性

中村学園大学平成24年

Intake of Calcium from Marine Resources for Prevention of Osteoporosis

（Abstract）In order to fill up the shortage of calcium intake,particular attention was paid to the absorbable calcium derived from fishes and she11fishes.The diets prepared from cuttlefish shell calcium(C-Ca),bonito head oil(fish oil)were administered to rats,and the bone metabolism and the bone modeling were investigated the calcium and inorganic phosphate contents and the measurement of the trabecular bone mineral density(BMD),the corticalBMD and the stress strain index(SSI)of rat femur.From these results the bone modeling was accelerated more effectively by the administration of cuttlefish calcium and fish oil,compared to the administration of control diet calcium. It is suggested that cuttlefish shell calcium was effective in bone modeling,and these are available as new calcium resources

Targeting abatacept-resistant T-helper-17 cells by aldehyde dehydrogenase inhibition

Summary: IL-17-producing helper T (Th17) cells are long-lived and serve as central effector cells in chronic autoimmune diseases. The underlying mechanisms of Th17 persistence remain unclear. We demonstrated that abatacept, a CD28 antagonist, effectively prevented the development of skin disease in a Th17-dependent experimental autoimmune dermatitis model. Abatacept selectively inhibited the emergence of IL-7R-negative effector-phenotype T cells while allowing the survival and proliferation of IL-7R+ memory-phenotype cells. The surviving IL-7R+ Th17 cells expressed genes associated with alcohol/aldehyde detoxification and showed potential to transdifferentiate into IL-7R-negative effector cells. Inhibiting aldehyde dehydrogenase reduced IL-7R+ Th17 cells in vivo, independently of CD28, and exhibited additive effects when combined with abatacept. Our findings suggest that CD28 blockade prevents inflammation without eliminating persistent memory cells. These remaining memory cells can be targeted by other drugs, such as aldehyde dehydrogenase inhibitors, to limit their survival, thereby facilitating the treatment of chronic autoimmune diseases