THE WIDENING CORN BASIS IN SOUTH DAKOTA: FACTORS AFFECTING AND THE IMPACT OF THE LOAN DEFICIENCY PAYMENT

Crop Production/Industries,

The Widening Corn Basis in South Dakota: Factors Affecting and the Impact of the Loan Deficiency Payment

This thesis examines factors affecting the local corn basis in South Dakota before and after the Federal Agricultural Improvement and Reform (FAIR) Act of 1996 in an attempt to identify why the local basis has widened in the years after the 1996 farm bill. The FAIR Act introduced the loan deficiency payment program as an alternative to putting grain under loan. This thesis will determine whether the loan deficiency payment has an affect [sic] on local corn basis through the construction of a model and testing of that model using ordinary least squares regression. Other possible factors affecting basis were identified through a review of literature. Theoretically, factors that have an affect [sic] on local corn basis are futures price, local cash price, local corn usage, transportation costs, local storage availability, yearly local corn production, and seasonality. The results of the regression analysis revealed that the loan deficiency payment accounts for approximately 32% of the widening of the South Dakota local corn basis. Other factors significantly affecting local corn basis are futures price, local supply and demand, and seasonality

Engineered human cytokine/antibody fusion proteins expand regulatory T cells and confer autoimmune disease protection

Low-dose human interleukin-2 (hIL-2) treatment is used clinically to treat autoimmune disorders due to the cytokine's preferential expansion of immunosuppressive regulatory T cells (Tregs). However, off-target immune cell activation and short serum half-life limit the clinical potential of IL-2 treatment. Recent work showed that complexes comprising hIL-2 and the anti-hIL-2 antibody F5111 overcome these limitations by preferentially stimulating Tregs over immune effector cells. Although promising, therapeutic translation of this approach is complicated by the need to optimize dosing ratios and by the instability of the cytokine/antibody complex. We leverage structural insights to engineer a single-chain hIL-2/F5111 antibody fusion protein, termed F5111 immunocytokine (IC), which potently and selectively activates and expands Tregs. F5111 IC confers protection in mouse models of colitis and checkpoint inhibitor-induced diabetes mellitus. These results provide a roadmap for IC design and establish a Treg-biased immunotherapy that could be clinically translated for autoimmune disease treatment

Engineered human cytokine/antibody fusion proteins expand regulatory T cells and confer autoimmune disease protection.

Low-dose human interleukin-2 (hIL-2) treatment is used clinically to treat autoimmune disorders due to the cytokine's preferential expansion of immunosuppressive regulatory T cells (Tregs). However, off-target immune cell activation and short serum half-life limit the clinical potential of IL-2 treatment. Recent work showed that complexes comprising hIL-2 and the anti-hIL-2 antibody F5111 overcome these limitations by preferentially stimulating Tregs over immune effector cells. Although promising, therapeutic translation of this approach is complicated by the need to optimize dosing ratios and by the instability of the cytokine/antibody complex. We leverage structural insights to engineer a single-chain hIL-2/F5111 antibody fusion protein, termed F5111 immunocytokine (IC), which potently and selectively activates and expands Tregs. F5111 IC confers protection in mouse models of colitis and checkpoint inhibitor-induced diabetes mellitus. These results provide a roadmap for IC design and establish a Treg-biased immunotherapy that could be clinically translated for autoimmune disease treatment