Prevalence and Predictors of Burnout Among Occupational Therapy Practitioners in the United States.

Importance: Identifying the extent and predictors of burnout among occupational therapy practitioners is important so strategies can be developed to reduce burnout and mitigate associated consequences within the profession.

Objective: To investigate the prevalence and determinants of burnout reported by U.S.

Susceptibility to diabetes is widely distributed in normal class IIu haplotype rats.

Aims/hypothesis: We did experiments to explore the pathways putatively leading to Type I (insulin-dependent) diabetes mellitus, and their association with the MHC locus, the major genetic determinant of disease susceptibility.

Methods: Normal MHC congenic rat strains that do not spontaneously develop diabetes or any other autoimmune syndrome were injected with the interferon-alpha inducer polyinosinic-polycytidylic acid (Poly IC).

Results: Insulitis and diabetes developed only in strains expressing Class II(u) genes and was independent of the Class I haplotype.

Islet cell membrane antigens activate diabetogenic CD4+ T-cells in the BB/Wor rat.

Type 1 diabetes is a major histocompatibility complex (MHC) class II-associated autoimmune disease mediated by beta-cell-specific T-cells and characterized by circulating autoantibodies to beta-cell molecules. In the BB/Wor diabetes-prone (DP) rat, type 1 diabetes develops spontaneously with an incidence of >90%. BB diabetes can be adoptively transferred to naive syngeneic or MHC class II-compatible rats with islet cell-activated T-cell lines derived from diabetic BB/Wor rats.

Kilham rat triggers T-cell-dependent autoimmune diabetes in multiple strains of rat.

Kilham rat virus (KRV) infection of BB/Wor diabetes-resistant (DR) RT1(u) rats induces autoimmune diabetes without direct cytolytic infection of pancreatic beta-cells and is a new model of virus-induced IDDM. To investigate genetic susceptibility to KRV-induced diabetes, major histocompatibility complex congenic and other inbred rats were infected with the virus and studied for the appearance of diabetes and insulitis. KRV infection alone induced insulitis, selective beta-cell necrosis, and diabetes in BB/Wor DR and LEW1.

A major histocompatibility complex class II restriction for BioBreeding/Worcester diabetes-inducing T cells.

Inbred diabetes-prone (DP) BioBreeding/Worcester (BB/Wor) (RT1u) rats develop spontaneous autoimmune diabetes, which, like human insulin-dependent diabetes mellitus, is mediated by autoreactive T lymphocytes. Breeding studies have shown an absolute requirement for at least one copy of the major histocompatibility complex (MHC) RT1u haplotype for spontaneous diabetes expression. Concanavalin A-activated spleen cells from acutely diabetic DP rats adoptively transfer diabetes only to recipients that express at least one RT1u haplotype.