Improving Inpatient Tobacco Treatment Measures: Outcomes Through Standardized Treatment, Care Coordination, and Electronic Health Record Optimization.

INTRODUCTION: The Centers for Disease Control and Prevention states that tobacco use is the largest and most preventable cause of disease and mortality in the United States. The Joint Commission implemented inpatient tobacco treatment measures (TTMs) in 2012 to encourage healthcare systems to create processes that help patients quit tobacco use through evidence-based care. METHODS: A tobacco cessation care delivery system was implemented at James A. Haley Veterans' Hospital and Clinics, which included: standardized pathways within the Veterans Health Administration (VHA) electronic health record system to improve nicotine replacement therapy ordering; evidence-based tobacco cessation counseling; and improved care coordination for tobacco cessation treatment through the use of technological innovation. RESULTS: Outcomes were obtained from the VHA quality metric reporting system known as Strategic Analytics for Improvement and Learning (SAIL). TOB-2 and TOB-3 (two Joint Commission inpatient TTMs) equivalent to tob20 and tob40 within SAIL improved by greater than 300% after implementation at James A. Haley Veterans' Hospital and Clinics. CONCLUSION: Implementation of a tobacco cessation care system at James A. Haley Veterans' Hospital and Clinics enhanced interdisciplinary coordination of tobacco cessation care and resulted in improvements of The Joint Commission inpatient TTMs by greater than threefold.

Advancing Order Set Design.

Order set design using evidence-based medicine, quality improvement techniques, and standardization increases the likelihood of provider order set adherence and potentially better patient outcomes.

Reduced Th1 and enhanced Th2 immunity after immunization with Alzheimer's beta-amyloid(1-42).

It has been demonstrated that immunization of transgenic mouse models of Alzheimer's disease (AD) with amyloid-beta(1-42) peptide (Abeta(1-42)) results in prevention of Abeta plaque formation and amelioration of established plaques in the brain. As the response of the T lymphocyte helper (Th) arm of the immune response had not yet been investigated after Abeta immunization, we i.p. immunized C57BL/6 mice with Abeta(1-42), Abeta(1-40), or phosphate-buffered saline (PBS), and examined markers of Th1 and Th2 immune responses in spleen and in splenocytes from these mice. Spleens from Abeta(1-42)-immunized mice demonstrated decreased interleukin-12 receptor beta chain expression compared to mice immunized with Abeta(1-40) or PBS. Consistently, following stimulation with concanavalin A or anti-CD3 antibody, primary splenocytes from Abeta(1-42)-immunized mice demonstrated elevated secretion of interleukin-4 and interleukin-10, and decreased levels of interferon-gamma. To validate this Th1-->Th2 shift in a transgenic mouse model of AD, we immunized Tg APP(sw) mice (line 2576) with Abeta(1-42) and found decreased Th1 (interleukin-2 and interferon-gamma) and elevated Th2 (interleukin-4 and interleukin-10) cytokines in their stimulated primary splenocytes. Interferon-gamma was markedly reduced and interleukin-10 was increased in blood plasma from these mice, effects that were associated with dramatically mitigated Abeta deposition after Abeta(1-42) immunization. Taken together, these results show enhanced Th2 and down-regulated Th1 immunity following immune challenge with Abeta(1-42).