Interprofessional Team Approach Using Standardized Patient Simulation to Facilitate Person-Centered Quality Healthcare in Home Hospice Care Setting.

Hospice care requires person-centered holistic approaches from interprofessional health care teams. Traditional curricular models include teaching hospice care in discipline-specific didactic settings. There are limited opportunities for prelicensure students to engage in real-life and hands-on hospice care. Students are often observers and lack meaningful interactions with patients, families, and interprofessional teams. Using "IPEC Core Competencies for Interprofessional Collaborative Practice" and "AACN CARES" as the framework, nursing and social work faculty collaborated to develop, implement, and evaluate an interprofessional home hospice simulation incorporating standardized patients. The purpose of this interprofessional simulation was to facilitate hands-on application of complex health care concepts in an authentic home hospice setting. Twenty-three Bachelor of Science in Nursing students and 10 Master of Social Work students participated as interprofessional teams to provide home hospice care for patients and families. Faculty evaluated the simulation experience through analysis of presimulation and postsimulation guided reflections, intrasimulation observations, and postsimulation debriefing. Evaluation indicated students gained a greater understanding of how to provide quality person-centered end-of-life care, increased comfort with assessing spiritual needs, increased confidence in initiating sensitive interactions, and greater appreciation for working in an interprofessional health care team. This interprofessional simulation provided a robust learning environment paving the way for future simulations incorporating additional members of the health care team.

Lethal giant discs, a novel C2-domain protein, restricts notch activation during endocytosis.

The Notch signaling pathway plays a central role in animal growth and patterning, and its deregulation leads to many human diseases, including cancer. Mutations in the tumor suppressor lethal giant discs (lgd) induce strong Notch activation and hyperplastic overgrowth of Drosophila imaginal discs. However, the gene that encodes Lgd and its function in the Notch pathway have not yet been identified. Here, we report that Lgd is a novel, conserved C2-domain protein that regulates Notch receptor trafficking. Notch accumulates on early endosomes in lgd mutant cells and signals in a ligand-independent manner. This phenotype is similar to that seen when cells lose endosomal-pathway components such as Erupted and Vps25. Interestingly, Notch activation in lgd mutant cells requires the early endosomal component Hrs, indicating that Hrs is epistatic to Lgd. These data suggest that Lgd affects Notch trafficking between the actions of Hrs and the late endosomal component Vps25. Taken together, our data identify Lgd as a novel tumor-suppressor protein that regulates Notch signaling by targeting Notch for degradation or recycling.

Results of the 2004 National Worksite Health Promotion Survey.

OBJECTIVES: We examined worksite health promotion programs, policies, and services to monitor the achievement of the Healthy People 2010 worksite-related goal of 75% of worksites offering a comprehensive worksite health promotion program. METHODS: We conducted a nationally representative, cross-sectional telephone survey of worksite health promotion programs stratified by worksite size and industry type. Techniques appropriate for analyzing complex surveys were used to compute point estimates, confidence intervals, and multivariate statistics. RESULTS: Worksites with more than 750 employees consistently offered more programs, policies, and services than did smaller worksites. Only 6.9% of responding worksites offered a comprehensive worksite health promotion program. Sites with a staff person dedicated to and responsible for health promotion were significantly more likely to offer a comprehensive program, and sites in the agriculture and mining or financial services sector were significantly less likely than those in other industry sectors to offer such a program. CONCLUSIONS: Increasing the number, quality, and types of health promotion programs at worksites, especially smaller worksites, remains an important public health goal.

Congruence of Organizational Self-Score and Audit-Based Organizational Assessments of Workplace Health Capabilities: An Analysis of the HealthLead Workplace Accreditation.

OBJECTIVE: The aim of this study was to provide descriptive characteristics of companies accredited as part of the HealthLead Workplace Accreditation and to assess congruence between data reported via online organizational self-assessment and third-party onsite audit. METHODS: Synthesized organizational level data collected through the HealthLead accreditation process (N = 22). Online self-assessment and onsite third-party audit data were compared using paired t-tests. RESULTS: Statistical tests revealed significantly higher onsite audit scores than organizational self-assessment scores. Descriptive analyses demonstrated that Outcomes Reporting was the lowest scoring area among all companies. Companies also varied widely in levels of Leadership Support for wellness. CONCLUSIONS: Gaps observed between organizational self-assessment and onsite audit scores were relatively stable across the sample, indicating that observed differences may be process related. Organizations awarded accreditation show a wide variation in Leadership Support, and Outcomes Reporting appears to be low across the sample.

A beta, aging, and Alzheimer's disease: a tale, models, and hypotheses.

In this paper we explore the potential functional role of the A beta peptides in the context of Alzheimer's disease (AD). We begin by defining the morphology of the amyloid deposits in relation to surrounding glial cells and, more importantly, in relation to the brain vasculature. Amyloid accumulation in the brain's microvasculature causes disturbances in the blood-brain barrier (BBB), and in larger arteries, impairment in control of regional cerebral blood flow due to myocyte degeneration. We postulate that the deposition of vascular amyloid may represent a hydrophobic protein plaster to seal leaks in the BBB, occasionally observed in aging and catastrophically common in AD. The vasoconstrictive activity of A beta may also be related to leaky vessels whereby decreasing the arterial diameter may also help to control breaches in the BBB. The admission of plasma neurotoxic proteins into the brain may be controlled by activation of microglia elicited by soluble A beta peptides creating a subtle, but permanent brain inflammatory reaction. We also delve into the influence that cholesterol metabolism may have in membrane topology and A beta production, and the close correlations that exist between cardiovascular disease and AD. Finally, we speculate about the possibility of a peripheral source of A beta that may, by crossing the BBB, contribute to the vascular and parenchymal deposits of A beta in the AD brain.

The human amyloid-beta precursor protein770 mutation V717F generates peptides longer than amyloid-beta-(40-42) and flocculent amyloid aggregates.

One of the familial forms of Alzheimer's disease (AD) encodes the amyloid-beta precursor protein (AbetaPP) substitution mutation V717F. This mutation is relevant to AD research, since it has been utilized to generate transgenic mice models to study AD pathology and therapeutic interventions. Amyloid beta (Abeta) peptides were obtained from the cerebral tissue of three familial AD subjects carrying the AbetaPP V717F mutation. A combination of ultracentrifugation, size-exclusion, and reverse-phase high performance liquid chromatography, tryptic and cyanogen bromide hydrolysis, amino acid analysis, and matrix-assisted laser desorption ionization and surface-enhanced laser desorption ionization mass spectrometry was used to characterize the familial AD mutant Abeta peptides. The AbetaPP V717F mutation, located 4-6 residues beyond the wild-type AbetaPP gamma-secretase cleavage site, yielded longer Abeta peptides with C termini between residues 43 and 54. In the cerebral cortex these peptides aggregated into thin water- and SDS-insoluble amyloid bundles that condensed into flocculent spherical plaques. In the leptomeningeal arteries the amyloid was deposited in moderate amounts and was primarily composed of the shorter and more soluble Abeta species ending at residues 40, 42, and 44. The single V717F mutation in AbetaPP results in distinctive and drastic changes in the length and tertiary structure of Abeta peptides, which appear to be responsible for the earlier clinical manifestations of dementia and death of these patients.

Cortical and leptomeningeal cerebrovascular amyloid and white matter pathology in Alzheimer's disease.

Alzheimer's disease (AD) is characterized by neurofibrillary tangles and by the accumulation of beta-amyloid (Abeta) peptides in senile plaques and in the walls of cortical and leptomeningeal arteries as cerebral amyloid angiopathy (CAA). There also is a significant increase of interstitial fluid (ISF) in cerebral white matter (WM), the pathological basis of which is largely unknown. We hypothesized that the accumulation of ISF in dilated periarterial spaces of the WM in AD correlates with the severity of CAA, with the total Abeta load in the cortex and with Apo E genotype. A total of 24 AD brains and 17 nondemented age-matched control brains were examined. CAA was seen in vessels isolated from brain by using EDTA-SDS lysis stained by Thioflavin-S. Total Abeta in gray matter and WM was quantified by immunoassay, ApoE genotyping by PCR, and dilatation of perivascular spaces in the WM was assessed by quantitative histology. The study showed that the frequency and severity of dilatation of perivascular spaces in the WM in AD were significantly greater than in controls (P< 0.001) and correlated with Abeta load in the cortex, with the severity of CAA, and with ApoE epsilon4 genotype. The results of this study suggest that dilation of perivascular spaces and failure of drainage of ISF from the WM in AD may be associated with the deposition of Abeta in the perivascular fluid drainage pathways of cortical and leptomeningeal arteries. This failure of fluid drainage has implications for therapeutic strategies to treat Alzheimer's disease.