Implementing evidence-based practice using an interprofessional team approach: part two.

The complexity inherent in the inpatient oncology population requires effective interprofessional collaboration and integrated evidence-based practice (EBP), drawing from each of the disciplines to achieve desired outcomes. Each member of the team lends a strength and expertise that, when combined, often results in outcomes greater than the sum of its parts (Hall & Weaver, 2001; Petri, 2010; Pullon & Fry, 2005). EBP promotes the use of research to solve issues raised in day-to-day nursing practice. This article provides an overview and summary of an evidence-based project to increase compliance of sequential compression devices (SCDs) in gynecologic oncology and urology patients on a post-surgical inpatient unit using the Plan, Do, Study, Act (PDSA) model for continuous quality improvement (CQI) (Institute for Innovation and Improvement, 2013).

Implementing evidence-based practice using an interprofessional team approach.

Translational research has been defined as "bench-to-bedside" research or "laboratory-to-clinical" research. Benefits to this type of research are that it fast tracks biomedical advances to improve the quality of care and life for patients with cancer (Callard, Rose, & Wykes, 2011). The challenge, however, is translating the research findings to the bedside in a timely fashion. Burns and Foley (2005) described an estimated 20-year delay in getting research findings translated to care delivery.

Use of the 13C-sucrose breath test to assess chemotherapy-induced small intestinal mucositis in the rat.

Mucositis is a debilitating side-effect of chemotherapy which affects the mucosa of the gastrointestinal tract, particularly the small intestine. Currently there are no simple, noninvasive methods to detect and monitor small intestinal function and the severity of mucosal damage. Activity of the brush-border enzyme sucrase provides an indicator of small intestinal absorptive function that remains relatively constant throughout life. Measuring 13CO2 levels in expired breath following ingestion of 13C-sucrose is a non-invasive marker of total intestinal sucrase activity. We evaluated the sucrose breath test (SBT) as an indicator of small intestinal injury and dysfunction, utilizing a rat model of chemotherapy-induced mucositis. SBT results reflected the time-course of damage and repair after methotrexate (MTX) treatment, with damage most severe 72 h after chemotherapy, and repair commencing after 96 h. SBT results correlated significantly with jejunal sucrase activity determined biochemically (r2= 0.89; p < 0.005). Moreover, calcium folinate ingested prior to chemotherapy totally prevented damage to the small intestinal mucosa induced by MTX, as assessed by the SBT in concert with structural, and biochemical indices. The SBT provides a simple, non-invasive, integrated measure of small intestinal damage and function. The SBT holds significant potential to monitor small intestinal function in cancer patients undergoing chemotherapy. This technique possesses further applicability to the screening of newly-developed agents for potential gastrointestinal toxicity including the development of new therapies targeted at minimising or preventing the onset of chemotherapy-induced mucositis.

Fibroblast growth factor 1: a key regulator of human adipogenesis.

Obesity, with its related problems, is recognized as the fastest growing disease epidemic facing the world, yet we still have limited insight into the regulation of adipose tissue mass in humans. We have previously shown that adipose-derived microvascular endothelial cells (MVECs) secrete a factor(s) that increases proliferation of human preadipocytes. We now demonstrate that coculture of human preadipocytes with MVECs significantly increases preadipocyte differentiation, evidenced by dramatically increased triacylglycerol accumulation and glycerol-3-phosphate dehydrogenase activity compared with controls. Subsequent analysis identified fibroblast growth factor (FGF)-1 as an adipogenic factor produced by MVECs. Expression of FGF-1 was demonstrated in MVECs but not in preadipocytes, while preadipocytes were shown to express FGF receptors 1-4. The proliferative effect of MVECs on human preadipocytes was blocked using a neutralizing antibody specific for FGF-1. Pharmacological inhibition of FGF-1 signaling at multiple steps inhibits preadipocyte replication and differentiation, supporting the key adipogenic role of FGF-1. We also show that 3T3-L1 cells, a highly efficient murine model of adipogenesis, express FGF-1 and, unlike human preadipocytes, display no increased differentiation potential in response to exogenous FGF-1. Conversely, FGF-1-treated human preadipocytes proliferate rapidly and differentiate with high efficiency in a manner characteristic of 3T3-L1 cells. We therefore suggest that FGF-1 is a key human adipogenic factor, and these data expand our understanding of human fat tissue growth and have significant potential for development of novel therapeutic strategies in the prevention and management of human obesity.