Development and validation testing of a weight management nutrition knowledge questionnaire for adults.

BACKGROUND/OBJECTIVES: Because no validated tool exists to assess nutrition knowledge regarding weight management we developed and tested the Weight Management Nutrition Knowledge Questionnaire (WMNKQ). SUBJECTS/METHODS: The questionnaire assesses nutrition knowledge in these categories: energy density of food, portion size/serving size, alcohol and sugar sweetened beverages, how food variety affects food intake, and reliable nutrition information sources. In total 60 questions were reviewed by 6 experts for face validity and quantitative analysis was used to assess item difficulty, item discrimination, internal consistency, inter-item-correlation, test-retest reliability, construct validity, criterion validity, and convergent validity. RESULTS: The final WMNKQ contained 43 items. Experts removed 3 of the original 60 questions and modified 41. Eighteen items did not meet criteria for item difficulty, item discrimination, and/or inter-item correlation; 4 were retained. The WMNKQ met criteria for internal consistency (Cronbach's alpha = 0.88), reliability (test-retest correlation ρ = 0.90, P < 0.0001), construct validity (known groups comparison) - dietitians scored 16% better (p < 0.0001) than information technology workers, and criterion validity (pre- to post-intervention improvement in knowledge scores = 11.2% (95% CI 9.8-12.5, p < 0.0001)). Participants younger than age 55 scored significantly better than those over age 55 (convergent validity). CONCLUSIONS: The WMNKQ measures how well nutrition principles of weight management are understood.

Methodology of a multispecialty outpatient Obesity Treatment Research Program.

Despite the large number of U.S. adults who overweight or obese, few providers have ready access to comprehensive lifestyle interventions, the cornerstone of medical obesity management. Our goal was to establish a research infrastructure embedded in a comprehensive lifestyle intervention treatment for obesity. The Obesity Treatment Research Program (OTRP) is a multi-specialty project at Mayo Clinic in Rochester, Minnesota designed to provide a high intensity, year-long, comprehensive lifestyle obesity treatment. The program includes a nutritional intervention designed to reduce energy intake, a physical activity program and a cognitive behavioral approach to increase the likelihood of long-term adherence. The behavioral intervention template incorporated the Diabetes Prevention Program and the Look AHEAD trial materials. The OTRP is consistent with national recommendations for the management of overweight and obesity in adults, but with embedded features designed to identify patient characteristics that might help predict outcomes, assure long-term follow up and support various research initiatives. Our goal was to develop approaches to understand whether there are patient characteristics that predict treatment outcomes.

Brivanib attenuates hepatic fibrosis in vivo and stellate cell activation in vitro by inhibition of FGF, VEGF and PDGF signaling.

BACKGROUND AND AIMS: Brivanib is a selective inhibitor of vascular endothelial growth factor receptor (VEGFR) and fibroblast growth factor receptor (FGFR) tyrosine kinases, which are both involved in mechanisms of liver fibrosis. We hypothesized that inhibition of VEGFR and FGFR by brivanib would inhibit liver fibrosis. We therefore examined the effect of brivanib on liver fibrosis in three mouse models of fibrosis. METHODS: In vivo, we induced liver fibrosis by bile duct ligation (BDL), chronic carbon tetrachloride (CCl4), and chronic thioacetamide (TAA) administration. Liver fibrosis was examined by immunohistochemistry and Western immunoblotting. In vitro, we used LX-2 human hepatic stellate cells (HSCs) to assess the effect of brivanib on stellate cell proliferation and activation. RESULTS: After in vivo induction with BDL, CCl4, and TAA, mice treated with brivanib showed reduced liver fibrosis and decreased expression of collagen Iα1 and α-smooth muscle actin in the liver. In vitro, brivanib decreased proliferation of HSCs induced by platelet-derived growth factor (PDGF), VEGF, and FGF. Brivanib also decreased stellate cell viability and inhibited PDGFBB-induced phosphorylation of its cognate receptor. CONCLUSION: Brivanib reduces liver fibrosis in three different animal models and decreases human hepatic stellate cell activation. Brivanib may represent a novel therapeutic approach to treatment of liver fibrosis and prevention of liver cancer.