The Influence of Education on the Nutritional Knowledge of Certified Fitness Professionals.

The American Fitness Industry has seen progressive success with recent increases in facility memberships and annual revenues of fitness centers. The number of fitness trainers and instructors in the United States has persisted this growth and is projected to grow over the next decade. However, only a few known studies have investigated the nutritional education of fitness professionals. This preliminary study explores the education and knowledge among certified fitness professions (CFPs) in the United States. A cross-sectional, descriptive survey design was utilized with a convenience sample of 120 female participants from the United States who were associated with a major fitness newsletter. The average age of the participants was 48.51 years (SD 12), and they had 14.85 years of experience (SD 10.16) and worked an average of 22.04 hours per week (SD 16.78). Most of the participants had some kind of college degree (96.2%) and held a group fitness certification (76.6%) or personal training certification (47.5%). Those with a nutrition certification were found to have significantly higher nutrition knowledge test scores on the 21 question test (18.2 ± 2.0 correct to 17.1 ± 1.9, p=0.04). Additionally, it is revealed that CFPs use the internet as a primary source for nutritional information and was the most frequently used source of nutrition information accessed. This pilot study suggests a more in-depth study would be beneficial to solidify the current results and could allow for more investigation into whether or not completion of nutrition coursework within formal earned degrees by CFPs positively influences their nutritional knowledge.

Allosteric inhibition of antiapoptotic MCL-1.

MCL-1 is an antiapoptotic BCL-2 family protein that has emerged as a major pathogenic factor in human cancer. Like BCL-2, MCL-1 bears a surface groove whose function is to sequester the BH3 killer domains of proapoptotic BCL-2 family members, a mechanism harnessed by cancer cells to establish formidable apoptotic blockades. Although drugging the BH3-binding groove has been achieved for BCL-2, translating this approach to MCL-1 has been challenging. Here, we report an alternative mechanism for MCL-1 inhibition by small-molecule covalent modification of C286 at a new interaction site distant from the BH3-binding groove. Our structure-function analyses revealed that the BH3 binding capacity of MCL-1 and its suppression of BAX are impaired by molecular engagement, a phenomenon recapitulated by C286W mutagenic mimicry in vitro and in mouse cells. Thus, we characterize an allosteric mechanism for disrupting the antiapoptotic BH3 binding activity of MCL-1, informing a new strategy for disarming MCL-1 in cancer.