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Students majoring in non-STEM fields often identify introductory biology courses as irrelevant and overly rigorous. Resistance to enroll in a required general education science course, coupled with negative attitudes toward the subject, can adversely affect the academic performance of students; this can especially be present in students from under-represented minority groups. Therefore, instructors have to intentionally design a curriculum that overcomes these factors as they educate non-major students enrolled in introductory biology. BioArt, a learning community, was formed between introductory biology and introduction to graphic design courses to improve the attitudes and academic performance of students in the biology course at a Historically Black College and University (HBCU). The BioArt model incorporated a common theme, project-based learning, and opportunities for experiential learning. To measure outcomes, traditional examinations, non-traditional assessments, failure/withdraw rates, and student attitudes were evaluated. Using this model, introductory biology became less intimidating, more relevant, and improved academic success among freshman minority students. Thus, the BioArt model can be utilized as an intervention at different institutions of higher learning.

Abstract The transforming growth factor-beta (TGF-β) superfamily consists of a variety of cytokines expressed in many different cell types including skeletal muscle. Members of this superfamily that are of particular importance in skeletal muscle are TGF-β1, mitogen-activated protein kinases (MAPKs), and myostatin. These signaling molecules play important roles in skeletal muscle homeostasis and in a variety of inherited and acquired neuromuscular disorders. Expression of these molecules is linked to normal processes in skeletal muscle such as growth, differentiation, regeneration, and stress response. However, chronic elevation of TGF-β1, MAPKs, and myostatin is linked to various features of muscle pathology, including impaired regeneration and atrophy. In this review, we focus on the aberrant signaling of TGF-β in various disorders such as Marfan syndrome, muscular dystrophies, sarcopenia, and critical illness myopathy. We also discuss how the inhibition of several members of the TGF-β signaling pathway has been implicated in ameliorating disease phenotypes, opening up novel therapeutic avenues for a large group of neuromuscular disorders.