Collectively Improving Our Teaching: Attempting Biology Department-wide Professional Development in Scientific Teaching.

Many efforts to improve science teaching in higher education focus on a few faculty members at an institution at a time, with limited published evidence on attempts to engage faculty across entire departments. We created a long-term, department-wide collaborative professional development program, Biology Faculty Explorations in Scientific Teaching (Biology FEST). Across 3 years of Biology FEST, 89% of the department's faculty completed a weeklong scientific teaching institute, and 83% of eligible instructors participated in additional semester-long follow-up programs. A semester after institute completion, the majority of Biology FEST alumni reported adding active learning to their courses. These instructor self-reports were corroborated by audio analysis of classroom noise and surveys of students in biology courses on the frequency of active-learning techniques used in classes taught by Biology FEST alumni and nonalumni. Three years after Biology FEST launched, faculty participants overwhelmingly reported that their teaching was positively affected. Unexpectedly, most respondents also believed that they had improved relationships with departmental colleagues and felt a greater sense of belonging to the department. Overall, our results indicate that biology department-wide collaborative efforts to develop scientific teaching skills can indeed attract large numbers of faculty, spark widespread change in teaching practices, and improve departmental relations.

Eicosapentaenoic acid prevents lipopolysaccharide-stimulated DNA binding of activator protein-1 and c-Jun N-terminal kinase activity.

Activator protein-1 (AP-1) is a transcription factor that plays an important role in regulating the expression of proinflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha). Many studies have shown that fish oil supplementation inhibits TNF-alpha production in mice and humans; however, the mechanisms remain unclear. In this study, the effects of eicosapentaenoic acid (EPA), a major n-3 fatty acid in fish oil, on lipopolysaccharide (LPS)-stimulated activation of AP-1 were investigated in human monocytic THP-1 cells. The results demonstrated that AP-1 DNA binding activity stimulated by LPS was suppressed by preincubating cells with EPA. Lipopolysaccharide-stimulated increase of c-Jun and c-Fos protein levels was also attenuated by EPA pretreatment. In addition, EPA pretreatment decreased LPS-induced c-Jun phosphorylation and c-Jun N-terminal kinase (JNK) activation. The results suggest that suppression of TNF-alpha expression by EPA may be partly mediated by its inhibitory effect on AP-1 activation.

Eicosapentaenoic acid prevents LPS-induced TNF-alpha expression by preventing NF-kappaB activation.

BACKGROUND: Many studies have shown that fish oil supplementation inhibits tumor necrosis factor-alpha (TNF-alpha) production in mice and human subjects; however, the mechanisms remain unclear. Nuclear factor-kappaB (NF-kappaB) is a transcription factor that plays an important role in controlling the expression of pro-inflammatory genes including TNF-alpha. Activation of NF-kappaB has been shown to mediate the maximal expression of TNF-alpha in human monocytes. NF-kappaB is kept in an inactive form in the cytoplasm by IkappaB, the inhibitory subunit of NF-kappaB complex. Phosphorylation and subsequent degradation of IkappaB lead to NF-kappaB activation. OBJECTIVES: The effect of eicosapentaenoic acid (EPA), a major n-3 fatty acid in fish oil, on the lipopolysaccharide (LPS)-induced expression of TNF-alpha and activation of NF-kappaB were investigated. The mechanism underlying EPA modulation of NF-kappaB activation was also studied. METHODS: Human monocytic THP-1 cells were pre-incubated with EPA and stimulated with LPS. The levels of secreted TNF-alpha were determined by ELISA. The DNA binding activity of NF-kappaB was analyzed by EMSA. The degradation and phosphorylation of IkappaB-alpha were examined by Western blot analysis. RESULTS: TNF-alpha production and expression induced by LPS were significantly decreased in cells pre-incubated with EPA. LPS-induced NF-kappaB activation, translocation of p65 subunit to the nucleus, phosphorylation and degradation of IkappaB-alpha were partially prevented by EPA. CONCLUSIONS: The results suggest that suppression of the TNF-alpha expression by EPA is partly attributed to its inhibitory effect on NF-kappaB activation. EPA appears to prevent NF-kappaB activation by preventing the phosphorylation of IkappaB-alpha.