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President Barack Obama's farewell address serves as a symbolic end to an eight-year tenure as president of the United States. The standard themes in Obama's public addresses have been hope and change, and the president continues to elaborate on those here. While describing accomplishments of his administration and thanking important people, Obama uses his last address as president to craft a narrative in three strands--past, present, and future--meant to inspire civic engagement in his audience. I use Burke's dramatistic pentad to discover how Obama rhetorically motivates his listeners towards this end. President Obama creates a sense of empowerment and audience identification with past American heroes by initially using purpose as a driving force, later emphasizing agency, and finally focusing on the agents who can accomplish the purpose. Obama's farewell address illustrates the importance of presidential farewell addresses to shape the politics to follow, in this case by persuading citizens to engage in democratic processes. [ABSTRACT FROM AUTHOR]

Murine studies have linked TGF-β signaling to emphysema, and human genome-wide association studies (GWAS) studies of lung function and COPD have identified associated regions near genes in the TGF-β superfamily. However, the functional regulatory mechanisms at these loci have not been identified. We performed the largest GWAS of emphysema patterns to date, identifying 10 GWAS loci including an association peak spanning a 200 kb region downstream from TGFB2 . Integrative analysis of publicly available eQTL, DNaseI, and chromatin conformation data identified a putative functional variant, rs1690789, that may regulate TGFB2 expression in human fibroblasts. Using chromatin conformation capture, we confirmed that the region containing rs1690789 contacts the TGFB2 promoter in fibroblasts, and CRISPR/Cas-9 targeted deletion of a ~ 100 bp region containing rs1690789 resulted in decreased TGFB2 expression in primary human lung fibroblasts. These data provide novel mechanistic evidence linking genetic variation affecting the TGF-β pathway to emphysema in humans., Competing Interests: MP, YH, FG, BP, RC, JP, VT, JC, XZ No competing interests declared, MC reports grants from GSK and personal fees from Genentech, CH reports personal fees from Mylan, personal fees from AstraZeneca, Concert Pharmaceuticals, 23andMe, grants from Novartis, and Boehringer-Ingelheim, GW reports grants and other support from Boehringer Ingelheim, PulmonX, BTG Interventional Medicine, Janssen Pharmaceuticals and GSK, SR reports receiving personal fees from Amgen, ES received honoraria from Novartis for Continuing Medical Education Seminars and grant and travel support from GlaxoSmithKline, RS reports personal fees from Boehringer Ingelheim, Eolo Medical and Toshiba, PC has received research support and consulting fees from GSK and Novartis, (© 2019, Parker et al.)

Background: Hepatic steatosis has been associated with chronic hepatitis C (CHC), but its prevalence, risk factors, and clinical significance remain to be determined., Aims: The present study determined the frequency of, and risk factors for hepatic steatosis and its association with activity and progression of CHC in a large cohort of U.S. patients., Methods: This is a retrospective study that utilized systematic chart review and statistical analyzes to investigate 324 U.S. patients with CHC from a university medical center and a regional VA medical center., Results: The frequency of hepatic steatosis was 66.0%. We demonstrated that not only being obese, but also overweight (i.e. body mass index > or =25 kg/m(2)) was independently associated with hepatic steatosis. In our cohort of patients with CHC, hepatic steatosis, especially grade II/III steatosis, was significantly associated with elevated aspartate aminotransferase at entry, persistently elevated alanine aminotransferase, and stage III/IV fibrosis. Grade II/III steatosis, was significantly associated with a higher histology activity index as well. Multivariate analysis indicated that steatosis, especially grade II/III steatosis, was independently associated with stage III/IV fibrosis., Conclusions: Being overweight/obese serves as an independent risk factor for hepatic steatosis in U.S. patients with CHC. Steatosis accelerates activity and progression of CHC, and is independently associated with stage III/IV hepatic fibrosis in these patients.