Leslie B. Adams

The human genome encodes the blueprint of life, but the function of the vast majority of its nearly three billion bases is unknown. The Encyclopedia of DNA Elements (ENCODE) project has systematically mapped regions of transcription, transcription factor association, chromatin structure and histone modification. These data enabled us to assign biochemical functions for 80% of the genome, in particular outside of the well-studied protein-coding regions. Many discovered candidate regulatory elements are physically associated with one another and with expressed genes, providing new insights into the mechanisms of gene regulation. The newly identified elements also show a statistical correspondence to sequence variants linked to human disease, and can thereby guide interpretation of this variation. Overall, the project provides new insights into the organization and regulation of our genes and genome, and is an expansive resource of functional annotations for biomedical research. © 2012 Macmillan Publishers Limited. All rights reserved.

e laboratory mouse is the premier mammalian model organism for the study of human disease, and it has played a vital role in both the annotation of the human genome and the study of gene function and regulation. Similar to humans, mice naturally develop diverse diseases that affect the hematologic, nervous, cardiovascular, endocrine, musculoskeletal, renal and other systems, providing excellent experimental paradigms for studying the pathogenesis of cancer, autoimmune disease, diabetes, obesity, atherosclerosis, hypertension, gastrointestinal disorders and diverse neurodegenerative states. Mouse models are currently available for hundreds of human disorders [1-4], spanning diverse quantitative and behavioral phenotypes and physiological systems. ese comprise both inbred strains and genetically engineered mutants, many of which have been extensively characterized. For these reasons, the mouse has emerged as a premier system for translating basic human genetic, genomic and physiologic research into paradigms for therapeutic development.

Men's tendency to delay health help-seeking is largely attributed to masculinity, but findings scarcely focus on African American men who face additional race-related, help-seeking barriers. Building principally on reactance theory, we test a hypothesized model situating racial discrimination, masculinity norms salience (MNS), everyday racism (ERD), racial identity, sense of control (SOC), and depressive symptomatology as key barriers to African American men's health help-seeking. A total of 458 African American men were recruited primarily from US barbershops in the Western and Southern regions. The primary outcome was Barriers to Help-Seeking Scale (BHSS) scores. The hypothesized model was investigated with confirmatory factor and path analysis with tests for measurement invariance. Our model fit was excellent [Formula: see text] CFI = 0.99; TLI = 1.00; RMSEA = 0.00, and 90% CI [0.00, 0.07] and operated equivalently across different age, income, and education strata. Frequent ERD and higher MNS contributed to higher BHHS scores. The relationship between ERD exposure and BHHS scores was partially mediated by diminished SOC and greater depressive symptomatology. Interventions aimed at addressing African American men's health help-seeking should not only address masculinity norms but also threats to sense of control, and negative psychological sequelae induced by everyday racism.