The risk of dying from lung cancer by race: a prospective cohort study in a biracial cohort in Charleston, South Carolina.

PURPOSE: Compared to European Americans (EAs), African Americans (AAs) suffer a disproportionate share of the lung cancer mortality burden. To investigate whether this disparity in lung cancer mortality is due to differential racial risks related to socioeconomic status (education, occupation), body mass index (BMI), hypertension, or cigarette smoking, we compared associations between these factors and lung cancer mortality by race in a biracial prospective cohort study. METHODS: The Charleston (South Carolina) Heart Study (N = 2,054) was established in 1960; 40% of the study participants are AAs. The participants have been followed up for mortality for 40 years. Using Cox proportional hazards models, we investigated whether there were racial differences in the associations between the study factors and lung cancer mortality. RESULTS: Cigarette smoking was the strongest lung cancer risk factor in both races. The association between cigarette smoking and lung cancer mortality was stronger in EAs than AAs (hazards ratio [HR] 26.1 vs. 7.6). In both races, men were at significantly greater risk than women and BMI was significantly inversely associated with lung cancer mortality. CONCLUSIONS: The evidence from the present study does not yield strong clues for the excess lung cancer mortality in AAs. Our results do not support the hypothesis that differential susceptibility to cigarette smoking is a major contributor to the racial disparity in lung cancer. This suggests we must expand our scope of inquiry beyond the factors included in the present study to fully understand why lung cancer mortality rates are greater in AAs than EAs.

Engineered early embryonic cardiac tissue retains proliferative and contractile properties of developing embryonic myocardium.

Embryonic myocardium has a high rate of cell proliferation and regulates cellular proliferation, contractile function, and myocardial architecture in response to changes in external mechanical loads. However, the small and complex three-dimensional (3D) structure of the embryonic myocardium limits our ability to directly investigate detailed relationships between mechanical load, contractile function, and cardiomyocyte proliferation. We developed a novel 3D engineered early embryonic cardiac tissue (EEECT) from early embryonic ventricular cells to test the hypothesis that EEECT retains the proliferative and contractile properties of embryonic myocardium. We combined freshly isolated White Leghorn chicken embryonic ventricular cells at Hamburger-Hamilton (HH) stage 31 (day 7 of a 46-stage, 21-day incubation period), collagen type I, and matrix factors to construct cylindrical-shaped EEECTs. We studied tissue architecture, cell proliferation patterns, and contractile function. We then generated engineered fetal cardiac tissue (EFCT) from HH stage 40 (day 14) fetal ventricular cells for direct comparison with EEECT. Tissue architecture was similar in EEECT and EFCT. EEECT maintained high cell proliferation patterns by culture day 12, whereas EFCT decreased cell proliferation rate by culture day 9 (P < 0.05). EEECT increased active contractile force from culture day 7 to day 12. The culture day 12 EEECT contractile response to the beta-adrenergic stimulation was less than culture day 9 EFCT (P < 0.05). Cyclic mechanical stretch stimulation induced myocardial hyperplasia in EEECT. Results indicate that EEECT retains the proliferative and contractile properties of developing embryonic myocardium and shows potential as a robust in vitro model of developing embryonic myocardium.