Objective: To investigate whether low-carbohydrate diets (LCDs) were associated with coronary artery calcium (CAC) progression. Approach and Results: We included the participants who completed computed tomography assessment of baseline CAC in 2000 to 2001 (year 15) and follow-up (year 20 or 25) and food frequency questionnaire (years 0, 7, and 20) in the CARDIA study (Coronary Artery Risk Development in Young Adults). CAC progression was defined as CAC >0 at follow-up among participants with baseline CAC of 0 and an annualized change of 10 or percent change of ≥10% for those with 0<baseline CAC<100 or baseline CAC≥100, respectively. Among 2226 included participants (age, 40.4±3.5 years; 45.4% men), the carbohydrate intake accounted for 47.8±6.5% of total energy, and 204 (9.2%) had CAC at baseline (year 15). Over a mean follow-up of 8.3 years, 591 (26.5%) participants had CAC progression. After adjustment for traditional cardiovascular risk factors and other dietary factors, carbohydrate intake as a percentage of total energy was inversely associated with the risk of CAC progression (hazard ratio, 0.731 [95% CI, 0.552–0.968]; P =0.029). Furthermore, the animal-based but not plant-based LCD score was significantly associated with a higher risk of CAC progression (animal-based LCD score: hazard ratio, 1.456 [95% CI, 1.015–2.089]; P =0.041; plant-based LCD score: hazard ratio, 1.016 [95% CI, 0.821–1.257]; P =0.884; both comparing extreme groups). Conclusions: LCDs starting at a young age are associated with an increased risk of subsequent CAC progression, particularly when animal protein or fat are chosen to replace carbohydrates. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT00005130.

Gold nanoparticles are emerging as promising biomedical tools due to their unique nanoscale characteristics. Our purpose was to synthesize a hollow-shaped gold nanoparticle and to investigate its effect on human aortic endothelial cells (HAECs) in vitro. Hollow gold nanoshells with average 35-nm diameters and 10-nm shell thickness were obtained by galvanic replacement using quasi-spherical nanosilver as sacrifice-template. Our results showed that hollow gold nanoshells in the culture medium could be internalized into the cytoplasm of HAECs. No cytotoxicity effect of hollow gold nanoshells on HAECs was observed within the test concentrations (0–0.8 μg/mL) and test exposure period (0–72 h) by tetrazolium dye assay. Meanwhile, the release of cell injury biomarker, lactate dehydrogenase, was not significantly higher than that from control cells (without hollow gold nanoshells). The concentrations of vasodilators, nitric oxide, and prostacyclin I-2 were not changed, but the vasoconstrictor endothelin-1 was decreased by hollow gold nanoshells treatment in HAECs. HAECs exposed to hollow gold nanoshells resulted in suppressing expressions of genes involved in apoptosis and activating expressions of genes of adhesion molecules. Moreover, we demonstrated by in vitro endothelial tube formation that hollow gold nanoshells (0.8 μg/mL) could not inhibit angiogenesis by the HAECs. Altogether, these results indicate that the structure and major function of HAECs would not be disrupted by hollow gold nanoshell treatment.