Throughput Optimized Implementations of QUAD

We present several software and hardware implementations of QUAD, a recently introduced stream cipher designed to be provably secure and practical to implement. The software implementations target both a personal computer and an ARM microprocessor. The hardware implementations target field programmable gate arrays. The purpose of our work was to first find the baseline performance of QUAD implementations, then to optimize our implementations for throughput. Our software implementations perform comparably to prior work. Our hardware implementations are the first known implementations to use random coefficients, in agreement with QUAD’s security argument, and achieve much higher throughput than prior implementations

The Star Formation History of the Large Magellanic Cloud

We present the first-ever global, spatially-resolved reconstruction of the star formation history (SFH) of the Large Magellanic Cloud (LMC), based on the application of our StarFISH analysis software to the multiband photometry of twenty million of its stars from the Magellanic Clouds Photometric Survey. The general outlines of our results are consistent with previously published results: following an initial burst of star formation, there was a quiescent epoch from approximately 12 to 5 Gyr ago. Star formation then resumed and has proceeded until the current time at an average rate of roughly 0.2 solar masses/yr, with temporal variations at the factor-of-two level. The re-ignition of star formation about 5 Gyr ago, in both the LMC and SMC, is suggestive of a dramatic event at that time in the Magellanic system. Among the global variations in the recent star formation rate are peaks at roughly 2 Gyr, 500 Myr, 100 Myr and 12 Myr. The peaks at 500 Myr and 2 Gyr are nearly coincident with similar peaks in the SFH of the Small Magellanic Cloud, suggesting a joint history for these galaxies extending back at least several Gyr. The chemical enrichment history recovered from our StarFISH analysis is in broad agreement with that inferred from the LMC's star cluster population, although our constraints on the ancient chemical enrichment history are weak. We conclude from the concordance between the star formation and chemical enrichment histories of the field and cluster populations that the field and cluster star formation modes are tightly coupled.Comment: 20 pages, with color figures. Accepted for publication in A

Mechanisms Underlying Acrolein-Mediated Inhibition of Chromatin Assembly

Acrolein is a major component of cigarette smoke and cooking fumes. Previously, we reported that acrolein compromises chromatin assembly; however, underlying mechanisms have not been defined. Here, we report that acrolein reacts with lysine residues, including lysines 5 and 12, sites important for chromatin assembly, on histone H4 in vitro and in vivo Acrolein-modified histones are resistant to acetylation, suggesting that the reduced H4K12 acetylation that occurs following acrolein exposure is probably due to the formation of acrolein-histone lysine adducts. Accordingly, the association of H3/H4 with the histone chaperone ASF1 and importin 4 is disrupted and the translocation of green fluorescent protein-tagged H3 is inhibited in cells exposed to acrolein. Interestingly, in vitro plasmid supercoiling assays revealed that treatment of either histones or ASF1 with acrolein has no effect on the formation of plasmid supercoiling, indicating that acrolein-protein adduct formation itself does not directly interfere with nucleosome assembly. Notably, exposure of histones to acrolein prior to histone acetylation leads to the inhibition of remodeling and spacing factor chromatin assembly, which requires acetylated histones for efficient assembly. These results suggest that acrolein compromises chromatin assembly by reacting with histone lysine residues at the sites critical for chromatin assembly and prevents these sites from physiological modifications

Tungsten-induced carcinogenesis in human bronchial epithelial cells

Metals such as arsenic, cadmium, beryllium, and nickel are known human carcinogens; however, other transition metals, such as tungsten (W), remain relatively uninvestigated with regard to their potential carcinogenic activity. Tungsten production for industrial and military applications has almost doubled over the past decade and continues to increase. Here, for the first time, we demonstrate tungsten's ability to induce carcinogenic related endpoints including cell transformation, increased migration, xenograft growth in nude mice, and the activation of multiple cancer-related pathways in transformed clones as determined by RNA sequencing. Human bronchial epithelial cell line (Beas-2B) exposed to tungsten developed carcinogenic properties. In a soft agar assay, tungsten-treated cells formed more colonies than controls and the tungsten-transformed clones formed tumors in nude mice. RNA-sequencing data revealed that the tungsten-transformed clones altered the expression of many cancer-associated genes when compared to control clones. Genes involved in lung cancer, leukemia, and general cancer genes were deregulated by tungsten. Taken together, our data show the carcinogenic potential of tungsten. Further tests are needed, including in vivo and human studies, in order to validate tungsten as a carcinogen to humans

Association between Exposure to Ambient Air Particulates and Metabolic Syndrome Components in a Saudi Arabian Population

Recent epidemiological evidence suggests that exposure to particulates may be a factor in the etiology of metabolic syndrome (MetS). In this novel study, we investigated the relationship between particulate levels and prevalence of MetS component abnormalities (hypertension, hyperglycemia, obesity) in a recruited cohort (N = 2025) in Jeddah, Saudi Arabia. We observed significant associations between a 10 μg/m3 increase in PM2.5 and increased risks for MetS (Risk Ratio (RR): 1.12; 95% Confidence Interval (CI): 1.06–1.19), hyperglycemia (RR: 1.08; 95% CI: 1.03–1.14), and hypertension (RR: 1.09; 95% CI: 1.04–1.14). PM2.5 from soil/road dust was found to be associated with hyperglycemia (RR: 1.12; 95% CI: 1.06–1.19) and hypertension (RR: 1.11; 95% CI: 1.05–1.18), while PM2.5 from traffic was associated with hyperglycemia (RR: 1.33; 95% CI: 1.05–1.71). We did not observe any health associations with source-specific mass exposures. Our findings suggest that exposure to specific elemental components of PM2.5, especially Ni, may contribute to the development of cardiometabolic disorders