Efficacy of monitoring and empirical predictive modeling at improving public health protection at Chicago beaches

Efforts to improve public health protection in recreational swimming waters have focused on obtaining real-time estimates of water quality. Current monitoring techniques rely on the time-intensive culturing of fecal indicator bacteria (FIB) from water samples, but rapidly changing FIB concentrations result in management errors that lead to the public being exposed to high FIB concentrations (type II error) or beaches being closed despite acceptable water quality (type I error). Empirical predictive models may provide a rapid solution, but their effectiveness at improving health protection has not been adequately assessed. We sought to determine if emerging monitoring approaches could effectively reduce risk of illness exposure by minimizing management errors. We examined four monitoring approaches (inactive, current protocol, a single predictive model for all beaches, and individual models for each beach) with increasing refinement at 14 Chicago beaches using historical monitoring and hydrometeorological data and compared management outcomes using different standards for decision-making. Predictability (R²) of FIB concentration improved with model refinement at all beaches but one. Predictive models did not always reduce the number of management errors and therefore the overall illness burden. Use of a Chicago-specific single-sample standard—rather than the default 235 E. coli CFU/100 ml widely used—together with predictive modeling resulted in the greatest number of open beach days without any increase in public health risk. These results emphasize that emerging monitoring approaches such as empirical models are not equally applicable at all beaches, and combining monitoring approaches may expand beach access.     

Microstructure and mechanical performance examination of 3D printed acrylonitrile butadiene styrene thermoplastic parts

Fused filament fabrication (FFF) is a process where thermoplastic materials are heated to its melting point and then extruded, layer by layer, to create a three dimensional printed part. Printing occurs in a layered manner, which leads to creation of voids (air gaps) in the 3D printed parts. These voids act as centers for crack initiation, propagation and therefore resulting bulk mechanical properties are lower. This paper focuses on microstructural characterization and analysis of fused filament fabricated tensile test coupons made from acrylonitrile butadiene styrene polymer, at various design conditions. Comparable tensile modulus with injection molded specimens was obtained for FFF design condition that is, slice height (0.1778 mm), raster width (0.4064 mm), raster to raster air gap (−0.0015 mm), contour to raster air gap (−0.0508 mm) and raster angle (0°). Scanning electron microscope studies provided an understanding as to why FFF processed specimens yielded lower failure strain and an insight into the presence of intralayer voids in specimens having lower tensile modulus. The study confirmed that though bulk mechanicals were affected by the combined effect of inter, intra and interfacial voids, intravoids had a predominant influence.     

Hydroxyl radical-induced hydrogen/deuterium exchange in amino acid carbon-hydrogen bonds

BB rats are used as models of autoimmune human IDDM. Genetic control of IDDM in both species is complex, including both major histocompatibility complex (MHC)-linked and non-MHC-linked genes. DP-BB rats develop IDDM spontaneously. Expression of disease in these animals requires homozygosity at the lyp locus, which causes lymphopenia. All genetic analyses of BB rat diabetes to date have backcrossed to the DP-BB strain or used (DP-BB x non-BB)F2 animals to ensure that a fraction of progeny are homozygous for lyp. Here we report the analysis of a backcross of the DP-BB rat to the histocompatible WF rat. Neither WF nor (WF x DP-BB)F1 animals develop spontaneous IDDM. However, 95% of (WF x DP-BB)F1 rats and a fraction of (WF x DP-BB) x WF backcross animals readily develop IDDM after treatment with polyinosinic:polycytidylic acid and a cytotoxic anti-RT6.1 monoclonal antibody. Using simple sequence length polymorphism analysis, we have mapped loci on chromosomes 4 and 13 that show significant linkage to IDDM expression and insulitis. The susceptibility locus on chromosome 4 is linked to, but not identical to, lyp. We propose a disease model for the BB rat that requires 1) the RT1u MHC haplotype for disease susceptibility, 2) a new locus on chromosome 4 for disease initiation (as measured by insulitis), 3) a new locus on chromosome 13 for disease progression in response to environmental perturbation, and 4) lyp for spontaneous expression of disease.     

Heritability of anxiety sensitivity: a twin study

OBJECTIVE: In attempting to explain the familial predisposition to panic disorder, most studies have focused on the heritability of physiologic characteristics (e.g., CO2 sensitivity). A heretofore unexplored possibility is that a psychological characteristic that predisposes to panic-anxiety sensitivity-might be inherited. In this study, the authors examined the heritability of anxiety sensitivity through use of a twin group. METHOD: Scores on the Anxiety Sensitivity Index were examined in a group of 179 monozygotic and 158 dizygotic twin pairs. Biometrical model fitting was conducted through use of standard statistical methods. RESULTS: Broad heritability estimate of the Anxiety Sensitivity Index as a unifactorial construct was 45%. Additive genetic effects and unique environmental effects emerged as the primary influences on anxiety sensitivity. There was no evidence of genetic discontinuity between normal and extreme scores on the Anxiety Sensitivity Index. CONCLUSIONS: This study suggests that one psychological risk factor for the development of panic disorder-anxiety sensitivity-may have a heritable component. As such, anxiety sensitivity should be considered in future research on the heritability of panic disorder.