DETERMINANTS OF UNSAFE HAMBURGER COOKING BEHAVIOR

We used a national hamburger preparation survey to estimate a simultaneous equation model of food safety knowledge, attitudes, and hamburger cooking behavior. The results suggest that food safety risk perceptions, palatability attributes, and food safety knowledge play important roles in determining food preparation behavior.Consumer/Household Economics, Food Consumption/Nutrition/Food Safety,

CONSUMER FOOD SAFETY BEHAVIOR: A CASE STUDY IN HAMBURGER COOKING AND ORDERING

More Americans are eating hamburgers more well-done than in the past, according to national surveys. This change reduced the risk of E. coli O157:H7 infection by an estimated 4.6 percent and reduced associated medical costs and productivity losses by an estimated $7.4 million annually. In a 1996 survey, respondents who were more concerned about the risk of foodborne illness cooked and ordered hamburgers more well-done than those who were less concerned. However, respondents who strongly preferred hamburgers less well-done cooked and ordered them that way, even after accounting for their concern about the risk of illness.hamburger doneness, ground beef, food safety, food safety education, E. coli O157:H7, consumer behavior, survey, risk, foodborne illness, risk perceptions, palatability, information, microbial pathogens, Food Consumption/Nutrition/Food Safety,

Vps54 Regulates Lifespan and Locomotor Behavior in Adult Drosophila Melanogaster

Vps54 is an integral subunit of the Golgi-associated retrograde protein (GARP) complex, which is involved in tethering endosome-derived vesicles to the trans-Golgi network (TGN). A destabilizing missense mutation in Vps54 causes the age-progressive motor neuron (MN) degeneration, muscle weakness, and muscle atrophy observed in the wobbler mouse, an established animal model for human MN disease. It is currently unclear how the disruption of Vps54, and thereby the GARP complex, leads to MN and muscle phenotypes. To develop a new tool to address this question, we have created an analogous model in Drosophila by generating novel loss-of-function alleles of the fly Vps54 ortholog (scattered/scat). We find that null scat mutant adults are viable but have a significantly shortened lifespan. Like phenotypes observed in the wobbler mouse, we show that scat mutant adults are male sterile and have significantly reduced body size and muscle area. Moreover, we demonstrate that scat mutant adults have significant age-progressive defects in locomotor function. Interestingly, we see sexually dimorphic effects, with scat mutant adult females exhibiting significantly stronger phenotypes. Finally, we show that scat interacts genetically with rab11 in MNs to control age-progressive muscle atrophy in adults. Together, these data suggest that scat mutant flies share mutant phenotypes with the wobbler mouse and may serve as a new genetic model system to study the cellular and molecular mechanisms underlying MN disease

FXS-Causing Point Mutations in FMRP Disrupt Neuronal Granule Formation and Function

Fragile X Syndrome (FXS) is a neurodevelopmental disorder caused by the disruption of Fragile X Mental Retardation Protein (FMRP) function in neurons, affecting nearly 1 in 7,500 individuals. Although FXS typically occurs from a complete loss of FMRP expression due to a CGG trinucleotide expansion within the 5’UTR of the FMR1 gene, single nucleotide polymorphisms (SNPs) within the KH domains of FMRP have been shown to severely disrupt FMRP function. FMRP is an RNA-binding translation repressor that interacts with ~4% of the neuronal transcriptome. Many target mRNAs encode for proteins important for regulating synaptic processes and modulate synaptic plasticity. It is likely that FMRP differentially regulates this large subset of mRNAs via its association with specific membraneless organelles (MLOs), or granules, that are each involved in regulating different processes of the transcript lifecycle. How FMRP forms and interacts with different MLOs however, is largely unknown. Here we show that multivalent interactions via the two canonical KH domains, KH1 and KH2, and the C-terminal intrinsically disordered region (IDR) function cooperatively to promote FMRP granule formation in Drosophila S2 cells. Two mutations within the KH domains of FMRP have been linked to severe forms of FXS. We were interested in determining whether these mutations disrupted the formation or function of FMRP-containing MLOs. Here we studied these missense point mutations, by making the orthologous mutations in the fly KH1 (Gly269Glu) and KH2 (Ile307Asn) domains. Within FRAP experiments of fly S2 cells we found that each of the KH point mutants destabilized the dynamic mobile fraction of FMRP granules, while having no impact on immobile fractions. The KH1 mutant in particular has an important function in granule formation and FMRP association with other MLOs involved in posttranscriptional regulation including stress granules and RNA Processing-bodies. Additionally, we found that the KH1 mutation is defective in FMRP-mediated translation, while the KH2 mutant has no effect. We also studied the impact of these mutations in Drosophila primary motor neurons (MNs) where FMRP associates with neuronal RNA transport granules (NGs). Within NGs FMRP is thought to translationally repress transcripts during their active transport from the soma out to the synapse. Interestingly, we found that the KH1 mutant severely disrupted the nucleation of FMRP-positive NGs. The KH2 mutant on the other hand destabilized NGs, impacting NG transport out in neurites. Interestingly, we found that these mutations had no impact on camkii transport, a well characterized FMRP target, suggesting that FMRP-NG association and RNA transport may not be functionally linked processes

Performance of compressed sensing for fluorine-19 magnetic resonance imaging at low signal-to-noise ratio conditions

PURPOSE: To examine the performance of compressed sensing (CS) in reconstructing low signal-to-noise ratio (SNR) (19)F MR signals that are close to the detection threshold and originate from small signal sources with no a priori known location. METHODS: Regularization strength was adjusted automatically based on noise level. As performance metrics, root-mean-square deviations, true positive rates (TPRs), and false discovery rates were computed. CS and conventional reconstructions were compared at equal measurement time and evaluated in relation to high-SNR reference data. (19)F MR data were generated from a purpose-built phantom and benchmarked against simulations, as well as from the experimental autoimmune encephalomyelitis mouse model. We quantified the signal intensity bias and introduced an intensity calibration for in vivo data using high-SNR ex vivo data. RESULTS: Low-SNR (19)F MR data could be reliably reconstructed. Detection sensitivity was consistently improved and data fidelity was preserved for undersampling and averaging factors of α = 2 or = 3. Higher α led to signal blurring in the mouse model. The improved TPRs at α = 3 were comparable to a 2.5-fold increase in measurement time. Whereas CS resulted in a downward bias of the (19)F MR signal, Fourier reconstructions resulted in an unexpected upward bias of similar magnitude. The calibration corrected signal-intensity deviations for all reconstructions. CONCLUSION: CS is advantageous whenever image features are close to the detection threshold. It is a powerful tool, even for low-SNR data with sparsely distributed (19)F signals, to improve spatial and temporal resolution in (19)F MR applications

LEED Holography applied to a complex superstructure: a direct view of the adatom cluster on SiC(111)-(3x3)

For the example of the SiC(111)-(3x3) reconstruction we show that a holographic interpretation of discrete Low Energy Electron Diffraction (LEED) spot intensities arising from ordered, large unit cell superstructures can give direct access to the local geometry of a cluster around an elevated atom, provided there is only one such prominent atom per surface unit cell. By comparing the holographic images obtained from experimental and calculated data we illuminate validity, current limits and possible shortcomings of the method. In particular, we show that periodic vacancies such as cornerholes may inhibit the correct detection of the atomic positions. By contrast, the extra diffraction intensity due to slight substrate reconstructions, as for example buckling, seems to have negligible influence on the images. Due to the spatial information depth of the method the stacking of the cluster can be imaged down to the fourth layer. Finally, it is demonstrated how this structural knowledge of the adcluster geometry can be used to guide the dynamical intensity analysis subsequent to the holographic reconstruction and necessary to retrieve the full unit cell structure.Comment: 11 pages RevTex, 6 figures, Phys. Rev. B in pres

The role of calcium ions in toxic cell injury.

Calcium ions have been increasingly implicated as a mediator of the mechanisms generating lethal cell injury under a variety of pathologic circumstances. An overview of the various roles suggested for such alterations in cellular calcium homeostasis is presented. The central role of plasma membrane damage in the genesis of irreversible cell injury is used to divide the postulated roles for calcium ions into two major mechanisms. On the one hand, calcium ions have been proposed as mediators of the functional consequences of plasma membrane injury. An influx of extracellular calcium ions across a damaged permeability barrier and down a steep concentration gradient may convert potentially reversible injury into irreversible injury. On the other hand, alterations in intracellular calcium homeostasis are postulated to participate in the mechanisms generating potentially lethal plasma membrane injury. The release of calcium stores sequestered within intracellular organelles raises the cytosolic concentration of free calcium, a process that may activate, in turn, a number of membrane-disruptive processes. The data supporting these two distinct actions of calcium are reviewed and discussed

A METHODOLOGY FOR SIMULATION AND ASSESSMENT OF CONCENTRATED SOLAR POWER PLANTS

A thermal analysis of Concentrated Solar Power plants is conducted considering parabolic trough collectors (PTC), linear Fresnel collectors using direct steam generation scheme (LFC-DSG) and central receiver system using both molten nitrate salts (CRS-MNS) direct steam generation (CRS-DSG). The plant capacities were ranged from 50 to 800 MWth and the analysis focuses on the environmental conditions of selected locations in South America. Thus, the study considers a parametric analysis of the main design parameter for different plant scales, in terms of the thermal performance indicators as solar field aperture area, power block rating capacity and plant annual efficiencies. The annual production of the plants is calculated by using the Transient System Simulation program (TRNSYS), which considers a new component library developed for that purpose. This library is based in the open access models developed by the U.S National Renewable Energy Laboratory and currently employed by the System Advisor Model (SAM) program. In addition, a new fluid properties subroutine compatible with TRNSYS codes standards was developed, which uses the freeware CoolProp library. These approaches allowed to modify and create new configurations for CSP plants, e.g. thermal storage for the DSG scheme

Cigarette Smoke Initiates Oxidative Stress-Induced Cellular Phenotypic Modulation Leading to Cerebral Aneurysm Pathogenesis.

OBJECTIVE: Cigarette smoke exposure (CSE) is a risk factor for cerebral aneurysm (CA) formation, but the molecular mechanisms are unclear. Although CSE is known to contribute to excess reactive oxygen species generation, the role of oxidative stress on vascular smooth muscle cell (VSMC) phenotypic modulation and pathogenesis of CAs is unknown. The goal of this study was to investigate whether CSE activates a NOX (NADPH oxidase)-dependent pathway leading to VSMC phenotypic modulation and CA formation and rupture. APPROACH AND RESULTS: In cultured cerebral VSMCs, CSE increased expression of NOX1 and reactive oxygen species which preceded upregulation of proinflammatory/matrix remodeling genes (MCP-1, MMPs [matrix metalloproteinase], TNF-α, IL-1β, NF-κB, KLF4 [Kruppel-like factor 4]) and downregulation of contractile genes (SM-α-actin [smooth muscle α actin], SM-22α [smooth muscle 22α], SM-MHC [smooth muscle myosin heavy chain]) and myocardin. Inhibition of reactive oxygen species production and knockdown of NOX1 with siRNA or antisense decreased CSE-induced upregulation of NOX1 and inflammatory genes and downregulation of VSMC contractile genes and myocardin. p47phox-/- NOX knockout mice, or pretreatment with the NOX inhibitor, apocynin, significantly decreased CA formation and rupture compared with controls. NOX1 protein and mRNA expression were similar in p47phox-/- mice and those pretreated with apocynin but were elevated in unruptured and ruptured CAs. CSE increased CA formation and rupture, which was diminished with apocynin pretreatment. Similarly, NOX1 protein and mRNA and reactive oxygen species were elevated by CSE, and in unruptured and ruptured CAs. CONCLUSIONS: CSE initiates oxidative stress-induced phenotypic modulation of VSMCs and CA formation and rupture. These molecular changes implicate oxidative stress in the pathogenesis of CAs and may provide a potential target for future therapeutic strategies