Australian SMEs waste to landfill

Landfill waste has a negative impact on the environment and small and medium sized enterprises (SMEs) are believed to be significant contributors. There is little government or scholarly research, however, quantifying the collective volume of waste SMEs send to landfill. Where studies do exist they measure total volumes (landfill and recycling combined) and/or do not distinguish between specific waste streams (e.g. wood) and subcategories (e.g. dust). This paper contributes to knowledge by giving insight into the collective volume of waste of 404 SMEs, reconceptualising SME waste into subcategories and by measuring landfill volumes. It presents findings from these 404 Australian SMEs which found that, in descending order, cardboard, paper, plastic wrap, wood dust and particleboard were the subcategories these SMEs sent to landfill in the greatest volumes. It also argues that this reconceptualisation, and associated data collection protocols, have the potential to enable scholars and policy makers to determine the waste subcategories to which SMEs contribute most, formulate targeted interventions and research or evaluate environmental outcomes. © 2014 © 2014 Environment Institute of Australia and New Zealand Inc

Capturing accelerometer outputs in healthy volunteers under normal and simulated-pathological conditions using ML classifiers

Wearable devices offer a possible solution for acquiring objective measurements of physical activity. Most current algorithms are derived using data from healthy volunteers. It is unclear whether such algorithms are suitable in specific clinical scenarios, such as when an individual has altered gait. We hypothesized that algorithms trained on healthy population will result in less accurate results when tested in individuals with altered gait. We further hypothesized that algorithms trained on simulated-pathological gait would prove better at classifying abnormal activity.We studied healthy volunteers to assess whether activity classification accuracy differed for those with healthy and simulated-pathological conditions. Healthy participants (n=30) were recruited from the University of Leeds to perform nine predefined activities under healthy and simulated-pathological conditions. Activities were captured using a wrist-worn MOX accelerometer (Maastricht Instruments, NL). Data were analyzed based on the Activity-Recognition-Chain process. We trained a Neural-Network, Random-Forests, k-Nearest-Neighbors (k-NN), Support-Vector-Machines (SVM) and Naive Bayes models to classify activity. Algorithms were trained four times; once with 'healthy' data, and once with 'simulated-pathological data' for each of activity-type and activity-task classification. In activity-type instances, the SVM provided the best results; the accuracy was 98.4% when the algorithm was trained and then tested with unseen data from the same group of healthy individuals. Accuracy dropped to 52.8% when tested on simulated-pathological data. When the model was retrained with simulated-pathological data, prediction accuracy for the corresponding test set was 96.7%. Algorithms developed on healthy data are less accurate for pathological conditions. When evaluating pathological conditions, classifier algorithms developed using data from a target sub-population can restore accuracy to above 95%.Clinical Relevance - This method remotely establishes health-related data of objective outcome measures of activities of daily living

A differential identity for Green functions

If P is a differential operator with constant coefficients, an identity is derived to calculate the action of exp(P) on the product of two functions. In many-body theory, P describes the interaction Hamiltonian and the identity yields a hierarchy of Green functions. The identity is first derived for scalar fields and the standard hierarchy is recovered. Then the case of fermions is considered and the identity is used to calculate the generating function for the Green functions of an electron system in a time-dependent external potential.Comment: 14 page

Two-Loop Calculations with Vertex Corrections in the Walecka Model

Two-loop corrections with scalar and vector form factors are calculated for nuclear matter in the Walecka model. The on-shell form factors are derived from vertex corrections within the framework of the model and are highly damped at large spacelike momenta. The two-loop corrections are evaluated first by using the one-loop parameters and mean fields and then by refitting the total energy/baryon to empirical nuclear matter saturation properties. The modified two-loop corrections are significantly smaller than those computed with bare vertices. Contributions from the anomalous isoscalar form factor of the nucleon are included for the first time. The effects of the implicit density dependence of the form factors, which arise from the shift in the baryon mass, are also considered. Finally, necessary extensions of these calculations are discussed.Comment: 29 pages in REVTeX, 18 figures, preprint IU/NTC 94-02 //OSU--94-11

Expression of ABCA4 in the retinal pigment epithelium and its implications for Stargardt macular degeneration.

Recessive Stargardt disease (STGD1) is an inherited blinding disorder caused by mutations in the Abca4 gene. ABCA4 is a flippase in photoreceptor outer segments (OS) that translocates retinaldehyde conjugated to phosphatidylethanolamine across OS disc membranes. Loss of ABCA4 in Abca4 -/- mice and STGD1 patients causes buildup of lipofuscin in the retinal pigment epithelium (RPE) and degeneration of photoreceptors, leading to blindness. No effective treatment currently exists for STGD1. Here we show by several approaches that ABCA4 is additionally expressed in RPE cells. (i) By in situ hybridization analysis and by RNA-sequencing analysis, we show the Abca4 mRNA is expressed in human and mouse RPE cells. (ii) By quantitative immunoblotting, we show that the level of ABCA4 protein in homogenates of wild-type mouse RPE is about 1% of the level in neural retina homogenates. (iii) ABCA4 immunofluorescence is present in RPE cells of wild-type and Mertk -/- but not Abca4 -/- mouse retina sections, where it colocalizes with endolysosomal proteins. To elucidate the role of ABCA4 in RPE cells, we generated a line of genetically modified mice that express ABCA4 in RPE cells but not in photoreceptors. Mice from this line on the Abca4 -/- background showed partial rescue of photoreceptor degeneration and decreased lipofuscin accumulation compared with nontransgenic Abca4 -/- mice. We propose that ABCA4 functions to recycle retinaldehyde released during proteolysis of rhodopsin in RPE endolysosomes following daily phagocytosis of distal photoreceptor OS. ABCA4 deficiency in the RPE may play a role in the pathogenesis of STGD1

Complement C3 variant and the risk of age-related macular degeneration

Background: Age-related macular degeneration is the most common cause of blindness in Western populations. Susceptibility is influenced by age and by genetic and environmental factors. Complement activation is implicated in the pathogenesis.Methods: We tested for an association between age-related macular degeneration and 13 single-nucleotide polymorphisms (SNPs) spanning the complement genes C3 and C5 in case subjects and control subjects from the southeastern region of England. All subjects were examined by an ophthalmologist and had independent grading of fundus photographs to confirm their disease status. To test for replication of the most significant findings, we genotyped a set of Scottish cases and controls.Results: The common functional polymorphism rs2230199 (Arg80Gly) in the C3 gene, corresponding to the electrophoretic variants C3S (slow) and C3F (fast), was strongly associated with age-related macular degeneration in both the English group (603 cases and 350 controls, P=5.9 x 10(sup -5)) and the Scottish group (244 cases and 351 controls, P=5.0 x 10(sup -5)). The odds ratio for age-related macular degeneration in C3 S/F heterozygotes as compared with S/S homozygotes was 1.7 (95% confidence interval [CI], 1.3 to 2.1); for F/F homozygotes, the odds ratio was 2.6 (95% CI, 1.6 to 4.1). The estimated population attributable risk for C3F was 22%.Conclusions: Complement C3 is important in the pathogenesis of age-related macular degeneration. This finding further underscores the influence of the complement pathway in the pathogenesis of this disease