Planar shape manipulation using approximate geometric primitives

We present robust algorithms for set operations and Euclidean transformations of curved shapes in the plane using approximate geometric primitives. We use a refinement algorithm to ensure consistency. Its computational complexity is \bigo(n\log n+k) for an input of size $n$ with k=\bigo(n^2) consistency violations. The output is as accurate as the geometric primitives. We validate our algorithms in floating point using sequences of six set operations and Euclidean transforms on shapes bounded by curves of algebraic degree~1 to~6. We test generic and degenerate inputs. Keywords: robust computational geometry, plane subdivisions, set operations

Food policies for physical and mental health

Noncommunicable diseases (NCDs) account for the largest burden of early mortality and are predicted to cost the global community more than US $30 trillion over the next 20 years. Unhealthy dietary habits, in large part driven by substantial changes to global food systems, are recognised as major contributors to many of the common NCDs, including cardiovascular disease, cancer and diabetes. Recent evidence now indicates that unhealthy diets are also risk factors for mental disorders, particularly depression and dementia. This affords substantial scope to leverage on the established and developing approaches to the nutrition-related NCDs to address the large global burden of these mental disorders and reinforces the imperative for governments take substantial actions in regards to improving the food environment and consequent population health via policy initiatives

'Maximising shareholder value’: a detailed insight into the corporate political activity of the Australian food industry

Objective: To gain deeper insight into the corporate political activity (CPA) of the Australian food industry from a public health perspective. Methods: Fifteen interviews with a purposive sample of current and former policy makers, public health advocates and academics who have closely interacted with food industry representatives or observed food industry behaviours. Results: All participants reported having directly experienced the CPA of the food industry during their careers, with the ‘information and messaging’ and ‘constituency building’ strategies most prominent. Participants expressed concern that food industry CPA strategies resulted in weakened policy responses to addressing diet-related disease. Conclusions: This study provides direct evidence of food industry practices that have the potential to shape public health-related policies and programs in Australia in ways that favour business interests at the expense of population health. Implications for public health: This evidence can inform policy makers and public health advocates and be used to adopt measures to ensure that public interests are put at the forefront as part of the policy development and implementation process

Synergy between type 1 fimbriae expression and C3 opsonisation increases internalisation of E. coli by human tubular epithelial cells

<p>Abstract</p> <p>Background</p> <p>Bacterial infection of the urinary tract is a common clinical problem with <it>E. coli </it>being the most common urinary pathogen. Bacterial uptake into epithelial cells is increasingly recognised as an important feature of infection. Bacterial virulence factors, especially fimbrial adhesins, have been conclusively shown to promote host cell invasion. Our recent study reported that C3 opsonisation markedly increases the ability of <it>E. coli </it>strain J96 to internalise into human proximal tubular epithelial cells via CD46, a complement regulatory protein expressed on host cell membrane. In this study, we further assessed whether C3-dependent internalisation by human tubular epithelial cells is a general feature of uropathogenic <it>E. coli </it>and investigated features of the bacterial phenotype that may account for any heterogeneity.</p> <p>Results</p> <p>In 31 clinical isolates of <it>E. coli </it>tested, C3-dependent internalisation was evident in 10 isolates. Type 1 fimbriae mediated-binding is essential for C3-dependent internalisation as shown by phenotypic association, type 1 fimbrial blockade with soluble ligand (mannose) and by assessment of a type 1 fimbrial mutant.</p> <p>Conclusion</p> <p>we propose that efficient internalisation of uropathogenic <it>E. coli </it>by the human urinary tract depends on co-operation between type 1 fimbriae-mediated adhesion and C3 receptor -ligand interaction.</p

Analysis of complement C4 loci in Caucasoids and Japanese with idiopathic membranous nephropathy

Analysis of complement C4 loci in Caucasoids and Japanese with idiopathic membranous nephropathy. Deletion of the HLA class III complement gene, C4A, has been linked with susceptibility to a number of autoimmune diseases. In this study, we show a strong positive association between C4A gene deletion and development of idiopathic membranous nephropathy (IMN) in European Caucasoids [patients, 17/27 (63%); healthy controls, 13/65 (20%); RR 6.8; P = 0.003]. To clarify whether C4A deletion is an independent risk factor for IMN or is increased secondarily to the Caucasoid HLA A1, B8, DR3 extended haplotype, we examined the frequency of C4A deletion in Japanese patients, in whom the disease is associated with another HLA haplotype (DR2-DQw1). Analysis of 31 Japanese patients and 46 healthy controls showed that C4A deletion was present in only one patient (3%) and one control (2%). In addition, examination of the C4B locus in Japanese patients showed that there was no significant increase in the estimated frequency of C4B deletion in patients against controls (31 vs. 27%) and no difference in the frequency of the C4B long gene (73 vs. 87%) or C4B short gene (77 vs. 78%). We conclude that although C4A deletion confers significant risk of IMN in Caucasoids, there is no significant association between C4 polymorphism, as detected here, and risk of IMN in Japanese. This suggests that either C4A deletion is irrelevant to the pathogenesis of IMN or that more than one genetic mechanism is involved

Effect of Dietary Composition of Weight Loss Diets on High Sensitivity C-Reactive Protein: The Randomized POUNDS LOST Trial

Overweight and obesity are associated with increased high sensitivity C-reactive protein (hsCRP) levels. The purpose of this study was to determine if weight loss diets differing in fat, protein, or carbohydrate composition differentially reduce hsCRP. POUNDS (Preventing Overweight Using Novel Dietary Strategies) LOST was a two-year trial of overweight and obese adults randomly allocated to one of four weight loss diets with targeted percentages of energy derived from fat, protein, and carbohydrates (20,15,65%;20,25,55%;40,15,45%;40,25,35%, respectively). hsCRP was measured at baseline, 6, and 24 months among 710 participants, and adiposity as measured by dual X-ray absorptiometry (N=340) or abdominal computed tomography (N=126) was correlated with hsCRP change. At 6 months, hsCRP was reduced in all trial participants by −24.7% (IQR +7%,−50%), weight by −6.7% (IQR −3%,−11%), and waist circumference by −6.0% (IQR −3%,−10%) (all P<.002), with no significant differences according to dietary composition. The percent change in hsCRP at 6 and 24 months correlated modestly with change in weight, waist circumference, fasting insulin, fasting glucose, HOMA, and most lipid levels. Reductions in hsCRP persisted despite an approximate 50% regain of weight by 24 months. The percent change in hsCRP at 24 months significantly correlated with changes in total body fat (r=0.42), total abdominal adiposity (r=0.52), subcutaneous abdominal adiposity (r=0.52), visceral adiposity (r=0.47), and hepatic tissue density (r=−0.34) (all P<0.0006). In conclusion, weight loss decreased hsCRP by similar magnitude, irrespective of dietary composition. Clinicians concerned about inflammation and cardiovascular risk should recommend weight loss diets most likely to succeed for their patients

FcγRIII and FcγRIV are indispensable for acute glomerular inflammation induced by switch variant monoclonal antibodies

The relative ability of IgG subclasses to cause acute inflammation, and the roles of specific effector mechanisms in this process is not clear. We explored this in an in vivo model of glomerular inflammation in the mouse. TNP was planted on the glomerular basement membrane after conjugation to nephrotoxic antibody. The relative nephritogenicity of anti-TNP switch-variant monoclonal antibodies was then explored and shown to be IgG2a>IgG2b, with no disease caused by IgG1. Using knockout mice, we showed that FcγRIII was necessary for both neutrophil influx and glomerular damage induced by IgG2a and IgG2b. Surprisingly IgG1 did not cause disease although it binds to FcγRIII. Using blocking antibodies, we showed that this was explained by an additional requirement for FcγRIV which does not bind to IgG1. IgG2a or IgG2b induced neutrophil influx was not affected by deficiency of either FcγRI or C3. Bone marrow chimeras were constructed to test the effect of combined deficiency of FcγRI and C3, and there was no effect on IgG2a or IgG2b mediated neutrophil influx. However, IgG2b-induced albuminuria and thrombosis was reduced in C3 deficient mice, showing an additional role for complement in IgG2b-mediated glomerular damage. The results show that IgG2a and IgG2b are the pathogenic subclasses in acute neutrophil-mediated glomerular inflammation, with an indispensible role for both FcγRIII and FcγRIV. In addition complement contributes to IgG2b induced glomerular injury