Project Energize: intervention development and 10 years of progress in preventing childhood obesity

Prevention of childhood obesity is a global priority. The school setting offers access to large numbers of children and the ability to provide supportive environments for quality physical activity and nutrition. This article describes Project Energize, a through-school physical activity and nutrition programme that celebrated its 10-year anniversary in 2015 so that it might serve as a model for similar practices, initiatives and policies elsewhere. The programme was envisaged and financed by the Waikato District Health Board of New Zealand in 2004 and delivered by Sport Waikato to 124 primary schools as a randomised controlled trial from 2005 to 2006. The programme has since expanded to include all 242 primary schools in the Waikato region and 70 schools in other regions, including 53,000 children. Ongoing evaluation and development of Project Energize has shown it to be sustainable (ongoing for >10 years), both effective (lower obesity, higher physical fitness) and cost effective (one health related cost quality adjusted life year between $18,000 and$30,000) and efficient ($45/child/year) as a childhood 'health' programme. The programme's unique community-based approach is inclusive of all children, serving a population that is 42 % Ma¯ori, the indigenous people of New Zealand. While the original nine healthy eating and seven quality physical activity goals have not changed, the delivery and assessment processes has been refined and the health service adapted over the 10 years of the programme existence, as well as adapted over time to other settings including early childhood education and schools in Cork in Ireland. Evaluation and research associated with the programme delivery and outcomes are ongoing. The dissemination of findings to politicians and collaboration with other service providers are both regarded as priorities

Resistivity due to a Domain Wall in Ferromagnetic Metal

The resistivity due to a domain wall in ferromagnetic metallic wire is calculated based on the linear response theory. The interaction between conduction electrons and the wall is expressed in terms of a classical gauge field which is introduced by the local gauge transformation in the electron spin space. It is shown that the wall contributes to the decoherence of electrons and that this quantum correction can dominate over the Boltzmann resisitivity, leading to a decrease of resisitivity by nucleation of a wall. The conductance fluctuation due to the motion of the wall is also investigated. The results are compared with recent experiments.Comment: 9 pages, 3 figure

Quantum Relaxation of Magnetisation in Magnetic Particles

At temperatures below the magnetic anisotropy energy, monodomain magnetic systems (small particles, nanomagnetic devices, etc.) must relax quantum mechanically. This quantum relaxation must be mediated by the coupling to both nuclear spins and phonons (and electrons if either particle or substrate is conducting. We analyze the effect of each of these couplings, and then combine them. Conducting systems can be modelled by a "giant Kondo" Hamiltonian, with nuclear spins added in as well. At low temperatures, even microscopic particles on a conducting substrate (containing only $10-50$ spins) will have their magnetisation frozen over millenia by a combination of electronic dissipation and the "degeneracy blocking" caused by nuclear spins. Raising the temperature leads to a sudden unblocking of the spin dynamics at a well defined temperature. Insulating systems are quite different. The relaxation is strongly enhanced by the coupling to nuclear spins. At short times the magnetisation of an ensemble of particles relaxes logarithmically in time, after an initial very fast decay; this relaxation proceeds entirely via the nuclear spins. At longer times phonons take over, but the decay rate is still governed by the temperature-dependent nuclear bias field acting on the particles - decay may be exponential or power-law depending on the temperature. The most surprising feature of the results is the pivotal role played by the nuclear spins. The results are relevant to any experiments on magnetic particles in which interparticle dipolar interactions are unimportant. They are also relevant to future magnetic device technology.Comment: 30 pages, RevTex, e:mail , Submitted to J.Low Temp.Phys. on 1 Nov. 199

Noise Probe of the Dynamic Phase Separation in La2/3Ca1/3MnO3

Giant Random Telegraph Noise (RTN) in the resistance fluctuation of a macroscopic film of perovskite-type manganese oxide La2/3Ca1/3MnO3 has been observed at various temperatures ranging from 4K to 170K, well below the Curie temperature (TC = 210K). The amplitudes of the two-level-fluctuations (TLF) vary from 0.01% to 0.2%. We use a statistical analysis of the life-times of the TLF to gain insight into the microscopic electronic and magnetic state of this manganite. At low temperature (below 30K) The TLF is well described by a thermally activated two-level model. An estimate of the energy difference between the two states is inferred. At higher temperature (between 60K and 170K) we observed critical effects of the temperature on the life-times of the TLF. We discuss this peculiar temperature dependence in terms of a sharp change in the free energy functional of the fluctuators. We attribute the origin of the RTN to be a dynamic mixed-phase percolative conduction process, where manganese clusters switch back and forth between two phases that differ in their conductivity and magnetization.Comment: 15 pages, PDF only, Phys. Rev. Lett. (in press

Speech delays and behavioral problems are the predominant features in individuals with developmental delays and 16p11.2 microdeletions and microduplications

Microdeletions and microduplications encompassing a ~593-kb region of 16p11.2 have been implicated as one of the most common genetic causes of susceptibility to autism/autism spectrum disorder (ASD). We report 45 microdeletions and 32 microduplications of 16p11.2, representing 0.78% of 9,773 individuals referred to our laboratory for microarray-based comparative genomic hybridization (aCGH) testing for neurodevelopmental and congenital anomalies. The microdeletion was de novo in 17 individuals and maternally inherited in five individuals for whom parental testing was available. Detailed histories of 18 individuals with 16p11.2 microdeletions were reviewed; all had developmental delays with below-average intelligence, and a majority had speech or language problems or delays and various behavioral problems. Of the 16 individuals old enough to be evaluated for autism, the speech/behavior profiles of seven did not suggest the need for ASD evaluation. Of the remaining nine individuals who had speech/behavior profiles that aroused clinical suspicion of ASD, five had formal evaluations, and three had PDD-NOS. Of the 19 microduplications with parental testing, five were de novo, nine were maternally inherited, and five were paternally inherited. A majority with the microduplication had delayed development and/or specific deficits in speech or language, though these features were not as consistent as seen with the microdeletions. This study, which is the largest cohort of individuals with 16p11.2 alterations reported to date, suggests that 16p11.2 microdeletions and microduplications are associated with a high frequency of cognitive, developmental, and speech delay and behavior abnormalities. Furthermore, although features associated with these alterations can be found in individuals with ASD, additional factors are likely required to lead to the development of ASD

Systems biology of platelet-vessel wall interactions

Platelets are small, anucleated cells that participate in primary hemostasis by forming a hemostatic plug at the site of a blood vessel's breach, preventing blood loss. However, hemostatic events can lead to excessive thrombosis, resulting in life-threatening strokes, emboli, or infarction. Development of multi-scale models coupling processes at several scales and running predictive model simulations on powerful computer clusters can help interdisciplinary groups of researchers to suggest and test new patient-specific treatment strategies

Chromosome microarray analysis as first-line test in pregnancies with a priori low risk for detection of submicroscopic chromosomal abnormalities

n this study, we aimed to explore the utility of chromosomal microarray analysis (CMA) in groups of pregnancies with a priori low risk for detection of submicroscopic chromosome abnormalities, usually not considered an indication for testing, in order to assess whether CMA improves the detection rate of prenatal chromosomal aberrations. A total of 3000 prenatal samples were processed in parallel using both whole-genome CMA and conventional karyotyping. The indications for prenatal testing included: advanced maternal age, maternal serum screening test abnormality, abnormal ultrasound findings, known abnormal fetal karyotype, parental anxiety, family history of a genetic condition and cell culture failure. The use of CMA resulted in an increased detection rate regardless of the indication for analysis. This was evident in high risk groups (abnormal ultrasound findings and abnormal fetal karyotype), in which the percentage of detection was 5.8% (7/120), and also in low risk groups, such as advanced maternal age (6/1118, 0.5%), and parental anxiety (11/1674, 0.7%). A total of 24 (0.8%) fetal conditions would have remained undiagnosed if only a standard karyotype had been performed. Importantly, 17 (0.6%) of such findings would have otherwise been overlooked if CMA was offered only to high risk pregnancies.The results of this study suggest that more widespread CMA testing of fetuses would result in a higher detection of clinically relevant chromosome abnormalities, even in low risk pregnancies. Our findings provide substantial evidence for the introduction of CMA as a first-line diagnostic test for all pregnant women undergoing invasive prenatal testing, regardless of risk factors

Allele-Specific Virulence Attenuation of the Pseudomonas syringae HopZ1a Type III Effector via the Arabidopsis ZAR1 Resistance Protein

Plant resistance (R) proteins provide a robust surveillance system to defend against potential pathogens. Despite their importance in plant innate immunity, relatively few of the ∼170 R proteins in Arabidopsis have well-characterized resistance specificity. In order to identify the R protein responsible for recognition of the Pseudomonas syringae type III secreted effector (T3SE) HopZ1a, we assembled an Arabidopsis R gene T–DNA Insertion Collection (ARTIC) from publicly available Arabidopsis thaliana insertion lines and screened it for plants lacking HopZ1a-induced immunity. This reverse genetic screen revealed that the Arabidopsis R protein HOPZ-ACTIVATED RESISTANCE 1 (ZAR1; At3g50950) is required for recognition of HopZ1a in Arabidopsis. ZAR1 belongs to the coiled-coil (CC) class of nucleotide binding site and leucine-rich repeat (NBS–LRR) containing R proteins; however, the ZAR1 CC domain phylogenetically clusters in a clade distinct from other related Arabidopsis R proteins. ZAR1–mediated immunity is independent of several genes required by other R protein signaling pathways, including NDR1 and RAR1, suggesting that ZAR1 possesses distinct signaling requirements. The closely-related T3SE protein, HopZ1b, is still recognized by zar1 Arabidopsis plants indicating that Arabidopsis has evolved at least two independent R proteins to recognize the HopZ T3SE family. Also, in Arabidopsis zar1 plants HopZ1a promotes P. syringae growth indicative of an ancestral virulence function for this T3SE prior to the evolution of recognition by the host resistance protein ZAR1. Our results demonstrate that the Arabidopsis resistance protein ZAR1 confers allele-specific recognition and virulence attenuation of the Pseudomonas syringae T3SE protein HopZ1a