992 resultados para show cause


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Victoria Nourse has observed that political debates about crime legislation are predictable and invariably one-sided because ‘no-one is “for” crime.’1 This certainly appears to be the case with regard to recent proposed changes to the Bail Act 1977 (‘the Act’) by the government of Victoria. The reforms were triggered by the case of Sean Price, an offender with a history of mental disorder, serious offending and lengthy incarceration who was on bail and subject to a supervision order when he murdered Masa Vukotic, raped another woman and assaulted a third person in March 2015. The Premier of Victoria, Daniel Andrews, stated that a bail system that allowed Price to be free and unmonitored was failing the community and pledged to repair ‘a system that is broken.’

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Police officers are exposed to impact noise coming from firearms, which may cause irreversible injuries to the hearing system.Aim: To evaluate the noise exposure in shooting stands during gunfire exercises, to analyze the acoustic impact of the noise produced by the firearms and to associate it with tonal audiometry results.Study design: Cross-sectional.Materials and methods: To measure noise intensity we used a digital sound level meter, and the acoustic analysis was carried out by means of the oscillations and cochlear response curves provided by the Praat software. 30 police officers were selected (27 males and 3 females).Results: The peak level measured was 113.1 dB(C) from a .40 pistol and 116.8 dB(C) for a .38 revolver. The values obtained for oscillation and Praat was 17.9 +/- 0.3 Barks, corresponding to the rate of 4,120 and 4,580 Hz. Audiometry indicated greater hearing loss at 4,000Hz in 86.7% of the cases.Conclusion: With the acoustic analysis it was possible to show cause and effect between the main areas of energy excitation of the cochlea (Praat cochlear response curve) and the frequencies of low hearing acuity.

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Utilizando dados observacionais de precipitação e temperatura do ar para o período de 1967 a 2008, do qual se elaborou a climatologia destas variáveis, e analisando as condições atmosféricas influenciadas pelo fenômeno ENOS, pretende-se identificar, caracterizar e analisar os efeitos térmicos espaciais na cidade de Belém-PA, a partir de dados meteorológicos de superfície e de imagens do sensor MODIS, o qual está disposto sobre a plataforma do satélite Aqua. Observou-se que, a média da precipitação anual foi de 2978,6 mm/ano, e que apresenta tendência de aumento ao longo dos anos, comportamento semelhante observou-se para a temperatura do ar. Em geral, os resultados mostram dois núcleos de maiores intensidade de temperaturas da superfície, um na cidade de Belém e outro na cidade vizinha, Ananindeua. Estes variam espacialmente e temporalmente de intensidade. Durante eventos de La Niña, o núcleo da ilha de calor fica localizado em bairros mais próximos a baía do Guajará, enquanto que durante eventos de El Niño estes bairros apresentam temperaturas mais amenas do que os bairros mais afastados dos corpos hídricos. Observou-se ainda que, a amplitude térmica da temperatura superficial entre áreas urbana e rural variam bastante, com a maior variação de 30,8°C e a menor de 16,8°C. Neste sentido, as maiores temperaturas da superfície foram observadas nos bairros com baixo NDVI, conseqüência de uma urbanização mais densa. As superfícies urbanas e as superfícies vegetadas apresentam relações de causa e efeito muito próximas, principalmente, durante o período menos chuvoso, isto pode ser percebido pela correlação que apresenta valor acima de 50%. Este estudo apresenta resultados que auxiliam no melhor entendimento do comportamento e dos efeitos térmicos espaciais e temporais na cidade de Belém, pois o uso de imagens do satélite é de fundamental importância para a identificação e caracterização das condições ambientais climáticas e ilhas de calor urbanas.

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Funding Some of author A’s research alluded to here was conducted while on a Leverhulme Senior Research Fellowship. Author B’s research is supported by the ESRC Research Centre XXX.

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The relationship between temperature and mortality is non-linear and the effect estimates depend on the threshold temperatures selected. However, little is known about whether threshold temperatures differ with age or cause of deaths in the Southern Hemisphere. We conducted polynomial distributed lag non-linear models to assess the threshold temperatures for mortality from all ages (Dall), aged from 15 to 64 (D15-64), 65- 84(D65-84), ≥85 years (D85+), respiratory (RD) and cardiovascular diseases (CVD) in Brisbane, Australia, 1996–2004. We examined both hot and cold thresholds, and the lags of up to 15 days for cold effects and 3 days for hot effects. Results show that for the current day, the cold threshold was 20°C and the hot threshold was 28°C for the groups of Dall, D15-64 and D85+. The cold threshold was higher (23°C) for the group of D65-84 and lower (21°C) for the group of CVD. The hot threshold was higher (29°C) for the group of D65-84 and lower (27°C) for the group of RD. Compared to the current day, for the cold effects of up to 15-day lags, the threshold was lower for the group of D15-64, and the thresholds were higher for the groups of D65-84, D85+, RD and CVD; while for the hot effects of 3-day lags, the threshold was higher for the group of D15-64 and the thresholds were lower for the groups of D65-84 and RD. Temperature thresholds appeared to differ with age and death categories. The elderly and deaths from RD and CVD were more sensitive to temperature stress than the adult group. These findings may have implications in the assessment of temperature-related mortality and development of weather/health warning systems.

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The life history strategies of massive Porites corals make them a valuable resource not only as key providers of reef structure, but also as recorders of past environmental change. Yet recent documented evidence of an unprecedented increase in the frequency of mortality in Porites warrants investigation into the history of mortality and associated drivers. To achieve this, both an accurate chronology and an understanding of the life history strategies of Porites are necessary. Sixty-two individual Uranium–Thorium (U–Th) dates from 50 dead massive Porites colonies from the central inshore region of the Great Barrier Reef (GBR) revealed the timing of mortality to have occurred predominantly over two main periods from 1989.2 ± 4.1 to 2001.4 ± 4.1, and from 2006.4 ± 1.8 to 2008.4 ± 2.2 A.D., with a small number of colonies dating earlier. Overall, the peak ages of mortality are significantly correlated with maximum sea-surface temperature anomalies. Despite potential sampling bias, the frequency of mortality increased dramatically post-1980. These observations are similar to the results reported for the Southern South China Sea. High resolution measurements of Sr/Ca and Mg/Ca obtained from a well preserved sample that died in 1994.6 ± 2.3 revealed that the time of death occurred at the peak of sea surface temperatures (SST) during the austral summer. In contrast, Sr/Ca and Mg/Ca analysis in two colonies dated to 2006.9 ± 3.0 and 2008.3 ± 2.0, suggest that both died after the austral winter. An increase in Sr/Ca ratios and the presence of low Mg-calcite cements (as determined by SEM and elemental ratio analysis) in one of the colonies was attributed to stressful conditions that may have persisted for some time prior to mortality. For both colonies, however, the timing of mortality coincides with the 4th and 6th largest flood events reported for the Burdekin River in the past 60 years, implying that factors associated with terrestrial runoff may have been responsible for mortality. Our results show that a combination of U–Th and elemental ratio geochemistry can potentially be used to precisely and accurately determine the timing and season of mortality in modern massive Porites corals. For reefs where long-term monitoring data are absent, the ability to reconstruct historical events in coral communities may prove useful to reef managers by providing some baseline knowledge on disturbance history and associated drivers.

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Bidirectional (anterograde and retrograde) motor-based intraflagellar transport (IFT) governs cargo transport and delivery processes that are essential for primary cilia growth and maintenance and for hedgehog signaling functions. The IFT dynein-2 motor complex that regulates ciliary retrograde protein transport contains a heavy chain dynein ATPase/motor subunit, DYNC2H1, along with other less well functionally defined subunits. Deficiency of IFT proteins, including DYNC2H1, underlies a spectrum of skeletal ciliopathies. Here, by using exome sequencing and a targeted next-generation sequencing panel, we identified a total of 11 mutations in WDR34 in 9 families with the clinical diagnosis of Jeune syndrome (asphyxiating thoracic dystrophy). WDR34 encodes a WD40 repeat-containing protein orthologous to Chlamydomonas FAP133, a dynein intermediate chain associated with the retrograde intraflagellar transport motor. Three-dimensional protein modeling suggests that the identified mutations all affect residues critical for WDR34 protein-protein interactions. We find that WDR34 concentrates around the centrioles and basal bodies in mammalian cells, also showing axonemal staining. WDR34 coimmunoprecipitates with the dynein-1 light chain DYNLL1 in vitro, and mining of proteomics data suggests that WDR34 could represent a previously unrecognized link between the cytoplasmic dynein-1 and IFT dynein-2 motors. Together, these data show that WDR34 is critical for ciliary functions essential to normal development and survival, most probably as a previously unrecognized component of the mammalian dynein-IFT machinery.

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Serum gamma-glutamyl transferase (GGT) activity is a marker of liver disease which is also prospectively associated with the risk of all-cause mortality, cardiovascular disease, type 2 diabetes and cancers. We have discovered novel loci affecting GGT in a genome-wide association study (rs1497406 in an intergenic region of chromosome 1, P = 3.9 x 10(-8); rs944002 in C14orf73 on chromosome 14, P = 4.7 x 10(-13); rs340005 in RORA on chromosome 15, P = 2.4 x 10(-8)), and a highly significant heterogeneity between adult and adolescent results at the GGT1 locus on chromosome 22 (maximum P(HET) = 5.6 x 10(-12) at rs6519520). Pathway analysis of significant and suggestive single-nucleotide polymorphism associations showed significant overlap between genes affecting GGT and those affecting common metabolic and inflammatory diseases, and identified the hepatic nuclear factor (HNF) family as controllers of a network of genes affecting GGT. Our results reinforce the disease associations of GGT and demonstrate that control by the GGT1 locus varies with age.

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Multiwavelength data indicate that the X-ray-emitting plasma in the cores of galaxy clusters is not cooling catastrophically. To a large extent, cooling is offset by heating due to active galactic nuclei (AGNs) via jets. The cool-core clusters, with cooler/denser plasmas, show multiphase gas and signs of some cooling in their cores. These observations suggest that the cool core is locally thermally unstable while maintaining global thermal equilibrium. Using high-resolution, three-dimensional simulations we study the formation of multiphase gas in cluster cores heated by collimated bipolar AGN jets. Our key conclusion is that spatially extended multiphase filaments form only when the instantaneous ratio of the thermal instability and free-fall timescales (t(TI)/t(ff)) falls below a critical threshold of approximate to 10. When this happens, dense cold gas decouples from the hot intracluster medium (ICM) phase and generates inhomogeneous and spatially extended Ha filaments. These cold gas clumps and filaments ``rain'' down onto the central regions of the core, forming a cold rotating torus and in part feeding the supermassive black hole. Consequently, the self-regulated feedback enhances AGN heating and the core returns to a higher entropy level with t(TI)/t(ff) > 10. Eventually, the core reaches quasi-stable global thermal equilibrium, and cold filaments condense out of the hot ICM whenever t(TI)/t(ff) less than or similar to 10. This occurs despite the fact that the energy from AGN jets is supplied to the core in a highly anisotropic fashion. The effective spatial redistribution of heat is enabled in part by the turbulent motions in the wake of freely falling cold filaments. Increased AGN activity can locally reverse the cold gas flow, launching cold filamentary gas away from the cluster center. Our criterion for the condensation of spatially extended cold gas is in agreement with observations and previous idealized simulations.

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The roles of myosin during muscle contraction are well studied, but how different domains of this protein are involved in myofibril assembly in vivo is far less understood. The indirect flight muscles (IFMs) of Drosophila melanogaster provide a good model for understanding muscle development and function in vivo. We show that two missense mutations in the rod region of the myosin heavy-chain gene, Mhc, give rise to IFM defects and abnormal myofibrils. These defects likely result from thick filament abnormalities that manifest during early sarcomere development or later by hypercontraction. The thick filament defects are accompanied by marked reduction in accumulation of flightin, a myosin binding protein, and its phosphorylated forms, which are required to stabilise thick filaments. We investigated with purified rod fragments whether the mutations affect the coiled-coil structure, rod aggregate size or rod stability. No significant changes in these parameters were detected, except for rod thermodynamic stability in one mutation. Molecular dynamics simulations suggest that these mutations may produce localised rod instabilities. We conclude that the aberrant myofibrils are a result of thick filament defects, but that these in vivo effects cannot be detected in vitro using the biophysical techniques employed. The in vivo investigation of these mutant phenotypes in IFM development and function provides a useful platform for studying myosin rod and thick filament formation generically, with application to the aetiology of human myosin rod myopathies. (C) 2012 Elsevier Ltd. All rights reserved.

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VCP (VCP/p97) is a ubiquitously expressed member of the AAA(+)-ATPase family of chaperone-like proteins that regulates numerous cellular processes including chromatin decondensation, homotypic membrane fusion and ubiquitin-dependent protein degradation by the proteasome. Mutations in VCP cause a multisystem degenerative disease consisting of inclusion body myopathy, Paget disease of bone, and frontotemporal dementia (IBMPFD). Here we show that VCP is essential for autophagosome maturation. We generated cells stably expressing dual-tagged LC3 (mCherry-EGFP-LC3) which permit monitoring of autophagosome maturation. We determined that VCP deficiency by RNAi-mediated knockdown or overexpression of dominant-negative VCP results in significant accumulation of immature autophagic vesicles, some of which are abnormally large, acidified and exhibit cathepsin B activity. Furthermore, expression of disease-associated VCP mutants (R155H and A232E) also causes this autophagy defect. VCP was found to be essential to autophagosome maturation under basal conditions and in cells challenged by proteasome inhibition, but not in cells challenged by starvation, suggesting that VCP might be selectively required for autophagic degradation of ubiquitinated substrates. Indeed, a high percentage of the accumulated autophagic vesicles contain ubiquitin-positive contents, a feature that is not observed in autophagic vesicles that accumulate following starvation or treatment with Bafilomycin A. Finally, we show accumulation of numerous, large LAMP-1 and LAMP-2-positive vacuoles and accumulation of LC3-II in myoblasts derived from patients with IBMPFD. We conclude that VCP is essential for maturation of ubiquitin-containing autophagosomes and that defect in this function may contribute to IBMPFD pathogenesis.

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Human papillomavirus type 16 proteins E6 and E7 have been shown to cause centrosome amplification and lagging chromosomes during mitosis. These abnormalities during mitosis can result in missegregation of the chromosomes, leading to chromosomal instability. Genomic instability is thought to be an essential part of the conversion of a normal cell to a cancer cell. We now show that E6 and E7 together cause polyploidy in primary human keratinocytes soon after these genes are introduced into the cells. Polyploidy seems to result from a spindle checkpoint failure arising from abrogation of the normal functions of p53 and retinoblastoma family members by E6 and E7, respectively. In addition, E6 and E7 cause deregulation of cellular genes such as Plk1, Aurora-A, cdk1, and Nek2, which are known to control the G2-M-phase transition and the ordered progression through mitosis.

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Animals often show behavioural plasticity with respect to predation risk but also show behavioural syndromes in terms of consistency of responses to different stimuli. We examine these features in the freshwater pearl mussel. These bivalves often aggregate presumably to reduce predation risk to each individual. Predation risk, however, will be higher in the presence of predator cues. Here we use dimming light, vibration and touch as novel stimuli to examine the trade-off between motivation to feed and motivation to avoid predation. We present two experiments that each use three sequential novel stimuli to cause the mussels to close their valves and hence cease feeding. We find that mussels within a group showed shorter closure times than solitary mussels, consistent with decreased vulnerability to predation in group-living individuals. Mussels exposed to the odour of a predatory crayfish showed longer closures than control mussels, highlighting the predator assessment abilities of this species. However, individuals showed significant consistency in their closure responses across the trial series, in line with behavioural syndrome theory. Our results show that bivalves trade-off feeding and predator avoidance according to predation risk but the degree to which this is achieved is constrained by behavioural consistency. © 2011 Elsevier B.V.