338 resultados para diesel common rail albero motore


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Numerous Abaqus [1] finite element analyses have been carried out using various plasticity models to investigate the effect of friction force on the rail head in relation to both the development of the accumulated plastic strain (PEEQ) and the changes in the depth of PEEQ distribution in the wheel-rail contact. The normal force distribution on the rail head was assumed to be Hertzian. The tangential force was implemented as a fraction of the normal force in the subroutine. Each analysis was carried out for a single pass and the effect of various friction coefficient values has been observed.

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This paper describes the work being conducted in the baseline rail level crossing project, supported by the Australian rail industry and the Cooperative Research Centre for Rail Innovation. The paper discusses the limitations of near-miss data for analysis obtained using current level crossing occurrence reporting practices. The project is addressing these limitations through the development of a data collection and analysis system with an underlying level crossing accident causation model. An overview of the methodology and improved data recording process are described. The paper concludes with a brief discussion of benefits this project is expected to provide the Australian rail industry.

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Migraine is a common neurological disorder characterised by temporary disabling attacks of severe head pain and associated disturbances. There is significant evidence to suggest a genetic aetiology to the disease however few causal mutations have been conclusively linked to the migraine subtypes Migraine with (MA) or without Aura (MO). The Potassium Channel, Subfamily K, member 18 (KCNK18) gene, coding the potassium channel TRESK, is the first gene in which a rare mutation resulting in a non-functional truncated protein has been identified and causally linked to MA in a multigenerational family. In this study, three common polymorphisms in the KCNK18 gene were analysed for genetic variation in an Australian case-control migraine population consisting of 340 migraine cases and 345 controls. No association was observed for the polymorphisms examined with the migraine phenotype or with any haplotypes across the gene. Therefore even though the KCNK18 gene is the only gene to be causally linked to MA our studies indicate that common genetic variation in the gene is not a contributor to MA.

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This thesis represents a major step forward in understanding the link between the development of combustion related faults in diesel engines and the generation of acoustic emissions. The findings presented throughout the thesis provide a foundation so that future diesel engine monitoring systems are able to more effectively detect and monitor developing faults. In undertaking this research knowledge concerning engine function and relevant failure mechanisms was combined with different modelling methods to generate a framework that was used to effectively identify fault related activity within acoustic emissions recorded from different engines.

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The process of building safer roads and roadsides needs to be managed to minimise risks to both the road using public and roadworkers. However, detailed and accurate data on fatalities and injuries at roadworks across Australia are not available. The lack of reliable safety records and consequent poor understanding of the hazards at roadworks motivated this research to examine the common trends in incidents and to understand workers' perceptions of the causes of incidents at roadworks. To achieve these aims, 66 roadworks personnel were interviewed in Queensland including road construction workers, traffic controllers, engineers, and managers. Qualitative analyses identified several major issues and themes. Vehicles driving into work areas, traffic controllers hit by vehicles, rear end crashes at roadwork approaches, and reversing incidents involving work vehicles and machinery were the most common types of incidents. Roadworkers perceived driver errors, such as violation of speed limits, distracted driving, and ignoring signage and traffic controllers' instructions as the main causes of the incidents.

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Migraine is a common, heterogeneous and heritable neurological disorder. Its pathophysiology is incompletely understood, and its genetic influences at the population level are unknown. In a population-based genome-wide analysis including 5,122 migraineurs and 18,108 non-migraineurs, rs2651899 (1p36.32, PRDM16), rs10166942 (2q37.1, TRPM8) and rs11172113 (12q13.3, LRP1) were among the top seven associations (P < 5 × 10(-6)) with migraine. These SNPs were significant in a meta-analysis among three replication cohorts and met genome-wide significance in a meta-analysis combining the discovery and replication cohorts (rs2651899, odds ratio (OR) = 1.11, P = 3.8 × 10(-9); rs10166942, OR = 0.85, P = 5.5 × 10(-12); and rs11172113, OR = 0.90, P = 4.3 × 10(-9)). The associations at rs2651899 and rs10166942 were specific for migraine compared with non-migraine headache. None of the three SNP associations was preferential for migraine with aura or without aura, nor were any associations specific for migraine features. TRPM8 has been the focus of neuropathic pain models, whereas LRP1 modulates neuronal glutamate signaling, plausibly linking both genes to migraine pathophysiology.

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Recent developments in genomic technologies have resulted in increased understanding of pathogenic mechanisms and emphasized the importance of central survival pathways. Here, we use a novel bioinformatic based integrative genomic profiling approach to elucidate conserved mechanisms of lymphomagenesis in the three commonest non-Hodgkin's lymphoma (NHL) entities: diffuse large B-cell lymphoma, follicular lymphoma, and B-cell chronic lymphocytic leukemia. By integrating genome-wide DNA copy number analysis and transcriptome profiling of tumor cohorts, we identified genetic lesions present in each entity and highlighted their likely target genes. This revealed a significant enrichment of components of both the apoptosis pathway and the mitogen activated protein kinase pathway, including amplification of the MAP3K12 locus in all three entities, within the set of genes targeted by genetic alterations in these diseases. Furthermore, amplification of 12p13.33 was identified in all three entities and found to target the FOXM1 oncogene. Amplification of FOXM1 was subsequently found to be associated with an increased MYC oncogenic signaling signature, and siRNA-mediated knock-down of FOXM1 resulted in decreased MYC expression and induced G2 arrest. Together, these findings underscore genetic alteration of the MAPK and apoptosis pathways, and genetic amplification of FOXM1 as conserved mechanisms of lymphomagenesis in common NHL entities. Integrative genomic profiling identifies common central survival mechanisms and highlights them as attractive targets for directed therapy.

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Patent foramen ovale (PFO) is associated with clinical conditions including cryptogenic stroke, migraine and varicose veins. Data from studies in humans and mouse suggest that PFO and the secundum form of atrial septal defect (ASDII) exist in an anatomical continuum of septal dysmorphogenesis with a common genetic basis. Mutations in multiple members of the evolutionarily conserved cardiac transcription factor network, including GATA4, cause or predispose to ASDII and PFO. Here, we assessed whether the most prevalent variant of the GATA4 gene, S377G, was significantly associated with PFO or ASD. Our analysis of world indigenous populations showed that GATA4 S377G was largely Caucasian-specific, and so subjects were restricted to those of Caucasian descent. To select for patients with larger PFO, we limited our analysis to those with cryptogenic stroke in which PFO was a subsequent finding. In an initial study of Australian subjects, we observed a weak association between GATA4 S377G and PFO/Stroke relative to Caucasian controls in whom ASD and PFO had been excluded (OR = 2.16; p = 0.02). However, in a follow up study of German Caucasians no association was found with either PFO or ASD. Analysis of combined Australian and German data confirmed the lack of a significant association. Thus, the common GATA4 variant S377G is likely to be relatively benign in terms of its participation in CHD and PFO/Stroke.

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Background Glutamate is the principal excitatory neurotransmitter in the central nervous system which acts by the activation of either ionotropic (AMPA, NMDA and kainate receptors) or G-protein coupled metabotropic receptors. Glutamate is widely accepted to play a major role in the path physiology of migraine as implicated by data from animal and human studies. Genes involved in synthesis, metabolism and regulation of both glutamate and its receptors could be, therefore, considered as potential candidates for causing/predisposing to migraine when mutated. Methods The association of polymorphic variants of GRIA1-GRIA4 genes which encode for the four subunits (GluR1-GluR4) of the alpha-amino-3- hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptor for glutamate was tested in migraineurs with and without aura (MA and MO) and healthy controls. Results Two variants in the regulative regions of GRIA1 (rs2195450) and GRIA3 (rs3761555) genes resulted strongly associated with MA (P = 0.00002 and P = 0.0001, respectively), but not associated with MO, suggesting their role in cortical spreading depression. Whereas the rs548294 variant in GRIA1 gene showed association primarily with MO phenotype, supporting the hypothesis that MA and MO phenotypes could be genetically related. These variants modify binding sites for transcription factors altering the expression of GRIA1 and GRIA3 genes in different conditions. Conclusions This study represents the first genetic evidence of a link between glutamate receptors and migraine.

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Migraine is a prevalent neurovascular disease with a significant genetic component. Linkage studies have so far identified migraine susceptibility loci on chromosomes 1, 4, 6, 11, 14, 19 and X. We performed a genome-wide scan of 92 Australian pedigrees phenotyped for migraine with and without aura and for a more heritable form of “severe” migraine. Multipoint non-parametric linkage analysis revealed suggestive linkage on chromosome 18p11 for the severe migraine phenotype (LOD*=2.32, P=0.0006) and chromosome 3q (LOD*=2.28, P=0.0006). Excess allele sharing was also observed at multiple different chromosomal regions, some of which overlap with, or are directly adjacent to, previously implicated migraine susceptibility regions. We have provided evidence for two loci involved in severe migraine susceptibility and conclude that dissection of the “migraine” phenotype may be helpful for identifying susceptibility genes that influence the more heritable clinical (symptom) profiles in affected pedigrees. Also, we concluded that the genetic aetiology of the common (International Headache Society) forms of the disease is probably comprised of a number of low to moderate effect susceptibility genes, perhaps acting synergistically, and this effect is not easily detected by traditional single-locus linkage analyses of large samples of affected pedigrees.

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Generally, the magnitude of pollutant emissions from diesel engines running on biodiesel fuel is ultimately coupled to the structure of respective molecules that constitutes the fuel. Previous studies demonstrated the relationship between organic fraction of PM and its oxidative potential. Herein, emissions from a diesel engine running on different biofuels were analysed in more detail to explore the role different organic fractions play in the measured oxidative potential. In this work, a more detailed chemical analysis of biofuel PM was undertaken using a compact Time of Flight Aerosol Mass Spectrometer (c-ToF AMS). This enabled a better identification of the different organic fractions that contribute to the overall measured oxidative potentials. The concentration of reactive oxygen species (ROS) was measured using a profluorescent nitroxide molecular probe 9-(1,1,3,3-tetramethylisoindolin-2-yloxyl-5-ethynyl)-10-(phenylethynyl)anthracene (BPEAnit). Therefore the oxidative potential of the PM, measured through the ROS content, although proportional to the total organic content in certain cases shows a much higher correlation with the oxygenated organic fraction as measured by the c-ToF AMS. This highlights the importance of knowing the surface chemistry of particles for assessing their health impacts. It also sheds light onto new aspects of particulate emissions that should be taken into account when establishing relevant metrics for assessing health implications of replacing diesel with alternative fuels.

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The issue of particle emissions from diesel engines is still a matter of concern due its deleterious effects both on human health and environment(Ristovski et al., 2012). Recently, International Agency for Research on Cancer (IARC) inclusion of diesel engine exhaust particles as carcinogenic to human health added a new margin on it. Apart from the use of after treatment technology, biodiesel is also considered as potential way to reduce particle emission alongside with other emissions(Xue, Grift, & Hansen, 2011). Global biodiesel production is still reasonably small compared to its counterpart fossil diesel, but even this small amount comes from a wide variety of feed stocks. Contrary to fossil diesel, the important physicochemical properties of biodiesel vary among different feed stocks(Hoekman, Broch, Robbins, Ceniceros, & Natarajan, 2012).

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A technique for analysing exhaust emission plumes from unmodified locomotives under real world conditions is described and applied to the task of characterizing plumes from railway trains servicing an Australian shipping port. The method utilizes the simultaneous measurement, downwind of the railway line, of the following pollutants; particle number, PM2.5 mass fraction, SO2, NOx and CO2, with the last of these being used as an indicator of fuel combustion. Emission factors are then derived, in terms of number of particles and mass of pollutant emitted per unit mass of fuel consumed. Particle number size distributions are also presented. The practical advantages of the method are discussed including the capacity to routinely collect emission factor data for passing trains and to thereby build up a comprehensive real world database for a wide range of pollutants. Samples from 56 train movements were collected, analyzed and presented. The quantitative results for emission factors are: EF(N)=(1.7±1)×1016 kg-1, EF(PM2.5)= (1.1±0.5) g·kg-1, EF(NOx)= (28±14) g·kg-1, and EF(SO2 )= (1.4±0.4) g·kg-1. The findings are compared with comparable previously published work. Statistically significant (p<α, α=0.05) correlations within the group of locomotives sampled were found between the emission factors for particle number and both SO2 and NOx.

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Australian authorities have set ambitious policy objectives to shift Australia’s current transport profile of heavy reliance on private motor cars to sustainable modes. Improving accessibility of public transport is a central component of that objective. Past studies on accessibility to public transport focus on walking time and/or waiting time. However, travellers’ perceptions of the interface leg journeys may depend not only on these direct and tangible factors but also on social and psychological factors. This paper extends previous research that identified five salient perspectives of rail access by means of a statement sorting activity and cluster analysis with a small sample of rail passengers in three Australian cities (Zuniga et al, 2013). This study collects a new data set including 144 responses from Brisbane and Melbourne to an online survey made up of a Likert-scaled statement sorting exercise and questionnaire. It employs factor analysis to examine the statement rankings and uncovers seven underlying factors in the exploratory manner, i.e., station, safety, access, transfer, service attitude, traveler’s physical activity levels, and environmental concern. Respondents from groups stratified by rail use frequency are compared in terms of their scores of those factors. Findings from this study indicate a need to re-conceptualize accessibility to intra-urban rail travel in agreement with current policy agenda, and to target behavioral intervention to multiple dimensions of accessibility influencing passengers’ travel choices. Arguments in this paper are not limited to intra-urban rail transit, but may also be relevant to public transport in general.