Developing and benchmarking native Linux applications on Android

Smartphones get increasingly popular where more and more smartphone platforms emerge. Special attention was gained by the open source platform Android which was presented by the Open Handset Alliance (OHA) hosting members like Google, Motorola, and HTC. Android uses a Linux kernel and a stripped-down userland with a custom Java VM set on top. The resulting system joins the advantages of both environments, while third-parties are intended to develop only Java applications at the moment. In this work, we present the benefit of using native applications in Android. Android includes a fully functional Linux, and using it for heavy computational tasks when developing applications can bring in substantional performance increase. We present how to develop native applications and software components, as well as how to let Linux applications and components communicate with Java programs. Additionally, we present performance measurements of native and Java applications executing identical tasks. The results show that native C applications can be up to 30 times as fast as an identical algorithm running in Dalvik VM. Java applications can become a speed-up of up to 10 times if utilizing JNI.

Pedestrian safety at level crossings : how the issue should be addressed?

• crashes at level crossings : pedestrians at higher risk • why pedestrian risky crossing lacks in understandng ? • systems approach – what benefits ? • what are the risk factors at play ? • focus group study: results and future implications

‘Doing’ social justice in early childhood : the potential of leadership

Early childhood education has long been connected with objectives related to social justice. Australian Early Childhood Education and Care (ECEC) has its roots in philanthropic and educational reform movements prevalent at the turn of the 20th century. More recently, with the introduction of the National Early Childhood Reform Agenda, early childhood education has once more been linked to the achievement of aims associated with redressing inequality and disadvantage. According to Jean-Marie, Normore and Brooks (2009), educational leaders have a moral and social obligation to foster equitable practices through advocating for traditionally marginalised and poorly served students while creating a new social order “...that subverts the long standing system that has privileged certain students while oppressing or neglecting others” (p.4). Drawing on extant literature, including data from two previously reported Australian studies in which leadership emerged as having a transformational impact on service delivery, this paper examines the potential of early childhood leadership to generate ‘socially just’ educational communities. With reference to critical theory, we argue that critically informed, intentional and strategic organisational leadership can play a pivotal role in creating changed circumstances and opportunities for children and families. Such leadership includes positional and distributed elements, articulation of values and beliefs, and collective action that is mindful and informed.

Role of serotonin via 5-HT2B receptors in the reinforcing effects of MDMA in mice

The amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) reverses dopamine and serotonin transporters to produce efflux of dopamine and serotonin, respectively, in regions of the brain that have been implicated in reward. However, the role of serotonin/dopamine interactions in the behavioral effects of MDMA remains unclear. We previously showed that MDMA-induced locomotion, serotonin and dopamine release are 5-HT(2B) receptor-dependent. The aim of the present study was to determine the contribution of serotonin and 5-HT(2B) receptors to the reinforcing properties of MDMA. We show here that 5-HT(2B) (-/-) mice do not exhibit behavioral sensitization or conditioned place preference following MDMA (10 mg/kg) injections. In addition, MDMA-induced reinstatement of conditioned place preference after extinction and locomotor sensitization development are each abolished by a 5-HT(2B) receptor antagonist (RS127445) in wild type mice. Accordingly, MDMA-induced dopamine D1 receptor-dependent phosphorylation of extracellular regulated kinase in nucleus accumbens is abolished in mice lacking functional 5-HT(2B) receptors. Nevertheless, high doses (30 mg/kg) of MDMA induce dopamine-dependent but serotonin and 5-HT(2B) receptor-independent behavioral effects. These results underpin the importance of 5-HT(2B) receptors in the reinforcing properties of MDMA and illustrate the importance of dose-dependent effects of MDMA on serotonin/dopamine interactions.

Serotonin 5-HT2B receptors are required for bone-marrow contribution to pulmonary arterial hypertension

Pulmonary arterial hypertension (PAH) is a progressive disease characterized by lung endothelial dysfunction and vascular remodeling. Recently, bone marrow progenitor cells have been localized to PAH lungs, raising the question of their role in disease progression. Independently, serotonin (5-HT) and its receptors have been identified as contributors to the PAH pathogenesis. We hypothesized that 1 of these receptors, 5-HT(2B), is involved in bone marrow stem cell mobilization that participates in the development of PAH and pulmonary vascular remodeling. A first study revealed expression of 5-HT(2B) receptors by circulating c-kit(+) precursor cells, whereas mice lacking 5-HT(2B) receptors showed alterations in platelets and monocyte-macrophage numbers, and in myeloid lineages of bone marrow. Strikingly, mice with restricted expression of 5-HT(2B) receptors in bone marrow cells developed hypoxia or monocrotaline-induced increase in pulmonary pressure and vascular remodeling, whereas restricted elimination of 5-HT(2B) receptors on bone marrow cells confers a complete resistance. Moreover, ex vivo culture of human CD34(+) or mice c-kit(+) progenitor cells in the presence of a 5-HT(2B) receptor antagonist resulted in altered myeloid differentiation potential. Thus, we demonstrate that activation of 5-HT(2B) receptors on bone marrow lineage progenitors is critical for the development of PAH.

Deconstructing antiobesity compound action : requirement of serotonin 5-HT2B receptors for dexfenfluramine anorectic effects

The now-banned anorectic molecule, dexfenfluramine, promotes serotonin release through a serotonin transporter-dependent mechanism, and it has been widely prescribed for the treatment of obesity. Previous studies have identified that 5-HT(2B) receptors have important roles in dexfenfluramine side effects, that is, pulmonary hypertension, plasma serotonin level regulation, and valvulopathy. We thus investigated a putative contribution of 5-HT(2B) receptors in dexfenfluramine-dependent feeding behavior in mice. Interestingly, the hypophagic response to dexfenfluramine (3-10 mg/kg) observed in wild-type mice (1-4 h) was eliminated in mice lacking 5-HT(2B) receptors (5-HT(2B)(-/-)). These findings were further validated by the lack of hypophagic response to dexfenfluramine in wild-type mice treated with RS127445, a highly selective and potent antagonist (pKi=8.22 ± 0.24). Using microdialysis, we observed that in 5-HT(2B)(-/-) awake mice, the dexfenfluramine-induced hypothalamic peak of serotonin release (1 h) was strongly reduced (fourfold) compared with wild type. Moreover, using hypothalamic synaptosomes, we established the serotonergic neuron autonomous properties of this effect: a strong serotonin release was observed upon dexfenfluramine stimulation of synaptosome preparation from wild type but not from mice lacking active 5-HT(2B) receptors. These findings strongly suggest that activation of presynaptic 5-HT(2B) receptors is a limiting step in the serotonin transporter dependent-releasing effect of dexfenfluramine, whereas other serotonin receptors act downstream with respect to feeding behavior.

Systems-based approach to investigate unsafe pedestrian behaviour at level crossings

Crashes at level crossings are a major issue worldwide. In Australia, as well as in other countries, the number of crashes with vehicles has declined in the past years, while the number of crashes involving pedestrians seems to have remained unchanged. A systematic review of research related to pedestrian behaviour highlighted a number of important scientific gaps in current knowledge. The complexity of such intersections imposes particular constraints to the understanding of pedestrians’ crossing behaviour. A new systems-based framework, called Pedestrian Unsafe Level Crossing framework (PULC) was developed. The PULC organises contributing factors to crossing behaviour on different system levels as per the hierarchical classification of Jens Rasmussen’s Framework for Risk Management. In addition, the framework adapts James Reason’s classification to distinguish between different types of unsafe behaviour. The framework was developed as a tool for collection of generalizable data that could be used to predict current or future system failures or to identify aspects of the system that require further safety improvement. To give it an initial support, the PULC was applied to the analysis of qualitative data from focus groups discussions. A total number of 12 pedestrians who regularly crossed the same level crossing were asked about their daily experience and their observations of others’ behaviour which allowed the extraction and classification of factors associated with errors and violations. Two case studies using Rasmussen’s AcciMap technique are presented as an example of potential application of the framework. A discussion on the identified multiple risk contributing factors and their interactions is provided, in light of the benefits of applying a systems approach to the understanding of the origins of individual’s behaviour. Potential actions towards safety improvement are discussed.

Direct observations of pedestrian unsafe crossing at urban Australian level crossings

The number of pedestrian victims at Australian and foreign level crossings has remained stable over the past decade and it continues to be a significant problem. To examine the factors contributing to pedestrians’ unsafe crossing behaviours, direct observations were conducted at three black spot urban level crossings in Brisbane for a total of 45 h during morning and afternoon peak. In total, 129 pedestrians transgressed the active controls. More transgressions were observed at the crossings located in more populated suburbs in close proximity to large shopping centres and school zones, whereas the smallest number of transgressions were observed at the least populated locations. In addition to characteristics associated with the larger socio-economic area, the patterns of transgression could be associated with the properties of the existing safety equipment and the design of each level crossing (i.e. location of the platforms, number of rail tracks). Indeed, the largest number of crossed unoccupied but “at risk” rail tracks (where a train could have passed), was observed at the crossing with the least transgressions. Contrary to previous findings, younger adults were the most frequent transgressors. School children and elderly were most likely to transgress in groups. Potential directions for future research and more effective measures are discussed.

Non-invasive MR imaging of inflammation in a patient with both asymptomatic carotid atheroma and an abdominal aortic aneurysm: A case report

Inflammation is a recognized risk factor for the vulnerable atherosclerotic plaque. USPIO-enhanced MRI imaging is a promising non-i nvasive method to identify high-risk atheromatous plaque inflammation in vivo in humans, in which areas of focal signal loss on MR images have been shown to correspond to the location of activated macrophages, typically at the shoulder regions of the plaque. This is the first report in humans describing simultaneous USPIO uptake within atheroma in two different arterial territories and again emphasises that atherosclerosis is a truly systemic disease. With further work, USPIO-enhanced MR imaging may be useful in identifying inflamed vulnerable atheromatous plaques in vivo, so refining patient selection for intervention and allowing appropriate early aggressive pharmacotherapy to prevent plaque rupture.