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Enabling children and youth’s well-being is widely valued by families and communities worldwide as an important outcome of schooling. However, whilst the concept of well-being in childhood has been widely studied, there is no general agreement about the structure and measurement of well-being in schooling contexts, nor in particular for Indigenous students who comprise some of the most educationally disadvantaged populations in the world. Hence there is a need to advance the conceptualization and development of better measures of well-being for schooling contexts. We theorized a multidimensional student well-being model and the Multidimensional Student Well-being (MSW) Instrument, grounded on recent research. We investigated its structure, measurement, and relation to correlates of well-being for a matched sample of 1,405 Australian students (Indigenous, N = 764; non-Indigenous, N = 641) at three time-points 10-12 months apart. Analyses supported an a priori multidimensional model of 6 higher-order domains of well-being, represented by 15 first-order factors. This structure was invariant across Indigenous and non-Indigenous, male and female, and primary and secondary schooling levels. Correlates provided support for convergent and discriminant validity. There was a downward trend in well-being over time, which calls for attention to multidimensional domains of students’ well-being to promote healthy development throughout school life and beyond. The results support a multidimensional model of student well-being appropriate for primary and secondary schooling and both Indigenous and non-Indigenous students.

Improving educational outcomes for Indigenous Australian students is a key strategy to helping Indigenous people reach their full potential. This has resulted in well-intentioned efforts by Australian educators and governments to ensure Indigenous children have positive school experiences. However, Indigenous students still lag behind their non-Indigenous counterparts in educational outcomes. This is particularly so for Indigenous students living in rural and remote parts of Australia where educational opportunities are limited, especially in high school. One solution to this problem has been to enrol these students in boarding schools in urban and metropolitan centres. While research on the success of boarding schools for Indigenous students is scarce, what little that does exist is not encouraging. The focus of this research was to examine the effects of boarding for Indigenous (n = 11) and non-Indigenous students’ (n = 158) wellbeing (N = 1423) in two large private boys’ schools. Participating students aged 12–18 years old completed a survey measuring wellbeing constructs on two occasions, 12 months apart. Non-Indigenous boys were generally higher in wellbeing compared with Indigenous boys. There was also evidence of improved social wellbeing beyond that of non-Indigenous boarders over time. Overall, while evidence of merit was weak, boarding schools may benefit their Indigenous students’ development in social wellbeing.

We investigated how satisfaction of the basic psychological needs at work was associated with the psychological and physical wellbeing of Indigenous and non-Indigenous employees both within and outside of the workplace. Participants included 1,146 Indigenous ( n = 559) and non-Indigenous Australians (60.9% female), aged 18 to 81 years ( Mage = 43.54) who were recruited through their employer or online advertisements. Structural equation modelling (SEM) was used to analyse the data, and Indigenous status and occupation type were investigated as moderators. Results revealed that independent of income, autonomy satisfaction was related to better physical and psychological health, satisfaction of the need for relatedness was associated with increased family and community thriving, and competence satisfaction was linked to decreased psychological distress. Results also showed that autonomy, competence, and relatedness need satisfaction was lower among Indigenous employees compared to non-Indigenous employees. Moderation analyses suggested that relatedness at work was especially important for non-Indigenous employees’ connection with their community, as were high levels of competence satisfaction for Indigenous employees. These findings are discussed in the context of self-determination theory and the implications for organizations wanting to improve the wellbeing of their Indigenous and non-Indigenous workforce.

Self-determination theory (SDT) posits universality without cross-cultural uniformity of the three basic psychological needs (autonomy, competence, and relatedness) which have been associated with desirable job outcomes. Yet these promising directions in theory and research have not been extended to Indigenous samples and different occupational types. This is unfortunate as Indigenous peoples globally remain the most disadvantaged on all socio-economic indicators, including employment. This study adopted a strengths-based approach to investigating associations between SDT’s need satisfaction and job outcomes in Australian Indigenous and non-Indigenous professionals and non-professionals. Participants included 1,146 Indigenous (48.8%) and non-Indigenous Australians (39.1% men), aged 18 to 81 years ( Mage = 43.54). Structural equation modeling (SEM) revealed that autonomy and competence need satisfaction were associated with multiple positive work outcomes and less job ambiguity, whereas satisfaction of the need for relatedness was associated with increased job satisfaction and greater resilience in the workplace. Moderation by Indigenous status and occupation type revealed few differences in the direction and strength of the associations between need satisfaction and job outcomes. However, non-professionals reported significantly lower satisfaction of all three needs, and Indigenous participants reported significantly lower levels of autonomy need satisfaction. As need satisfaction was shown to be equally beneficial for all workers regardless of culture or occupation type, these findings highlight the need for employers to invest more in cultivating the need satisfaction of their Indigenous and non-professional staff. Overall, the results extend upon previous research by demonstrating that SDT is generalizable to an Australian Indigenous population and that workplace need satisfaction is important for Indigenous and non-professional employee outcomes.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive disease which leads to significant morbidity and mortality from respiratory failure. The two drugs currently approved for clinical use slow the rate of decline in lung function but have not been shown to halt disease progression or reverse established fibrosis. Thus, new therapeutic targets are needed. Endothelial injury and the resultant vascular permeability are critical components in the response to tissue injury and are present in patients with IPF. However, it remains unclear how vascular permeability affects lung repair and fibrosis following injury. Lipid mediators such as sphingosine-1-phosphate (S1P) are known to regulate multiple homeostatic processes in the lung including vascular permeability. We demonstrate that endothelial cell–(EC) specific deletion of the S1P receptor 1 (S1PR1) in mice (EC-S1pr1(−/−)) results in increased lung vascular permeability at baseline. Following a low-dose intratracheal bleomycin challenge, EC-S1pr1(−/−) mice had increased and persistent vascular permeability compared with wild-type mice, which was strongly correlated with the amount and localization of resulting pulmonary fibrosis. EC-S1pr1(−/−) mice also had increased immune cell infiltration and activation of the coagulation cascade within the lung. However, increased circulating S1P ligand in ApoM-overexpressing mice was insufficient to protect against bleomycin-induced pulmonary fibrosis. Overall, these data demonstrate that endothelial cell S1PR1 controls vascular permeability in the lung, is associated with changes in immune cell infiltration and extravascular coagulation, and modulates the fibrotic response to lung injury.

In contemporary times, there are children who suffer from limited access to resources, even in some developed countries. In Australia, because of its vast landscape, students in rural and remote locations suffer from a variety of disadvantages. Due to limited resources available in their local environment, students in remote locations do not achieve to their best potential. This chapter illustrates how information and communication technology (ICT) may enable educators to engage students in interactive learning activities online. The study is part of a collaborative research project known as Ngara Wumara in Aboriginal language, which means “cultivating capabilities” in English, funded by the Australian Research Council (LP140100481). As part of the research project, interviews were conducted with children who worked in a circus, their parents, and other adults, who traveled with the circus from place to place. As their special circumstances prevented them from attending school on a regular basis, the children attended a virtual project-based learning program via Google Classroom. Interview data showed that ICT can expand accessibility to collaborative learning for students who have limited opportunities in a traditional classroom. However, effective virtual classroom environments require adequate technical and infrastructure support, which should be the government’s priority in distance education.

Pulmonary fibrosis is thought to result from dysregulated wound repair after repetitive lung injury. Many cellular responses to injury involve rearrangements of the actin cytoskeleton mediated by the two isoforms of the Rho-associated coiled-coil-forming protein kinase (ROCK), ROCK1 and ROCK2. In addition, profibrotic mediators such as transforming growth factor-β, thrombin, and lysophosphatidic acid act through receptors that activate ROCK. Inhibition of ROCK activation may be a potent therapeutic strategy for human pulmonary fibrosis. Pharmacological inhibition of ROCK using nonselective ROCK inhibitors has been shown to prevent fibrosis in animal models; however, the specific roles of each ROCK isoform are poorly understood. Furthermore, the pleiotropic effects of this kinase have raised concerns about on-target adverse effects of ROCK inhibition such as hypotension. Selective inhibition of one isoform might be a better-tolerated strategy. In the present study, we used a genetic approach to determine the roles of ROCK1 and ROCK2 in a mouse model of bleomycin-induced pulmonary fibrosis. Using ROCK1- or ROCK2-haploinsufficient mice, we found that reduced expression of either ROCK1 or ROCK2 was sufficient to protect them from bleomycin-induced pulmonary fibrosis. In addition, we found that both isoforms contribute to the profibrotic responses of epithelial cells, endothelial cells, and fibroblasts. Interestingly, ROCK1- and ROCK2-haploinsufficient mice exhibited similar protection from bleomycin-induced vascular leak, myofibroblast differentiation, and fibrosis; however, ROCK1-haploinsufficient mice demonstrated greater attenuation of epithelial cell apoptosis. These findings suggest that selective inhibition of either ROCK isoform has the potential to be an effective therapeutic strategy for pulmonary fibrosis.

Maladaptive wound healing responses to chronic tissue injury result in organ fibrosis. Fibrosis, which entails excessive extracellular matrix (ECM) deposition and tissue remodeling by activated myofibroblasts, leads to loss of proper tissue architecture and organ function; however, the molecular mediators of myofibroblast activation have yet to be fully identified. Here we identify soluble ephrin-B2 (sEphrin-B2) as a new profibrotic mediator in lung and skin fibrosis. We provide molecular, functional and translational evidence that the ectodomain of membrane-bound ephrin-B2 is shed from fibroblasts into the alveolar airspace after lung injury. Shedding of sEphrin-B2 promotes fibroblast chemotaxis and activation via EphB3 and/or EphB4 receptor signaling. We found that mice lacking ephrin-B2 in fibroblasts are protected from skin and lung fibrosis and that a disintegrin and metalloproteinase 10 (ADAM10) is the major ephrin-B2 sheddase in fibroblasts. ADAM10 expression is increased by transforming growth factor (TGF)-β1, and ADAM10-mediated sEphrin-B2 generation is required for TGF-β1-induced myofibroblast activation. Pharmacological inhibition of ADAM10 reduces sEphrin-B2 levels in bronchoalveolar lavage and prevents lung fibrosis in mice. Consistent with the mouse data, ADAM10-sEphrin-B2 signaling is upregulated in fibroblasts from human subjects with idiopathic pulmonary fibrosis. These results uncover a new molecular mechanism of tissue fibrogenesis and identify sEphrin-B2, its receptors EphB3 and EphB4 and ADAM10 as potential therapeutic targets in the treatment of fibrotic diseases.

Given the variety of stakeholders involved in cases within family drug courts, efficient communication and information sharing, which are needed to support decision-making, can be quite challenging. Through a case study in one family drug court system, this research employed an action research approach to improve the information sharing process following the Lean Six Sigma methodology. The solutions implemented through this study contributed to improving the quality of the services provided by this court system and its overall productivity. In addition, this research extends our knowledge about methods for improving court systems from which others can learn to guide future improvement efforts.

Maladaptive wound healing responses to chronic tissue injury result in organ fibrosis. Fibrosis, which entails excessive extracellular matrix (ECM) deposition and tissue remodelling by activated myofibroblasts, leads to loss of proper tissue architecture and organ function; however the molecular mediators of myofibroblast activation remain to be fully identified. Here we identify soluble ephrin-B2 as a novel pro-fibrotic mediator in lung and skin fibrosis. We provide molecular, functional and translational evidence that the ectodomain of membrane-bound ephrin-B2 is shed from fibroblasts into the alveolar airspace after lung injury. Shedding of soluble ephrin-B2 (sEphrin-B2) promotes fibroblast chemotaxis and activation via EphB3/EphB4 receptor signaling. We found that mice lacking ephrin-B2 in fibroblasts are protected from skin and lung fibrosis and that a distintegrin and metalloproteinase 10 (ADAM10) is the major ephrin-B2 sheddase in fibroblasts. ADAM10 is induced by transforming growth factor-β1 (TGF-β1), and ADAM10-mediated sEphrin-B2 generation is required for TGF-β1–induced myofibroblast activation. Pharmacological inhibition of ADAM10 reduces sEphrin-B2 levels in bronchoalveolar lavage and prevents lung fibrosis in mice. Consistent with the mouse data, ADAM10/sEphrin-B2 signaling is upregulated in fibroblasts from human subjects with idiopathic pulmonary fibrosis. These results uncover a new molecular mechanism of tissue fibrogenesis and identify sEphrin-B2, its receptors Eph3/Eph4, and ADAM10 as potential therapeutic targets in the treatment of fibrotic diseases.

Background and Rationale: The actin cytoskeleton directs many pro-fibrotic cellular responses in pulmonary fibrosis, including epithelial cell apoptosis, endothelial cell barrier disruption and fibroblast migration and differentiation. The Rho kinases ROCK1 and ROCK2 regulate the actin cytoskeleton, making them logical targets for anti-fibrotic therapy. We used a genetic approach to identify the …

Lysophosphatidic acid (LPA) signaling through one of its receptors, LPA1, contributes to both the development and the pathological remodeling after injury of many organs. Because we found previously that LPA-LPA1 signaling contributes to pulmonary fibrosis, here we investigated whether this pathway is also involved in lung development. Quantitative assessment of lung architecture of LPA1-deficient knock-out (KO) and wild-type (WT) mice at 3, 12, and 24 weeks of age using design-based stereology suggested the presence of an alveolarization defect in LPA1 KO mice at 3 weeks, which persisted as alveolar numbers increased in WT mice into adulthood. Across the ages examined, the lungs of LPA1 KO mice exhibited decreased alveolar numbers, septal tissue volumes, and surface areas, and increased volumes of the distal airspaces. Elastic fibers, critical to the development of alveolar septa, appeared less organized and condensed and more discontinuous in KO alveoli starting at P4. Tropoelastin messenger RNA expression was decreased in KO lungs, whereas expression of matrix metalloproteinases degrading elastic fibers was either decreased or unchanged. These results are consistent with the abnormal lung phenotype of LPA1 KO mice, being attributable to reduced alveolar septal formation during development, rather than to increased septal destruction as occurs in the emphysema of chronic obstructive pulmonary disease. Peripheral septal fibroblasts and myofibroblasts, which direct septation in late alveolarization, demonstrated reduced production of tropoelastin and matrix metalloproteinases, and diminished LPA-induced migration, when isolated from LPA1 KO mice. Taken together, our data suggest that LPA-LPA1 signaling is critically required for septation during alveolarization.

Objectives:An earlier study by Franklin and Doran (2009) provided the first evidence that coaching benefits objective performance as assessed by evaluators’ blind to participation in coaching. This study examines the efficacy of two coaching programmes on independently evaluated academic performance 12 and 18 months after the completion of coaching.Design:A double-blind controlled trial in which participants were randomly allocated to either a Preparation, Action, Adaptive Learning (PAAL), or a Self-regulation co-coaching programme with blind assessment of subsequent academic performance. A third no-treatment condition was used for additional comparison and control of expectancy effects.Methods:Two structurally identical seven-week co-coaching programmes were run. The Self-regulation condition focused on the development of study and coping skills, whilst the PAAL condition additionally focused on preparation for change and adaptive learning. Fifty-two volunteer first-year university students were randomly assigned to either a PAAL (N=27) or Self-regulation (N=25) co-coaching programme. Academic results 12 and 18 months after completing the brief coaching programme are compared with a control group of students (N=2183 at 12 months, 2063 at 18 months.) who did not participate in the programme.Results:Relative to the no treatment control group, PAAL participants consistently performed some 10 per cent better in independently assessed academic performance at both the 12-month follow-up (71.04 per cent vs. 61.29 per cent) (p=Conclusion:Both co-coaching conditions were associated with increases in blindly assessed academic performance, however, only those in the PAAL condition performed significantly better 12 and 18 months after the completion of the brief coaching programme. The effects of the PAAL coaching method need to be evaluated in other areas where outcomes may be objectively and blindly assessed.