ATAD3 Proteins: Unique Mitochondrial Proteins Essential for Life in Diverse Eukaryotic Lineages.

ATAD3 proteins (ATPase family AAA domain-containing protein 3) are unique mitochondrial proteins that arose deep in the eukaryotic lineage but that are surprisingly absent from the Fungi and Amoebozoa. These ~600 amino acid proteins are anchored in the inner mitochondrial membrane and are essential in metazoans and Arabidopsis thaliana. ATAD3s comprise a C-terminal AAA+ matrix domain and an ATAD3_N domain that is located primarily in the inner membrane space but potentially extends into cytosol to interact with the ER. Sequence and structural alignments indicate ATAD3 proteins are most similar to classic chaperone unfoldases in AAA+ family, suggesting that they operate in mitochondrial protein quality control. A. thaliana has four ATAD3 genes in two distinct clades that appear first in the seed plants, and both clades are essential for viability. The four genes are generally coordinately expressed, and transcripts are highest in growing apices and imbibed seeds. Plants with disrupted ATAD3 have reduced growth, aberrant mitochondrial morphology, diffuse nucleoids and reduced oxidative phosphorylation complex I. These and other pleiotropic phenotypes are also observed in ATAD3 mutants in metazoans. Here we discuss the distribution of ATAD3 proteins as they have evolved in the plant kingdom, their unique structure, what we know about their function in plants, and the challenges in determining their essential roles in mitochondria.

Estrogen Receptor ß Contributes to Both Hypertension and Hypothalamic Plasticity in a Mouse Model of Peri-Menopause.

Hypertension susceptibility in women increases at the transition to menopause, termed perimenopause, a state characterized by erratic estrogen fluctuation and extended hormone cycles. Elucidating the role of estrogen signaling in the emergence of hypertension during perimenopause has been hindered by animal models that are confounded by abrupt estrogen cessation or effects of aging. In the present study, accelerated ovarian failure (AOF) in estrogen receptor ß (ERß) reporter mice was induced by 4-vinylcyclohexene diepoxide in young mice to model early-stage ovarian failure (peri-AOF) characteristic of peri-menopause. It was found that administering ERß agonists suppressed elevated blood pressure in a model of neurogenic hypertension induced by angiotensin II (AngII) in peri-AOF, but not in age-matched male mice. It was also found that ERß agonist administration in peri-AOF females, but not males, suppressed the heightened NMDAR signaling and reactive oxygen production in ERß neurons in the hypothalamic paraventricular nucleus (PVN), a critical neural regulator of blood pressure. It was further shown that deleting ERß in the PVN of gonadally intact females produced a phenotype marked by a sensitivity to AngII hypertension. These results suggest that ERß signaling in the PVN plays an important role in blood pressure regulation in female mice and contributes to hypertension susceptibility in females at an early stage of ovarian failure comparable to human perimenopause.

Estrogen Effects on Cognitive and Synaptic Health Over the Lifecourse.

Estrogen facilitates higher cognitive functions by exerting effects on brain regions such as the prefrontal cortex and hippocampus. Estrogen induces spinogenesis and synaptogenesis in these two brain regions and also initiates a complex set of signal transduction pathways via estrogen receptors (ERs). Along with the classical genomic effects mediated by activation of ER α and ER ß, there are membrane-bound ER α, ER ß, and G protein-coupled estrogen receptor 1 (GPER1) that can mediate rapid nongenomic effects. All key ERs present throughout the body are also present in synapses of the hippocampus and prefrontal cortex. This review summarizes estrogen actions in the brain from the standpoint of their effects on synapse structure and function, noting also the synergistic role of progesterone. We first begin with a review of ER subtypes in the brain and how their abundance and distributions are altered with aging and estrogen loss (e.g., ovariectomy or menopause) in the rodent, monkey, and human brain. As there is much evidence that estrogen loss induced by menopause can exacerbate the effects of aging on cognitive functions, we then review the clinical trials of hormone replacement therapies and their effectiveness on cognitive symptoms experienced by women. Finally, we summarize studies carried out in nonhuman primate models of age- and menopause-related cognitive decline that are highly relevant for developing effective interventions for menopausal women. Together, we highlight a new understanding of how estrogen affects higher cognitive functions and synaptic health that go well beyond its effects on reproduction.

Biallelic variants in HPDL, encoding 4-hydroxyphenylpyruvate dioxygenase-like protein, lead to an infantile neurodegenerative condition.

PURPOSE: Dioxygenases are oxidoreductase enzymes with roles in metabolic pathways necessary for aerobic life. 4-hydroxyphenylpyruvate dioxygenase-like protein (HPDL), encoded by HPDL, is an orphan paralogue of 4-hydroxyphenylpyruvate dioxygenase (HPD), an iron-dependent dioxygenase involved in tyrosine catabolism. The function and association of HPDL with human diseases remain unknown. METHODS: We applied exome sequencing in a cohort of over 10,000 individuals with neurodevelopmental diseases. Effects of HPDL loss were investigated in vitro and in vivo, and through mass spectrometry analysis. Evolutionary analysis was performed to investigate the potential functional separation of HPDL from HPD. RESULTS: We identified biallelic variants in HPDL in eight families displaying recessive inheritance. Knockout mice closely phenocopied humans and showed evidence of apoptosis in multiple cellular lineages within the cerebral cortex. HPDL is a single-exonic gene that likely arose from a retrotransposition event at the base of the tetrapod lineage, and unlike HPD, HPDL is mitochondria-localized. Metabolic profiling of HPDL mutant cells and mice showed no evidence of altered tyrosine metabolites, but rather notable accumulations in other metabolic pathways. CONCLUSION: The mitochondrial localization, along with its disrupted metabolic profile, suggests HPDL loss in humans links to a unique neurometabolic mitochondrial infantile neurodegenerative condition.

Plant small heat shock proteins - evolutionary and functional diversity.

Small heat shock proteins (sHSPs) are an ubiquitous protein family found in archaea, bacteria and eukaryotes. In plants, as in other organisms, sHSPs are upregulated by stress and are proposed to act as molecular chaperones to protect other proteins from stress-induced damage. sHSPs share an 'α-crystallin domain' with a ß-sandwich structure and a diverse N-terminal domain. Although sHSPs are 12-25 kDa polypeptides, most assemble into oligomers with ≥ 12 subunits. Plant sHSPs are particularly diverse and numerous; some species have as many as 40 sHSPs. In angiosperms this diversity comprises ≥ 11 sHSP classes encoding proteins targeted to the cytosol, nucleus, endoplasmic reticulum, chloroplasts, mitochondria and peroxisomes. The sHSPs underwent a lineage-specific gene expansion, diversifying early in land plant evolution, potentially in response to stress in the terrestrial environment, and expanded again in seed plants and again in angiosperms. Understanding the structure and evolution of plant sHSPs has progressed, and a model for their chaperone activity has been proposed. However, how the chaperone model applies to diverse sHSPs and what processes sHSPs protect are far from understood. As more plant genomes and transcriptomes become available, it will be possible to explore theories of the evolutionary pressures driving sHSP diversification.

Interventions for preventing obesity in children.

BACKGROUND: Prevention of childhood obesity is an international public health priority given the significant impact of obesity on acute and chronic diseases, general health, development and well-being. The international evidence base for strategies to prevent obesity is very large and is accumulating rapidly. This is an update of a previous review. OBJECTIVES: To determine the effectiveness of a range of interventions that include diet or physical activity components, or both, designed to prevent obesity in children. SEARCH METHODS: We searched CENTRAL, MEDLINE, Embase, PsychINFO and CINAHL in June 2015. We re-ran the search from June 2015 to January 2018 and included a search of trial registers. SELECTION CRITERIA: Randomised controlled trials (RCTs) of diet or physical activity interventions, or combined diet and physical activity interventions, for preventing overweight or obesity in children (0-17 years) that reported outcomes at a minimum of 12 weeks from baseline. DATA COLLECTION AND ANALYSIS: Two authors independently extracted data, assessed risk-of-bias and evaluated overall certainty of the evidence using GRADE. We extracted data on adiposity outcomes, sociodemographic characteristics, adverse events, intervention process and costs. We meta-analysed data as guided by the Cochrane Handbook for Systematic Reviews of Interventions and presented separate meta-analyses by age group for child 0 to 5 years, 6 to 12 years, and 13 to 18 years for zBMI and BMI. MAIN RESULTS: We included 153 RCTs, mostly from the USA or Europe. Thirteen studies were based in upper-middle-income countries (UMIC: Brazil, Ecuador, Lebanon, Mexico, Thailand, Turkey, US-Mexico border), and one was based in a lower middle-income country (LMIC: Egypt). The majority (85) targeted children aged 6 to 12 years.Children aged 0-5 years: There is moderate-certainty evidence from 16 RCTs (n = 6261) that diet combined with physical activity interventions, compared with control, reduced BMI (mean difference (MD) -0.07 kg/m2, 95% confidence interval (CI) -0.14 to -0.01), and had a similar effect (11 RCTs, n = 5536) on zBMI (MD -0.11, 95% CI -0.21 to 0.01). Neither diet (moderate-certainty evidence) nor physical activity interventions alone (high-certainty evidence) compared with control reduced BMI (physical activity alone: MD -0.22 kg/m2, 95% CI -0.44 to 0.01) or zBMI (diet alone: MD -0.14, 95% CI -0.32 to 0.04; physical activity alone: MD 0.01, 95% CI -0.10 to 0.13) in children aged 0-5 years.Children aged 6 to 12 years: There is moderate-certainty evidence from 14 RCTs (n = 16,410) that physical activity interventions, compared with control, reduced BMI (MD -0.10 kg/m2, 95% CI -0.14 to -0.05). However, there is moderate-certainty evidence that they had little or no effect on zBMI (MD -0.02, 95% CI -0.06 to 0.02). There is low-certainty evidence from 20 RCTs (n = 24,043) that diet combined with physical activity interventions, compared with control, reduced zBMI (MD -0.05 kg/m2, 95% CI -0.10 to -0.01). There is high-certainty evidence that diet interventions, compared with control, had little impact on zBMI (MD -0.03, 95% CI -0.06 to 0.01) or BMI (-0.02 kg/m2, 95% CI -0.11 to 0.06).Children aged 13 to 18 years: There is very low-certainty evidence that physical activity interventions, compared with control reduced BMI (MD -1.53 kg/m2, 95% CI -2.67 to -0.39; 4 RCTs; n = 720); and low-certainty evidence for a reduction in zBMI (MD -0.2, 95% CI -0.3 to -0.1; 1 RCT; n = 100). There is low-certainty evidence from eight RCTs (n = 16,583) that diet combined with physical activity interventions, compared with control, had no effect on BMI (MD -0.02 kg/m2, 95% CI -0.10 to 0.05); or zBMI (MD 0.01, 95% CI -0.05 to 0.07; 6 RCTs; n = 16,543). Evidence from two RCTs (low-certainty evidence; n = 294) found no effect of diet interventions on BMI.Direct comparisons of interventions: Two RCTs reported data directly comparing diet with either physical activity or diet combined with physical activity interventions for children aged 6 to 12 years and reported no differences.Heterogeneity was apparent in the results from all three age groups, which could not be entirely explained by setting or duration of the interventions. Where reported, interventions did not appear to result in adverse effects (16 RCTs) or increase health inequalities (gender: 30 RCTs; socioeconomic status: 18 RCTs), although relatively few studies examined these factors.Re-running the searches in January 2018 identified 315 records with potential relevance to this review, which will be synthesised in the next update. AUTHORS' CONCLUSIONS: Interventions that include diet combined with physical activity interventions can reduce the risk of obesity (zBMI and BMI) in young children aged 0 to 5 years. There is weaker evidence from a single study that dietary interventions may be beneficial.However, interventions that focus only on physical activity do not appear to be effective in children of this age. In contrast, interventions that only focus on physical activity can reduce the risk of obesity (BMI) in children aged 6 to 12 years, and adolescents aged 13 to 18 years. In these age groups, there is no evidence that interventions that only focus on diet are effective, and some evidence that diet combined with physical activity interventions may be effective. Importantly, this updated review also suggests that interventions to prevent childhood obesity do not appear to result in adverse effects or health inequalities.The review will not be updated in its current form. To manage the growth in RCTs of child obesity prevention interventions, in future, this review will be split into three separate reviews based on child age.

Feasibility and development of a cariogenic diet scale for epidemiological research.

BACKGROUND: Diet cariogenicity plays a major role as both a protective and risk factor in the development of early childhood caries (ECC). AIM: Develop a scale measuring the cariogenicity of foods and beverages and employ it to describe the cariogenicity of young children's diets and predict dental caries outcomes. DESIGN: Scores of cariogenicity and consumption frequency were applied to food frequency questionnaire (FFQ) collected from an Australian children's cohort study with three time-points of data. One-way ANOVA, with post hoc Tukey test compared mean cariogenic scale measured at 18 months between the subsample of children with caries classification at age 5 years. RESULTS: At 6 months, children's mean cariogenic score was 10.05, increasing to 34.18 at 12 and 50.00 at 18 months. Mean cariogenic scale score at 18 months was significantly higher in children with advanced disease at 5 years (mean scale score: 59.0 ± 15.9) compared to those that were healthy (mean score 47.7 ± 17.5, P = 0.007) or had mild-moderate disease (mean score 48.2 ± 17.3, P = 0.008). CONCLUSIONS: The cariogenic diet scale provides a useful indication of the increasing cariogenicity of children's diets with age and highlights the incorporation of discretionary choice foods and beverages into the diets of young children much earlier than nutritionally recommended.

Redistribution of NMDA Receptors in Estrogen-Receptor-ß-Containing Paraventricular Hypothalamic Neurons following Slow-Pressor Angiotensin II Hypertension in Female Mice with Accelerated Ovarian Failure.

Hypertension in male and aging female rodents is associated with glutamate-dependent plasticity in the hypothalamus, but existing models have failed to capture distinct transitional menopausal phases that could have a significant impact on the synaptic plasticity and emergent hypertension. In rodents, accelerated ovarian failure (AOF) induced by systemic injection of 4-vinylcyclohexane diepoxide mimics the estrogen fluctuations seen in human menopause including the perimenopause transition (peri-AOF) and postmenopause (post-AOF). Thus, we used the mouse AOF model to determine the impact of slow-pressor angiotensin II (AngII) administration on blood pressure and on the subcellular distribution of obligatory N-methyl-D-aspartate (NMDA) receptor GluN1 subunits in the paraventricular hypothalamic nucleus (PVN), a key estrogen-responsive cardiovascular regulatory area. Estrogen-sensitive neuronal profiles were identified in mice expressing enhanced green fluorescent protein under the promoter for estrogen receptor (ER) ß, a major ER in the PVN. Slow-pressor AngII increased arterial blood pressure in mice at peri- and post-AOF time points. In control oil-injected (nonhypertensive) mice, AngII decreased the total number of GluN1 in ERß-containing PVN dendrites. In contrast, AngII resulted in a reapportionment of GluN1 from the cytoplasm to the plasma membrane of ERß-containing PVN dendrites in peri-AOF mice. Moreover, in post-AOF mice, AngII increased total GluN1, dendritic size and radical production in ERß-containing neurons. These results indicate that unique patterns of hypothalamic glutamate receptor plasticity and dendritic structure accompany the elevated blood pressure in peri- and post-AOF time points. Our findings suggest the possibility that distinct neurobiological processes are associated with the increased blood pressure during perimenopausal and postmenopausal periods.

Cluster randomised trial of a school-community child health promotion and obesity prevention intervention: findings from the evaluation of fun 'n healthy in Moreland!

BACKGROUND: Multi-level, longer-term obesity prevention interventions that focus on inequalities are scarce. Fun 'n healthy in Moreland! aimed to improve child adiposity, school policies and environments, parent engagement, health behaviours and child wellbeing. METHODS: All children from primary schools in an inner urban, culturally diverse and economically disadvantaged area in Victoria, Australia were eligible for participation. The intervention, fun 'n healthy in Moreland!, used a Health Promoting Schools Framework and provided schools with evidence, school research data and part time support from a Community Development Worker to develop health promoting strategies. Comparison schools continued as normal. Participants were not blinded to intervention status. The primary outcome was change in adiposity. Repeated cross-sectional design with nested longitudinal subsample. RESULTS: Students from twenty-four primary schools (clusters) were randomised (aged 5-12 years at baseline). 1426 students from 12 intervention schools and 1539 students from 10 comparison schools consented to follow up measurements. Despite increased prevalence of healthy weight across all schools, after 3.5 years of intervention there was no statistically significant difference between trial arms in BMI z score post-intervention (Mean (sd): Intervention 0.68(1.16); Comparison: 0.72(1.12); Adjusted mean difference (AMD): -0.05, CI: -0.19 to 0.08, p = 0.44). Children from intervention schools consumed more daily fruit serves (AMD: 0.19, CI:0.00 to 0.37, p = 0.10), were more likely to have water (AOR: 1.71, CI:1.05 to 2.78, p = 0.03) and vegetables (AOR: 1.23, CI: 0.99 to 1.55, p = 0.07), and less likely to have fruit juice/cordial (AOR: 0.58, CI:0.36 to 0.93, p = 0.02) in school lunch compared to children in comparison schools. More intervention schools (8/11) had healthy eating and physical activity policies compared with comparison schools (2/9). Principals and schools highly valued the approach as a catalyst for broader positive school changes. The cost of the intervention per child was $65 per year. CONCLUSION: The fun n healthy in Moreland! intervention did not result in statistically significant differences in BMI z score across trial arms but did result in greater policy implementation, increased parent engagement and resources, improved child self-rated health, increased fruit, vegetable and water consumption, and reduction in sweet drinks. A longer-term follow up evaluation may be needed to demonstrate whether these changes are sustainable and impact on childhood overweight and obesity. CLINICAL TRIAL REGISTRATION: ACTRN12607000385448 (Date submitted 31/05/2007; Date registered 23/07/2007; Date last updated 15/12/2009).

'Yarning up with Koori kids' - hearing the voices of Australian urban Indigenous children about their health and well-being.

OBJECTIVE: Australian Indigenous children experience some of the most substantial health inequalities globally. In this context, research regarding their health and well-being has overemphasised physical illnesses with limited exploration of a diverse range of dimensions and determinants, particularly those based on Indigenous holistic understandings of health and well-being. This deficit-based approach has thus missed many strengths and assets of Indigenous children. This research aimed to gain insight into the perspectives of Indigenous children about their health and well-being in an urban setting in Australia. It joins a limited international literature examining views and experiences of non-majority children. DESIGN: Participatory and qualitative child-friendly research methods were utilised. The project was developed in partnership with Indigenous community organisations and members. Photo-elicitation activities and focus groups were conducted with 31 Indigenous children aged 8-12 years. Qualitative data were analysed thematically, combining focus group and interview data. RESULTS: It was evident an urban Indigenous child perspective of health and well-being includes rich understandings of the interconnectedness of physical, social-emotional and cultural dimensions of holism, as well as the integral importance of family and community relationships. The study also found that specific worries regarding loss of loved ones and racism were highly salient in Indigenous children's lives. CONCLUSION: The overwhelming conclusion to be drawn from this research is that Indigenous children in urban areas need ongoing recognition of both their agency and resilience in the face of adversity, within a wider context of historical and contemporary racialisation and racism.

A Cultural Competence Organizational Review for Community Health Services: Insights From a Participatory Approach.

Cultural competence is an important aspect of health service access and delivery in health promotion and community health. Although a number of frameworks and tools are available to assist health service organizations improve their services to diverse communities, there are few published studies describing organizational cultural competence assessments and the extent to which these tools facilitate cultural competence. This article addresses this gap by describing the development of a cultural competence assessment, intervention, and evaluation tool called the Cultural Competence Organizational Review (CORe) and its implementation in three community sector organizations. Baseline and follow-up staff surveys and document audits were conducted at each participating organization. Process data and organizational documentation were used to evaluate and monitor the experience of CORe within the organizations. Results at follow-up indicated an overall positive trend in organizational cultural competence at each organization in terms of both policy and practice. Organizations that are able to embed actions to improve organizational cultural competence within broader organizational plans increase the likelihood of sustainable changes to policies, procedures, and practice within the organization. The benefits and lessons learned from the implementation of CORe are discussed.

G-protein-coupled estrogen receptor 1 is anatomically positioned to modulate synaptic plasticity in the mouse hippocampus.

Both estrous cycle and sex affect the numbers and types of neuronal and glial profiles containing the classical estrogen receptors α and ß, and synaptic levels in the rodent dorsal hippocampus. Here, we examined whether the membrane estrogen receptor, G-protein-coupled estrogen receptor 1 (GPER1), is anatomically positioned in the dorsal hippocampus of mice to regulate synaptic plasticity. By light microscopy, GPER1-immunoreactivity (IR) was most noticeable in the pyramidal cell layer and interspersed interneurons, especially those in the hilus of the dentate gyrus. Diffuse GPER1-IR was found in all lamina but was most dense in stratum lucidum of CA3. Ultrastructural analysis revealed discrete extranuclear GPER1-IR affiliated with the plasma membrane and endoplasmic reticulum of neuronal perikarya and dendritic shafts, synaptic specializations in dendritic spines, and clusters of vesicles in axon terminals. Moreover, GPER1-IR was found in unmyelinated axons and glial profiles. Overall, the types and amounts of GPER1-labeled profiles were similar between males and females; however, in females elevated estrogen levels generally increased axonal labeling. Some estradiol-induced changes observed in previous studies were replicated by the GPER agonist G1: G1 increased PSD95-IR in strata oriens, lucidum, and radiatum of CA3 in ovariectomized mice 6 h after administration. In contrast, estradiol but not G1 increased Akt phosphorylation levels. Instead, GPER1 actions in the synapse may be due to interactions with synaptic scaffolding proteins, such as SAP97. These results suggest that although estrogen's actions via GPER1 may converge on the same synaptic elements, different pathways are used to achieve these actions.

Mental Health Following Separation in a Disaster: The Role of Attachment.

Short-term separation from close family members during a disaster is a highly salient event for those involved. Yet, its subsequent impact on mental health has received little empirical attention. One relevant factor may be attachment style, which influences patterns of support-seeking under threatening conditions. Individuals (N = 914) affected by the 2009 Victorian bushfires in southeastern Australia were assessed for disaster experiences, depression, posttraumatic stress disorder (PTSD) symptoms, and attachment style 3-4 years after the fires. Using multigroup structural equation modelling, individuals who reported separation from close family members during the bushfires (n = 471) were compared to those who reported no separation (n = 443). Cross-sectional results indicated that separated individuals had higher levels of PTSD symptoms. Furthermore, attachment anxiety was more strongly positively associated with depression among separated (b = 0.62) versus not separated individuals (b = 0.32). Unexpectedly, among separated individuals, attachment avoidance had a statistically weaker association with depression (b = 0.17 vs. b = 0.35) and with PTSD symptoms (b = 0.06 vs. b = 0.22). These results suggest that attachment anxiety amplifies a negative reaction to separation; meanwhile, for avoidant individuals, separation in times of danger may facilitate defensive cognitive processes.

Impact of family structure and socio-demographic characteristics on child health and wellbeing in same-sex parent families: A cross-sectional survey.

UNLABELLED: Children with same-sex attracted parents develop well in terms of their health and wellbeing. There are many recognised factors that have an impact on child health, in general, including individual, family and wider social mediators. The aim of this study is to determine the impact of family structure and socio-demographic characteristics on child health and wellbeing in Australian same-sex parent families. METHODS: A cross-sectional survey of self-identified same-sex attracted parents from across Australia was used to collect information on child health and wellbeing between May and December 2012. Mixed-effects multiple linear regression models were used to identify associations between family structure/socio-demographic characteristics and child wellbeing. Child health outcomes were measured using the Child Health Questionnaire and the Strengths and Difficulties Questionnaire. RESULTS: In same-sex parent families, biological relationships, parental gender and parental education were not significantly associated with health and wellbeing. Parental income, rurality and stable parental relationships were associated with health and wellbeing, and living in a single-parent household was associated with poorer wellbeing. CONCLUSIONS: Stable dual parent families offer good outcomes for children with same-sex attracted parents. Family processes are most important. This study does not support the assertion that children require both male and female parents, nor that biological relationships are essential to health and wellbeing. This study provides scientific data from a cross-sectional Australian-based study to describe and understand health determinants for children in family contexts that comprise same-sex parent and all family contexts. It recommends equitable, stigma-free family support.

Socioeconomic and health factors associated with kindergarten retention in Australian children.

AIM: We aimed to identify key socioeconomic and health factors that are associated with a child's likelihood of being retained in kindergarten prior to commencing first year of school in Australian children. METHODS: We used data linked from the School Entrant Health Questionnaire administered to children commencing school in 2012 (N = 42 002). Kindergarten retention here is defined by children accessing a second year of funded kindergarten prior to commencing school. We used logistic regression analysis to estimate the strength of associations between a range of socioeconomic and health factors to the likelihood of kindergarten retention. RESULTS: Of the 25 289 children included in our analysis, 903 (3.6%) had a second year of funded kindergarten prior to commencing school. In comparison, 1680 children out of 42 002 in the Kinder-School Entrant Health Questionnaire dataset had a second year of funded kindergarten (4.0%). From our final regression model, the highest association was found in children whose parents reported a history of speech and language difficulties (odds ratio 2.25, 95% confidence interval (1.91-2.66)) (adjusting for a range of demographic, health and developmental factors). Similarly, children from an indigenous background were twice as likely to be retained in kindergarten compared with those with a non-indigenous background (odds ratio 2.06 (1.17-3.64)). CONCLUSION: This analysis adds to the evidence base that children who are more socially disadvantaged as well as children with health difficulties, particularly speech and language difficulties, are more likely to be retained in kindergarten.

A snapshot of the scope of obesity prevention practice in Australia.

Community-based initiatives (CBIs) that build capacity and promote healthy environments hold promise for preventing obesity and non-communicable disease, however their characteristics remain poorly understood and lessons are learned in isolation. This limits understanding of likely effectiveness of CBIs; the potential for actively supporting practice; and the translation of community-based knowledge into policy. Building on an initial survey (2010), an online survey was launched (2013) with the aim to describe the reach and characteristics of Australian CBIs and identify and evaluate elements known to contribute to best practice, effectiveness and sustainability. Responses from 104 CBIs were received in 2013. Geographic location generally reflected population density in Australia. Duration of CBIs was short-term (median 3 years; range 0.2-21.0 years), delivered mostly by health departments and local governments. Median annual funding had more than doubled since the 2010 survey, but average staffing had not increased. CBIs used at least two strategy types, with a preference for individual behaviour change strategies. Targeting children was less common (31%) compared with the 2010 survey (57%). Logic models and theory were used in planning, but there was low use of research evidence and existing prevention frameworks. Nearly, all CBIs had an evaluation component (12% of budget), but dissemination was limited. This survey provides information on the scope and varied quality of the current obesity prevention investment in Australia. To boost the quality and effectiveness of CBIs, further support systems may be required to ensure that organizations adopt upstream, evidence-informed approaches; and integrate CBIs into systems, policies and environments.

Natural history of dental caries in very young Australian children.

BACKGROUND: Whilst the global burden of caries is increasing, the trajectory of decay in young children and the point at which prevention should occur has not been well established. AIM: To identify the 'natural history' of dental caries in early childhood. DESIGN: A birth cohort study was established with 467 mother/child dyads followed at 1, 6, 12, 18, and 36 months of age. Parent-completed surveys captured demographic, social, and behavioural data, and oral examinations provided clinical and data. RESULTS: Eight per cent of children (95% confidence interval (CI): 5-12%) at 18 months and 23% (95% CI: 18-28%) at 36 months experienced decay. Interesting lesion behaviour was found between 18 and 36 months, with rapid development of new lesions on sound teeth (70% of teeth, 95% CI: 63-76%) and regression of many lesions from non-cavitated lesions to sound (23% of teeth, 95% CI: 17-30%). Significant associations were found between soft drink consumption and lesion progression. CONCLUSIONS: Findings suggest optimal time periods for screening and prevention of a disease which significantly impacts multiple health and well-being outcomes across the life course.

The association between self-reported diet quality and health-related quality of life in rural and urban Australian adolescents.

OBJECTIVE: This study examines the relationship between diet quality and health-related quality of life (HRQoL) in rural and urban Australian adolescents, and gender differences. DESIGN: Cross-sectional. SETTING: Secondary schools. PARTICIPANTS: 722 rural and 422 urban students from 19 secondary schools. MAIN OUTCOME MEASURES: Self-report dietary-related behaviours, demographic information, HRQoL (AQoL-6D) were collected. Healthy and unhealthy diet quality scores were calculated; multiple linear regression investigated associations between diet quality and HRQoL. RESULTS: Compared to urban students, rural students had higher HRQoL, higher healthy diet score, lower unhealthy diet score, consumed less soft drink and less frequently, less takeaway and a higher proportion consumed breakfast (P < 0.05). Overall, males had higher unhealthy diet score, poorer dietary behaviours but a higher HRQoL score compared to females (P < 0.05). In all students, final regression models indicated: a unit increase in healthy diet score was associated with an increase in HRQoL (unstandardised coefficient(B)±standard error(SE); B = 0.02 ± 0.01(SE); P < 0.02); and a unit increase in unhealthy diet scores was associated with a decrease in HRQoL (-0.01 ± 0.00; P < 0.05). In rural students alone, a unit increase in unhealthy diet score was associated with a decrease in HRQoL (B = -0.01 ± 0.00; P = 0.002), and in urban students a unit increase in healthy diet score was associated with an increase in HRQoL (B = 0.02 ± 0.00; P < 0.001). CONCLUSIONS: Cross-sectional associations between diet quality and HRQoL were observed. Dietary modification may offer a target to improve HRQoL and general well-being; and consequently the prevention and treatment of adolescent health problems. Such interventions should consider gender and locality.

The Influence of Social Disadvantage on Children's Emotional and Behavioral Difficulties at Age 4-7 Years.

OBJECTIVE: To examine associations between indicators of social disadvantage and emotional and behavioral difficulties in children aged 4-7 years. STUDY DESIGN: This cross-sectional study was based on data collected in a questionnaire completed by parents of children enrolled in their first year of school in Victoria, Australia, in 2010. Just over 57000 children participated (86% of children enrolled), of whom complete data were available for 38955 (68% of the dataset); these children formed the analysis sample. The outcome measure was emotional and behavioral difficulties, assessed by the Strengths and Difficulties Questionnaire Total Difficulties score. Logistic regression analyses were undertaken. RESULTS: Having a concession card (a government-issued card enabling access to subsidized goods and services, particularly in relation to medical care, primarily for economically vulnerable households) was the strongest predictor of emotional and behavioral difficulties (OR, 2.71; 95% CI, 2.39-3.07), followed by living with 1 parent and the parent's partner or not living with either parent (OR, 1.93; 95% CI, 1.58-2.37) and having a mother who did not complete high school (OR, 1.27; 95% CI, 1.11-1.45). CONCLUSION: These findings may assist schools and early childhood practitioners in identifying young children who are at increased risk of emotional and behavioral difficulties, to provide these children, together with their parents and families, with support from appropriate preventive interventions.

Female protection from slow-pressor effects of angiotensin II involves prevention of ROS production independent of NMDA receptor trafficking in hypothalamic neurons expressing angiotensin 1A receptors.

Renin­angiotensin system overactivity, upregulation of postsynaptic NMDA receptor function, and increased reactive oxygen species (ROS) production in the hypothalamic paraventricular nucleus (PVN) are hallmarks of angiotensin II (AngII)-induced hypertension, which is far more common in young males than in young females. We hypothesize that the sex differences in hypertension are related to differential AngII-induced changes in postsynaptic trafficking of the essential NMDA receptor GluN1 subunit and ROS production in PVN cells expressing angiotensin Type 1a receptor (AT1aR). We tested this hypothesis using slow-pressor (14-day) infusion of AngII (600 ng/kg/min) in mice, which elicits hypertension in males but not in young females. Two-month-old male and female transgenic mice expressing enhanced green fluorescent protein (EGFP) in AT1aR-containing cells were used. In males, but not in females, AngII increased blood pressure and ROS production in AT1aR­EGFP PVN cells at baseline and following NMDA treatment. Electron microscopy showed that AngII increased cytoplasmic and total GluN1­silver-intensified immunogold (SIG) densities and induced a trend toward an increase in near plasmalemmal GluN1­SIG density in AT1aR­EGFP dendrites of males and females. Moreover, AngII decreased dendritic area and diameter in males, but increased dendritic area of small (<1 µm) dendrites and decreased diameter of large (>1 µm) dendrites in females. Fluorescence microscopy revealed that AT1aR and estrogen receptor ß do not colocalize, suggesting that if estrogen is involved, its effect is indirect. These data suggest that the sexual dimorphism in AngII-induced hypertension is associated with sex differences in ROS production in AT1aR-containing PVN cells but not with postsynaptic NMDA receptor trafficking.