Fatherhood and mental illness: a review of key issues

Researchers have traditionally paid little attention to the intersections between men’s mental illness and family life. Recently, however, this has been changing. This paper provides practitioners and policy-makers with a broad overview of some of the key issues identified in the growing literature on paternal mental illness. Key messages Compared to many other life stages, the transition to fatherhood and the early years of childrearing are periods in which men are at a substantially increased risk of experiencing psychological distress. The children of men with a mental illness are more likely than other children to experience internalising (i.e., emotional) and externalising (i.e., behavioural) problems, as well as to be diagnosed with a mental illness themselves. Parenting behaviour is one of the mechanisms by which parental mental illness may translate into problem outcomes in children. Fathers with a mental illness are more likely than other fathers to show low levels of parental engagement, warmth and appropriate monitoring. The scarce qualitative literature exploring fathers\u27 experiences of mental illness suggests that fatherhood is central to the image many men have of themselves - their experience of mental illness and their paternal identity are inextricably linked. Stigma is a significant source of suffering for many people with mental health concerns. Fathers with a mental illness can be subject to unique forms of stigma, which can influence their perceptions and experiences in a number of ways. Psychiatric and welfare service providers in Australia and internationally have often struggled to effectively engage fathers, either failing to see men as members of a family unit, or failing to offer services tailored to their specific needs

Family structure and child maltreatment: Do some family types place children at greater risk?

Reviewing current research on family structures, this paper aims to assist practitioners and policy-makers who work with children and families to make evidence-informed decisions. This paper reviews the research on whether some family structures expose children to a higher risk of child maltreatment than others. It aims to assist practitioners and policy-makers who work with children and families to make evidence-informed decisions. Key messages The research on whether particular family structures place children at higher risk of maltreatment has produced complex and often ambiguous results. While most of the available research suggests that children in sole-mother families and step families tend to be at higher risk of maltreatment than those in married families, not all findings are consistent. In general, much of the perceived relationship between family structure and child maltreatment can be explained by factors such as poverty, substance misuse and domestic violence. There is no single cause of child maltreatment. Rather, maltreatment reflects the effects of multiple, dynamic, interrelated and, often, cumulative risk factors. Sole-mother families, sole-father families, and step or blended families are overrepresented in Australia\u27s child protection systems. However, there are a number of limitations to the Australian child protection data, which must be noted when interpreting this finding. Although family structure is an easily identifiable risk factor for child maltreatment, its influence can easily be - and is often - exaggerated. It is important that practitioners and policy-makers look further and identify other risk factors that may be more conducive to intervention. Downloads. Online: Family structure and child maltreatment: Do some family types place children at greater risk? Download printable version (PDF 190 KB) Download EPUB version (66 KB) | About EPU

The good practice guide to Child Aware Approaches: keeping children safe and well

Abstract: Child Aware Approaches is a grassroots initiative that engages civil society to develop local approaches, actions and initiatives to keep children safe and well, recognising that protecting children is a shared responsibility. This paper defines Child Aware Approaches, outlines the philosophies and principles underpinning this strategy, and offers case study examples of how the principles can be applied in practice. This paper is intended for service managers and practitioners working with vulnerable children and families, particularly those working in adult-focused service sectors. Key messages: There has been growing awareness that parental problems such as substance misuse, mental illness and family or domestic violence, are often related to negative outcomes for children. This paper is intended as a practical resource for organisations, practitioners and individuals working in social services (particularly services for children, families and adults) to put the needs, views and aspirations of children and young people at the heart of actions to improve child and family wellbeing and safety. The paper explains the five core philosophies and 10 key principles underpinning Child Aware Approaches, to provide practical guidance for those working with vulnerable children and families and to inform policies, procedures and practices within organisations. Each principle can be considered from multiple perspectives (e.g., at the organisational, managerial and practitioner levels). Practice considerations are provided as examples to inspire thought and discussion of the different levels at which action may be required in applying the principles of Child Aware Approaches. Case study examples highlight the diversity of innovative and creative ways in which the principles of Child Aware Approaches have been applied in a variety of settings and situations

International approaches to child protection: what can Australia learn?

The provision of child protection services varies considerably across the world. This paper offers a broad overview of some of the main approaches to child protection used internationally. Using examples from Canada, Sweden, Belgium and the Gaza Strip, it offers policy-makers the chance to reflect on the strengths and weaknesses of different approaches, as well as how these examples might be used to inspire improvements within the Australian context. One way in which policy-makers can reflect critically on Australia’s child protection systems is to develop knowledge of the ways in which different jurisdictions around the world structure and conduct child protection services, and condsider how this knowledge may be relevant to the Australian context. It is often argued that there are two broad orientations to child protection: the “child protection” orientation (evident in Australia, the United States, and the United Kingdom) and the “family service” orientation (of many European countries, including Belgium, Sweden and Denmark). Attempts to respond to rising demand have seen countries that have traditionally possessed a child protection orientation (e.g., Australia) increasingly move towards a family service orientation. A third orientation to child protection has been employed by “child-focused community-based groups”, which have emerged in emergency, transitional and developmental contexts, most notably in Africa and Asia. As country-level service systems are embedded in complex cultural, social and historical contexts, it is not always possible to determine whether different approaches are “evidence-based”, “promising” or “untested”. However, it is possible to identify the strengths and limitations of each service model, as well as their potential applicability to the Australian context

Access to early childhood education in Australia: insights from a qualitative study

Based on interviews with 94 parents in Victoria, South Australia, Tasmania, and Western Australia, this report investigates parents\u27 knowledge of and attitudes towards early childhood education. Executive summary This report documents the background, methodology and findings from the Access to Early Childhood Education (AECE): Qualitative Study, undertaken by the Australian Institute of Family Studies (AIFS) and commissioned by the then Department of Education, Employment and Workplace Relations (DEEWR; now the Department of Education) on behalf of the Early Childhood Data Subgroup (ECDSG). This research was commissioned within the context of the National Partnership Agreement on Early Childhood Education (NP ECE), which jointly committed the Commonwealth and all state and territory governments to achieving universal access to preschool by 2013. The AECE Qualitative Study was undertaken in order to develop a qualitative evidence base about how the concept of “access” to early childhood education (ECE) is defined and understood, and to explore what reasons and barriers exist in relation to access to ECE. A qualitative framework was chosen for this study to enable more in-depth study of any barriers to ECE, and/or factors that lead to parents making particular decisions about their children’s use of ECE. &nbsp

Basic science232. Certolizumab pegol prevents pro-inflammatory alterations in endothelial cell function

Background: Cardiovascular disease is a major comorbidity of rheumatoid arthritis (RA) and a leading cause of death. Chronic systemic inflammation involving tumour necrosis factor alpha (TNF) could contribute to endothelial activation and atherogenesis. A number of anti-TNF therapies are in current use for the treatment of RA, including certolizumab pegol (CZP), (Cimzia ®; UCB, Belgium). Anti-TNF therapy has been associated with reduced clinical cardiovascular disease risk and ameliorated vascular function in RA patients. However, the specific effects of TNF inhibitors on endothelial cell function are largely unknown. Our aim was to investigate the mechanisms underpinning CZP effects on TNF-activated human endothelial cells. Methods: Human aortic endothelial cells (HAoECs) were cultured in vitro and exposed to a) TNF alone, b) TNF plus CZP, or c) neither agent. Microarray analysis was used to examine the transcriptional profile of cells treated for 6 hrs and quantitative polymerase chain reaction (qPCR) analysed gene expression at 1, 3, 6 and 24 hrs. NF-κB localization and IκB degradation were investigated using immunocytochemistry, high content analysis and western blotting. Flow cytometry was conducted to detect microparticle release from HAoECs. Results: Transcriptional profiling revealed that while TNF alone had strong effects on endothelial gene expression, TNF and CZP in combination produced a global gene expression pattern similar to untreated control. The two most highly up-regulated genes in response to TNF treatment were adhesion molecules E-selectin and VCAM-1 (q 0.2 compared to control; p > 0.05 compared to TNF alone). The NF-κB pathway was confirmed as a downstream target of TNF-induced HAoEC activation, via nuclear translocation of NF-κB and degradation of IκB, effects which were abolished by treatment with CZP. In addition, flow cytometry detected an increased production of endothelial microparticles in TNF-activated HAoECs, which was prevented by treatment with CZP. Conclusions: We have found at a cellular level that a clinically available TNF inhibitor, CZP reduces the expression of adhesion molecule expression, and prevents TNF-induced activation of the NF-κB pathway. Furthermore, CZP prevents the production of microparticles by activated endothelial cells. This could be central to the prevention of inflammatory environments underlying these conditions and measurement of microparticles has potential as a novel prognostic marker for future cardiovascular events in this patient group. Disclosure statement: Y.A. received a research grant from UCB. I.B. received a research grant from UCB. S.H. received a research grant from UCB. All other authors have declared no conflicts of interes

Search for dark matter produced in association with bottom or top quarks in √s = 13 TeV pp collisions with the ATLAS detector

A search for weakly interacting massive particle dark matter produced in association with bottom or top quarks is presented. Final states containing third-generation quarks and miss- ing transverse momentum are considered. The analysis uses 36.1 fb−1 of proton–proton collision data recorded by the ATLAS experiment at √s = 13 TeV in 2015 and 2016. No significant excess of events above the estimated backgrounds is observed. The results are in- terpreted in the framework of simplified models of spin-0 dark-matter mediators. For colour- neutral spin-0 mediators produced in association with top quarks and decaying into a pair of dark-matter particles, mediator masses below 50 GeV are excluded assuming a dark-matter candidate mass of 1 GeV and unitary couplings. For scalar and pseudoscalar mediators produced in association with bottom quarks, the search sets limits on the production cross- section of 300 times the predicted rate for mediators with masses between 10 and 50 GeV and assuming a dark-matter mass of 1 GeV and unitary coupling. Constraints on colour- charged scalar simplified models are also presented. Assuming a dark-matter particle mass of 35 GeV, mediator particles with mass below 1.1 TeV are excluded for couplings yielding a dark-matter relic density consistent with measurements

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely

SARS-CoV-2 Omicron is an immune escape variant with an altered cell entry pathway

Vaccines based on the spike protein of SARS-CoV-2 are a cornerstone of the public health response to COVID-19. The emergence of hypermutated, increasingly transmissible variants of concern (VOCs) threaten this strategy. Omicron (B.1.1.529), the fifth VOC to be described, harbours multiple amino acid mutations in spike, half of which lie within the receptor-binding domain. Here we demonstrate substantial evasion of neutralization by Omicron BA.1 and BA.2 variants in vitro using sera from individuals vaccinated with ChAdOx1, BNT162b2 and mRNA-1273. These data were mirrored by a substantial reduction in real-world vaccine effectiveness that was partially restored by booster vaccination. The Omicron variants BA.1 and BA.2 did not induce cell syncytia in vitro and favoured a TMPRSS2-independent endosomal entry pathway, these phenotypes mapping to distinct regions of the spike protein. Impaired cell fusion was determined by the receptor-binding domain, while endosomal entry mapped to the S2 domain. Such marked changes in antigenicity and replicative biology may underlie the rapid global spread and altered pathogenicity of the Omicron variant

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation