Domestic and Family Violence Affecting Children and Young People from Culturally and Racially Marginalized Migrant Backgrounds in Australia: A Scoping Review of Child Experiences and Service Responses.

In Australia, children and families from culturally and racially marginalized (CARM) migrant backgrounds experience a range of compounding structural and interpersonal factors that limit help-seeking and exacerbate the impacts of domestic and family violence (DFV). This scoping review examines the current state of knowledge on how children and young people from CARM migrant backgrounds experience DFV, and the services that respond to DFV including child protection services. A systematic search was conducted across PsycINFO, MEDLINE, and CINAHL databases and Google Scholar, alongside a complementary grey literature search. Articles were included in the review if participants were from CARM migrant backgrounds, and the article included information related to children and young people's experiences of DFV, and the DFV service system. The review found 19 articles that met selection criteria. Due to limited research on this topic in Australia, most articles focused on children and young people's experiences shared through parental, carer or service provider perspectives. To our knowledge, this is the first scoping review to examine how children and young people from CARM migrant backgrounds experience DFV. Findings demonstrate children and young people are victim-survivors of multiple forms of DFV. Children and young people's engagement with the DFV service system is often accompanied by feelings of fear and distrust. Findings suggest that to strengthen system responses to DFV, services must build their capability to implement intersectional approaches that simultaneously support the safety and well-being of both the child and the non-violent parent or carer.

Facilitators and Barriers to the Implementation of a School-Based Intervention for Anxiety.

School-based cognitive behavioural interventions for anxiety are found to be effective, but there is a lack of research on their implementation in real world settings. The current study aims to explore the facilitators and barriers to the implementation of a school-based intervention for anxiety through a qualitative process evaluation. Evaluation of the implementation of Let's Introduce Anxiety Management (LIAM), a six-session school-based cognitive behavioural intervention, was conducted. LIAM was implemented by non-mental health professionals trained and coached on the model. Semi-structured interviews with stakeholders (N = 15) were analysed with grounded theory and framework analysis. Forty-one practitioners were trained and coached on LIAM, with thirty-five children and young people receiving the intervention. Facilitators (e.g. systemic collaboration, self-efficacy and an enabling context) and barriers (e.g. the exclusivity of the intervention and a lack of systemic understanding) to implementation emerged as themes. Implementing school-based interventions is complex and requires the involvement of multiple stakeholders.

The Borrelia afzelii outer membrane protein BAPKO_0422 binds human factor-H and is predicted to form a membrane-spanning ß-barrel.

The deep evolutionary history of the Spirochetes places their branch point early in the evolution of the diderms, before the divergence of the present day Proteobacteria. As a spirochete, the morphology of the Borrelia cell envelope shares characteristics of both Gram-positive and Gram-negative bacteria. A thin layer of peptidoglycan, tightly associated with the cytoplasmic membrane, is surrounded by a more labile outer membrane (OM). This OM is rich in lipoproteins but with few known integral membrane proteins. The outer membrane protein A (OmpA) domain is an eight-stranded membrane-spanning ß-barrel, highly conserved among the Proteobacteria but so far unknown in the Spirochetes. In the present work, we describe the identification of four novel OmpA-like ß-barrels from Borrelia afzelii, the most common cause of erythema migrans (EM) rash in Europe. Structural characterization of one these proteins (BAPKO_0422) by SAXS and CD indicate a compact globular structure rich in ß-strand consistent with a monomeric ß-barrel. Ab initio molecular envelopes calculated from the scattering profile are consistent with homology models and demonstrate that BAPKO_0422 adopts a peanut shape with dimensions 25×45 Å (1 Å=0.1 nm). Deviations from the standard C-terminal signature sequence are apparent; in particular the C-terminal phenylalanine residue commonly found in Proteobacterial OM proteins is replaced by isoleucine/leucine or asparagine. BAPKO_0422 is demonstrated to bind human factor H (fH) and therefore may contribute to immune evasion by inhibition of the complement response. Encoded by chromosomal genes, these proteins are highly conserved between Borrelia subspecies and may be of diagnostic or therapeutic value.

Anti-NMDA receptor encephalitis: a cause of acute psychosis and catatonia.

Anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis is a newly described form of encephalitis associated with prominent psychiatric symptoms at onset. Recognition of the symptom complex is the key to diagnosis. Most patients with anti-NMDAR encephalitis develop a multistage illness that progresses from initial psychiatric symptoms to memory disturbance, seizures, dyskinesia, and catatonia. Psychiatric manifestations include anxiety, mania, social withdrawal, and psychosis (i.e., delusions, hallucinations, disorganized behavior). The disorder is more common in females (80%), in approximately half of whom it is associated with an underlying ovarian teratoma. Treatment involves immunosuppression, with steroids and intravenous immunoglobulin considered first line. The disorder is particularly relevant to psychiatrists, because most patients are initially seen by psychiatric services. Psychiatrists should consider anti-NMDAR encephalitis in patients presenting with psychosis as well as dyskinesia, seizures, and/or catatonia, especially if there is no history of a psychiatric disorder. We present the case of a 37-year-old woman who demonstrated many of the key clinical features of this potentially treatable disorder.

Reproducibility of 24-h post-exercise changes in energy intake in overweight and obese women using current methodology.

Direct observation(s) of energy intake (EI) via buffet meals served in the laboratory are often carried out within short-term exercise intervention studies. The reproducibility of values obtained has not been assessed either under resting control conditions or post-exercise, in overweight and obese females. A total of fourteen sedentary, pre-menopausal females (BMI 30.0 (SD 5.1) kg/m²) completed four trials; two exercise and two control. Each trial lasted 24 h spanning over 2 d; conducted from afternoon on day 1 and morning on day 2. An exercise session to expend 1.65 MJ was completed on day 1 of exercise trials, and three buffet meals were served during each trial. Reproducibility of post-exercise changes in energy and macronutrient intakes was assessed at each individual buffet meal by intraclass correlation coefficient (r(i)). Only the r(i) values for post-exercise changes in energy (r(i) 0.44 (95 % CI - 0.03, 0.77), P = 0.03) and fat intake (r(i) 0.51 (95 % CI 0.04, 0.81), P = 0.02) at the lunch buffet meal achieved statistical significance; however, these r i values were weak and had large associated 95 % CI, which indicates a large degree of variability associated with these measurements. Energy and macronutrient intakes at the breakfast and evening buffet meals were not reproducible. This study concludes that the frequently used laboratory-based buffet meal method of assessing EI does not produce reliable, reproducible post-exercise changes in EI in overweight and obese women.

NICU noise and the preterm infant.

Premature infants in the NICU are often exposed to continuous loud noise despite research documenting the presence and damaging effects of noise on the preterm infant's development. Excessive auditory stimulation creates negative physiologic responses such as apnea and fluctuations in heart rate, blood pressure, and oxygen saturation. Preterm infants exposed to prolonged excessive noise are also at increased risk for hearing loss, abnormal brain and sensory development, and speech and language problems. Reducing noise levels in the NICU can improve the physiologic stability of sick neonates and therefore enlarge the potential for infant brain development. Recommendations include covering incubators with blankets, removing noisy equipment from the incubator environment, implementing a quiet hour, educating staff to raise awareness, and encouraging staff to limit conversation near infants.

NCR-1 and NCR-2, the C. elegans homologs of the human Niemann-Pick type C1 disease protein, function upstream of DAF-9 in the dauer formation pathways.

Mutations in the human NPC1 gene cause most cases of Niemann-Pick type C (NP-C) disease, a fatal autosomal recessive neurodegenerative disorder. NPC1 is implicated in intracellular trafficking of cholesterol and glycolipids, but its exact function remains unclear. The C. elegans genome contains two homologs of NPC1, ncr-1 and ncr-2, and an ncr-2; ncr-1 double deletion mutant forms dauer larvae constitutively (Daf-c). We have analyzed the phenotypes of ncr single and double mutants in detail, and determined the ncr gene expression patterns. We find that the ncr genes function in a hormonal branch of the dauer formation pathway upstream of daf-9 and daf-12, which encode a cytochrome P450 enzyme and a nuclear hormone receptor, respectively. ncr-1 is expressed broadly in tissues with high levels of cholesterol, whereas expression of ncr-2 is restricted to a few cells. Both Ncr genes are expressed in the XXX cells, which are implicated in regulating dauer formation via the daf-9 pathway. Only the ncr-1 mutant is hypersensitive to cholesterol deprivation and to progesterone, an inhibitor of intracellular cholesterol trafficking. Our results support the hypothesis that ncr-1 and ncr-2 are involved in intracellular cholesterol processing in C. elegans, and that a sterol-signaling defect is responsible for the Daf-c phenotype of the ncr-2; ncr-1 mutant.

EGF receptor signalling protects smooth-cuticle cells from apoptosis during Drosophila ventral epidermis development.

Patterning of the Drosophila ventral epidermis is a tractable model for understanding the role of signalling pathways in development. Interplay between Wingless and EGFR signalling determines the segmentally repeated pattern of alternating denticle belts and smooth cuticle: spitz group genes, which encode factors that stimulate EGFR signalling, induce the denticle fate, while Wingless signalling antagonizes the effect of EGFR signalling, allowing cells to adopt the smooth-cuticle fate. Medial fusion of denticle belts is also a hallmark of spitz group genes, yet its underlying cause is unknown. We have studied this phenotype and discovered a new function for EGFR signalling in epidermal patterning. Smooth-cuticle cells, which are receiving Wingless signalling, are nevertheless dependent on EGFR signalling for survival. Reducing EGFR signalling results in apoptosis of smooth-cuticle cells between stages 12 and 14, bringing adjacent denticle regions together to result in denticle belt fusions by stage 15. Multiple factors stimulate EGFR signalling to promote smooth-cuticle cell survival: in addition to the spitz group genes, Rhomboid-3/roughoid, but not Rhomboid-2 or -4, and the neuregulin-like ligand Vein also function in survival signalling. Pointed mutants display the lowest frequency of fusions, suggesting that EGFR signalling may inhibit apoptosis primarily at the post-translational level. All ventral epidermal cells therefore require some level of EGFR signalling; high levels specify the denticle fate, while lower levels maintain smooth-cuticle cell survival. This strategy might guard against developmental errors, and may be conserved in mammalian epidermal patterning.

Drosophila necrotic mutations mirror disease-associated variants of human serpins.

Polymerization of members of the serpin superfamily underlies diseases as diverse as cirrhosis, angioedema, thrombosis and dementia. The Drosophila serpin Necrotic controls the innate immune response and is homologous to human alpha(1)-antitrypsin. We show that necrotic mutations that are identical to the Z-deficiency variant of alpha(1)-antitrypsin form urea-stable polymers in vivo. These necrotic mutations are temperature sensitive, which is in keeping with the temperature-dependent polymerization of serpins in vitro and the role of childhood fevers in exacerbating liver disease in Z alpha-antitrypsin deficiency. In addition, we identify two nec mutations homologous to an antithrombin point mutation that is responsible for neonatal thrombosis. Transgenic flies carrying an S>F amino-acid substitution equivalent to that found in Siiyama-variant antitrypsin (nec(S>F.UAS)) fail to complement nec-null mutations and demonstrate a dominant temperature-dependent inactivation of the wild-type nec allele. Taken together, these data establish Drosophila as a powerful system to study serpin polymerization in vivo.

Orbit/Mast, the CLASP orthologue of Drosophila, is required for asymmetric stem cell and cystocyte divisions and development of the polarised microtubule network that interconnects oocyte and nurse cells during oogenesis.

Drosophila oocyte differentiation is preceded by the formation of a polarised 16-cell cyst from a single progenitor stem cell as a result of four rounds of asymmetric mitosis followed by incomplete cytokinesis. We show that the Orbit/Mast microtubule-associated protein is required at several stages in the formation of such polarised 16-cell cysts. In wild-type cysts, the Orbit/Mast protein not only associates with the mitotic spindle and its poles, but also with the central spindle (spindle remnant), ring canal and fusome, suggesting it participates in interactions between these structures. In orbit mutants, the stem cells and their associated fusomes are eventually lost as Orbit/Mast protein is depleted. The mitotic spindles of those cystocytes that do divide are either diminutive or monopolar, and do not make contact with the fusome. Moreover, the spindle remnants and ring canals fail to differentiate correctly in such cells and the structure of fusome is compromised. The Orbit/Mast protein thus appears to facilitate multiple interactions of the fusome with mitotic spindles and ring canals. This ensures correct growth of the fusome into a branched asymmetrically distributed organelle that is pre-determinative of 16-cell cyst formation and oocyte fate specification. Finally the Orbit/Mast protein is required during mid-oogenesis for the organisation of the polarised microtubule network inside the 16-cell cyst that ensures oocyte differentiation. The localisation of CLIP-190 to such microtubules and to the fusome is dependent upon Orbit/Mast to which it is complexed.