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The Australian disability workforce has grown, and there is compelling evidence that peer work has a number of valuable impacts. Despite these apparent opportunities, there continue to be high levels of unemployment among people with disability and failure to draw on the assets of people with disability in Australian workplaces. To understand these ostensible missed opportunities, this study examined the ways in which lived experience was described as an asset in disability workforce recruitment. Advertisements for positions in New South Wales, Australia, that referred to lived experience or peer work and disability were collected over a 3‐month period. Through a process of content analysis, we found that there were more employment opportunities for people with lived experience of mental illness than for other types of disability. Community engagement was a key function, and peer workers were described as complementary to professionals. Recruitment processes for lived experience jobs were not necessarily accessible. We recommend systemic reforms to facilitate recognition of lived experience as a valuable criterion for disability sector employment and to harness the benefits of a disability peer workforce. [ABSTRACT FROM AUTHOR]

Research on imitation in infancy has primarily focused on "what" and "when" infants imitate. More recently, however, the question why infants imitate has received renewed attention, partly motivated by the finding that infants sometimes selectively imitate the actions of others and sometimes faithfully imitate, or overimitate, the actions of others. The present study evaluates the hypothesis that this varying imitative behavior is related to infants' social traits. To do so, we assessed faithful and selective imitation longitudinally at 12 and 15 months, and extraversion at 15 months. At both ages, selective imitation was dependent on the causal structure of the act. From 12 to 15 months, selective imitation decreased while faithful imitation increased. Furthermore, infants high in extraversion were more faithful imitators than infants low in extraversion. These results demonstrate that the onset of faithful imitation is earlier than previously thought, but later than the onset of selective imitation. The observed relation between extraversion and faithful imitation supports the hypothesis that faithful imitation is driven by the social motivations of the infant. We call this relation the King Louie Effect: like the orangutan King Louie in "The Jungle Book," infants imitate faithfully due to a growing interest in the interpersonal nature of interactions.

Previous studies have reported that infants selectively reproduce observed actions and have argued that this selectivity reflects understanding of intentions and goals, or goal-directed imitation. We reasoned that if selective imitation of goal-directed actions reflects understanding of intentions, infants should demonstrate stability across perceptually and causally dissimilar imitation tasks. To this end, we employed a longitudinal within-participants design to compare the performance of 37 infants on two imitation tasks, with one administered at 13 months and one administered at 14 months. Infants who selectively imitated goal-directed actions in an object-cued task at 13 months also selectively imitated goal-directed actions in a vocal-cued task at 14 months. We conclude that goal-directed imitation reflects a general ability to interpret behavior in terms of mental states. (Contains 1 figure and 1 table.)

Introduction: Down syndrome (DS) is associated with immune dysregulation and a high risk of early onset Alzheimer's disease (AD). Complement is a key part of innate immunity and driver of pathological inflammation, including neuroinflammation in AD. Complement dysregulation has been reported in DS; however, the pattern of dysregulation and its relationship to AD risk is unclear. Methods: Plasma levels of 14 complement biomarkers were measured in 71 adults with DS and 46 controls to identify DS‐associated dysregulation; impact of apolipoprotein E (APOE) ε4 genotype, single nucleotide polymorphisms (SNPs) in CLU and CR1, and dementia on complement biomarkers was assessed. Results: Plasma levels of complement activation products (TCC, iC3b), proteins (C1q, C3, C9), and regulators (C1 inhibitor, factor H, FHR4, clusterin) were significantly elevated in DS versus controls while FI and sCR1 were significantly lower. In DS with AD (n = 13), C3 and FI were significantly decreased compared to non‐AD DS (n = 58). Neither APOE genotype nor CLU SNPs impacted complement levels, while rs6656401 in CR1 significantly impacted plasma sCR1 levels. Conclusions: Complement is dysregulated in DS, likely reflecting the generalized immune dysregulation state; measurement may help identify inflammatory events in individuals with DS. Complement biomarkers differed in DS with and without AD and may aid diagnosis and/or prediction. Highlights: Complement is significantly dysregulated in plasma of people with DS who show changes in levels of multiple complement proteins compared to controls.People with DS and dementia show evidence of additional complement dysregulation with significantly lower levels of C3 and factor I compared to those without dementia.rs6656401 in CR1 was associated with significantly elevated sCR1 plasma levels in DS. [ABSTRACT FROM AUTHOR]

In this article, we use a collaborative approach to autoethnography to explore experiences of power in relation to our identities as people with disabilities and/or mental illnesses. We draw on elements of Bronfenbrenner's ecological systems framework to consider how we enact our own power or struggle against systemic power in making meaning of our lives. As a team of lived experience researchers we wrote, shared and thematically analysed a series of narratives about our personal (microsystem) and institutional (macrosystem) relationships. Through this research process we were able to identify common experiences of being resilient in the face of institutions that dehumanised and problematised us and tried to render us voiceless—exerting 'power over'. In contrast, reflections on our personal relationships highlighted experiences of reciprocity, respect and autonomy that energised our efforts towards meaningful and powerful identities—'power with'. We conclude that by generating strength through our own advocacy, perseverance and caring relationships, we engage dynamics (mesosystem) of empowerment and identity to resist oppressive power at structural levels. This exemplifies the importance of person-centred social work premised on self-determination, autonomy and dignity, and socially just social work that advocates for equitability and fights structural discrimination. [ABSTRACT FROM AUTHOR]

Complement, a critical defence against pathogens, has been implicated as a driver of pathology in COVID‐19. Complement activation products are detected in plasma and tissues and complement blockade is considered for therapy. To delineate roles of complement in immunopathogenesis, we undertook the largest comprehensive study of complement in COVID‐19 to date, comprehensive profiling of 16 complement biomarkers, including key components, regulators and activation products, in 966 plasma samples from 682 hospitalized COVID‐19 patients collected across the hospitalization period as part of the UK ISARIC4C (International Acute Respiratory and Emerging Infection Consortium) study. Unsupervised clustering of complement biomarkers mapped to disease severity and supervised machine learning identified marker sets in early samples that predicted peak severity. Compared to healthy controls, complement proteins and activation products (Ba, iC3b, terminal complement complex) were significantly altered in COVID‐19 admission samples in all severity groups. Elevated alternative pathway activation markers (Ba and iC3b) and decreased alternative pathway regulator (properdin) in admission samples were associated with more severe disease and risk of death. Levels of most complement biomarkers were reduced in severe disease, consistent with consumption and tissue deposition. Latent class mixed modelling and cumulative incidence analysis identified the trajectory of increase of Ba to be a strong predictor of peak COVID‐19 disease severity and death. The data demonstrate that early‐onset, uncontrolled activation of complement, driven by sustained and progressive amplification through the alternative pathway amplification loop is a ubiquitous feature of COVID‐19, further exacerbated in severe disease. These findings provide novel insights into COVID‐19 immunopathogenesis and inform strategies for therapeutic intervention. [ABSTRACT FROM AUTHOR]

The importance of collaborative practice between those who provide services to children with special educational needs is now regarded as essential and is supported strongly by the UK government. However, joint working is often difficult to implement, despite the goodwill of all involved. This paper describes a pilot study aimed at developing collaboration between a local education authority and a National Health Service (NHS) Trust. It reports on the results of the evaluation and discusses aspects of the project that facilitated collaborative working between the various parties involved. (Contains 3 tables.)

Severe bacterial or viral infections can induce a state of immune hyperactivation that can culminate in a potentially lethal cytokine storm. The classic example is toxic shock syndrome, a life-threatening complication of Staphylococcus aureus or Streptococcus pyogenes infection, which is driven by potent toxins known as superantigens (SAgs). SAgs are thought to promote immune evasion via the promiscuous activation of T cells, which subsequently become hyporesponsive, and act by cross-linking major histocompatibility complex class II molecules on antigen-presenting cells to particular β-chain variable (TRBV) regions of αβ T cell receptors (TCRs). Although some of these interactions have been defined previously, our knowledge of SAg-responsive TRBV regions is incomplete. In this study, we found that CD4+ and CD8+ T cells expressing TRBV12-3/12-4+ TCRs were highly responsive to streptococcal pyrogenic exotoxin C (SpeC) and toxic shock syndrome toxin-1 (TSST-1). In particular, SpeC and TSST-1 specifically induced effector cytokine production and the upregulation of multiple coinhibitory receptors among TRBV12-3/12-4+ CD4+ and CD8+ memory T cells, and importantly, these biological responses were dependent on human leukocyte antigen (HLA)-DR. Collectively, these data provided evidence of functionally determinative and therapeutically relevant interactions between SpeC and TSST-1 and CD4+ and CD8+ memory T cells expressing TRBV12-3/12-4+ TCRs, mediated via HLA-DR. In peripheral blood mononuclear cells from healthy human donors, the superantigens SpeC and TSST-1 are shown to specifically activate TRBV12-3/12-4+ memory T cells. [ABSTRACT FROM AUTHOR]

Context Differences of sex development (DSD) represent a wide range of conditions presenting at different ages to various health professionals. Establishing a diagnosis, supporting the family, and developing a management plan are important. Objective We aimed to better understand the presentation and prevalence of pediatric DSD. Methods A retrospective, observational cohort study was undertaken in a single tertiary pediatric center of all children and young people (CYP) referred to a DSD multidisciplinary team over 25 years (1995-2019). In total, 607 CYP (520 regional referrals) were included. Data were analyzed for diagnosis, sex-assignment, age and mode of presentation, additional phenotypic features, mortality, and approximate point prevalence. Results Among the 3 major DSD categories, sex chromosome DSD was diagnosed in 11.2% (68/607) (most commonly 45,X/46,XY mosaicism), 46,XY DSD in 61.1% (371/607) (multiple diagnoses often with associated features), while 46,XX DSD occurred in 27.7% (168/607) (often 21-hydroxylase deficiency). Most children (80.1%) presented as neonates, usually with atypical genitalia, adrenal insufficiency, undescended testes or hernias. Those presenting later had diverse features. Rarely, the diagnosis was made antenatally (3.8%, n = 23) or following incidental karyotyping/family history (n = 14). Mortality was surprisingly high in 46,XY children, usually due to complex associated features (46,XY girls, 8.3%; 46,XY boys, 2.7%). The approximate point prevalence of neonatal referrals for investigation of DSD was 1 in 6347 births, and 1 in 5101 overall throughout childhood. Conclusion DSD represent a diverse range of conditions that can present at different ages. Pathways for expert diagnosis and management are important to optimize care. [ABSTRACT FROM AUTHOR]