Simulation-based education improves student self-efficacy in physiotherapy assessment and management of paediatric patients.

BACKGROUND: The Australian Physiotherapy Council mandates that physiotherapy clinical education be sufficient to produce graduates who are competent to practice across the lifespan. Due to a lack of opportunities for paediatric clinical placements, there is a risk of graduates not having the opportunity to develop competency in paediatric physiotherapy. To address this risk, simulation-based education (SBE) has been proposed as an educational strategy to address the placement shortfall. Despite encouraging evidence for its use in physiotherapy education, there is limited evidence supporting its use specifically in paediatric populations. The aims of this research were to investigate the effect of SBE on student self-efficacy in the physiotherapy assessment and management of paediatric clients, and to determine student satisfaction with SBE as a learning strategy. METHODS: Three interactive SBE sessions were run during the undergraduate paediatric physiotherapy unit at the campus of one Australian university. Self-efficacy was surveyed before and after each session, to determine confidence in clinical skills, clinical decision-making, treatment preparation and planning, communication skills; evaluating and modifying interventions, and interprofessional practice. Student satisfaction with SBE as a learning strategy was surveyed after the final SBE session. RESULTS: For the 164 participants included in this study, self-efficacy survey response rate varied from 77 to 96% for each session. Significant increases in mean student self-efficacy were recorded for all questions (p <  0.001). A total of 139 (85%) responded to the learning reactionnaire with 78.6% indicating they were very satisfied with SBE as a learning strategy. Written comments from 41 participants identified 'experience' as the primary theme. CONCLUSION: SBE had a significant positive effect on student self-efficacy in the physiotherapy assessment and management of paediatric patients. Students also perceived SBE to be a valuable learning experience. Future research is needed to investigate whether the improvement in self-efficacy achieved through SBE translates into improved student performance during workplace-based clinical placements.

Linguistic ostracism causes prejudice: Support for a serial mediation effect.

This research investigated the effects of linguistic ostracism, defined as any communication setting in which a target individual (or group) is ostracized by another individual (or group) in a language that the target has extremely limited ability to understand. Participants were included or ostracized by their group members during a computer-mediated group discussion. Half of the ostracized participants were linguistically ostracized via their group members conversing with one another in a language the participant did not know well (Spanish Ostracism: SO), or in a language the participant did know well (English Ostracism: EO). SO participants reported feeling less similar than both included and EO participants. SO participants also reported being angrier and expressed more prejudice than included participants (and EO participants using effect size estimates). Results also provided support for the hypothesized serial mediation model. Findings are discussed in terms of implications for intergroup relations.

Construct validity of the need to belong scale: mapping the nomological network.

Nine studies examined the construct validity of the Need to Belong Scale. The desire for acceptance and belonging correlated with, but was distinct from, variables that involve a desire for social contact, such as extraversion and affiliation motivation. Furthermore, need to belong scores were not related to insecure attachment or unfulfilled needs for acceptance. Need to belong was positively correlated with extraversion, agreeableness, and neuroticism and with having an identity that is defined in terms of social attributes. Need to belong was associated with emotional reactions to rejection, values involving interpersonal relationships, and subclinical manifestations of certain personality disorders.

Changes in sources and perceived quality of social supports among formerly homeless persons receiving assertive community treatment services.

We recruited a sample of individuals who were formerly homeless that received assertive community treatment (ACT) services to assess differences in their sources and perceived quality of social support related to changes in their residence status. Standardized questionnaires were administered to 22 participants via face-to-face interviews, including various measures of social support and relationship quality. Results indicated that participants mentioned ACT staff members significantly more often than any other relationship category (e.g., friends or family) as sources of social support. Participants also indicated that the quality of their relationships with ACT staff members was significantly better than relationships maintained before and during their homelessness. These findings indicate that ACT staff can serve as social supports for clients on their caseloads, and they further suggest that clients perceive these worker-consumer relationships to be of high quality. Implications related to community integration are discussed.

Evaluation of the contributions of ADAMs 9, 12, 15, 17, and 19 to heart development and ectodomain shedding of neuregulins beta1 and beta2.

Defects in heart development are the most common congenital abnormalities in humans, providing a strong incentive to learn more about the underlying causes. Previous studies have implicated the metalloprotease-disintegrins ADAMs (a disintegrin and metalloprotease) 17 and 19 as well as heparin binding EGF-like growth factor (HB-EGF) and neuregulins in heart development in mice. Here, we show that mice lacking both ADAMs 17 and 19 have exacerbated defects in heart development compared to mice lacking either ADAM, providing the first evidence for redundant or compensatory functions of ADAMs in development. Moreover, we identified additional compensatory or redundant roles of ADAMs 9 and 19 in morphogenesis of the mitral valve and cardiac outflow tract. Cell biological studies designed to address the functions of these ADAMs in shedding of HB-EGF uncovered a contribution of ADAM19 to this process, but this was only evident in the absence of the major HB-EGF sheddase, ADAM17. In addition, ADAM17 emerged as the major sheddase for neuregulins beta1 and beta2 in mouse embryonic fibroblasts. These results raise the possibility that ADAMs 9, 17, and 19 contribute to heart development in humans and have implications for understanding the mechanisms underlying congenital heart disease.

Metalloprotease-disintegrin ADAM8: expression analysis and targeted deletion in mice.

ADAM8 (a disintegrin and metalloprotease 8, also referred to as MS2/CD156a) is a membrane-anchored metalloprotease that was first identified in a macrophage cell line and has been implicated in neurodegenerative diseases. Here, we evaluated the expression of ADAM8 during mouse development and generated mice lacking ADAM8 (Adam8-/- mice). During early mouse development, ADAM8 is expressed by maternal cells in the decidua and by trophoblast derivatives of the embryo but not in the derivatives of the inner cell mass. At later stages, prominent expression of ADAM8 is seen in the embryo proper, in the gonadal ridge, thymus, developing cartilage and bone, brain and spinal cord, and in the mesenchyme in close proximity to the branch point between the jugular vein and developing lymphatic vessels. Examination of Adam8-/- mice, however, revealed no major defects in these or other structures during development or in adult tissues and no evident pathological phenotypes.

Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligands.

All ligands of the epidermal growth factor receptor (EGFR), which has important roles in development and disease, are released from the membrane by proteases. In several instances, ectodomain release is critical for activation of EGFR ligands, highlighting the importance of identifying EGFR ligand sheddases. Here, we uncovered the sheddases for six EGFR ligands using mouse embryonic cells lacking candidate-releasing enzymes (a disintegrin and metalloprotease [ADAM] 9, 10, 12, 15, 17, and 19). ADAM10 emerged as the main sheddase of EGF and betacellulin, and ADAM17 as the major convertase of epiregulin, transforming growth factor alpha, amphiregulin, and heparin-binding EGF-like growth factor in these cells. Analysis of adam9/12/15/17-/- knockout mice corroborated the essential role of adam17-/- in activating the EGFR in vivo. This comprehensive evaluation of EGFR ligand shedding in a defined experimental system demonstrates that ADAMs have critical roles in releasing all EGFR ligands tested here. Identification of EGFR ligand sheddases is a crucial step toward understanding the mechanism underlying ectodomain release, and has implications for designing novel inhibitors of EGFR-dependent tumors.

Induction and patterning of the primitive streak, an organizing center of gastrulation in the amniote.

The primitive streak is the organizing center for amniote gastrulation. It defines the future embryonic midline and serves as a conduit of cell migration for germ layer formation. The migration patterns of endodermal and mesodermal precursors through the streak have been studied in great detail. Additional new breakthroughs recently have revealed the cell biological and molecular mechanisms that govern streak induction and patterning. These findings include (1) identification of the ontogeny and inductive signals of streak precursors, (2) the potential cellular mechanism of streak extension, and (3) the molecular and functional diversification along the anterior-posterior and mediolateral axes within the primitive streak. These findings indicate that amniote embryos initiate gastrulation by using both evolutionarily conserved and divergent mechanisms. The data also provide a foundation for understanding how the midline axis is defined and maintained during gastrulation of the amniotes.

Cell death along the embryo midline regulates left-right sidedness.

During embryogenesis, left-right sidedness is established by asymmetric expression of laterality genes. A recent model predicts the presence of a functional midline that divides the left side of the embryonic disc from the right side, separating left- and right-inducing signals. We show evidence that this midline is formed from a distinct population of cells within the primitive streak. Cells in the dorsal midline of the chick primitive streak display unique expression of the gastrulation markers fgf-8 and brachyury. These midline cells are fated to die, and dead cells remain in the midline during gastrulation. Inhibition of midline cell death compromises the early expression of laterality genes, such as shh and nodal and randomizes the direction of heart looping. We suggest that cell death along the primitive streak midline is a novel mechanism involved in the regulation of left-right asymmetry during early embryogenesis.