Development prediction of sagittal itermaxillary relations in patients with complete unilateral cleft lip and palate during puberty

The main objective was to find a predictive model for the development of the jaw in patients with the most frequent facial cleft malformation, i.e. complete unilateral cleft lip and palate (UCLPc) by means of multivariate methods. This prediction is urgently needed from the clinical aspect. It will make it possible to provide early detection for patients at risk of adverse development. The study is based on a long-term X-ray cephalometric follow-up of 73 boys with UCLPc during puberty. Prediction was performed by methods of multiple regression and regression partitioning trees. The best equation predicts the intermaxillary relations at 15 years of age with high reliability (determination coefficient R2 = 0.822). The model was successfully verified statistically. In clinical practice, we suggest the use of a simple method of regression partitioning trees where the measurement of only 1 to 4 dimensions in a ten-year-old patient would suffice to achieve a reliable reading of the ANB angle at 15 years of age from a tree diagram.     

Child protection contact among children of culturally and linguistically diverse backgrounds: A South Australian linked data study

Aim

To describe the cumulative incidence of child protection (CP) system contact, maltreatment type, source of reports to age 7 years, and socio-demographic characteristics for culturally and linguistically diverse (CALD) Australian children.

Methods

We used CP, education, health, and birth registrations data for children followed from birth up to age 7 from the South Australian Better Evidence, Better Outcomes, Linked Data (SA BEBOLD) platform. Participants: SA born children enrolled in their first year of school from 2009 to 2015 (n = 76 563). CALD defined as non-Aboriginal or Torres Strait Islander, spoken language other than English, Indigenous or Sign, or had at least one parent born in a non-English speaking country. Outcomes measures: For CALD and non-CALD children, we estimated the cumulative incidence (risk) of CP contacts up to age 7, relative risk and risk differences for all levels of CP contact from notification to out-of-home care (OOHC), primary maltreatment type, reporter type, and socio-economic characteristics. Sensitivity analyses explored different population selection criteria and CALD definitions.

Results

By age 7, 11.2% of CALD children had ‘screened-in’ notifications compared to 18.8% of non-CALD (risk difference [RD] 7.6 percentage points (95% confidence interval: 6.9–8.3)), and 0.6% of CALD children experienced OOHC compared to 2.2% of non-CALD (RD 1.6 percentage points (95% confidence interval: 1.3–1.8)). Emotional abuse was the most common substantiated maltreatment type for CALD and neglect for non-CALD. Among both groups, the most common reporter sources were police and education sector. Socio-economic characteristics were broadly similar. Sensitivity analyses results were consistent with primary analyses.

Conclusion

By age 7, CALD children had lower risk of contact with all levels of CP. Estimates based on primary and sensitivity analyses suggested CALD children were 5–9 percentage points less likely to have a report screened-in, and from 1.0 to 1.7 percentage points less likely to have experienced OOHC.     

Multistakeholder Etiological Explanation Agreement and Adolescent/Parent Treatment Engagement

Client–therapist consensus has been hypothesized to be an important element of culturally competent care. However, little is known about the relationship between explanatory model agreement and treatment engagement, particularly for services involving adolescents, where both parent and youth perspectives may need to be considered. This longitudinal study collected youth, parent, and therapist survey data on etiological beliefs as well as therapist-rated treatment engagement related to a culturally diverse sample of 285 outpatient mental health service-using youth (aged 12–18, M = 14.06 at Time 1 interview; 40% female). Youth–therapist and parent–therapist agreement on beliefs about the etiology of the youth’s mental health problems were examined in relationship to later treatment engagement. Although parent–therapist agreement was unrelated to parent engagement, youth–therapist coendorsement of etiological beliefs predicted overall youth treatment engagement. In addition, youth–therapist agreement significantly predicted specific aspects of youth engagement: client–therapist interaction, communication/openness, and client’s perceived usefulness of treatment. Results speak to the importance of agreement between therapist and youth upon key issues related to the youth’s problems in mental health treatment settings and support facilitation of consensus as a component of culturally competent care. Differences between findings for youth and parents suggest that therapeutic relationships may vary for different stakeholders, indicating a need to consider individual perspectives and contributions separately.     

Craniofacial dysmorphology in 22q11.2 deletion syndrome by 3D laser surface imaging and geometric morphometrics: Illuminating the developmental relationship to risk for psychosis

Persons with 22q11.2 deletion syndrome (22q11.2DS) are characterized inter alia by facial dysmorphology and greatly increased risk for psychotic illness. Recent studies indicate facial dysmorphology in adults with schizophrenia. This study evaluates the extent to which the facial dysmorphology of 22q11.2DS is similar to or different from that evident in schizophrenia. Twenty‐one 22q11.2DS‐sibling control pairs were assessed using 3D laser surface imaging. Geometric morphometrics was applied to 30 anatomical landmarks, 480 geometrically homologous semi‐landmarks on curves and 1720 semi‐landmarks interpolated on each 3D facial surface. Principal component (PC) analysis of overall shape space indicated PC2 to strongly distinguish 22q11.2DS from controls. Visualization of PC2 indicated 22q11.2DS and schizophrenia to be similar in terms of overall widening of the upper face, lateral displacement of the eyes/orbits, prominence of the cheeks, narrowing of the lower face, narrowing of nasal prominences and posterior displacement of the chin; they differed in terms of facial length (increased in 22q11.2DS, decreased in schizophrenia), mid‐face and nasal prominences (displaced upwards and outwards in 22q11.2DS, less prominent in schizophrenia); lips (more prominent in 22q11.2DS; less prominent in schizophrenia) and mouth (open mouth posture in 22q11.2DS; closed mouth posture in schizophrenia). These findings directly implicate dysmorphogenesis in a cerebral‐craniofacial domain that is common to 22q11.2DS and schizophrenia and which may repay further clinical and genetic interrogation in relation to the developmental origins of psychotic illness. © 2015 The Authors. American Journal of Medical Genetics Part A Published by Wiley Periodicals, Inc.     

Recruiting and retaining couples for an HIV prevention intervention: lessons learned from the PARTNERS project

Intervening with both members of a couple has been recommended as an important strategy for human immunodeficiency virus prevention. Analyses of focus groups and in-depth interviews with project personnel involved in recruitment and retention for the Partners Against Risk-Taking: A Networking and Evaluation Research Study project identified, at the termination of the project, barriers and facilitators to recruiting couples. Barriers included logistical problems of coordinating two people's schedules, sensitivity of the topic and challenges related to recruitment efforts focused on one partner only. Strategies to overcome such barriers were to increase availability of project personnel and recruit both partners simultaneously, with recruitment teams consisting of men and women. Challenges related to recruiting and retaining couples remain significant and should be considered before undertaking couples interventions.     

Glutamatergic regulation prevents hippocampal-dependent age-related cognitive decline through dendritic spine clustering

The dementia of Alzheimer’s disease (AD) results primarily from degeneration of neurons that furnish glutamatergic corticocortical connections that subserve cognition. Although neuron death is minimal in the absence of AD, age-related cognitive decline does occur in animals as well as humans, and it decreases quality of life for elderly people. Age-related cognitive decline has been linked to synapse loss and/or alterations of synaptic proteins that impair function in regions such as the hippocampus and prefrontal cortex. These synaptic alterations are likely reversible, such that maintenance of synaptic health in the face of aging is a critically important therapeutic goal. Here, we show that riluzole can protect against some of the synaptic alterations in hippocampus that are linked to age-related memory loss in rats. Riluzole increases glutamate uptake through glial transporters and is thought to decrease glutamate spillover to extrasynaptic NMDA receptors while increasing synaptic glutamatergic activity. Treated aged rats were protected against age-related cognitive decline displayed in nontreated aged animals. Memory performance correlated with density of thin spines on apical dendrites in CA1, although not with mushroom spines. Furthermore, riluzole-treated rats had an increase in clustering of thin spines that correlated with memory performance and was specific to the apical, but not the basilar, dendrites of CA1. Clustering of synaptic inputs is thought to allow nonlinear summation of synaptic strength. These findings further elucidate neuroplastic changes in glutamatergic circuits with aging and advance therapeutic development to prevent and treat age-related cognitive decline.Cognitive decline often occurs with aging in rodents (1), nonhuman primates (2), and humans (3). Memory loss (4) and executive impairment (5) are of the most functional importance, mediated primarily by the hippocampus and related areas of the medial temporal lobe and the prefrontal cortex (PFC), respectively. The neural circuits vulnerable to aging are composed of glutamatergic pyramidal neurons that furnish corticocortical connections between the association cortices as well as the excitatory hippocampal connections (2, 6). Dendritic spine changes, which appear to be the primary site of structural plasticity in the adult brain (7), occur in the pyramidal neurons of the PFC (5) and in the hippocampus (8, 9) with aging and correlate with behavioral decline. Spines form the postsynaptic component of most excitatory synapses in the cerebral cortex and are capable of rapid formation, expansion, contraction, and elimination (10, 11).Synaptic glutamatergic activity is neuroprotective and critical for long-term potentiation (LTP) and memory formation, whereas extrasynaptic NMDA receptor activity promotes long-term depression and excitotoxicity (12, 13). There is some evidence that astrocytic glutamate transporters decrease with aging (14, 15), and consequently reduce glutamate uptake (14, 16, 17). Reduced glutamate uptake can lead to glutamate spillover to the extrasynaptic space with electrophysiological repercussions (14). The potential use of glutamate modulators as a therapeutic target to regulate the synaptic age-related glutamatergic dysregulation in those vulnerable neural circuits remains to be further investigated.Riluzole is a glutamate modulator that decreases glutamate release (18) and facilitates astrocytic glutamate uptake (19–21). These actions have been suggested to increase glutamate-glutamine cycling, enhancing synaptic glutamatergic activity while preventing excessive glutamate overflow to the extrasynaptic space in rodents (21, 22) and humans (23). Riluzole has also been shown to increase oxidative metabolism with mitochondrial enhancing properties (24) and to increase BDNF expression (25). We hypothesized that improved regulation of the glutamatergic synapse with the glutamate modulator riluzole would promote synaptic NMDA receptor activation while preventing extrasynaptic NMDA activity, thereby protecting against age-related cognitive decline, through induction of neuroplastic changes in the hippocampus and PFC. An important neuroplastic mechanism is clustering of dendritic spines because it significantly empowers neural circuits with nonlinear summation of synaptic inputs (26, 27) and is dependent on neuronal activity (28, 29). For this study, we focused on pyramidal neurons within CA1 and pyramidal neurons in layer 3 of the prelimbic region of medial PFC, an area where we have demonstrated age-related spine loss in middle-aged animals previously (30).