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Social determinants of health have a significant effect on health and wellbeing. There is increasing recognition of the need for health professionals to measure and address the social determinants affecting the health and wellbeing of their clients, yet efforts to do so are hampered by the lack of a validated, brief self-report measure that covers a range of determinants in a single measure. This study aimed to develop and conduct initial validation of a measure of social determinants of health, the Steps to Better Health Questionnaire (STBH-Q). Construct validity was assessed via factorial validity using exploratory factor analysis and second order confirmatory factor analysis (CFA), followed by convergent validity against the EQ-5D-5L quality of life measure. Reliability was assessed by exploring internal consistency. A convenience sampling approach was used, and 330 Australian adults aged 18 and over completed the survey. This initial validation suggests an underlying structure of STBH-Q consisting of Access; Employment, FinancesEducation; Safety; PhysicalMental Health; and FamilyChildhood, confirmed by second-order CFA. Results of convergent validity testing with the EQ-5D-5L demonstrated significant correlations of modest to moderate strength with the instrument as a whole and with the sub-scales in the expected direction. Cronbach's alpha for the five scales ranged from 0.561 to 0.827. Further development and validation of the STBH-Q is needed to explore alternative questions regarding social connection and habits/addictions and add additional items to factors with only two items.Health and wellbeing are influenced by a range of factors, including the circumstances in which we are born and live our lives, called social determinants of health. It is important to measure social determinants of health at an individual level so they can be addressed, yet existing questionnaires tend to focus on a limited number of determinants or are time consuming and complex for individuals to fill in. We developed a simple measure of social determinants of health that can be easily completed and conducted a study to determine the validity and reliability of the questionnaire. We found that the questionnaire is a valid and reliable measure of social determinants of health.

In North America, nest site competition from invasive cavity-nesting birds can limit the opportunities for successful nesting by native birds. Managing invasive species is costly and complex, requiring input from biologists, decision makers, and the public. An informed and engaged public can play an important role in mitigating the negative effects of invasive avian species. However, little is known regarding the publics’ knowledge, attitudes, and behaviors toward non-native bird species. We examined the association between participating in a citizen science project and enjoyment, knowledge, and management of two non-native avian species in North America: European starlings (Sturnus vulgaris) and house sparrows (Passer domesticus). We administered a pre and post survey to 947 people who monitor nest boxes in the United States and Canada, 30% of whom were also reporting their observations to NestWatch, a citizen science project focused on nesting birds. We found that NestWatch participants were more likely to have negative views of non-native species, score higher on bird identification tasks, and manage for invasive species than non-participants. The most important predictor for undertaking management activities was respondents' perceptions of whether they believed non-native birds to be a problem at the continental scale, underscoring the important role of individual factors such as perception. Our study also highlights the important role citizen science may play in shaping attitudes and behaviors and increasing knowledge. We propose a conceptual model describing the mechanisms by which citizen science can be leveraged for management of invasive species.

Background Congenital malformations involving the Mullerian ducts are observed in around 5% of infertile women. Complete aplasia of the uterus, cervix, and upper vagina, also termed Mullerian aplasia or Mayer–Rokitansky–Kuster–Hauser (MRKH) syndrome, occurs with an incidence of around 1 in 4500 female births, and occurs in both isolated and syndromic forms. Previous reports have suggested that a proportion of cases, especially syndromic cases, are caused by variation in copy number at different genomic loci. Methods In order to obtain an overview of the contribution of copy number variation to both isolated and syndromic forms of Mullerian aplasia, copy number assays were performed in a series of 63 cases, of which 25 were syndromic and 38 isolated. Results A high incidence (9/63, 14%) of recurrent copy number variants in this cohort is reported here. These comprised four cases of microdeletion at 16p11.2, an autism susceptibility locus not previously associated with Mullerian aplasia, four cases of microdeletion at 17q12, and one case of a distal 22q11.2 microdeletion. Microdeletions at 16p11.2 and 17q12 were found in 4/38 (10.5%) cases with isolated Mullerian aplasia, and at 16p11.2, 17q12 and 22q11.2 (distal) in 5/25 cases (20%) with syndromic Mullerian aplasia. Conclusion The finding of microdeletion at 16p11.2 in 2/38 (5%) of isolated and 2/25 (8%) of syndromic cases suggests a significant contribution of this copy number variant alone to the pathogenesis of Mullerian aplasia. Overall, the high incidence of recurrent copy number variants in all forms of Mullerian aplasia has implications for the understanding of the aetiopathogenesis of the condition, and for genetic counselling in families affected by it.

Four lines of evidence, proceeding from correlational outcomes to findings from true experiments, are reviewed as preliminary support for the hypothesis that learning is increased when students attempt to construct explanatory answers to questions about to-be-learned content (i.e., answers requiring inferential transformation of questioned material). The lines of evidence are as follows: (a) When students generate explanatory answers to questions as part of learning in a group, better learning occurs for students doing the explaining. (b) Manipulations that increase student generation of explanations to questions during group interaction increase learning. (e) Attempting: to predict the content of upcoming text by responding to prequestions (including explanatory justifications for predicted answers) increases learning of prequestioned content. (d) Attempting to explain the significance of to-be-learned facts increases learning of those facts. Requiring learners to construct explanatory answers about new ...

This study explored whether or not standard administration and scoring of conventional articulation tests accurately identified children as phonologically disordered and whether or not information from these tests established severity level and programming needs. Results of standard scoring procedures from the Assessment of Phonological Processes-Revised, the Goldman-Fristoe Test of Articulation, the Photo Articulation Test, and the Weiss Comprehensive Articulation Test were compared for 20 phonologically impaired children. All tests identified the children as phonologically delayed/disordered, but the conventional tests failed to clearly and consistently differentiate varying severity levels. Conventional test results also showed limitations in error sensitivity, ease of computation for scoring procedures, and implications for remediation programming. The use of some type of rule-based analysis for phonologically impaired children is highly recommended.

Intestinal malrotation is well covered in the surgical literature from the point of view of operative management, but few reviews to date have attempted to provide a comprehensive examination of the topic from the point of view of aetiology, in particular genetic aetiology. Following a brief overview of molecular embryology of midgut rotation, we present in this article instances of and case reports and case series of intestinal malrotation in which a genetic aetiology is likely. Autosomal dominant, autosomal recessive, X-linked and chromosomal forms of the disorder are represented. Most occur in syndromic form, that is to say, in association with other malformations. In many instances, recognition of a specific syndrome is possible, one of several examples discussed being the recently described association of intestinal malrotation with alveolar capillary dysplasia, due to mutations in the forkhead box transcription factor FOXF1. New advances in sequencing technology mean that the identification of the genes mutated in these disorders is more accessible than ever, and paediatric surgeons are encouraged to refer to their colleagues in clinical genetics where a genetic aetiology seems likely.

Alveolar capillary dysplasia with misalignment of pulmonary veins (ACD/MPV) is a rare, neonatally lethal developmental disorder of the lung with defining histologic abnormalities typically associated with multiple congenital anomalies (MCA). Using array CGH analysis, we have identified six overlapping microdeletions encompassing the FOX transcription factor gene cluster in chromosome 16q24.1q24.2 in patients with ACD/MPV and MCA. Subsequently, we have identified four different heterozygous mutations (frameshift, nonsense, and no-stop) in the candidate FOXF1 gene in unrelated patients with sporadic ACD/MPV and MCA. Custom-designed, high-resolution microarray analysis of additional ACD/MPV samples revealed one microdeletion harboring FOXF1 and two distinct microdeletions upstream of FOXF1, implicating a position effect. DNA sequence analysis revealed that in six of nine deletions, both breakpoints occurred in the portions of Alu elements showing eight to 43 base pairs of perfect microhomology, suggesting replication error Microhomology-Mediated Break-Induced Replication (MMBIR)/Fork Stalling and Template Switching (FoSTeS) as a mechanism of their formation. In contrast to the association of point mutations in FOXF1 with bowel malrotation, microdeletions of FOXF1 were associated with hypoplastic left heart syndrome and gastrointestinal atresias, probably due to haploinsufficiency for the neighboring FOXC2 and FOXL1 genes. These differences reveal the phenotypic consequences of gene alterations in cis.