Can Social Cognitive Theory Influence Breakfast Frequency in an Institutional Context: A Qualitative Study.

Breakfast is considered an important meal, especially for people who are about to commence a long or demanding workday, and for roles that may involve physical tasks and a requirement to remain alert and vigilant in potentially high-risk situations. This study looks at breakfast consumption influences within two workplace institutional settings, namely military and mining. Semi-structured interviews were conducted with military personnel (n = 12) and mining employees (n = 12) to understand their breakfast consumption behaviour at work and at home, and the associated behavioural influences. The interview questions were framed by social cognitive theory. Overall, cognitive and environmental influences were the most prominent influences on breakfast consumption, less evident were behavioural influences. A negative stereotype of workplace institutional food services emerged as one of the most significant barriers to breakfast consumption for those already at work. Considerations of environmental influences on behaviour may need to be broadened beyond physical barriers and social influences, to include perceptions of the behavioural environment. Programs that aim to increase breakfast consumption must create areas where their employees want to go. Food systems need to ensure nutritious, quality, and appealing food is available. Interventions need to increase participants' knowledge, improve their attitudes, and create positive expectations for breakfast.

A systematic review of interventions to increase breakfast consumption: a socio-cognitive perspective.

OBJECTIVE: Regular breakfast skipping is related to unhealthy dietary behaviours, such as consuming an overall poorer quality diet and lower rates of physical activity, both of which are linked to a higher BMI. Adolescent breakfast skippers struggle with mental focus, sleep issues and lower grades. Solutions that can be implemented to overcome breakfast skipping are needed. DESIGN: A systematic literature review was undertaken to identify programmes that aimed to increase breakfast eating. Following the PRISMA framework, studies were sourced to examine details of behaviour change, evidence of theory use and other important programme learnings and outcomes. SETTING: Breakfast consumption empirical studies published from 2000 onwards. PARTICIPANTS: Nineteen empirical studies that aimed to improve breakfast eating behaviour. RESULTS: Out of the nineteen studies examined, ten studies reported an increase in breakfast consumption frequency for the entire study group or subgroups. Seven studies found no change, one was inconclusive and one observed a decrease in breakfast frequency. Positive changes to the dietary quality of breakfast were observed in five of the studies that did not observe increased frequency of breakfast consumption. Only six studies reported using theory in the intervention. CONCLUSIONS: This evidence review points needed to extend theory application to establish a reliable evidence base that can be followed by practitioners seeking to increase breakfast eating rates in their target population.

Mutations in the gene encoding IFT dynein complex component WDR34 cause Jeune asphyxiating thoracic dystrophy.

Bidirectional (anterograde and retrograde) motor-based intraflagellar transport (IFT) governs cargo transport and delivery processes that are essential for primary cilia growth and maintenance and for hedgehog signaling functions. The IFT dynein-2 motor complex that regulates ciliary retrograde protein transport contains a heavy chain dynein ATPase/motor subunit, DYNC2H1, along with other less well functionally defined subunits. Deficiency of IFT proteins, including DYNC2H1, underlies a spectrum of skeletal ciliopathies. Here, by using exome sequencing and a targeted next-generation sequencing panel, we identified a total of 11 mutations in WDR34 in 9 families with the clinical diagnosis of Jeune syndrome (asphyxiating thoracic dystrophy). WDR34 encodes a WD40 repeat-containing protein orthologous to Chlamydomonas FAP133, a dynein intermediate chain associated with the retrograde intraflagellar transport motor. Three-dimensional protein modeling suggests that the identified mutations all affect residues critical for WDR34 protein-protein interactions. We find that WDR34 concentrates around the centrioles and basal bodies in mammalian cells, also showing axonemal staining. WDR34 coimmunoprecipitates with the dynein-1 light chain DYNLL1 in vitro, and mining of proteomics data suggests that WDR34 could represent a previously unrecognized link between the cytoplasmic dynein-1 and IFT dynein-2 motors. Together, these data show that WDR34 is critical for ciliary functions essential to normal development and survival, most probably as a previously unrecognized component of the mammalian dynein-IFT machinery.

Short-rib polydactyly and Jeune syndromes are caused by mutations in WDR60.

Short-rib polydactyly syndromes (SRPS I-V) are a group of lethal congenital disorders characterized by shortening of the ribs and long bones, polydactyly, and a range of extraskeletal phenotypes. A number of other disorders in this grouping, including Jeune and Ellis-van Creveld syndromes, have an overlapping but generally milder phenotype. Collectively, these short-rib dysplasias (with or without polydactyly) share a common underlying defect in primary cilium function and form a subset of the ciliopathy disease spectrum. By using whole-exome capture and massive parallel sequencing of DNA from an affected Australian individual with SRPS type III, we detected two novel heterozygous mutations in WDR60, a relatively uncharacterized gene. These mutations segregated appropriately in the unaffected parents and another affected family member, confirming compound heterozygosity, and both were predicted to have a damaging effect on the protein. Analysis of an additional 54 skeletal ciliopathy exomes identified compound heterozygous mutations in WDR60 in a Spanish individual with Jeune syndrome of relatively mild presentation. Of note, these two families share one novel WDR60 missense mutation, although haplotype analysis suggested no shared ancestry. We further show that WDR60 localizes at the base of the primary cilium in wild-type human chondrocytes, and analysis of fibroblasts from affected individuals revealed a defect in ciliogenesis and aberrant accumulation of the GLI2 transcription factor at the centrosome or basal body in the absence of an obvious axoneme. These findings show that WDR60 mutations can cause skeletal ciliopathies and suggest a role for WDR60 in ciliogenesis.

Directed evaluation of enterotoxigenic Escherichia coli autotransporter proteins as putative vaccine candidates.

BACKGROUND: Enterotoxigenic Escherichia coli (ETEC) is a major diarrheal pathogen in developing countries, where it accounts for millions of infections and hundreds of thousands of deaths annually. While vaccine development to prevent diarrheal illness due to ETEC is feasible, extensive effort is needed to identify conserved antigenic targets. Pathogenic Escherichia coli, including ETEC, use the autotransporter (AT) secretion mechanism to export virulence factors. AT proteins are comprised of a highly conserved carboxy terminal outer membrane beta barrel and a surface-exposed amino terminal passenger domain. Recent immunoproteomic studies suggesting that multiple autotransporter passenger domains are recognized during ETEC infection prompted the present studies. METHODOLOGY: Available ETEC genomes were examined to identify AT coding sequences present in pathogenic isolates, but not in the commensal E. coli HS strain. Passenger domains of the corresponding autotransporters were cloned and expressed as recombinant antigens, and the immune response to these proteins was then examined using convalescent sera from patients and experimentally infected mice. PRINCIPAL FINDINGS: Potential AT genes shared by ETEC strains, but absent in the E. coli commensal HS strain were identified. Recombinant passenger domains derived from autotransporters, including Ag43 and an AT designated pAT, were recognized by antibodies from mice following intestinal challenge with H10407, and both Ag43 and pAT were identified on the surface of ETEC by flow cytometry. Likewise, convalescent sera from patients with ETEC diarrhea recognized Ag43 and pAT, suggesting that these proteins are expressed during both experimental and naturally occurring ETEC infections and that they are immunogenic. Vaccination of mice with recombinant passenger domains from either pAT or Ag43 afforded protection against intestinal colonization with ETEC. CONCLUSIONS: Passenger domains of conserved autotransporter proteins could contribute to protective immune responses that develop following infection with ETEC, and these antigens consequently represent potential targets to explore in vaccine development.

Phenomenon of declining anxiety sensitivity scores: a controlled investigation.

BACKGROUND: Repeated administration of anxiety sensitivity measures can often produce declining scores, even in ostensible control groups, which is a significant concern for researchers. The reasons for these changes are as yet unknown, but could be because of regression to the mean in samples selected on extreme scores, exposure to general information about anxiety contained in psychiatric interviews, or mere exposure to anxiety sensitivity information. METHODS: This study sought to experimentally evaluate these potential explanations using a comprehensive measure of anxiety sensitivity and its subcomponents, a non-anxiety sensitivity measure (self-esteem), and participants representing the full spectrum of anxiety sensitivity. RESULTS: Results indicated significant decreases in anxiety sensitivity scores (but not self-esteem scores) that could not be accounted for by regression to the mean or exposure to information about anxiety in general. CONCLUSIONS: Several potential explanations for these findings are reviewed and implications for research study designs are discussed.