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Unintentional injuries are a leading cause of child death. The present study evaluated the effectiveness of a behavioral injury prevention program for children aged 3-18 years and their caregivers. To accommodate families during the Coronavirus-19 pandemic, training was modified to be delivered virtually. Forty-one children aged 3-18 years and 14 parents/caregivers of children aged 3-5 years attended one of several 4-hour online injury prevention training sessions directed toward residents of Washington state. Training was targeted to three different developmental stages (ages 3-5, 6-12 and 13-18 years). Study outcomes included knowledge about injury prevention strategies, perceived vulnerability for injury, self-efficacy to engage in safety behaviors and behavioral intentions to be safe. Following training, participants showed improved self-efficacy to stay safe, excellent knowledge about the learned material and increased behavioral intention to engage safely. There was minimal change in perceived vulnerability to injury among children; caregivers of young children felt their children were somewhat less vulnerable to injury following the training. Almost all participants said they would recommend the program to others. Results suggest that a virtual behavioral training program delivered remotely is feasible and may be effective to create behavior change and reduce child injury risk. Given its scalability and reach, such programs are recommended for further study, refinement and, if demonstrated effective in larger-scale controlled trials, dissemination to address the leading cause of child mortality in the United States, unintentional injury.

Fungi can have important beneficial and detrimental effects on animals, yet our understanding of the diversity and function of most bee-associated fungi is poor. Over 2 million bumblebee colonies are traded globally every year, but the presence and transport of viable fungi within them is unknown. Here, we explored whether any culturable fungi could be isolated from commercial bumblebee nests. We collected samples of various substrates from within 14 bumblebee colonies, including the honey, honey cup wall, egg cup wall, and frass then placed them on agar and recorded any growth. Fungal morphotypes were then subcultured and their ITS region sequenced for identification. Overall, we cultured 11 fungal species from the various nest substrates. These included both pathogenic and non-pathogenic fungi, such as Aspergillus sp., Penicillium sp., and Candida sp. Our results provide the first insights into the diversity of viable fungal communities in commercial bumblebee nests. Further research is needed to determine if these fungi are unique to commercial colonies or prevalent in wild bumblebee nests, and crucially to determine the ecological and evolutionary implications of these fungi in host colonies.

For security and justice professionals (e.g., police officers, lawyers, judges), the thousands of peer-reviewed articles on nonverbal communication represent important sources of knowledge. However, despite the scope of the scientific work carried out on this subject, professionals can turn to programs, methods, and approaches that fail to reflect the state of science. The objective of this article is to examine (i) concepts of nonverbal communication conveyed by these programs, methods, and approaches, but also (ii) the consequences of their use (e.g., on the life or liberty of individuals). To achieve this objective, we describe the scope of scientific research on nonverbal communication. A program (SPOT; Screening of Passengers by Observation Techniques), a method (the BAI; Behavior Analysis Interview) and an approach (synergology) that each run counter to the state of science are examined. Finally, we outline five hypotheses to explain why some organizations in the fields of security and justice are turning to pseudoscience and pseudoscientific techniques. We conclude the article by inviting these organizations to work with the international community of scholars who have scientific expertise in nonverbal communication and lie (and truth) detection to implement evidence-based practices.

Summary: Cardiac surgery requiring cardiopulmonary bypass is associated with postoperative acute kidney injury and neurocognitive disorders, including delirium. Intra‐operative inflammation and/or impaired tissue perfusion/oxygenation are thought to be contributors to these outcomes. It has been hypothesised that these problems may be ameliorated by the highly selective α2‐agonist, dexmedetomidine. We tested the effects of dexmedetomidine on renal and cerebral microcirculatory tissue perfusion, oxygenation and histology in a clinically relevant ovine model. Sixteen sheep were studied while conscious, after induction of anaesthesia and during 2 h of cardiopulmonary bypass. Eight sheep were allocated randomly to receive an intravenous infusion of dexmedetomidine (0.4–0.8 μg.kg‐1.h‐1) from induction of anaesthesia to the end of cardiopulmonary bypass, and eight to receive an equivalent volume of matched placebo (0.9% sodium chloride). Commencement of cardiopulmonary bypass decreased renal medullary tissue oxygenation in the placebo group (mean (95%CI) 5.96 (4.24–7.23) to 1.56 (0.84–2.09) kPa, p = 0.001), with similar hypoxic levels observed in the dexmedetomidine group (6.33 (5.33–7.07) to 1.51 (0.33–2.39) kPa, p = 0.002). While no differences in kidney function (i.e. reduced creatinine clearance) were evident, a greater incidence of histological renal tubular injury was observed in sheep receiving dexmedetomidine (7/8 sheep) compared with placebo (2/8 sheep), p = 0.041. Graded on a semi‐quantitative scale (0–3), median (IQR [range]) severity of histological renal tubular injury was higher in the dexmedetomidine group compared with placebo (1.5 (1–2 [0–3]) vs. 0 (0–0.3 [0–1]) respectively, p = 0.013). There was no difference in cerebral tissue microglial activation (neuroinflammation) between the groups. Dexmedetomidine did not reduce renal medullary hypoxia or cerebral neuroinflammation in sheep undergoing cardiopulmonary bypass. [ABSTRACT FROM AUTHOR]

Research and theory in nonverbal communication have made great advances toward understanding the patterns and functions of nonverbal behavior in social settings. Progress has been hindered, we argue, by presumptions about nonverbal behavior that follow from both received wisdom and faulty evidence. In this article, we document four persistent misconceptions about nonverbal communication—namely, that people communicate using decodable body language; that they have a stable personal space by which they regulate contact with others; that they express emotion using universal, evolved, iconic, categorical facial expressions; and that they can deceive and detect deception, using dependable telltale clues. We show how these misconceptions permeate research as well as the practices of popular behavior experts, with consequences that extend from intimate relationships to the boardroom and courtroom and even to the arena of international security. Notwithstanding these misconceptions, existing frameworks of nonverbal communication are being challenged by more comprehensive systems approaches and by virtual technologies that ambiguate the roles and identities of interactants and the contexts of interaction. [ABSTRACT FROM AUTHOR]

Background/Objectives: The available evidence from randomised controlled trials suggests that vitamin B12 supplementation does not improve neurologic function in older people with marginal but not deficient Vitamin B12 status. This secondary analysis used data from the Older People and Enhanced Neurological function (OPEN) randomised controlled trial to assess whether baseline vitamin B12 status or change in vitamin B12 status over 12 months altered the effectiveness of dietary vitamin B12 supplementation on neurologic function in asymptomatic older people with depleted vitamin B12 status at study entry. Subjects/Methods: Vitamin B12 status was measured as serum concentrations of vitamin B12, holotranscobalamin, homocysteine and via a composite indicator (cB12). Neurological function outcomes included eleven electrophysiological measures of sensory and motor components of peripheral and central nerve function. Linear regression analyses were restricted to participants randomised into the intervention arm of the OPEN trial (n=91). Results: Analyses revealed an inconsistent pattern of moderate associations between some measures of baseline vitamin B12 status and some neurological responses to supplementation. The directions of effect varied and heterogeneity in effect across outcomes could not be explained according to type of neurological outcome. There was no evidence of differences in the neurological response to vitamin B12 supplementation according to change from baseline over 12 months in any indicator of B12 status. Conclusions: This secondary analysis of high-quality data from the OPEN trial provides no evidence that baseline (or change from baseline) vitamin B12 status modifies the effect of vitamin B12 supplementation on peripheral or central nerve conduction among older people with marginal vitamin B12 status. There is currently insufficient evidence of efficacy for neurological function to support population-wide recommendations for vitamin B12 supplementation in healthy asymptomatic older people with marginal vitamin B12 status., Author(s): L M Miles [sup.1] , E Allen [sup.1] , R Clarke [sup.2] , K Mills [sup.3] , R Uauy [sup.1] , A D Dangour [sup.1] Author Affiliations: (1) Department [...]

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease affecting spinal cord motoneurons (MN) with an associative connection to Frontotemporal Lobar Dementia (FTLD). The endoplasmic reticulum (ER) bound Sigma-1 Receptor (S1R) chaperone protein localizes to specialized ER cisternae within 10 nm of the plasma membrane in spinal cord ventral horn cholinergic post synaptic C-terminals. Removal of the S1R gene in the Superoxide Dismutase-1 (SOD-1) mouse model of ALS exacerbated the neurodegenerative condition and resulted in a significantly reduced longevity when compared to the SOD-1/S1R wild type (WT) mouse. The proposed amelioration of the ALS phenotype by the S1R is likely due to a “brake” on excitation of the MN as evidenced by a reduction in action potential generation in the MN of the WT when compared to the S1R KO mouse MN. Although the precise signal transduction pathway(s) regulated by the S1R in the MN has/have not been elucidated at present, it is likely that direct or indirect functional interactions occur between the S1R in the ER cisternae with voltage gated potassium channels and/or with muscarinic M2 receptor signaling in the post synaptic plasma membrane. Possible mechanisms for regulation of MN excitability by S1R are discussed.

Background: HIV prevention research projects often apply 'empowerment' approaches to achieve scientific goals and redress power imbalances between the study team and marginalized communities, particularly communities of color. Simultaneously, there have been calls for both scientific leadership and study methods that recognize the role of systemic racism within study team and the power differentials between study leadership and the communities. Methods: ETOILE, Experiences of Tensions in Organizations and Interventions Leveraged for Empowerment and Prevention, is a French-American cooperative project to explore and characterize how researchers in France and the US have addressed tensions related to race/racism-related power imbalances within two empowerment-based HIV prevention projects and how these tensions influence study implementation. Each project involved has predominately white leadership and predominately Black (US) or Black African/Black French (France) staff and community representatives. ETOILE applies reflexive, comparative, qualitative process evaluation methods to identify how tensions related to race/racism-related power imbalances manifest in various aspects of the study. Originally planned as a face-to-face intervisitation between French and US teams, we have conducted with three semi-structured, web-based group interviews, where study scientific leadership, staff, and community representatives, discussed within-project power relations, representation in study leadership and the role of race/racism, privilege and voice, related to community location, education and status. Interviews were conducted via Zoom and Skype and transcribed. Analysis is ongoing. Results: Preliminary analyses have identified several overarching themes, including racialized organization of labor within each team; resistance to sharing power; need for strategies and opportunities for Black scholars in HIV prevention research; the role of country-specific history and contexts; and need for white researchers to systematically undo marginalization of black researchers. Conclusions: Failing to reflexively consider the role of within study team-based, race/racism-related power imbalances in empowerment-based HIV prevention research may threaten the integrity and impact of the research and potentially reinforce the social conditions the research may be attempting to mitigate. Our hope is that by identifying how these tensions emerge in our own research and engaging in a structured analysis of the similarities and differences across contexts, we will identify best practices that reduce race/racism-related power imbalances and advance both in US and French HIV prevention research., OA17.04 T. Albritton (1); K.B. Coulibaly (2); I. Zoumenou (3); M. Paige (1); C. Davis (4); S. Carillon (5); D. Matthews (1); P. Saintonge Austin (6); L. Miles (1); V. [...]

Summary: In the intravenous iron therapy to treat iron deficiency anaemia in patients undergoing major abdominal surgery (PREVENTT) trial, the use of intravenous iron did not reduce the need for blood transfusion or reduce patient complications or length of hospital stay. As part of the trial protocol, serum was collected at randomisation and on the day of surgery. These samples were analysed in a central laboratory for markers of iron deficiency. We performed a secondary analysis to explore the potential interactions between pre‐operative markers of iron deficiency and intervention status on the trial outcome measures. Absolute iron deficiency was defined as ferritin <30 μg.l−1; functional iron deficiency as ferritin 30–100 μg.l−1 or transferrin saturation < 20%; and the remainder as non‐iron deficient. Interactions were estimated using generalised linear models that included different subgroup indicators of baseline iron status. Co‐primary endpoints were blood transfusion or death and number of blood transfusions, from randomisation to 30 days postoperatively. Secondary endpoints included peri‐operative change in haemoglobin, postoperative complications and length of hospital stay. Most patients had iron deficiency (369/452 [82%]) at randomisation; one‐third had absolute iron deficiency (144/452 [32%]) and half had functional iron deficiency (225/452 [50%]). The change in pre‐operative haemoglobin with intravenous iron compared with placebo was greatest in patients with absolute iron deficiency, mean difference 8.9 g.l−1, 95%CI 5.3–12.5; moderate in functional iron deficiency, mean difference 2.8 g.l−1, 95%CI −0.1 to 5.7; and with little change seen in those patients who were non‐iron deficient. Subgroup analyses did not suggest that intravenous iron compared with placebo reduced the likelihood of death or blood transfusion at 30 days differentially across subgroups according to baseline ferritin (p = 0.33 for interaction), transferrin saturation (p = 0.13) or in combination (p = 0.45), or for the number of blood transfusions (p = 0.06, 0.29, and 0.39, respectively). There was no beneficial effect of the use of intravenous iron compared with placebo, regardless of the metrics to diagnose iron deficiency, on postoperative complications or length of hospital stay. [ABSTRACT FROM AUTHOR]

Hirschsprung's disease (HSCR) is characterized by aganglionosis from failure of neural crest cell (NCC) migration to the distal hindgut. Up to 40% of HSCR patients suffer Hirschsprung's-associated enterocolitis (HAEC), with an incidence that is unchanged from the pre-operative to the post-operative state. Recent reports indicate that signaling pathways involved in NCC migration may also be involved in the development of secondary lymphoid organs. We hypothesize that gastrointestinal (GI) mucosal immune defects occur in HSCR that may contribute to enterocolitis. EdnrB was deleted from the neural crest (EdnrBNCC-/-) resulting in mutants with defective NCC migration, distal colonic aganglionosis and the development of enterocolitis. The mucosal immune apparatus of these mice was interrogated at post-natal day (P) 21-24, prior to histological signs of enterocolitis. We found that EdnrBNCC-/- display lymphopenia of their Peyer's Patches, the major inductive site of GI mucosal immunity. EdnrBNCC-/- Peyer's Patches demonstrate decreased B-lymphocytes, specifically IgM+IgDhi (Mature) B-lymphocytes, which are normally activated and produce IgA following antigen presentation. EdnrBNCC-/- animals demonstrate decreased small intestinal secretory IgA, but unchanged nasal and bronchial airway secretory IgA, indicating a gut-specific defect in IgA production or secretion. In the spleen, which is the primary source of IgA-producing Mature B-lymphocytes, EdnrBNCC-/- animals display decreased B-lymphocytes, but an increase in Mature B-lymphocytes. EdnrBNCC-/- spleens are also small and show altered architecture, with decreased red pulp and a paucity of B-lymphocytes in the germinal centers and marginal zone. Taken together, these findings suggest impaired GI mucosal immunity in EdnrBNCC-/- animals, with the spleen as a potential site of the defect. These findings build upon the growing body of literature that suggests that intestinal defects in HSCR are not restricted to the aganglionic colon but extend proximally, even into the ganglionated small intestine and immune cells.