Behavioural response of Sea Lamprey (Petromyzon marinus) to acoustic stimuli in a laboratory and field setting

Sea lamprey are invasive in the Laurentian Great Lakes and parasitically feed on valued fishes. Migration barriers and selective pesticides are used to control sea lamprey, but there is a desire to develop additional control tools such as traps with deterrents. Sound has been used as a deterrent for other invasive species but its potential for manipulating sea lamprey behavior in natural stream conditions remains untested. The behavioural threshold for sea lamprey nor a behavioural comparison of life stages has also not been established. Here, behavioral responses of upstream migrating adult sea lamprey in response to low frequency sounds of 70 or 90 Hz was tracked in a small stream using passive integrated transponder (PIT) telemetry. The low frequency sounds shifted sea lamprey distribution with up to 30% more sea lamprey detected on PIT antennas without sound compared to PIT antennas with sound playing. The same frequency tones were used for behavioral responses of adult and juvenile sea lamprey and were tracked in a lab setup. The low frequency sounds changed the sea lampreys behaviour with juvenile and adult sea lamprey showing similar swimming behavioural thresholds and twitch (startle) behavioural thresholds for both frequencies. Future studies could continue testing low frequency sounds in natural setting for use as a natural deterrent at sea lamprey barriers to push sea lamprey toward traps at different life stages and continued studies in a lab setting could be useful for knowledge of the behaviour of sea lamprey to apply to traps for population control

Creating positive spaces using the WELL Building standard™

An accessible practitioner's guide to help inspire architects & designers to understand and practice according to the principles of the globally emerging WELL Building certification standard

Caring and conflicted: mothers' ethical judgements about consumption

Literature on consumer ethics tends to focus on issues within the public sphere, such as the environment, and treats other drivers of consumption decisions, such as family, as non-moral concerns. Consequently, an attitude– behaviour gap is viewed as a straightforward failure by consumers to act ethically. We argue that this is based upon a view of consumer behaviour as linear and unproblematic, and an approach to moral reasoning, arising from a stereotypically masculine understanding of morality, which foregrounds abstract principles. By demonstrating the importance of context to consumption decisions and articulating the impact of caring relationships, we highlight how such decisions are both complex and situated. This is particularly evident for decisions involving the needs of others, as occurs in family life. We argue that the incorporation of care ethics provides both theoretical insights and a more complete account of consumer ethics. This is explored empirically through an investigation of the ethical dilemmas arising from consumption decisions made by mothers of young children. Such decisions juxtapose an ethical consumption orientation (representing impartial concerns) with care for one’s child. Therefore, what has been previously considered a failure to act ethically may in fact be the outcome of complex decision making, which involves competing ethical considerations. We discuss the implications of our findings for theory and practice and how this approach to consumer ethics could be applied more widely

Inhibition of Adipogenesis by the c-Myc Oncoprotein

Enforced expression of c-myc in many cell types is associated with inhibition of terminal differentiation. However, the mechanism by which this occurs remains unclear. In order to address this issue we therefore exploited the ability of c-Myc to block differentiation in the 3T3-L1 cell line, a well characterised in vitro model of adipogenesis. Analysis of 3T3-L1 lines constitutively expressing an avian c-myc transgene revealed an inability to undergo morphological changes or accumulate cytoplasmic triglyceride, which was dependent upon the integrity of the Myc leucine zipper. In order to define the point at which adipogenesis was inhibited we analysed patterns of gene expression during the differentiation programme. This study demonstrated that the Myc block was associated with repression of the late stage markers C/EBPalpha, PPARgamma2, aP2 and SCD1. C/EBPa and PPARgamma2 are key transcriptional regulators of adipogenesis that co-ordinate the expression of genes required for lipid metabolism, including aP2 and SCD1. Hence, repression of these factors provides a molecular basis for the inability of Myc-expressing cell lines to undergo morphological differentiation. Interestingly, a 3T3-L1 clone that had spontaneously lost the ability to differentiate displayed a similar profile of gene expression. However, subtle differences indicated that this block occurred via a different mechanism. Surprisingly, low levels of c-Myc were sufficient to inhibit 3T3-L1 differentiation and this was not associated with transformation or the capacity to undergo apoptosis. Additionally, the continued presence of c-Myc did not alter the ability of the 3T3-L1 line to undergo a number of defined cell cycle events during the early phases of the differentiation programme. Hence, inhibition of adipogenesis was unlikely to reflect altered cell cycle control. It had been proposed that c-Myc inhibits adipogenesis by preventing entry into a differentiation-specific growth arrest (GD) that is both irreversible and a prerequisite for terminal differentiation. However, we were unable to characterise the Gd state by either conventional criteria or by analysis of factors known to mediate cell cycle withdrawal in other differentiation systems. Indeed, irreversible cell cycle exit was only apparent in mature adipocytes, suggesting this was a consequence of terminal differentiation rather than the driving force. Thus, c-Myc did not inhibit adipogenesis by precluding entry into Go- Finally, treatment with 10% foetal calf serum (PCS) was sufficient to rescue Myc-mediated inhibition of adipogenesis but had no effect on the differentiation- defective clone. Abrogation of the Myc block was associated with restoration of the late stage markers, accounting for the ability of the Myc-expressing lines to accumulate lipid in the presence of PCS. Whilst the active component(s) present in PCS have yet to be fully defined, it is likely that growth hormone may be partly responsible for this phenomenon. We therefore conclude that c-Myc inhibits adipogenesis by repressing the expression of master transcription factors. However, this effect is dependent upon external factors, since FCS rescues the phenotype

Realising curriculum possibilities in Wales: Teachers’ initial experiences of re-imagining secondary physical education

This paper provides insight into secondary Physical Education (PE) teachers’ experiences of beginning to re-imagine secondary physical education provision in light of the new Curriculum for Wales, 2022 (CfW). Data were generated through analysis of semi-structured interviews (n = 5) with secondary PE teachers who participated in three workshops which uses a design-thinking methodology. Informed by Ball and colleagues’ conceptualisation of policy work, findings draw attention towards how engagement in the workshops provided a foundation for the participants to begin interpretation and translation of the new CfW and consider re-imagining existing PE provision within the school context. Participants’ interpretations of the new CfW centred around health and physical activity provision which were shaped by a connection with a range of health and physical activity stakeholders. This enabled participants to translate their ideas from the workshops into pedagogical practices within the school context. The paper concludes by suggesting secondary PE teacher’s realisation of the new CfW would be enhanced through opportunities to further integrate disciplinary ideas from health, sport, physical activity, and education across national and global contexts

Copper- and zinc-bearing composite membranes for periodontal repair

Periodontitis (inflammation and destruction of the tooth attachment apparatus) is one of the most widespread diseases in the world. Polymer-bioactive glass composite membranes can be used for the guided tissue regeneration (GTR) of diseased periodontal structures. GTR involves the placement of the membrane to exclude soft epithelial and gingival tissues from the exposed tooth in order to facilitate the regeneration of the more slow-growing periodontal ligament and hard tissues. Bioactive glasses incorporating antimicrobial ions such as silver, zinc and copper have been shown to resist biomaterial-centred infection; although, the presence of these metal ions is reported to reduce bioactivity in some instances. Chitosan, a biodegradable carbohydrate polymer, is a popular choice for GTR membranes as its structure resembles that of bone extracellular matrix. In the present study, copper- and/or zinc-bearing bioactive glasses were prepared by the sol-gel process and incorporated into chitosan membranes by solvent-casting. The in vitro bioactivity and degradation rates of the chitosan-bioactive glass membranes were evaluated with respect to their potential use as GTR membranes

RhoJ/TCL Regulates Endothelial Motility and Tube Formation and Modulates Actomyosin Contractility and Focal Adhesion Numbers

Objective—RhoJ/TCL was identified by our group as an endothelial-expressed Rho GTPase. The aim of this study was to determine its tissue distribution, subcellular localization, and function in endothelial migration and tube formation. Methods and Results—Using in situ hybridization, RhoJ was localized to endothelial cells in a set of normal and cancerous tissues and in the vasculature of mouse embryos; endogenous RhoJ was localized to focal adhesions by immunofluorescence. The proangiogenic factor vascular endothelial growth factor activated RhoJ in endothelial cells. Using either small interfering (si)RNA-mediated knockdown of RhoJ expression or overexpression of constitutively active RhoJ (daRhoJ), RhoJ was found to positively regulate endothelial motility and tubule formation. Downregulating RhoJ expression increased focal adhesions and stress fibers in migrating cells, whereas daRhoJ overexpression resulted in the converse. RhoJ downregulation resulted in increased contraction of a collagen gel and increased phospho–myosin light chain, indicative of increased actomyosin contractility. Pharmacological inhibition of Rho-kinase (which phosphorylates myosin light chain) or nonmuscle myosin II reversed the defective tube formation and migration of RhoJ knockdown cells. Conclusion—RhoJ is endothelial-expressed in vivo, activated by vascular endothelial growth factor, localizes to focal adhesions, regulates endothelial cell migration and tube formation, and modulates actomyosin contractility and focal adhesion numbers