A systematic review of the health and well-being impacts of school gardening: synthesis of quantitative and qualitative evidence

Background: School gardening programmes are increasingly popular, with suggested benefits including healthier eating and increased physical activity. Our objectives were to understand the health and well-being impacts of school gardens and the factors that help or hinder their success. Methods: We conducted a systematic review of quantitative and qualitative evidence (PROSPERO CRD42014007181). We searched multiple databases and used a range of supplementary approaches. Studies about school gardens were included if they reported on physical or mental health or well-being. Quantitative studies had to include a comparison group. Studies were quality appraised using appropriate tools. Findings were narratively synthesised and the qualitative evidence used to produce a conceptual framework to illustrate how benefits might be accrued. Results: Evidence from 40 articles (21 quantitative studies; 16 qualitative studies; 3 mixed methods studies) was included. Generally the quantitative research was poor. Evidence for changes in fruit and vegetable intake was limited and based on self-report. The qualitative research was better quality and ascribed a range of health and well-being impacts to school gardens, with some idealistic expectations for their impact in the long term. Groups of pupils who do not excel in classroom activities were thought to particularly benefit. Lack of funding and over reliance on volunteers were thought to threaten success, while involvement with local communities and integration of gardening activities into the school curriculum were thought to support success. Conclusion: More robust quantitative research is needed to convincingly support the qualitative evidence suggesting wide ranging benefits from school gardens

Making the Case for “Whole System” Approaches Integrating Public Health and Housing

This is the final version. Available on open from MDPI via the DOI in this recordHousing conditions have been an enduring focus for public health activity throughout the modern public health era. However, the nature of the housing and health challenge has changed in response to an evolution in the understanding of the diverse factors influencing public health. Today, the traditional public health emphasis on the type and quality of housing merges with other wider determinants of health. These include the neighbourhood, community, and “place” where a house is located, but also the policies which make access to a healthy house possible and affordable for everyone. Encouragingly, these approaches to policy and action on housing have the potential to contribute to the “triple win” of health and well-being, equity, and environmental sustainability. However, more effective housing policies (and in public health in general) that adopt more systemic approaches to addressing the complex interactions between health, housing, and wider environment are needed. This paper illustrates some of the key components of the housing and health challenge in developed countries, and presents a conceptual model to co-ordinate activities that can deliver the “triple win.” This is achieved by offering a perspective on how to navigate more effectively, inclusively and across sectors when identifying sustainable housing interventions.This research was supported in part by funding provided by: (1) the South West Academic Health Science Network (grant number SW AHSN G005) and the European Regional Development Fund (grant number SZ07660) for the SMARTLINE Project; (2) the Eaga Charitable Trust; (3) the National Institute for Health Research Health Protection Research Unit (NIHR HPRU) in Environmental Change and Health at the London School of Hygiene and Tropical Medicine in partnership with Public Health England, and in collaboration with the University of Exeter, University College London, and the Met Office; and (4) the European Commission Horizon 2020 funded INHERIT project, coordinated by EuroHealthNet (grant number 667364)

Non-peptidic antagonists of the CGRP receptor, BIBN4096BS and MK-0974, interact with the calcitonin receptor-like receptor via methionine-42 and RAMP1 via tryptophan-74

The receptor for calcitonin gene-related peptide (CGRP) has been the target for the development of novel small molecule antagonists for the treatment of migraine. Two such antagonists, BIBN4096BS and MK-0974, have shown great promise in clinical trials and hence a deeper understanding of the mechanism of their interaction with the receptor is now required. The structure of the CGRP receptor is unusual since it is comprised of a hetero-oligomeric complex between the calcitonin receptor-like receptor (CRL) and an accessory protein (RAMP1). Both the CLR and RAMP1 components have extracellular domains which interact with each other and together form part of the peptide-binding site. It seems likely that the antagonist binding site will also be located on the extracellular domains and indeed Trp-74 of RAMP1 has been shown to form part of the binding site for BIBN4096BS. However, despite a chimeric study demonstrating the role of the N-terminal domain of CLR in antagonist binding, no specific residues have been identified. Here we carry out a mutagenic screen of the extreme N-terminal domain of CLR (residues 23-63) and identify a mutant, Met-42-Ala, which displays 48-fold lower affinity for BIBN4096BS and almost 900-fold lower affinity for MK-0974. In addition, we confirm that the Trp-74-Lys mutation at human RAMP1 reduces BIBN4096BS affinity by over 300-fold and show for the first time a similar effect for MK-0974 affinity. The data suggest that the non-peptide antagonists occupy a binding site close to the interface of the N-terminal domains of CLR and RAMP1

CGRP, adrenomedullin and adrenomedullin 2 display endogenous GPCR agonist bias in primary human cardiovascular cells.

Agonist bias occurs when different ligands produce distinct signalling outputs when acting at the same receptor. However, its physiological relevance is not always clear. Using primary human cells and gene editing techniques, we demonstrate endogenous agonist bias with physiological consequences for the calcitonin receptor-like receptor, CLR. By switching the receptor-activity modifying protein (RAMP) associated with CLR we can "re-route" the physiological pathways activated by endogenous agonists calcitonin gene-related peptide (CGRP), adrenomedullin (AM) and adrenomedullin 2 (AM2). AM2 promotes calcium-mediated nitric oxide signalling whereas CGRP and AM show pro-proliferative effects in cardiovascular cells, thus providing a rationale for the expression of the three peptides. CLR-based agonist bias occurs naturally in human cells and has a fundamental purpose for its existence. We anticipate this will be a starting point for more studies into RAMP function in native environments and their importance in endogenous GPCR signalling

Common and Distinct Roles of Juvenile Hormone Signaling Genes in Metamorphosis of Holometabolous and Hemimetabolous Insects

Insect larvae metamorphose to winged and reproductive adults either directly (hemimetaboly) or through an intermediary pupal stage (holometaboly). In either case juvenile hormone (JH) prevents metamorphosis until a larva has attained an appropriate phase of development. In holometabolous insects, JH acts through its putative receptor Methoprene-tolerant (Met) to regulate Krüppel-homolog 1 (Kr-h1) and Broad-Complex (BR-C) genes. While Met and Kr-h1 prevent precocious metamorphosis in pre-final larval instars, BR-C specifies the pupal stage. How JH signaling operates in hemimetabolous insects is poorly understood. Here, we compare the function of Met, Kr-h1 and BR-C genes in the two types of insects. Using systemic RNAi in the hemimetabolous true bug, Pyrrhocoris apterus, we show that Met conveys the JH signal to prevent premature metamorphosis by maintaining high expression of Kr-h1. Knockdown of either Met or Kr-h1 (but not of BR-C) in penultimate-instar Pyrrhocoris larvae causes precocious development of adult color pattern, wings and genitalia. A natural fall of Kr-h1 expression in the last larval instar normally permits adult development, and treatment with an exogenous JH mimic methoprene at this time requires both Met and Kr-h1 to block the adult program and induce an extra larval instar. Met and Kr-h1 therefore serve as JH-dependent repressors of deleterious precocious metamorphic changes in both hemimetabolous and holometabolous juveniles, whereas BR-C has been recruited for a new role in specifying the holometabolous pupa. These results show that despite considerable evolutionary distance, insects with diverse developmental strategies employ a common-core JH signaling pathway to commit to adult morphogenesis

Bostonia: The Boston University Alumni Magazine. Volume 9

Founded in 1900, Bostonia magazine is Boston University's main alumni publication, which covers alumni and student life, as well as university activities, events, and programs

The importance of structured noise in the generation of self-organizing tissue patterns through contact-mediated cell–cell signalling

Lateral inhibition provides the basis for a self-organizing patterning system in which distinct cell states emerge from an otherwise uniform field of cells. The development of the microchaete bristle pattern on the notum of the fruitfly, Drosophila melanogaster, has long served as a popular model of this process. We recently showed that this bristle pattern depends upon a population of dynamic, basal actin-based filopodia, which span multiple cell diameters. These protrusions establish transient signalling contacts between non-neighbouring cells, generating a type of structured noise that helps to yield a well-ordered and spaced pattern of bristles. Here, we develop a general model of protrusion-based patterning to analyse the role of noise in this process. Using a simple asynchronous cellular automata rule-based model we show that this type of structured noise drives the gradual refinement of lateral inhibition-mediated patterning, as the system moves towards a stable configuration in which cells expressing the inhibitory signal are near-optimally packed. By analysing the effects of introducing thresholds required for signal detection in this model of lateral inhibition, our study shows how filopodia-mediated cell–cell communication can generate complex patterns of spots and stripes, which, in the presence of signalling noise, align themselves across a patterning field. Thus, intermittent protrusion-based signalling has the potential to yield robust self-organizing tissue-wide patterns without the need to invoke diffusion-mediated signalling