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This article covers recent National Institute for Health and Care Excellence guidance relevant to public health. The article includes an overview of key public health aspects of the Community pharmacy: promoting health and wellbeing guideline, summarizing recommendations for commissioners and health promoting organizations and professionals around the potential to integrate community pharmacies into wider health and care pathways.

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OBJECTIVES: The National Institute for Health and Care Excellence, jointly with Public Health England, have developed a guideline on outdoor air pollution and its links to health. The guideline makes recommendations on local interventions that can help improve air quality and prevent a range of adverse health outcomes associated with road-traffic-related air pollution. METHODS: The guideline was based on a rigorous assessment of the scientific evidence by an independent advisory committee, with input from public health professionals and other professional groups. The process included systematics reviews of the literature, expert testimonies and stakeholder consultation. RESULTS: The guideline includes recommendations for local planning, clean air zones, measures to reduce emissions from public sector transport services, smooth driving and speed reduction, active travel, and awareness raising. CONCLUSIONS: The guideline recommends taking a number of actions in combination, because multiple interventions, each producing a small benefit, are likely to act cumulatively to produce significant change. These actions are likely to bring multiple public health benefits, in addition to air quality improvements.

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AIM: To examine how effectively forwards citation searching with Web of Science (WOS) or Google Scholar (GS) identified evidence to support public health guidance published by the National Institute for Health and Care Excellence. METHOD: Forwards citation searching was performed using GS on a base set of 46 publications and replicated using WOS. OUTCOMES: WOS and GS were compared in terms of recall; precision; number needed to read (NNR); administrative time and costs; and screening time and costs. Outcomes for all publications were compared with those for a subset of highly important publications. RESULTS: The searches identified 43 relevant publications. The WOS process had 86.05% recall and 1.58% precision. The GS process had 90.7% recall and 1.62% precision. The NNR to identify one relevant publication was 63.3 with WOS and 61.72 with GS. There were nine highly important publications. WOS had 100% recall, 0.38% precision and NNR of 260.22. GS had 88.89% recall, 0.33% precision and NNR of 300.88. Administering the WOS results took 4 h and cost £88-£136, compared with 75 h and £1650-£2550 with GS. CONCLUSION: WOS is recommended over GS, as citation searching was more effective, while the administrative and screening times and costs were lower.

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Excessive mucus production has been linked to many of the pathologic features of respiratory diseases, including obstruction of the airways, decline in lung function, increased rates of mortality, and increased infections. The mucins, MUC5AC and MUC5B, contribute to the viscoelastic properties of mucus, and are found at elevated levels in the airways of individuals with chronic respiratory diseases. The T helper type 2 cell cytokine, IL-13, is known to regulate MUC5AC expression in goblet cells of the airways, although much less is known about the regulation of MUC5B expression. In a study to further understand the mediators of MUC5AC and MUC5B expression, neuregulin (NRG) 1beta1 was identified as novel regulator of goblet cell formation in primary cultures of human bronchial epithelial cells (HBECs). NRG1beta1 increased expression of MUCAC and MUC5B proteins in a time- and dose-dependent fashion in HBEC cultures. NRG1beta1-induced expression of MU5AC and MUC5B was shown to involve v-erb-b2 erythroblastic leukemia viral oncogene homolog (ErbB) and ErbB3 receptors, but not ErbB4 receptors. Treatment of HBECs with inhibitors of p38 mitogen-activated protein kinase, extracellular signal-regulated kinase1/2, and phosphatidylinositol 3-kinase indicated that these kinases were involved in NRG1beta1-induced MUC5AC and MUC5B expression. Additionally, NRG1beta1 was shown to induce the phosphorylation of the ErbB2 receptor, AKT, and extracellular signal-regulated kinase 1/2. NRG1beta1 protein was found increased in the airways of antigen-challenged mice, together with increases in MUC5AC and MUC5B message. Together, these data indicate that NRG1beta1 is a novel mediator of MUC5AC and MUC5B expression in HBECs, and may represent a novel therapeutic target for mucus hypersecretion in respiratory diseases.

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Using a bioinformatics approach, we have isolated a novel G-protein-coupled receptor (GPCR), R527, and have demonstrated that this receptor shows no significant homology to previously deorphanized GPCRs. Quantitative reverse transcription-polymerase chain reaction analysis of the expression of GPCR R527 indicated a very high level of mRNA expression in eosinophils, with high expression also detected in neutrophils and lung macrophages. Stable cell lines were generated expressing this receptor together with the G-protein alpha-subunit G alpha(16). These cells were used to screen an agonist collection in a calcium mobilization assay and 5-oxo-6E,8Z,11Z,14Z-eicosatetraenoic acid (5-oxo-ETE) was identified as a putative ligand. 5(S)-hydroxyperoxy-6E,8Z,11Z,14Z-eicosatetraenoic acid was also shown to activate the receptor, whereas the leukotrienes LTB(4), LTC(4), LTD(4), and LTE(4) failed to elicit a response. In cAMP assays, pertussis toxin reversed the inhibitory effects of 5-oxo-ETE on cAMP production, indicating that the receptor is G alpha(i)-coupled. The GPCR R527 shows pharmacological properties similar to those of the previously described 5-oxo-ETE receptor expressed on eosinophils, neutrophils, and monocytes. These cell types show chemotactic responses to 5-oxo-ETE, and this eicosanoid has been proposed to play a key role in the inflammatory response. The molecular identification of a receptor binding 5-oxo-ETE will expand our understanding of the physiological role of this mediator and may provide new therapeutic opportunities.

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