Removal of sugar sweetened beverages from sale in a hospital setting-Consumer opinion and influence on purchasing behavior.

ISSUE ADDRESSED: This study investigated the impact of removing sugar sweetened beverages (SSBs) from sale in a regional health service. Drink purchasing patterns were measured by product ordering data. Consumer opinion regarding the intervention, self-reported packaged drink purchase and consumption were also explored. METHODS: Packaged drinks were classified into two categories, SSB or non-SSB and drink types. Drink sales were determined by the collection of product ordering data for all packaged drink types sold, six months prior to and twelve months after the removal of SSBs. A consumer survey was undertaken six months after SSB removal to assess consumer opinion regarding SSB removal, self-reported SSB consumption and purchase. Descriptive and Wilcoxon rank-sum tests analyses assessed differences in packaged drinks purchase, self-reported SSB consumption and purchase. Open-ended survey responses were thematically analysed. RESULTS: The median monthly number of juices, and diet drinks ordered increased significantly (P = .05). 59% of the survey respondents regularly consumed SSBs and 58% agreed or strongly agreed with removing SSBs from sale. However, some consumers felt it was a removal of their freedom of choice. CONCLUSIONS: Removing SSBs from sale can result in consumers making healthier purchases. There was support for the initiative as it is seen as the responsibility of the health service to role model healthy eating behaviours. SO WHAT?: This study indicates removal of SSBs from sale is a promising health promotion intervention that can contribute to positive behaviour change, and potentially influence longer-term health and wellbeing.

High-resolution within-sewer SARS-CoV-2 surveillance facilitates informed intervention.

To assist in the COVID-19 public health guidance on a college campus, daily composite wastewater samples were withdrawn at 20 manhole locations across the University of Colorado Boulder campus. Low-cost autosamplers were fabricated in-house to enable an economical approach to this distributed study. These sample stations operated from August 25th until November 23rd during the fall 2020 semester, with 1512 samples collected. The concentration of SARS-CoV-2 in each sample was quantified through two comparative reverse transcription quantitative polymerase chain reactions (RT-qPCRs). These methods were distinct in the utilization of technical replicates and normalization to an endogenous control. (1) Higher temporal resolution compensates for supply chain or other constraints that prevent technical or biological replicates. (2) The data normalized by an endogenous control agreed with the raw concentration data, minimizing the utility of normalization. The raw wastewater concentration values reflected SARS-CoV-2 prevalence on campus as detected by clinical services. Overall, combining the low-cost composite sampler with a method that quantifies the SARS-CoV-2 signal within six hours enabled actionable and time-responsive data delivered to key stakeholders. With daily reporting of the findings, wastewater surveillance assisted in decision making during critical phases of the pandemic on campus, from detecting individual cases within populations ranging from 109 to 2048 individuals to monitoring the success of on-campus interventions.

Nebulized anti-IL-13 monoclonal antibody Fab' fragment reduces allergen-induced asthma.

IL-13 is a prototypic T helper type 2 cytokine and a central mediator of the complex cascade of events leading to asthmatic phenotype. Indeed, IL-13 plays key roles in IgE synthesis, bronchial hyperresponsiveness, mucus hypersecretion, subepithelial fibrosis, and eosinophil infiltration. We assessed the potential efficacy of inhaled anti-IL-13 monoclonal antibody Fab' fragment on allergen-induced airway inflammation, hyperresponsiveness, and remodeling in an experimental model of allergic asthma. Anti-IL-13 Fab' was administered to mice as a liquid aerosol generated by inExpose inhalation system in a tower allowing a nose-only exposure. BALB/c mice were treated by PBS, anti-IL-13 Fab', or A33 Fab' fragment and subjected to ovalbumin exposure for 1 and 5 weeks (short-term and long-term protocols). Our data demonstrate a significant antiasthma effect after nebulization of anti-IL-13 Fab' in a model of asthma driven by allergen exposure as compared with saline and nonimmune Fab fragments. In short- and long-term protocols, administration of the anti-IL-13 Fab' by inhalation significantly decreased bronchial responsiveness to methacholine, bronchoalveolar lavage fluid eosinophilia, inflammatory cell infiltration in lung tissue, and many features of airway remodeling. Levels of proinflammatory mediators and matrix metalloprotease were significantly lower in lung parenchyma of mice treated with anti-IL-13 Fab'. These data demonstrate that an inhaled anti-IL-13 Fab' significantly reduces airway inflammation, hyperresponsiveness, and remodeling. Specific neutralization of IL-13 in the lungs using an inhaled anti-IL-13 Fab' could represent a novel and effective therapy for the treatment of asthma.

Monoclonal antibodies for the treatment of asthma.

Asthma is a chronic inflammatory disease of the airways which can have a detrimental effect on quality of life and in extreme cases cause death. Although the majority of patients can control their asthma symptoms with a combination of steroids and beta agonists there is still a group of patients whose asthma remains symptomatic despite the best available treatment. These severe asthmatic patients represent the unmet medical need in asthma and are the focus of those developing novel monoclonal antibody based drugs. The complex networks of cytokines and cells involved in the pathology of asthma provide plenty of scope for intervention with monoclonal antibody based drugs which are able to block cytokine or chemokine receptor interactions, deplete cells expressing a specific receptor or block cell/cell interactions. At present anti-IgE (Xolair©) is the only monoclonal antibody based drug approved for the treatment of asthma. However, a number of other antibody based drugs have been clinically tested in asthma including anti-IL-5, anti-IL-4, anti-IL-13, anti-TNFα, anti-CCR3, anti-CCR4 and anti-OX40L. This review will examine the development of these monoclonal antibody based therapies. Since many of these therapies have targeted key pathways in asthma pathology these studies provide information on patient stratification and asthma pathology.

Neutralisation of interleukin-13 in mice prevents airway pathology caused by chronic exposure to house dust mite.

BACKGROUND: Repeated exposure to inhaled allergen can cause airway inflammation, remodeling and dysfunction that manifests as the symptoms of allergic asthma. We have investigated the role of the cytokine interleukin-13 (IL-13) in the generation and persistence of airway cellular inflammation, bronchial remodeling and deterioration in airway function in a model of allergic asthma caused by chronic exposure to the aeroallergen House Dust Mite (HDM). METHODOLOGY/PRINCIPAL FINDINGS: Mice were exposed to HDM via the intranasal route for 4 consecutive days per week for up to 8 consecutive weeks. Mice were treated either prophylactically or therapeutically with a potent neutralising anti-IL-13 monoclonal antibody (mAb) administered subcutaneously (s.c.). Airway cellular inflammation was assessed by flow cytometry, peribronchial collagen deposition by histocytochemistry and airway hyperreactivity (AHR) by invasive measurement of lung resistance (R(L)) and dynamic compliance (C(dyn)). Both prophylactic and therapeutic treatment with an anti-IL-13 mAb significantly inhibited (P<0.05) the generation and maintenance of chronic HDM-induced airway cellular inflammation, peribronchial collagen deposition, epithelial goblet cell upregulation. AHR to inhaled methacholine was reversed by prophylactic but not therapeutic treatment with anti-IL-13 mAb. Both prophylactic and therapeutic treatment with anti-IL-13 mAb significantly reversed (P<0.05) the increase in baseline R(L) and the decrease in baseline C(dyn) caused by chronic exposure to inhaled HDM. CONCLUSIONS/SIGNIFICANCE: These data demonstrate that in a model of allergic lung disease driven by chronic exposure to a clinically relevant aeroallergen, IL-13 plays a significant role in the generation and persistence of airway inflammation, remodeling and dysfunction.