Social support, educational, and behavioral modification interventions for improving household disaster preparedness in the general community-dwelling population: a systematic review and meta-analysis

Background: The efficacy of household emergency preparedness interventions for community-dwelling, non-institutionalized people is largely unknown. Objective: To ascertain the state of the science on social support, educational, and behavioral modification interventions to improve all-hazard household disaster preparedness. Design: Systematic review and meta-analysis. Methods: Databases, trial registers, reports, and websites were searched, and citation trails followed utilizing replicable methods. Individual, cluster, and cross-over randomized controlled trials of non-institutionalized, community-dwelling populations and non-randomized controlled trials, controlled before-after, and program evaluation studies were included. At least two review authors independently screened each potentially relevant study for inclusion, extracted data, and assessed the risk of bias. Risk of bias was assessed using Cochrane’s RoB2 tool for randomized studies and ROBINS-I tool for nonrandomized studies. Meta-analyses were applied using a random-effects model. Where meta-analysis was not indicated, results were synthesized using summary statistics of intervention effect estimates and vote counting based on effect direction. The evidence was rated using GRADE. Results: 17 studies were included with substantial methodological and clinical diversity. No intervention effect was observed for preparedness supplies (OR = 6.12, 95% 0.13 to 284.37) or knowledge (SMD = 0.96, 95% CI −0.15 to 2.08) outcomes. A small positive effect (SMD = 0.53, 95% CI 0.16 to 0.91) was observed for preparedness behaviors, with very low certainty of evidence. No studies reported adverse effects from the interventions. Conclusion: Research designs elucidating the efficacy of practical yet complex and multi- faceted social support, educational, and behavioral modification interventions present substantial methodological challenges where rigorous study design elements may not match the contextual public health priority needs and resources where interventions were delivered. While the overall strength of the evidence was evaluated as low to very low, we acknowledge the valuable and informative work of the included studies. The research represents the seminal work in this field and provides an important foundation for the state of the science of household emergency preparedness intervention effectiveness and efficacy. The findings are relevant to disaster preparedness practice and research, and we encourage researchers to continue this line of research, using these studies and this review to inform ongoing improvements in study designs

Social support, educational, and behavioral modification interventions for improving household disaster preparedness in the general community-dwelling population

Objectives: This is a protocol for a Cochrane Review (intervention). The objectives are as follows: To ascertain the state of the science on social support, educational, and behavioural modification interventions to improve all‐hazard household disaster preparedness The PICO research question is as follows: in the general, non‐institutionalised, community‐dwelling population (P), do social support, educational, and behavioural modification interventions (I) compared to no intervention or usual mass public service messaging (C) improve all‐hazard household disaster preparedness behaviours, supplies, and/or knowledge (O) To assess whether social support, educational, and behavioural modification interventions have effects on healthcare utilisation (emergency department utilisation, hospitalisation, morbidity), mortality, and mental health or physical functioning post disaster

Hacking the Immune Response to Infection in Chronic Obstructive Pulmonary Disease

Efforts to treat chronic diseases are often obstructed by the complexity of the biological mechanisms supporting pathology. Here, we apply a novel method for discrete logical modeling of biological systems to the problem of infectious exacerbations in chronic obstructive pulmonary disease (COPD), using data from human clinical studies to constrain the selection of decisional logic parameters. We obtained two candidate models satisfactorily adhering to the available data. A predicted resting state with no activation of inflammatory markers was supported natively in one model, and could be induced following onset of an exacerbation episode in either model by applying targeted suppression of IL-4 concurrently with at least one additional inflammatory marker including IL-IB. Recapitulating a failed clinical trial of anakinra, suppression of IL-IB alone was not predicted to be sufficient. Instead, these results suggest that the efficacy of IL-IB suppression in the treatment of COPD might be improved by the added concurrent suppression of IL-4 and CCL4 or IL-4 and IL-17A

Impaired Innate COPD Alveolar Macrophage Responses and Toll-Like Receptor-9 Polymorphisms

<div><p>Background</p><p>Dysfunctional innate responses of alveolar macrophages to nontypeable <i>Haemophilus influenzae</i>, <i>Moraxella catarrhalis</i> and <i>Streptococcus pneumoniae</i> contribute to morbidity in chronic obstructive pulmonary disease (COPD). Our earlier studies discovered impaired COPD alveolar macrophage responses to Toll-like receptor (TLR) ligands of nontypeable <i>H</i>. <i>influenzae</i> and provide rationale for further evaluation of TLR signaling. While the role of TLR single nucleotide polymorphisms is increasingly recognized in inflammatory diseases, TLR single nucleotide polymorphisms in COPD have only recently been explored. We hypothesized that specific TLR polymorphisms are associated with dysfunctional innate immune COPD alveolar macrophage responses and investigated polymorphisms of TLR2(Arg753Gln), TLR4(Thr399Ile; Asp299Gly), and TLR9(T1486C; T1237C).</p><p>Methods</p><p>DNA was purified from cells of 1) healthy nonsmokers (n = 20); 2) COPD ex-smokers (n = 83); 3) COPD active smokers (n = 93). DNA amplifications (polymerase chain reaction) were performed for each SNP. Alveolar macrophages from each group were incubated with nontypeable <i>H</i>. <i>influenzae</i>, <i>M</i>. <i>catarrhalis</i> and <i>S</i>. <i>pneumoniae</i>. Cytokine induction of macrophage supernatants was measured and the association with TLR single nucleotide polymorphism expression was determined.</p><p>Results</p><p>No significant inter-group differences in frequency of any TLR SNP existed. However both TLR9 single nucleotide polymorphisms were expressed in high frequency. Among COPD ex-smokers, diminished IL-8 responsiveness to nontypeable <i>H</i>. <i>influenzae</i>, <i>M</i>. <i>catarrhalis</i> and <i>S</i>. <i>pneumoniae</i> was strongly associated with carriage of TLR9(T1237C) (p = 0.02; p = 0.008; p = 0.02), but not TLR9(T1486C). Carriage of TLR9(T1237C), but not TLR9(T1486C), correlated with diminished FEV₁%predicted (p = 0.037).</p><p>Conclusion</p><p>Our results demonstrate a notable association of TLR9(T1237C) expression with dysfunctional innate alveolar macrophage responses to respiratory pathogens and with severity of COPD.</p></div

IL-17 Is a Key Regulator of Mucin-Galectin-3 Interactions in Asthma

Mucus hypersecretion and chronic airway inflammation are standard characteristics of several airway diseases, such as chronic obstructive pulmonary disease and asthma. Increased mucus secretion from increased mucin gene expression in the airway epithelium is associated with poor prognosis and mortality. We previously showed that the absence of tissue inhibitor of metalloproteinase 1 (TIMP-1) enhances lung inflammation, airway hyperreactivity, and lung remodeling in asthma in an ovalbumin (OVA) asthma model of TIMP-1 knockout (TIMPKO) mice as compared to wild-type (WT) controls and mediated by increased galectin-3 (Gal-3) levels. Additionally, we have shown that in the lung epithelial cell line A549, Gal-3 inhibition increases interleukin-17 (IL-17) levels, leading to increased mucin expression in the airway epithelium. Therefore, in the current study, we further examined the relationship between Gal-3 and the production of IL-17-axis cytokines and critical members of the mucin family in the murine TIMPKO asthma model and the lung epithelium cell line A549. While Gal-3 may regulate a Th1/Th2 response, IL-17 could stimulate the mucin genes, MUC5B and MUC5AC. Gal-3 and IL-17 interactions induce mucus expression in OVA-sensitized mice. We conclude that Gal-3 may play an essential role in the pathogenesis of asthma, and modulation of Gal-3 may prove helpful in the treatment of this disease

Single nucleotide polymorphisms of TLR’s.

<p>PCR-based RFLP’s were performed with genomic DNA from each participant. Representative agarose gels of shown for: TLR9 (T1237C) (Panel A), TLR9 (T1486C) (Panel B), TLR4 (Thr399Ile) (Panel C), TLR4 (Asp299Gly) (Panel D) and TLR2 (Arg753Gln) (Panel E). Numbers in left margin of each gel correspond to DNA ladder base pairs. Lanes with restriction fragments for heterozygotes and homozygotes of each SNP are distinguishable from restriction fragments for wildtypes. Representative patient samples are shown in each lane of each panel.</p

Demographic characteristics: Bronchoscopy participants.

<p>^a p≤0.05—nonsmokers vs. COPD ex-smokers</p><p>^b p≤0.05—nonsmokers vs. COPD active smokers</p><p>^c p≤0.05 –COPD ex-smokers vs. COPD active smokers</p><p>^# GOLD classification is as detailed in the Global Initiative for Chronic Obstructive Lung Disease [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0134209#pone.0134209.ref024" target="_blank">24</a>].</p><p>Data are expressed as mean±SEM.</p

TLR9 SNPs and FEV₁%predicted.

<p>Correlation of FEV₁%predicted and expression of TLR9 wildtype (dark shading) compared with (T1237C) (light shading) is shown in left panel. Correlation of FEV₁%predicted and expression of TLR9 wildtype (dark shading) compared with TLR9 (T1486C) (striped shading) is shown in right panel. Results are given for all COPD participants.</p