Search

Background Determining which therapies fall under the umbrella of complementary, alternative, and/or integrative medicine (CAIM) is difficult for several reasons. An operational definition is dynamic, and changes depending on both historical time period and geographical location, with many countries integrating or considering their traditional system(s) of medicine as conventional care. We have previously reported the first operational definition of CAIM informed by a systematic search. In the present study, we have developed a bibliographic database keyword search strategy for CAIM based on this operational definition, in order to standardize research involving systematic searches such as systematic reviews and bibliometric analyses. Methods Using the finalised operational definition of CAIM's 604 therapies, a single keyword search strategy was developed for the most common bibliographic databases, including those searchable on the OVID platform (e.g., MEDLINE, EMBASE, PsycINFO, AMED), the EBSCO platform (e.g., ERIC, CINAHL), Scopus, and Web of Science. The Therapeutic Research Center's “Natural Medicines” database was searched for all 604 therapies, and each item's scientific name and/or synonym was included as a phrase to the search strategy. Results This developed bibliographic database search strategy provides a standardised list of CAIM terms that may be searched on bibliographic databases including those found on the OVID platform (e.g., MEDLINE, EMBASE, PsycINFO, AMED), the EBSCO platform (e.g., ERIC, CINAHL), Scopus, and Web of Science. Conclusion Researchers can select relevant terms for their CAIM study and insert the keywords or phrases into these databases to receive all accessible data. This search technique can simply be copied and pasted into the search bar of each database to identify research by keywords, which is the most inclusive, or by words in the article title, which is more selective. Given its versatility across multiple commonly used academic platforms/databases, it is expected that this search strategy will be of great value to those conducting research on CAIM topics involving systematic searches.

Rhinovirus (RV) exposure evokes exacerbations of asthma that markedly impact morbidity and mortality worldwide. The mechanisms by which RV induces airway hyperresponsiveness (AHR) or by which specific RV serotypes differentially evoke AHR remain unknown. We posit that RV infection evokes AHR and inflammatory mediator release, which correlate with degrees of RV infection. Furthermore, we posit that rhinovirus C-induced AHR requires paracrine or autocrine mediator release from epithelium that modulates agonist-induced calcium mobilization in human airway smooth muscle. In these studies, we used an ex vivo model to measure bronchoconstriction and mediator release from infected airways in human precision cut lung slices to understand how RV exposure alters airway constriction. We found that rhinovirus C15 (RV-C15) infection augmented carbachol-induced airway narrowing and significantly increased release of IP-10 (IFN-γ-induced protein 10) and MIP-1β (macrophage inflammatory protein-1β) but not IL-6. RV-C15 infection of human airway epithelial cells augmented agonist-induced intracellular calcium flux and phosphorylation of myosin light chain in co-cultured human airway smooth muscle to carbachol, but not after histamine stimulation. Our data suggest that RV-C15-induced structural cell inflammatory responses are associated with viral load but that inflammatory responses and alterations in agonist-mediated constriction of human small airways are uncoupled from viral load of the tissue.