BackgroundSurface water contaminated with human waste may transmit urogenital schistosomiasis (UGS). Water-related activities that allow skin exposure place people at risk, but public health practitioners know little about why some communities with access to improved water infrastructure have substantial surface water contact with infectious water bodies. Community-based mixed-methods research can provide critical information about water use and water infrastructure improvements.MethodsOur mixed-methods study assessed the context of water use in a rural community endemic for schistosomiasis.ResultsEighty-seven (35.2 %) households reported using river water but not borehole water; 26 (10.5 %) reported using borehole water but not river water; and 133 (53.8 %) households reported using both water sources. All households are within 1 km of borehole wells, but tested water quality was poor in most wells. Schistosomiasis is perceived by study households (89.3 %) to be a widespread problem in the community, but perceived schistosomiasis risk fails to deter households from river water usage. Hematuria prevalence among schoolchildren does not differ by household water use preference. Focus group data provides context for water preferences. Demand for improvements to water infrastructure was a persistent theme; however, roles and responsibilities with respect to addressing community water and health concerns are ill-defined.ConclusionsCollectively, our study illustrates how complex attitudes towards water resources can affect which methods will be appropriate to address schistosomiasis.
Background: Wheezing disorders are prominent in former preterm infants beyond the neonatal period. Objectives: We used a neonatal mouse model to investigate the time course of airway hyperreactivity in response to mild (40% oxygen) or severe (70% oxygen) neonatal hyperoxia. Methods: After hyperoxic exposure during the first week of postnatal life, we measured changes in airway reactivity using the in vitro living lung slice preparation at the end of exposure [postnatal day 8 (P8)] and 2 weeks later (P21). This was accompanied by measures of smooth muscle actin, myosin light chain (MLC) and alveolar morphology. Results: Neither mild nor severe hyperoxia exposure affected airway reactivity to methacholine at P8 compared to normoxic controls. In contrast, airway reactivity was enhanced at P21 in mice exposed to mild (but not severe) hyperoxia, 2 weeks after exposure ended. This was associated with increased airway α-smooth muscle actin expression at P21 after 40% oxygen exposure without a significant increase in MLC. Alveolar morphology via radial alveolar counts was comparably diminished by both 40 and 70% oxygen at both P8 and P21. Conclusions: These data demonstrate that early mild hyperoxia exposure causes a delayed augmentation of airway reactivity, suggesting a long-term alteration in the trajectory of airway smooth muscle development and consistent with resultant symptomatology.
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