RESUMEN
This study demonstrates that students in kindergarten through eighth grade can use the XpressCollect nasal swab to self-collect a specimen under the guidance of a teacher. This phased study was conducted with parents, teachers, and students. Phases 1 and 2 were conducted as interviews with teachers and parents to assess the suitability of the XpressCollect for children in kindergarten through eighth grade. Additionally, teacher and parent feedback was obtained to develop and optimize the instructional materials for subsequent phases. In Phases 3 and 4, teachers guided small groups and full classes of students through the sample collection process with XpressCollect. The samples collected by the students were sent to a laboratory to analyze the effectiveness of specimen self-collection based on the presence of ribonuclease P (RNase P) on each nasal swab. The presence of RNase P enables disease determination; thus, student samples were analyzed for adequate or inadequate sampling. All students in kindergarten through eighth grade are capable of self-collecting an anterior nares specimen with XpressCollect, as the laboratory results identified acceptable RNase P Ct values for the samples collected in a classroom setting.
RESUMEN
Cigarette smoke (CS) exposure is a major risk factor for the development of emphysema, a common disease characterized by loss of cells comprising the lung parenchyma. The mechanisms of cell injury leading to emphysema are not completely understood but are thought to involve persistent cytotoxic or mutagenic DNA damage induced by CS. Using complementary cell culture and mouse models of CS exposure, we investigated the role of the DNA repair protein, xeroderma pigmentosum group C (XPC), on CS-induced DNA damage repair and emphysema. Expression of XPC was decreased in mouse lungs after chronic CS exposure and XPC knockdown in cultured human lung epithelial cells decreased their survival after CS exposure due to activation of the intrinsic apoptosis pathway. Similarly, cell autophagy and apoptosis were increased in XPC-deficient mouse lungs and were further increased by CS exposure. XPC deficiency was associated with structural and functional changes characteristic of emphysema, which were worsened by age, similar to levels observed with chronic CS exposure. Taken together, these findings suggest that repair of DNA damage by XPC plays an important and previously unrecognized role in the maintenance of alveolar structures. These findings support that loss of XPC, possibly due to chronic CS exposure, promotes emphysema development and further supports a link between DNA damage, impaired DNA repair, and development of emphysema.
