Driving with Parkinson\u27s Disease: Exploring Lived Experience

A growing body of literature has explored the impact of Parkinson\u27s disease (PD) on fitness to drive. As such, evidence now supports the use of specific clinical tests for screening purposes, the predictive validity of risk impressions, and the critical driving errors that predict on-road pass/fail outcomes in this population. However, little is known about the lived experiences of persons with PD as they navigate driving-related concerns such as driving impairments, cessation, potential threats to independence, and community mobility. This qualitative secondary data analysis aimed to explore the driving-related lived experiences of persons with PD. We utilized summative content analysis to identify themes related to driving from transcribed interviews with nineteen community-dwelling individuals with PD who participated in the primary study. Five themes emerged within the analysis: (1) the meaning and significance of driving; (2) driving cessation; (3) modified driving behaviors; (4) factors affecting driving; and (5) accessibility. Participants identified driving as an activity that holds significant importance-both directly (i.e., as a primary activity) and as a means for enabling other activities. This study lays the foundation for the development of client-centred and evidence-informed driving interventions for individuals with PD, as well as the development of driving retirement programs

Embryonic protein NODAL regulates the breast tumor microenvironment by reprogramming cancer-derived secretomes

The tumor microenvironment (TME) is an important mediator of breast cancer progression. Cancer-associated fibroblasts constitute a major component of the TME and may originate from tissue-associated fibroblasts or infiltrating mesenchymal stromal cells (MSCs). The mechanisms by which cancer cells activate fibroblasts and recruit MSCs to the TME are largely unknown, but likely include deposition of a pro-tumorigenic secretome. The secreted embryonic protein NODAL is clinically associated with breast cancer stage and promotes tumor growth, metastasis, and vascularization. Herein, we show that NODAL expression correlates with the presence of activated fibroblasts in human triple-negative breast cancers and that it directly induces Cancer-associated fibroblasts phenotypes. We further show that NODAL reprograms cancer cell secretomes by simultaneously altering levels of chemokines (e.g., CXCL1), cytokines (e.g., IL-6) and growth factors (e.g., PDGFRA), leading to alterations in MSC chemotaxis. We therefore demonstrate a hitherto unappreciated mechanism underlying the dynamic regulation of the TME