Cancer survivorship care in Colombia is of increasing importance. International survivorship initiatives and studies show that continuing symptoms, psychological distress, and late effects impact the quality of life for survivors. Priorities for quality survivorship according to Colombian patients and clinicians are unknown. We undertook a nominal consensus approach with 24 participants using virtual meeting technology to identify the priorities for cancer survivorship. We applied an iterative approach conducted over eight weeks with five workshops and one patient focus group followed by a priority setting survey. The consensus group established six main themes, which were subsequently evaluated by experts: (i) symptoms and secondary effects of cancer; (ii) care coordination to increase patient access and integration of cancer care; (iii) psychosocial support after cancer treatment; (iv) mapping information resources and available support services for long-term cancer care; (v) identifying socioeconomic and regional inequalities in cancer survival to improve care and outcomes; and (vi) health promotion and encouraging lifestyle change. The order of priorities differed between clinicians and patients: patients mentioned psychosocial support as the number one priority, and clinicians prioritized symptoms and surveillance for cancer recurrence. Developing survivorship care needs consideration of both views, including barriers such as access to services and socioeconomic disparities.
Endothelial dysfunction is an early marker for cardiovascular diseases. Hyperglycemia induces endothelial dysfunction, increasing the production of reactive oxygen species. Platelet-derived growth factor C stimulates angiogenesis and revascularization in ischemic tissues of diabetic mice and promotes the migration of progenitors and mature ECs to injury sites; however, the molecular mechanisms of its actions are not described yet. Here, we evaluated the effect of PDGF-C on oxidative stress induced by HG. Human aortic endothelial cells were grown in glucose concentrations ranging from 5 mmol/L to 35 mmol/L for 1 to 24 h. Treatment with 50 ng/mL PDGF-C was done for 1 to 3 h. Cytosolic and mitochondrial ROS were measured by fluorometry, and the expression of antioxidant enzymes was evaluated by Western blot. Nrf2 and Keap1 expression was assessed by real-time PCR. High glucose induced mitochondrial ROS production. PDGF-C diminished the oxidative stress induced by high glucose, increasing SOD2 expression and SOD activity, and modulating the Keap1 expression gene. These results give new evidence about the mitochondrial antioxidant effect that PDGF-C could exert on endothelial cells exposed to high glucose and its considerable role as a therapeutic target in diabetes.
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