Purpose: To study patient follow-up after they engage in a teleretinal screening program and to understand potential barriers to care. Methods: This was a retrospective analysis and a prospective study of telephone-based patient interviews of outpatients screened for diabetic retinopathy (DR) through a teleretinal referral system. Results: Of 2761 patients screened through a teleretinal referral program, 123 (4.5%) had moderate nonproliferative DR (NPDR), 83 (3.0%) had severe NPDR, and 31 (1.1%) had proliferative DR. Of the 114 patients with severe NPDR or worse, 67 (58.8%) saw an ophthalmologist within 3 months of referral. Eighty percent of interviewed patients reported they were not aware of the need for follow-up eye appointments. Conclusions: Of patients with severe retinopathy or worse, 58.8% presented for in-person evaluation and treatment within 3 months of screening. Although this result was negatively affected by factors related to the COVID-19 pandemic, key elements of patient education and improved referral strategies to facilitate in-person treatment are essential to improving follow-up after patients engage in telescreening.
The chimeric protein Bcr/Abl has been connected to several signalling pathways such as AKT, JNK or ERK1/2. Here, we present evidence showing that Bcr/Abl is able to modulate the p38 MAPK pathway. Transient transfection experiments indicated that over-expression of Bcr/Abl in 293T is able to activate p38 MAPK or induce p73 stabilization, suggesting that c-Abl and Bcr/Abl share some biological substrates. Interestingly, the control exerted by Bcr/Abl on the p38 MAPK pathway was not only mediated by the tyrosine kinase activity of Bcr/Abl. In fact, Bcr alone is able to induce P38 MAPK activation specifically through MKK3. Supporting these observations Chronic Myeloid Leukaemia-derived K562 cells or BaF 3 cells stably transfected with Bcr/Abl showed higher levels of phosphorylated p38 MAPK compared to Bcr/Abl-negative cells. Interestingly, Bcr/Abl-negative cells activated p38 MAPK in response to Ara-C, while Bcr/Abl-positive cells were unable to activate p38 MAPK. Furthermore, inhibition of p38 MAPK activation by SKF860002 induces a resistant phenotype in Bcr/Abl negative cells. Our results demonstrate that the interference of Bcr/Abl in the p38 MAPK pathway is a key mechanism for explaining resistance to Ara-C in Bcr/abl positive cells.
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