Abstract: Background: Type 2 Diabetes Mellitus affects patients’ quality of life. The my ePRO app was constructed to collect patient-reported outcomes in an investigator free study - DePRO study. We aimed to describe the qualitative and quantitative feedback received during user experience testing in a diabetes mellitus type 2 focus group. Methods: Metformin containing drug taking patients aged 18 years or older completed a 37-item qualitative questionnaire as the quantitative 6 scales and 26 items containing User Experience Questionnaire (UEQ) in a single focus group interview. The qualitative interview addressed feedback to 1) the download of the app, 2) scanning the 2D matrix code, 3) informed consent form, 4) demographic questionnaire and the 3 PRO instruments EQ-5D-5L, SDSCA and DTSQ. Results: Nine T2DM patients, 3 female and 6 male, aged 55-88 years were interviewed for 45 to 65 minutes. Patients expressed their need of lay language within the app, criticized the length of the informed consent form, the amount of health information, missed pictures of the drugs they scanned and judged the questions to income and education as too indiscreet. As positive feedback patient reported that everything was fine, the questions were self-explaining and could be read without glasses. The UEC scales (mean; variances) Perspicuity (0.722; 1.73), Efficiency (0.5; 0.89) and Novelty (0.25; 1.13) were rated neutral, Attractiveness (0.854: 0.63), Dependability (1.031; 0.1) and Stimulation (1.094; 0.39) represent a positive evaluation. Discussion: User experience testing provided insight into usage, challenges and areas of improvement of my ePRO app in a type 2 Diabetes Mellitus focus group. User experiences were implemented in the final app. The quantitative feedback was compared to a benchmark data set, to which the my ePRO app means were below average in all scales. Understanding patient view, leads to a better design of health apps and study conduct.Abstract: Background: Type 2 Diabetes Mellitus affects patients’ quality of life. The my ePRO app was constructed to collect patient-reported outcomes in an investigator free study - DePRO study. We aimed to describe the qualitative and quantitative feedback received during user experience testing in a diabetes mellitus type 2 focus group. Methods: Metformin...Show More
Abstract: Ischemic postconditioning was induced by brief cycles of ischemia/reperfusion (I/R) at the end of ischemia scavenge brain tissues from I/R injury in several animal models. However, the relationship between ischemic postconditioning and gap junction (GJ) yet to be explored. Here, we investigated whether the beneficial effect of hypoxic postconditioning involves in decrease of GJ function via establishing the hypoxia/reoxygenation (H/R) model with astrocytes to mimic the cerebral I/R. The primary astrocytes were exposed to 8 h hypoxia/24 h reoxygenation. Hypoxic postconditioning (HPC) was induced by 3 cycles of 10 min reoxygenation/10 min hypoxia after 8 h hypoxia. Before H/R, the retinoid acid was added for 24 h, and oleamide was applied for 1 h. Parachute dye coupling assay was used to evaluate GJ function. The viability and apoptosis of astrocytes was detected by MTT, flow cytometry and Hoechst 33258 staining, respectively. Finally, the Protein expression of Cx43, Bcl-2 and Bax was tested by western blotting, while the effect of Cx43-siRNA to H/R injury and HPC was explored by Cx43-siRNA transfection. It was found that HPC attenuated the expected increase in GJ function during reperfusion increased astrocyte viability and inhibit apoptosis. Compared with H/R group, the HPC group exhibit an increased expression of Cx43 and Bcl-2 protein, but decrease in Bax. Moreover, the pretreatment with retinoid strengthened the effect of ischemic/hypoxic postconditioning, while oleamide weakened it. We attributed these effects to the inhibited gap junctional intercellular communication (GJIC) induced by HPC through inhibition of Cx43 expression on cell surface, indicating that HPC protects astrocytes from H/R injury.Abstract: Ischemic postconditioning was induced by brief cycles of ischemia/reperfusion (I/R) at the end of ischemia scavenge brain tissues from I/R injury in several animal models. However, the relationship between ischemic postconditioning and gap junction (GJ) yet to be explored. Here, we investigated whether the beneficial effect of hypoxic postcondition...Show More