Adaptation and validation of standardized aphasia tests in different languages: Lessons from the Boston diagnostic aphasia examination - Short form in Greek

The aim of the current study was to adapt the Boston Diagnostic Aphasia Examination - Short Form (BDAE-SF) [1] to the Greek language and culture, determine the influence of demographic variables on performance and in particular the effects of age and education, develop normative data, and examine the discriminative validity of the test for acute stroke patients. A sample of 129 community healthy adults participated in the study (66 women), covering a broad range of ages and education levels so as to maximize representation of the Greek population and be able to examine the effects of age and education in language performance. Regression models showed that, overall, younger and more educated individuals presented higher performance on several subtests. Normative data for the Greek population are presented in percentile tables. Neurological patients' performance was compared to that of the neurologically intact population using Wilcoxon's rank sum test and for the most part was found to be significantly inferior, indicating good discriminant validity of the test. Qualitative errors of patients diagnosed with aphasia on the test are presented, and limitations and generalizable strengths of this adaptation are discussed. © 2009/2010 - IOS Press and the authors

Chronic Empagliflozin Treatment Reduces Myocardial Infarct Size in Nondiabetic Mice through STAT-3-Mediated Protection on Microvascular Endothelial Cells and Reduction of Oxidative Stress

Aims: Empagliflozin (EMPA) demonstrates cardioprotective effects on diabetic myocardium but its infarct-sparing effects in normoglycemia remain unspecified. We investigated the acute and chronic effect of EMPA on infarct size after ischemia-reperfusion (I/R) injury and the mechanisms of cardioprotection in nondiabetic mice. Results: Chronic oral administration of EMPA (6 weeks) reduced myocardial infarct size after 30 min/2 h I/R (26.5% ± 3.9% vs 45.8% ± 3.3% in the control group, p < 0.01). Body weight, blood pressure, glucose levels, and cardiac function remained unchanged between groups. Acute administration of EMPA 24 or 4 h before I/R did not affect infarct size. Chronic EMPA treatment led to a significant reduction of oxidative stress biomarkers. STAT-3 (signal transducer and activator of transcription 3) was activated by Y(705) phosphorylation at the 10th minute of R, but it remained unchanged at 2 h of R and in the acute administration protocols. Proteomic analysis was employed to investigate signaling intermediates and revealed that chronic EMPA treatment regulates several pathways at reperfusion, including oxidative stress and integrin-related proteins that were further evaluated. Superoxide dismutase and vascular endothelial growth factor were increased throughout reperfusion. EMPA pretreatment (24 h) increased the viability of human microvascular endothelial cells in normoxia and on 3 h hypoxia/1 h reoxygenation and reduced reactive oxygen species production. In EMPA-treated murine hearts, CD31-/VEGFR2-positive endothelial cells and the pSTAT-3(Y705) signal derived from endothelial cells were boosted at early reperfusion. Innovation: Chronic EMPA administration reduces infarct size in healthy mice via the STAT-3 pathway and increases the survival of endothelial cells. Conclusion: Chronic but not acute administration of EMPA reduces infarct size through STAT-3 activation independently of diabetes mellitus. © Copyright 2021, Mary Ann Liebert, Inc., publishers 2021