Melodic Intonation Therapy might have a positive effect on the communication skills of stroke survivors with nonfluent aphasia as measured by the CAL questionnaire. A full-scale trial with at least 27 patients per group is necessary to confirm these results.

Preliminary data suggest that ex vivo T cell-depleted matched related donor (MRD) hematopoietic stem cell transplantation (HSCT) is feasible and confers a clinically beneficial reduction in graft-versus-host disease. Classically, T cell-depleted grafts were associated with reduction of the graft-versus-leukemia (GVL) effect because of delayed T cell immune reconstitution. However, natural killer (NK) cell alloreactivity is also critical for an early GVL effect as well as for lymphocyte immune reconstitution. Here, we study the role of NK cells in MRD T cell-depleted HSCT, which is still poorly understood. Given that MRD ligands for inhibitory killer cell immunoglobulin-like receptors (KIRs) are matched, we focused on activating KIR receptors. We retrospectively analyzed KIR genotyping in patients and MRDs in 40 ex vivo T cell-depleted pediatric HSCTs. The log-rank test and Cox proportional risk test were performed to correlate genotype with clinical outcome (relapse rate, disease-free survival, and overall survival) and immune reconstitution. The statistical analysis revealed poorer overall survival when donors have a KIR-B content score of ≥2, a best/better subtype, or present the KIR2DS1 gene. The patient's relapse rate was higher when donors present the KIR2DL5A gene, as well as a poorer probability of disease-free survival when the donor is classified with a best/better subtype. Regarding immune reconstitution, donor KIR haplotype A or the presence of inhibitory KIR genes promote best recovery of T lymphocytes, whereas donor KIR haplotype B or the presence of activating KIR genes confer better expansion of NK cells. These findings suggest that the selection of MRDs with an inhibitory KIR phenotype improve T cell expansion as well as the clinical outcome after pediatric ex vivo T cell-depleted HSCT.

Lack of response to conventional treatment for glucose management in acute IS is frequent and associated with poor outcomes.

Background and purpose The aim was to identify whether post‐stroke hyperglycaemia (PSH) influences the levels of circulating biomarkers of brain damage and repair, and to explore whether these biomarkers mediate the effect of PSH on the ischaemic stroke (IS) outcome. Methods This was a secondary analysis of the Glycaemia in Acute Stroke II study. Biomarkers of inflammation, prothrombotic activity, endothelial dysfunction, blood–brain barrier rupture, cell death and brain repair processes were analysed at 24–48 h (baseline) and 72–96 h (follow‐up) after IS. The associations of the biomarkers and stroke outcome (modified Rankin Scale score at 3 months) based on the presence of PSH were compared. Results A total of 174 patients participated in this sub‐study. Brain‐derived neurotrophic factor (BDNF) at admission was negatively correlated with glucose levels. PSH was associated with a trend toward higher levels of endothelial progenitor cells (EPCs) at baseline. The EPCs in the PSH group then decreased in the follow‐up samples (−8.5 ± 10.3) compared with the non‐PSH group (4.7 ± 7.33; P = 0.024). However, neither BDNF nor EPC values had correlation with the 3‐month outcome. Higher interleukin‐6 at follow‐up was associated with poor outcomes (modified Rankin Scale > 2) independently of PSH. Conclusion Post‐stroke hyperglycaemia appears to be associated with a negative regulation of BDNF and a different reaction in EPC levels. However, neither BDNF nor EPCs showed significant mediation of the PSH association with IS outcome, and only higher interleukin‐6 in the follow‐up samples (72–96 h) was related to poor outcomes, independently of PSH status. Further studies are needed to achieve definite conclusions.