Poor responses to tyrosine kinase inhibitors in a child with precursor B‐cell acute lymphoblastic leukemia with SNX2‐ABL1 chimeric transcript

In addition to BCR, various rare fusion partners for the ABL1 gene have been reported in leukemia. We have identified the fusion gene SNX2‐ABL1 in a pediatric case of acute lymphoblastic leukemia (ALL), which has only once previously been reported in an adult patient. Cytogenetic analysis detected this fusion gene arising from a t(5;9)(q22;q34) translocation. ALL cells carrying a SNX2‐ABL1 fusion exhibited a BCR‐ABL1+ ALL‐like gene expression profile. The patient poorly responded to dasatinib but partially responded to imatinib. Treatment using tyrosine kinase inhibitors requires further investigation to optimize the genotype‐based treatment stratification for patients with SNX2‐ABL1 fusion.     

Intraclass correlation coefficient of trunk muscle thicknesses in different positions measured using ultrasonography

[Purpose] This study aimed to clarify the required number of measurements to calculate trunk muscle thickness at each position. [Participants and Methods] The participants were 30 elderly males aged >65 years. The right lumbar multifidus (L2), lumbar multifidus (L5), erector spinae, transversus abdominis, internal oblique, and external oblique muscle thicknesses were measured on longitudinal images obtained using ultrasonography in the lying, sitting, and standing positions. Two measurement values for each muscle thickness was used to calculate the intraclass correlation coefficient (1.1–1.5). [Results] The intraclass correlation coefficients of the abdominal muscle thickness measurements with “great reliabilities” were as follows: 1.3–1.5 for the external oblique muscle and 1.2–1.5 for the internal oblique and transversus abdominis muscles in the lying position; 1.3–1.5 for the external oblique and transversus abdominis muscles and 1.2–1.5 for the internal oblique muscle in the sitting position; the intraclass correlation coefficient in the standing position was 1.5 for the external oblique muscle 1.1–1.5 for the internal oblique muscle and 1.3–1.5 for the transversus abdominis muscle. In all the positions, the intraclass correlation coefficient of the measurements of the back-muscle thicknesses ranged from 1.1 to 1.5 for the right lumbar multifidus (L2), lumbar multifidus (L5), and erector spinae. [Conclusion] Depending on the posture, the abdominal muscles require multiple measurements, whereas the back muscles only require a single measurement.Key words: Intraclass correlation coefficient, Trunk muscle thicknesses, Ultrasonography     

The melatonin metabolite N1‐acetyl‐5‐methoxykynuramine facilitates long‐term object memory in young and aging mice

Melatonin (MEL) has been reported to enhance cognitive processes, making it a potential treatment for cognitive decline. However, the role of MEL’s metabolites, N1‐acetyl‐N2‐formyl‐5‐methoxykynuramine (AFMK) and N1‐acetyl‐5‐methoxykynuramine (AMK), in these effects are unknown. The current study directly investigated the acute effects of systemic MEL, AFMK, and AMK on novel object recognition. We also analyzed MEL, AFMK, and AMK levels in hippocampus and temporal lobe containing the perirhinal cortex following systemic MEL and AMK treatment. AMK administered post‐training had a more potent effect on object memory than MEL and AFMK. AMK was also able to rescue age‐associated declines in memory impairments when object memory was tested up to 4 days following training. Results from administering AMK at varying times around the training trial and the metabolism time course in brain tissue suggest that AMK’s memory‐enhancing effects reflect memory consolidation. Furthermore, inhibiting the MEL‐to‐AMK metabolic pathway disrupted object memory at 24 hours post‐training, suggesting that endogenous AMK might play an important role in long‐term memory formation. This is the first study to report that AMK facilitates long‐term object memory performance in mice, and that MEL crosses the blood‐brain barrier and is immediately converted to AMK in brain tissue. Overall, these results support AMK as a potential therapeutic agent to improve or prevent memory decline.