The effect of finite pore length on ion structure and charging.

Nanoporous supercapacitors play an important role in modern energy storage systems, and their modeling is essential to predict and optimize the charging behaviour. Two classes of models have been developed that consist of finite and infinitely long pores. Here, we show that although both types of models predict qualitatively consistent results, there are important differences emerging due to the finite pore length. In particular, we find that the ion density inside a finite pore is not constant, but increases linearly from the pore entrance to the pore end, where the ions form a strongly layered structure. This hinders a direct quantitative comparison between the two models. In addition, we show that although the ion density between the electrodes changes appreciably with the applied potential, this change has a minor effect on charging. Our simulations also reveal a complex charging behaviour, which is adsorption-driven at high voltages, but it is dominated either by co-ion desorption or by adsorption of both types of ions at low voltages, depending on the ion concentration.

The detection of SRSF2 mutations in routinely processed bone marrow biopsies is useful in the diagnosis of chronic myelomonocytic leukemia.

Diagnosis of chronic myelomonocytic leukemia (CMML) is based on a combination of clinical, laboratory, and morphological parameters, including persistent peripheral blood monocytosis. Recently, mutations of serine/arginine-rich splicing factor 2 (SRSF2) have been identified in 40% to 50% of CMMLs and occasionally in other myeloid disorders. In this study, we established a robust assay for the detection of SRSF2 mutations in decalcified, paraffin-embedded bone marrow (BM) biopsies and investigated its diagnostic utility. BM biopsies of 78 patients with myeloid neoplasms, including 36 CMMLs, 22 myelodysplastic syndromes (MDS), and 20 Ph- myeloproliferative neoplasms (MPN) were analyzed. The region around hot spot P95 in exon 1 of SRSF2 was amplified and bidirectionally sequenced. In addition, a restriction fragment length polymorphism analysis was established. The JAK2 V617F mutation was investigated by allele-specific polymerase chain reaction. SRSF2 mutations were identified in 16 (44%) of 36 CMMLs, including 1 of 3 cases with associated systemic mastocytosis, 4 (20%) of 20 Ph- MPN, and 1 (4.5%) of 22 MDS. Restriction fragment length polymorphism analysis detected all mutations with the exception of a single P95A. Of note, 2 cases of JAK2 V617F+ primary myelofibrosis with SRSF2 mutation initially were diagnosed as CMML based on significant peripheral blood monocytosis. In CMML, no correlation with histopathology and/or clinical parameters was observed, but SRSF2 mutations were associated with normal karyotype (P < .001). In summary, SRSF2 mutations are frequent in CMML and a useful diagnostic feature demonstrable in BM biopsies, allowing a definitive diagnosis for cases with minimal dysplasia and normal karyotype. The role of SRSF2 mutations in cases with hybrid features between primary myelofibrosis and CMML needs further investigation.