Recurrent somatic mutation of SRSF2, one of the RNA splicing machinery genes, has been identified in a substantial proportion of patients with myelodysplastic syndrome (MDS). However, the clinical and biologic characteristics of MDS with this mutation remain to be addressed. In this study, 34 (14.6%) of the 233 MDS patients were found to have SRSF2 mutation. SRSF2 mutation was closely associated with male sex (P ‫؍‬ .001) and older age (P < .001). It occurred concurrently with at least 1 additional mutation in 29 patients (85.3%) and was closely associated with RUNX1, IDH2, and ASXL1 mutations (P ‫؍‬ .004, P < .001, and P < .001, respectively). Patients with SRSF2 mutation had an inferior overall survival (P ‫؍‬ .010), especially in the lower risk patients. Further exploration showed that the prognostic impact of SRSF2 mutation might be attributed to its close association with old age. Sequential analyses in 173 samples from 66 patients showed that all SRSF2-mutated patients retained their original mutations, whereas none of the SRSF2-wild patients acquired a novel mutation during disease evolution. IntroductionPre-mRNA needs splicing process to become mature mRNA for further translation into proteins. The splicing of pre-mRNA, a highly regulated cascade of processes, is important for gene expression and genetic diversity; more than 90% of human genes undergo alternative splicing to make various protein isoforms for different biologic functions. 1,2 SRSF2, located at 17q25.1, encodes serine/arginine-rich splicing factor 2 that belongs to the serine/ arginine-rich protein family, important for splice-site selection, spliceosome assembly, and both constitutive and alternative splicing. 3 Recently, through next-generation whole exome sequencing, recurrent somatic mutations involving the RNA splicing machinery were identified in a substantial proportion of patients with myelodysplastic syndrome (MDS), 4-7 a myeloid hematopoietic disorder characterized by ineffective hematopoiesis, cytopenias, and risk of transformation to acute leukemia. 8,9 Among these mutations, the clinical relevance of 2 prevalent mutations, U2AF35 4,6,10 and SF3B1, 4,5,7,[11][12][13][14] have been explored. Mutations in SRSF2 also have been reported in MDS patients, 4,7,10,15,16 but studies concerning the clinical correlations of the mutations are limited. In addition, the interaction of SRSF2 mutation with other genetic alternations in MDS patients and its stability during disease progression remain to be determined.The pathogenesis of MDS has not been clearly identified; genomic damage with accumulation of genetic aberrations, 8,17 deregulated or autoreactive immune responses, 18,19 and abnormal bone marrow (BM) microenvironment 20,21 might all contribute to the development and progression of this preleukemic disease. Because the regulation of RNA splicing is important for normal cell function, genetic alternation in SRSF2 may play an important role in the pathogenesis of MDS. 4 Here, we aimed to define the clinical correlations of SRSF2 mut...

We aimed to analyze clinical impacts of the U2AF1 mutation on patients with myelodysplastic syndrome (MDS) and its stability during disease progression. We checked mutation status of the U2AF1 by direct sequencing in 478 de novo MDS patients and correlated with the clinical characteristics and outcomes. We also sequentially analyzed the U2AF1 mutation in 421 samples from 142 patients to determine its stability during the disease courses. Thirty-six patients (7.5%) were found to have U2AF1 mutations, which occurred more frequently in younger patients (P 5 0.033). U2AF1 mutation was an independent poor-risk factor for overall survival (OS) in all patients (P 5 0.030) and younger patients (P 5 0.041). U2AF1 mutation could also predict shorter time-to-leukemia transformation (TTL) in younger patients (P 5 0.020). In addition, U2AF1 mutation was associated with shorter TTL in lower-risk MDS patients. Sequential analyses showed all original U2AF1 mutations in U2AF1-mutated patients were retained during follow-ups unless complete remission was achieved, whereas none of the U2AF1-wild patients acquired a novel mutation during disease evolution. U2AF1 mutation is more prevalent in younger MDS patients and associated with inferior outcomes although it is stable during the clinical course. The mutation may be used as a biomarker for risk stratification. Am. J. Hematol. 88:E277-E282,

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This study proposes a promising silicon (Si) solar cell structure for reducing the potential induced degradation (PID) of crystalline Si solar cells. Phosphorous silicate glass (PSG) layers were carefully designed on an emitter layer, and the thickness of these layers (d PSG ) was controlled by adjusting the diffusion temperature and time. The results show that the power loss remarkably decreased from 31% (d PSG = 0 nm) to 11% (d PSG = 22.3 nm) and further decreased to less than 5% after a 48-h PID test when d PSG In recent years, the number of large photovoltaic (PV) systems for generating high electricity has increased. Such PV systems contain numerous high power PV modules. Therefore, the durability of a PV module is imperative.1 The potential induced degradation (PID) of crystalline silicon (Si) solar cells, first observed by Sunpower in 2005, has drawn considerable attention in recent years. [2][3][4][5][6] This is because the local electrical short-circuiting of the pn-junction in a Si solar cell occurs under high voltage stress, which leads to a substantial reduction in the power of a module. 7Several approaches can be used to prevent PID from cell to module levels. For example, leakage current can be reduced by changing the cover glass and encapsulation materials. [8][9][10] However, applying these approaches increases the cost drastically and may cause the efficiency of solar cells to deteriorate. The soda-lime cover glass and ethylene vinyl acetate (EVA) are still the most widely used and low-cost packaging materials for solar modules. Strong demand has necessitated the modification of the antireflective layers or emitter layers in PID-resistant solar cells. However, risks should be noticed that an efficiency of a solar cell and throughput may be reduced.This study proposes a promising Si solar cell structure for reducing the PID of solar cells without influencing their efficiency and throughput. Phosphorous silicate glass (PSG) layers were carefully designed on an emitter layer to determine how they affect the efficiencies of solar cells before and after PID. A current-voltage (I-V) tester was used to determine PV parameters. An ellipseometer and transmission electron microscope (TEM) were used to measure the thicknesses of the PSG layers. Secondary ion mass spectrometry (SIMS) was used to obtain concentration profiles of Si, sodium (Na), phosphorus (P), oxygen, and nitrogen. Figure 1 shows the process flow in this study as well as the structure of a solar cell with a PSG layer. Solar-grade and monocrystalline Si wafers with a size and resistivity of 5 in 2 and 0.5-3.0 ·cm, respectively, were used in this study. These wafers were processed using the following procedures: texturization by using an alkaline solution, P diffusion by using POCl 3 as a precursor, removing PSG layers by using a dilute HF solution (for standard solar cells only), depositing SixNy films as antireflection coatings by using a plasma enhanced chemical vapor deposition, and forming front and rear contacts by performing screen-p...