Attention network training promotes selective attention of children with low socioeconomic status.

The objectives of this study were to evaluate the difference of selective attention efficiency between children with low and high socioeconomic status (SES) and the promotional effect of attention network training (an attention network test was used as the training task) on selective attention in children with the low SES. A total of 139 10- to 12-year-old children participated in two experiments (71 in Experiment 1 and 68 in Experiment 2). The results suggest that selective attention and switch ability of children with high SES are better than those of children with low SES. After attention network training, selective attention, switch ability, and working memory of low-SES children improved significantly. The findings provide evidence that attention network training could enhance selective attention in low-SES children and that the beneficial training effect could also transfer to switch ability and working memory. The research may provide a promising method to compensate cognitive delay of low-SES children.

Calycosin may Alleviate Ang II-Induced Pro-proliferative Effects on Glomerular Mesangial Cells via Partially Inhibiting Autophagy and ERK Signaling Pathway.

Over-expression of angiotensin II (Ang II) is an important reason for the development of chronic kidney disease. Calycosin is the active component of traditional Chinese medicine astragali radix. The present work aims to explore whether calycosin could affect the growth and apoptosis ability of the Ang II treated glomerular mesangial cells and the underlying mechanism. Human glomerular mesangial cells (GMCs) were cultured and treated by Ang II and 0, 0.1, 1, or 10 µM calycosin, and the viability and proliferation of the cells were determined by methyl thiazolyl tetrazolium (MTT) and 5-ethynil-2'-deoxyuridine (EdU) staining; moreover, the apoptosis of the cells was examined by flow cytometry assay; furthermore, the expression levels of extracellular signal-regulated kinase (ERK), p-ERK, anti-apoptotic factor Bcl-2, as well as pro-apoptotic factor Bax have been examined by Western blot (WB) methods; finally, the expression of autophagic markers in each group was examined by WB and immunocytochemistry methods. We found that Ang II increased viability and proliferation, meanwhile inhibited apoptosis of the GMCs; furthermore, 1 and 10 µM calycosin significantly inhibited the growth and promoted the apoptosis of the GMCs treated by Ang II; moreover, calycosin also inhibited ERK signaling in mesangial cells activated by Ang II treatment; Finally, calycosin could inhibit Ang II induced autophagy of GMCs in a dose-dependent manner. In conclusion, calycosin may alleviate Ang II-induced pro-proliferative and anti-apoptotic effects on glomerular mesangial cells at least partially via inhibiting autophagy and ERK signaling pathway, suggesting that calycosin may function as a potential alternative medication for the management of chronic kidney diseases.

Affinity Feature Strengthening for Accurate, Complete and Robust Vessel Segmentation.

Vessel segmentation is crucial in many medical image applications, such as detecting coronary stenoses, retinal vessel diseases and brain aneurysms. However, achieving high pixel-wise accuracy, complete topology structure and robustness to various contrast variations are critical and challenging, and most existing methods focus only on achieving one or two of these aspects. In this paper, we present a novel approach, the affinity feature strengthening network (AFN), which jointly models geometry and refines pixel-wise segmentation features using a contrast-insensitive, multiscale affinity approach. Specifically, we compute a multiscale affinity field for each pixel, capturing its semantic relationships with neighboring pixels in the predicted mask image. This field represents the local geometry of vessel segments of different sizes, allowing us to learn spatial- and scale-aware adaptive weights to strengthen vessel features. We evaluate our AFN on four different types of vascular datasets: X-ray angiography coronary vessel dataset (XCAD), portal vein dataset (PV), digital subtraction angiography cerebrovascular vessel dataset (DSA) and retinal vessel dataset (DRIVE). Extensive experimental results demonstrate that our AFN outperforms the state-of-the-art methods in terms of both higher accuracy and topological metrics, while also being more robust to various contrast changes.

Differential expression of long non-coding RNA and mRNA in children with Henoch-Schönlein purpura nephritis.

Long non-coding RNAs (lncRNAs) serve an essential role in regulating immunological functions. However, their impact on Henoch-Schönlein purpura nephritis (HSPN), has remained elusive. The present study determined the expression of lncRNAs and mRNAs in the peripheral blood of 6 children with HSPN and recruited 4 healthy children for comparative study. High-throughput sequencing revealed outstanding differences in lncRNA and mRNA expression, which were verified through reverse transcription-quantitative polymerase chain reaction. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses were used to investigate the associated biological functions and possible mechanisms of lncRNAs and mRNAs in HSPN. A total of 820 differentially expressed lncRNAs between the two groups were identified, of which 34 were upregulated and 786 were downregulated. Simultaneously, a total of 3,557 mRNAs were also identified to be differentially expressed, of which 1,232 were upregulated and 2,325 were downregulated. The results revealed that the expression of lncRNAs including ENST00000378432, ENST00000571370, uc001kfc.1 and uc010qna.2 was decreased in HSPN patients compared with that in healthy controls. These lncRNAs were associated with the p53 signaling pathway and apoptosis-associated genes (AKT2, tumor protein 53, phosphatase and tensin homolog and FAS). Further studies of those lncRNAs will be performed to elucidate their functions in apoptosis. Complete raw data files were deposited in the Gene Expression Omnibus (GEO) at National Center for Biotechnology information under the GEO accession no. GSE102114 (www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE102114).