Entropy Weight Measure Model of Online Influential Users’ Relative Social Capital

Based on the perspectives of information resource management and social capital measurement, this paper studies how influential users acquire, accumulate, and use their social capital in social networks to explore the general rules, which enterprises use influential users’ relative competitiveness in their topic areas of expertise to advertise precisely. The paper describes the social capital differences among influential users by introducing and calculating users’ relative social capital. Results show that user’s social capital values in different fields are dissimilar, and the scope and intensity of social capital among different users are relative. The proposed method is proved to be effective and reasonable

Information Entropy-based Social Capital Measure Method of Online Influential Users

Measuring online user influence is a major research topic in social marketing performance maximization. In this study, we comprehensively investigate how online influential users gain, accumulate, and use their social capital from the perspective of information resource management and social capital measurement. First, we define the social capital of online influential users and the attribute characters and relationships reflected fully by personality and sociality index data. We then construct a social capital measurement indicator system and information entropy model of online users. After the calculations of this model, we finally forma social capital measure method of online influential users. The rationality and validity of proposed model are tested by experimental study on real datasets

Aggregation formation mediated anoikis resistance of BEL7402 hepatoma cells.

Anoikis resistance is the prerequisite of cancer cells metastasis. Elucidation of the mechanism of anoikis resistance remains a significant challenge. We reported here a model to mimic anoikis resistant process of hepatoma cells in vitro. Experimental results indicated cell to cell aggregation could mediate anoikis resistance of BEL7402 hepatoma cells. Further investigation of these aggregations indicated the biological properties changed greatly after the hepatoma cells lost their anchorage. Aggregation forming process could be separated into three distinct phases according to their biological characteristics, comprising of premature phase, mature phase and postmature phase. Mature phase aggregations have the premium state of cell viability and may mimic the metastatic cells in the circulating system. Biological properties of these three phases aggregations were studied in details including morphological alteration, cell viability and microarray expression profiles. It indicated there was a great upregulation of adhesion molecules during the process of aggregation formation and the cell to cell contact in the aggregation may be mediated independent of calcium involved adhesion pathway. This model might shed light on the anoikis resistance mechanism of hepatoma cells and help to develop new therapies that may target the anoikis resistant hepatoma cells in the metastasis process

The anaphase promoting complex impacts repair choice by protecting ubiquitin signalling at DNA damage sites

Double-strand breaks (DSBs) are repaired through two major pathways, homology-directed recombination (HDR) and non-homologous end joining (NHEJ). While HDR can only occur in S/G2, NHEJ can happen in all cell cycle phases (except mitosis). How then is the repair choice made in S/G2 cells? Here we provide evidence demonstrating that APCCdh1 plays a critical role in choosing the repair pathways in S/G2 cells. Our results suggest that the default for all DSBs is to recruit 53BP1 and RIF1. BRCA1 is blocked from being recruited to broken ends because its recruitment signal, K63-linked poly-ubiquitin chains on histones, is actively destroyed by the deubiquitinating enzyme USP1. We show that the removal of USP1 depends on APCCdh1 and requires Chk1 activation known to be catalysed by ssDNA-RPA-ATR signalling at the ends designated for HDR, linking the status of end processing to RIF1 or BRCA1 recruitment.We thank S.-Y. Lin (MD Anderson Cancer Center) for cell lines; J. Rosen (Baylor College of Medicine) for reagents; H. Masai (Tokyo Metropolitan Institute of Medical Science) for U2OS-Fucci cell line; D. Durocher (University of Toronto) for HeLa-Fucci cell line; E. Citterio (Netherlands Cancer Institute) for GFP-USP3 construct; M.S.Y. Huen (The University of Hong Kong) for RNF168 antibody. This work was performed with facilities and instruments in the Imaging Core of National Center for Protein Science (Beijing), the Cytometry and Cell Sorting Core at Baylor College of Medicine with funding from the NIH (P30 AI036211, P30 CA125123 and S10 RR024574), the Integrated Microscopy Core at Baylor College of Medicine with funding from the NIH (HD007495, DK56338 and CA125123), and the John S. Dunn Gulf Coast Consortium for Chemical Genomics. We also thank other members of the Zhang lab for helpful discussion and support. This work was supported in part by an international collaboration grant (# 2013DFB30210) and a 973 Project grant (# 2013CB910300) from Chinese Minister of Science and Technology, in part by a Chinese National Natural Science Foundation grant (# 81171920), in part by a grant from The Committee of Science and Technology of Beijing Municipality, China (# Z141100000214015), and in part by NIH grants CA116097 and CA122623 to P.Z. J.J. is supported by grants from National Institutes of Health (R01GM102529) and the Welch Foundation (AU-1711). S.H. is supported by grants (# 81272488 and 81472795) from Chinese National Natural Science Foundation. Y.Z. is supported by grants from the National Natural Scientific Foundation of China (No. 81430055), Programs for Changjiang Scholars and Innovative Research Team in University (No. IRT_15R13).S

Nuclear Receptor Coactivator 2 Promotes Human Breast Cancer Cell Growth by Positively Regulating the MAPK/ERK Pathway

As a member of the p160 steroid receptor coactivator (SRC) family, nuclear receptor coactivator 2 (NCOA2) is known to play essential roles in many physiological and pathological processes, including development, endocrine regulation, and tumorigenesis. However, the biological function of NCOA2 in breast cancer is not fully understood. We found that the copy number of the NCOA2 gene was frequently amplified in four breast cancers datasets, varying from 6 to 10%, and the mRNA levels of NCOA2 were also upregulated in 11% of the sequenced cases/patients (TCGA provisional dataset). Next, we confirmed that NCOA2 silencing significantly suppressed cell proliferation in different breast cancer cell lines, by inducing cell cycle arrest and apoptosis. Mechanistically, whole-transcriptome sequencing (RNA-Seq) analysis showed that NCOA2 depletion leads to downregulation of the MAPK/ERK signaling cascade, possibly via downregulating NCOA2's downstream target RASEF. In conclusion, our results suggest NCOA2 as a potential target of therapeutics against breast cancer

Wartość prognostyczna współczynnika płytki krwi/limfocyty w ostrym zespole wieńcowym: przegląd systematyczny z metaanalizą

Background and aim: The aim of this study was to investigate whether the platelet-to-lymphocyte ratio (PLR) is an independent predictor of all-cause mortality and cardiovascular (CV) events in patients with acute coronary syndrome (ACS). Methods: PubMed, Embase, and the Cochrane Library were searched for relevant cohort studies regarding the association between PLR and outcomes of patients with ACS. Either a random- or a fixed-effect model was used for pooling data. Results: Eight studies involving 6627 patients with ACS were included. The cut-off PLR value for defining risk groups was 150, and patients were assigned to the low (≤ 150) or high (> 150) PLR groups. The pooled relative risk (RR) values of in-hospital and long-term mortality were 2.15 (95% CI [confidence interval] 1.73–2.67; p < 0.00001) and 2.27 (95% CI 1.35–3.80; p = 0.002), respectively, comparing the high and the low PLR groups. Compared with the low PLR group, the high PLR group had a significantly increased risk of in-hospital (RR 1.95; 95% CI 1.30–2.91; p = 0.001) and long-term (RR 1.50; 95% CI 1.08–2.09; p = 0.01) major adverse CV events. Conclusions: Elevated PLR was found to be a predictor of all-cause mortality and CV events.Wstęp i cel: Badanie przeprowadzono w celu ustalenia, czy współczynnik płytki krwi/limfocyty (PLR) jest niezależnym czynnikiem predykcyjnym śmiertelności całkowitej i zdarzeń sercowo-naczyniowych u chorych z ostrym zespołem wieńcowym (ACS). Metody: Przeszukano bazy danych PubMed, Embase i Cochrane Library w celu pozyskania odpowiednich badań kohortowych zawierających informacje dotyczące związku między PLR a punktami końcowymi u pacjentów z ACS. Do analizy połączonych danych użyto modelu z efektami losowymi lub z efektami stałymi. Wyniki: Do metaanalizy włączono 8 badań obejmujących 6627 osób z ACS. Wartość progowa PLR przyjęta na potrzeby definiowania ryzyka wynosiła 150, a chorych przydzielano do grupy niskiego (≤ 150) lub wysokiego (> 150) PLR. Oszacowane w analizie łączonych danych ryzyko względne (RR) zgonu wewnątrzszpitalnego i zgonu w perspektywie długoterminowej (porównanie grup z wysokimi i niskimi wartościami PLR) wynosiło odpowiednio 2,15 (95% przedział ufności [CI] 1,73–2,67; p < 0,00001) i 2,27 (95% CI 1,35–3,80; p = 0,002). W porównaniu z grupą niskich wartości PLR, osoby z wysokimi wartościami PLR charakteryzowały się istotnie wyższym ryzykiem zgonu wewnątrzszpitalnego (RR 1,95; 95% CI 1,30–2,91; p = 0,001) i wyższym ryzykiem długookresowym poważnych niepożądanych zdarzeń sercowo-naczyniowych (RR 1,50; 95% CI 1,08–2,09; p = 0,01). Wnioski: Stwierdzono, że podwyższona wartość PLR jest czynnikiem predykcyjnym śmiertelności całkowitej i zdarzeń sercowo-naczyniowych

Evapotranspiration on Natural and Reclaimed Coral Islands in the South China Sea

Studies of evapotranspiration on remote tropical coral islands are important to explore and sustain scarce freshwater resources. However, there is a significant knowledge gap between research to evaluate evapotranspiration based on remote sensing methods and the influences of different land use types on water dynamics on reclaimed coral islands. This study applied the remote-sensing-based Vegetation Interfaces Processes (VIP-RS) model to estimate actual evapotranspiration (ETa) on Zhaoshu Island, Yongxing Island, and Yongshu Island in the South China Sea from 2016 to 2019. The results showed that the average annual ETa of Zhaoshu Island, Yongxing Island, and Yongshu Island was 685 mm, 530 mm, and 210 mm, respectively. Annual transpiration (Ec) and soil evaporation (Es) exhibited similar patterns on the natural islands; however, Es controlled the water consumption on the reclaimed islands. Water dynamics exhibited seasonal fluctuations due to the uneven distribution of precipitation (PRP). However, ETa of the natural islands was higher than PRP in the dry season, indicating vegetation has to absorb water from the groundwater to sustain growth. The results also agreed with the analysis of dominant driving factors based on partial correlation analysis, which demonstrated that the Normalized Difference Vegetation Index (NDVI) is the most important factor that influences ETa, while relative humidity (RH) controlled the bare land or sparsely vegetated areas on the reclaimed islands. The setting of different land use types showed that vegetation and built-up or hardened roads took control of evapotranspiration and rainwater collection, respectively, which play important roles in water dynamics on corals islands. The evaluation of ETa based on a remote-sensing-based model overcame the difficulty in fieldwork observation, which improves the certainty and accuracy at a spatial scale. In addition, it gave us a new reference to protect and manage scarce freshwater resources properly