Mesothelial- and epithelial-derived FGF9 have distinct functions in the regulation of lung development

Fibroblast growth factor (FGF) 9 is a secreted signaling molecule that is expressed in lung mesothelium and epithelium and is required for lung development. Embryos lacking FGF9 show mesenchymal hypoplasia, decreased epithelial branching and, by the end of gestation, hypoplastic lungs that cannot support life. Mesenchymal FGF signaling interacts with β-catenin-mediated WNT signaling in a feed-forward loop that functions to sustain mesenchymal FGF responsiveness and mesenchymal WNT/β-catenin signaling. During pseudoglandular stages of lung development, Wnt2a and Wnt7b are the canonical WNT ligands that activate mesenchymal WNT/β-catenin signaling, whereas FGF9 is the only known ligand that signals to mesenchymal FGF receptors (FGFRs). Here, we demonstrate that mesothelial- and epithelial-derived FGF9, mesenchymal Wnt2a and epithelial Wnt7b have unique functions in lung development in mouse. Mesothelial FGF9 and mesenchymal WNT2A are principally responsible for maintaining mesenchymal FGF-WNT/β-catenin signaling, whereas epithelial FGF9 primarily affects epithelial branching. We show that FGF signaling is primarily responsible for regulating mesenchymal proliferation, whereas β-catenin signaling is a required permissive factor for mesenchymal FGF signaling

Understanding the user display names across social networks

The display names that an individual uses in various online social networks always contain some redundant information because some people tend to use the similar names across different networks to make them easier to remember or to build their online reputation. In this paper, we aim to measure the redundant information between different display names of the same individual. Based on the cross-site linking function, we first develop a specific distributed crawler to extract the display names that individuals select for different social networks, and we give an overview on the display names we extracted. Then we measure and analyze the redundant information in three ways: length similarity, character similarity and letter distribution similarity, comparing with display names of different individuals. We also analyze the evolution of redundant information over time. We find 45% of users tend to use the same display name across OSNs. Our findings also demonstrate that display names of the same individual show high similarity. The evolution analysis results show that redundant information is time-independent. Awareness of the redundant information between the display names can benefit many applications, such as user identification across social networks

Study on measurement model of lignin content in pulp after alkaline extraction

Because kappa number cannot accurately represent the lignin content in the pulp after alkaline extraction, lead to the excessive dosage of bleaching chemicals added and the pollutant content increases. In order to accurately determine the dosage of bleaching agent, reduce pollutant emissions, a prediction model of lignin content of pulp was established by analyzing the correlation between lignin content and alkaline extraction conditions in this paper. The results show that the established soft sensor model can accurately measure lignin content, it is helpful to determine the amount of bleaching agent more accurately, reduce pollutant generation after pulp bleaching

Overexpression of CDC25C affects the cell cycle of ovarian granulosa cells from adult and young goats

Background: CDC25 is a dual-specificity phosphatase that was first identified in the yeast Schizosaccharomyces pombe as a cell cycle-defective mutant. Although CDC25 is involved in the cell cycle of ovarian granulosa cells, the CDC25 signaling pathway has not been clarified fully. To explore the role of CDC25C in the cell cycle of goat ovarian granulosa cells, a CDC25C-overexpressing vector, pCMV-HA-CDC25C, was constructed and transfected into granulosa cells from adult and young white goats from Jiangsu Nantong. RT-PCR was used to measure CDC25C, CDK1, and WEE1 gene expression levels, and flow cytometry was used to distinguish ovarian granulosa cells in different phases of the cell cycle. Progesterone and estradiol levels in transfected ovarian granulosa cells were also measured. Results: In adult goat follicular granulosa cells transfected with pCMV-HA-CDC25C, CDC25C expression increased significantly, which greatly increased the relative gene expression levels of both CDK1 and WEE1. Additionally, progesterone and estradiol levels were increased in goat follicular granulosa cells overexpressing CDC25C. And the cell cycle results showed that transfection of pCMV-HA-CDC25C leads to a higher proportion of cells in S phase compared to the no vector-transfected groups. Conclusions: The results of this study indicated that the overexpression of CDC25C may increase the gene expression levels of both WEE1 and CDK1 in S phase and accelerate the transition of cells from G1 phase to S phase

A deep dive into user display names across social networks

The display names from an individual across Online Social Networks (OSNs) always contain abundant information redundancies because most users tend to use one main name or similar names across OSNs to make them easier to remember or to build their online reputation. These information redundancies are of great benefit to information fusion across OSNs. In this paper, we aim to measure these information redundancies between different display names of the same individual. Based on the cross-site linking function of Foursquare, we first develop a distributed crawler to extract the display names that individuals used in Facebook, Twitter and Foursquare, respectively. We construct three display name datasets across three OSNs, and measure the information redundancies in three ways: length similarity, character similarity and letter distribution similarity. We also analyze the evolution of redundant information over time. Finally, we apply the measurement results to the user identification across OSNs. We find that (1) more than 45% of users tend to use the same display name across OSNs; (2) the display names of the same individual for different OSNs show high similarity; (3) the information redundancies of display names are time-independent; (4) the AUC values of user identification results only based on display names are more than 0.9 on three datasets

The protective role of DOT1L in UV-induced melanomagenesis

The DOT1L histone H3 lysine 79 (H3K79) methyltransferase plays an oncogenic role in MLL-rearranged leukemogenesis. Here, we demonstrate that, in contrast to MLL-rearranged leukemia, DOT1L plays a protective role in ultraviolet radiation (UVR)-induced melanoma development. Specifically, the DOT1L gene is located in a frequently deleted region and undergoes somatic mutation in human melanoma. Specific mutations functionally compromise DOT1L methyltransferase enzyme activity leading to reduced H3K79 methylation. Importantly, in the absence of DOT1L, UVR-induced DNA damage is inefficiently repaired, so that DOT1L loss promotes melanoma development in mice after exposure to UVR. Mechanistically, DOT1L facilitates DNA damage repair, with DOT1L-methylated H3K79 involvement in binding and recruiting XPC to the DNA damage site for nucleotide excision repair (NER). This study indicates that DOT1L plays a protective role in UVR-induced melanomagenesis

Plexin-B1 silencing inhibits ovarian cancer cell migration and invasion

BACKGROUND: Elevated Plexin-B1 expression has been found in diverse human cancers and in non-neoplastic tissues, and it mediates diverse biological and pathological activities. However, whether or not Plexin-B1 expression is involved in human ovarian tumors remains unclear. In the present study, Plexin-B1 expression was explored in benign and malignant human ovarian tumor tissues. In addition, the impact of Plexin-B1 expression on ovarian cancer cell proliferation, migration and invasion were investigated in vitro. METHODS: Plexin-B1 expression was analyzed in normal and benign ovarian tissues and serous ovarian tumors (both borderline and malignant) by immunohistochemical staining, as well as in four human ovarian cancer cell lines (A2780, C13*, SKOV3, and OV2008) by RT-PCR and western blot analyses. Furthermore, endogenous Plexin-B1 expression was suppressed by Plexin-B1 siRNA in SKOV3 cells, which overexpress Plexin-B1. Protein levels of Plexin-B1, AKT and AKT(Ser473 )were examined by western blot analysis. Cell proliferation, migration and invasion were measured with MTT, wound healing and boyden chamber assays, respectively, and the cytoskeleton was monitored via F-actin staining. RESULTS: Expression levels of Plexin-B1 protein were significantly higher in serous ovarian carcinomas than in normal ovaries or benign ovarian neoplasms, and in the former, Plexin-B1 expression was positively correlated with lymphatic metastasis, and the membrane and cytoplasm of cancer cells stained positively. SKOV3 cells displayed the highest Plexin-B1 expression at both the mRNA and protein levels among the four tested human ovarian cancer cell lines and was selected as a cell model for further in vitro experiments. Plexin-B1 siRNA significantly suppressed phosphorylation of AKT at Ser473 in SKOV3 cells, but it did not alter total AKT expression. In addition, silencing of Plexin-B1 in SKOV3 cells inhibited cell migration and invasion and reorganized the cytoskeleton, whereas cell proliferation was not affected. CONCLUSION: Plexin-B1 expression correlates with malignant phenotypes of serous ovarian tumors, probably via phosphorylation of AKT at Ser473, suggesting that Plexin-B1 might be a useful biomarker and/or a novel therapeutic target

Stochastic and deterministic drivers of seasonal variation of fungal community in tobacco field soil

Background The soil fungal community plays an important role in global carbon cycling and shows obvious seasonal variations, however, drivers, particularly stochastic drivers, of the seasonal variation in the fungal community have never been addressed in sufficient detail. Methods We investigated the soil fungal community variation between summer growing (SG) and winter fallow (WF) stage, through high throughput sequencing of internal transcribed spacer (ITS) amplicons. Subsequently, we assessed the contribution of different ecological processes to community assembly using null-model-based statistical framework. Results The results showed that the fungal community diversity decreased significantly after tobacco cropping in the SG stage and the composition showed a clear turnover between the WF and SG stages. The variation in community composition was largely attributable to the presence of a small portion of Dothideomycetes in the WF stage that dominated the soil fungal community in the SG stage. The organic matter, temperature, and water content were the main deterministic factors that regulated the fungal community; these factors explained 34.02% of the fungal community variation. Together with the result that the fungal community was mainly assembled by the dispersal process, our results suggested that the stochastic factors played important roles in driving the seasonal variation of fungal community. The dispersal limitation dominated the fungal community assembly during the WF stage when homogenizing dispersal was the main assembly process of the fungal community in the SG stage. Thus, we proposed that the dispersal processes are important drivers for seasonal variation of fungal community in tobacco planted soil

Expression of the Inhibitory Receptor TIGIT Is Up-Regulated Specifically on NK Cells With CD226 Activating Receptor From HIV-Infected Individuals

Natural killer (NK) cells are important for maintenance of innate immune system stability and serve as a first line of defense against tumors and virus infections; they can act either directly or indirectly and are regulated via co-operation between inhibitory and stimulatory surface receptors. The recently reported inhibitory receptor, TIGIT, can be expressed on the NK cell surface; however, the expression level and function of TIGIT on NK cells during HIV infection is unknown. In this study, for the first time, we investigated the expression and function of TIGIT in NK cells from HIV-infected individuals. Our data demonstrate that the level of TIGIT is higher on NK cells from patients infected with human immunodeficiency virus (HIV) compared with HIV-negative healthy controls. TIGIT expression is inversely correlated with CD4+ T cell counts and positively correlated with plasma viral loads. Additionally, levels of the TIGIT ligand, CD155, were higher on CD4+ T cells from HIV-infected individuals compared with those from healthy controls; however, there was no difference in the level of the activating receptor, CD226, which recognizes the same ligands as TIGIT. Furthermore, TIGIT was found to specifically up-regulated on CD226+ NK cells in HIV-infected individuals, and either rIL-10, or rIL-12 + rIL-15, could induce TIGIT expression on these cells. In addition, high TIGIT expression inhibited the production of interferon-gamma (IFN-γ) by NK cells, while TIGIT inhibition restored IFN-γ production. Overall, these results highlight the important role of TIGIT in NK cell function and suggest a potential new avenue for the development of therapeutic strategies toward a functional cure for HIV

SCARB2/LIMP-2 Regulates IFN Production of Plasmacytoid Dendritic Cells by Mediating Endosomal Translocation of TLR9 and Nuclear Translocation of IRF7

Scavenger receptor class B, member 2 (SCARB2) is essential for endosome biogenesis and reorganization and serves as a receptor for both β-glucocerebrosidase and enterovirus 71. However, little is known about its function in innate immune cells. In this study, we show that, among human peripheral blood cells, SCARB2 is most highly expressed in plasmacytoid dendritic cells (pDCs), and its expression is further upregulated by CpG oligodeoxynucleotide stimulation. Knockdown of SCARB2 in pDC cell line GEN2.2 dramatically reduces CpG-induced type I IFN production. Detailed studies reveal that SCARB2 localizes in late endosome/lysosome of pDCs, and knockdown of SCARB2 does not affect CpG oligodeoxynucleotide uptake but results in the retention of TLR9 in the endoplasmic reticulum and an impaired nuclear translocation of IFN regulatory factor 7. The IFN-I production by TLR7 ligand stimulation is also impaired by SCARB2 knockdown. However, SCARB2 is not essential for influenza virus or HSV-induced IFN-I production. These findings suggest that SCARB2 regulates TLR9-dependent IFN-I production of pDCs by mediating endosomal translocation of TLR9 and nuclear translocation of IFN regulatory factor 7