Improving the CALA\u27s Social Media Experience: The First CALA Social Media Survey

The Chinese American Librarians Association (CALA) currently uses three social media channels, CALA Facebook, WeChat, and YouTube. In order to improve their presence and better serve the CALA members, CALA\u27s first social media survey was conducted at the end of 2016 to seek feedback from its members and friends. This poster will present the background information for the survey, its methodology, findings, recommendations and follow-up. 18 questions were compiled, added to LimeSurvey and distributed to the CALA members via its Listserv. These questions attempted to address the users\u27 social media usage, participation level, time spent on the CALA\u27s social media channels, and their perception and experience of these channels, including their understanding of the main functions of these channels, whether they felt a sense of community in these channels, and how likely they are to share information. In addition, they were also asked to provide feedback about possible future directions of the CALA’s social media in regards to the possibility of creating additional channels, the desirable content categories, and their preferred language. The responses were analyzed and illustrated using Excel. A list of recommendations were made, including experimenting with ways to get members more involved in the social networking arena by creating a private Facebook group, WeChat public account, or LinkedIn group. The ultimate goal is to encourage members to participate and engage with each other on the CALA’s social media channels. The survey was coordinated by the CALA Social Media Group and follow-up efforts will be addressed. Session photos are available at the CALA\u27s Facebook page: https://www.facebook.com/CALA-Chinese-American-Librarians-Association-281336511932864

DHRL-FNMR: An Intelligent Multicast Routing Approach Based on Deep Hierarchical Reinforcement Learning in SDN

The optimal multicast tree problem in the Software-Defined Networking (SDN) multicast routing is an NP-hard combinatorial optimization problem. Although existing SDN intelligent solution methods, which are based on deep reinforcement learning, can dynamically adapt to complex network link state changes, these methods are plagued by problems such as redundant branches, large action space, and slow agent convergence. In this paper, an SDN intelligent multicast routing algorithm based on deep hierarchical reinforcement learning is proposed to circumvent the aforementioned problems. First, the multicast tree construction problem is decomposed into two sub-problems: the fork node selection problem and the construction of the optimal path from the fork node to the destination node. Second, based on the information characteristics of SDN global network perception, the multicast tree state matrix, link bandwidth matrix, link delay matrix, link packet loss rate matrix, and sub-goal matrix are designed as the state space of intrinsic and meta controllers. Then, in order to mitigate the excessive action space, our approach constructs different action spaces at the upper and lower levels. The meta-controller generates an action space using network nodes to select the fork node, and the intrinsic controller uses the adjacent edges of the current node as its action space, thus implementing four different action selection strategies in the construction of the multicast tree. To facilitate the intelligent agent in constructing the optimal multicast tree with greater speed, we developed alternative reward strategies that distinguish between single-step node actions and multi-step actions towards multiple destination nodes

Functional Analysis of the Melanin-Associated Gene CmMR1 in Coniothyrium minitans

Coniothyrium minitans is a sclerotial parasite, which has been investigated for commercial control of crop diseases caused by Sclerotinia sclerotiorum. Previously, we obtained a T-DNA insertional mutant, ZS-1TN24363, which did not produce melanin during conidiation. To understand the function of melanin in C. minitans, we cloned the gene that was disrupted by the T-DNA insertion, and found that this gene, called CmMR1, encoded a putative protein of 1,011 amino acids, which is a homolog of the transcription factor MR. Full-length CmMR1 contains 3,167 bp, with three exons and two introns. To confirm that the disrupted gene is responsible for the melanin-deficiency of the mutant, CmMR1 was disrupted and three targeted knockout mutants were obtained. Biological assays showed that the phenotype of the targeted knockout mutants was similar to that of the T-DNA insertional mutant. Furthermore, gene complementation confirmed that CmMR1 is responsible for the mutant phenotype. CmMR1 disruption did not affect hyphal growth, conidiation, and parasitization of C. minitans, however, the ROS accumulation increased and tolerance to UV light decreased significantly in the mutants. Our result may enhance the understanding of melanin in the ecology of C. minitans on molecular level

Transcriptomic analysis of mRNA expression and alternative splicing during mouse sex determination

Mammalian sex determination hinges on sexually dimorphic transcriptional programs in developing fetal gonads. A comprehensive view of these programs is crucial for understanding the normal development of fetal testes and ovaries and the etiology of human disorders of sex development (DSDs), many of which remain unexplained. Using strand-specific RNA-sequencing, we characterized the mouse fetal gonadal transcriptome from 10.5 to 13.5 days post coitum, a key time window in sex determination and gonad development. Our dataset benefits from a greater sensitivity, accuracy and dynamic range compared to microarray studies, allows global dynamics and sex-specificity of gene expression to be assessed, and provides a window to non-transcriptional events such as alternative splicing. Spliceomic analysis uncovered female-specific regulation of Lef1 splicing, which may contribute to the enhanced WNT signaling activity in XX gonads. We provide a user-friendly visualization tool for the complete transcriptomic and spliceomic dataset as a resource for the field

Gene Regulation and Epigenetic Remodeling in Murine Embryonic Stem Cells by c-Myc

BACKGROUND:The Myc oncoprotein, a transcriptional regulator involved in the etiology of many different tumor types, has been demonstrated to play an important role in the functions of embryonic stem (ES) cells. Nonetheless, it is still unclear as to whether Myc has unique target and functions in ES cells. METHODOLOGY/PRINCIPAL FINDINGS:To elucidate the role of c-Myc in murine ES cells, we mapped its genomic binding sites by chromatin-immunoprecipitation combined with DNA microarrays (ChIP-chip). In addition to previously identified targets we identified genes involved in pluripotency, early development, and chromatin modification/structure that are bound and regulated by c-Myc in murine ES cells. Myc also binds and regulates loci previously identified as Polycomb (PcG) targets, including genes that contain bivalent chromatin domains. To determine whether c-Myc influences the epigenetic state of Myc-bound genes, we assessed the patterns of trimethylation of histone H3-K4 and H3-K27 in mES cells containing normal, increased, and reduced levels of c-Myc. Our analysis reveals widespread and surprisingly diverse changes in repressive and activating histone methylation marks both proximal and distal to Myc binding sites. Furthermore, analysis of bulk chromatin from phenotypically normal c-myc null E7 embryos demonstrates a 70-80% decrease in H3-K4me3, with little change in H3-K27me3, compared to wild-type embryos indicating that Myc is required to maintain normal levels of histone methylation. CONCLUSIONS/SIGNIFICANCE:We show that Myc induces widespread and diverse changes in histone methylation in ES cells. We postulate that these changes are indirect effects of Myc mediated by its regulation of target genes involved in chromatin remodeling. We further show that a subset of PcG-bound genes with bivalent histone methylation patterns are bound and regulated in response to altered c-Myc levels. Our data indicate that in mES cells c-Myc binds, regulates, and influences the histone modification patterns of genes involved in chromatin remodeling, pluripotency, and differentiation