Automatic Image Annotation Based on Particle Swarm Optimization and Support Vector Clustering

With the progress of network technology, there are more and more digital images of the internet. But most images are not semantically marked, which makes it difficult to retrieve and use. In this paper, a new algorithm is proposed to automatically annotate images based on particle swarm optimization (PSO) and support vector clustering (SVC). The algorithm includes two stages: firstly, PSO algorithm is used to optimize SVC; secondly, the trained SVC algorithm is used to annotate the image automatically. In the experiment, three datasets are used to evaluate the algorithm, and the results show the effectiveness of the algorithm

A Continuum Model for Dislocation Climb

Dislocation climb plays an important role in understanding plastic deformation of metallic materials at high temperature. In this paper, we present a continuum formulation for dislocation climb velocity based on densities of dislocations. The obtained continuum formulation is an accurate approximation of the Green's function based discrete dislocation dynamics method (Gu et al. J. Mech. Phys. Solids 83:319-337, 2015). The continuum dislocation climb formulation has the advantage of accounting for both the long-range effect of vacancy bulk diffusion and that of the Peach-Koehler climb force, and the two longrange effects are canceled into a short-range effect (integral with fast-decaying kernel) and in some special cases, a completely local effect. This significantly simplifies the calculation in the Green's function based discrete dislocation dynamics method, in which a linear system has to be solved over the entire system for the long-range effect of vacancy diffusion and the long-range Peach-Koehler climb force has to be calculated. This obtained continuum dislocation climb velocity can be applied in any available continuum dislocation dynamics frameworks. We also present numerical validations for this continuum climb velocity and simulation examples for implementation in continuum dislocation dynamics frameworks

Regulation of the stability and transcriptional activity of NFATc4 by ubiquitination

AbstractNuclear factor of activated T cells (NFATc4) has been implicated as a critical regulator of the cardiac development and hypertrophy. However, the mechanisms for regulating NFATc4 stability and transactivation remain unclear. We showed that NFATc4 protein was predominantly ubiquitinated through the formation of Lysine 48-linked polyubiquitin chains, and this modification decreased NFATc4 protein levels and its transcriptional activity. Furthermore, activation of GSK3β markedly enhanced NFATc4 ubiquitination and decreased its transactivation, whereas inhibition of GSK3β had opposite effects. Importantly, ubiquitination and phosphorylation induced by GSK3β repressed NFATc4-dependent cardiac-specific gene expression. These results demonstrate that the ubiquitin–proteasome system plays an important role in regulating NFATc4 stability and transactivation.Structured summaryMINT-6798349:NFATc4 (uniprotkb:Q14934) physically interacts (MI:0218) with Ubiquitin (uniprotkb:P62988) by anti bait coimmunoprecipitation (MI:0006)MINT-6798334:NFATc4 (uniprotkb:Q14934) physically interacts (MI:0218) with Ubiquitin (uniprotkb:P62988) by anti tag coimmunoprecipitation (MI:0007)MINT-6798321:Ubiquitin (uniprotkb:P62988) physically interacts (MI:0218) with NFATc4 (uniprotkb:Q14934) by pull down (MI:0096

Baicalin suppresses colorectal cancer cell proliferation, potentially via ARRDC4: Bioinformatics and experimental analysis

Colorectal cancer (CRC) is a malignant digestive tumor mostly prevalent among adolescents and has great proliferation potential. Baicalin is a flavonoid derived from the dried root of Scutellaria baicalensis, it has tumor-suppressing effects on various kinds of tumors. Although baicalin has been shown to regulate genes associated with CRC, its role in cancer proliferation remains poorly illustrated. In this work, we evaluated the effect of baicalin on the proliferative ability of three CRC cell lines using a cell counting kit-8 assay. Furthermore, we screened for differentially expressed genes in HCT-116 cells using baicalin-treated samples and control samples on a gene expression profile microarray. We identified 19 genes were identified significantly downregulated by baicalin, which may potentially play an indispensable role in the proliferation of HCT-116 cells. High-content screening evaluated whether silencing the 19 genes affected HCT-116 cell growth. The results showed that knocking down ARRDC4 exhibited the most potent inhibition of cell proliferation. ARRDC4 expression was knocked down by transfecting CRC cells with lentiviral shRNA. MTT assay, Caspase-Glo 3/7 assay and immunohistochemistry analysis were performed to explore the effects of baicalin on proliferation and apoptosis of CRC cells. Besides, RT-PCR showed that the expression levels of ARRDC4 mRNA decreased significantly in HCT-116 cells after baicalin treatment. In conclusion, these findings indicated that baicalin may attenuated the expression of ARRDC4 via regulating the levels of LCN2, Claudin-2 and GSTA4 to inhibit HCT-116 cell proliferation. The theoretical underpinnings for the investigation of the pharmacological effects of baicalin in the treatment of human CRC were also established in this study

DNMT3A and TET1 cooperate to regulate promoter epigenetic landscapes in mouse embryonic stem cells

Abstract Background DNA methylation is a heritable epigenetic mark, enabling stable but reversible gene repression. In mammalian cells, DNA methyltransferases (DNMTs) are responsible for modifying cytosine to 5-methylcytosine (5mC), which can be further oxidized by the TET dioxygenases to ultimately cause DNA demethylation. However, the genome-wide cooperation and functions of these two families of proteins, especially at large under-methylated regions, called canyons, remain largely unknown. Results Here we demonstrate that DNMT3A and TET1 function in a complementary and competitive manner in mouse embryonic stem cells to mediate proper epigenetic landscapes and gene expression. The longer isoform of DNMT3A, DNMT3A1, exhibits significant enrichment at distal promoters and canyon edges, but is excluded from proximal promoters and canyons where TET1 shows prominent binding. Deletion of Tet1 increases DNMT3A1 binding capacity at and around genes with wild-type TET1 binding. However, deletion of Dnmt3a has a minor effect on TET1 binding on chromatin, indicating that TET1 may limit DNA methylation partially by protecting its targets from DNMT3A and establishing boundaries for DNA methylation. Local CpG density may determine their complementary binding patterns and therefore that the methylation landscape is encoded in the DNA sequence. Furthermore, DNMT3A and TET1 impact histone modifications which in turn regulate gene expression. In particular, they regulate Polycomb Repressive Complex 2 (PRC2)-mediated H3K27me3 enrichment to constrain gene expression from bivalent promoters. Conclusions We conclude that DNMT3A and TET1 regulate the epigenome and gene expression at specific targets via their functional interplay

DNMT3A-coordinated splicing governs the stem state switch towards differentiation in embryonic and haematopoietic stem cells

Upon stimulation by extrinsic stimuli, stem cells initiate a programme that enables differentiation or self-renewal. Disruption of the stem state exit has catastrophic consequences for embryogenesis and can lead to cancer. While some elements of this stem state switch are known, major regulatory mechanisms remain unclear. Here we show that this switch involves a global increase in splicing efficiency coordinated by DNA methyltransferase 3 alpha (DNMT3A), an enzyme typically involved in DNA methylation. Proper activation of murine and human embryonic and haematopoietic stem cells depends on messenger RNA processing, influenced by DNMT3A in response to stimuli. DNMT3A coordinates splicing through recruitment of the core spliceosome protein SF3B1 to RNA polymerase and mRNA. Importantly, the DNA methylation function of DNMT3A is not required and loss of DNMT3A leads to impaired splicing during stem cell turnover. Finally, we identify the spliceosome as a potential therapeutic target in DNMT3A-mutated leukaemias. Together, our results reveal a modality through which DNMT3A and the spliceosome govern exit from the stem state towards differentiation.Ramabadran et al. identify a DNA methylation-independent role for DNMT3A in stem cell activation, mediated through recruitment of SF3B1 and splicing regulation

Additional file 2: of DNMT3A and TET1 cooperate to regulate promoter epigenetic landscapes in mouse embryonic stem cells

Table S1. List of oligonucleotides: guide sgRNAs and primers. (PDF 52 Kb