1,2-Di-2-pyridylethyl­ene–phenyl­succinic acid (1/1)

In the title 1:1 adduct, C10H10O4·C12H10N2, the two components are linked by O—H⋯N hydrogen bonds to form a one-dimensional chain. The dihedral angle between the pyridine rings is 15.68 (8)° These chains are further inter­connected by weak inter­molecular C—H⋯O hydrogen bonds and weak C—H⋯π inter­actions to generate a three-dimensional network

Increased nucleotide polymorphic changes in the 5'-untranslated region of δ-catenin (CTNND2) gene in prostate cancer

Cancer pathogenesis involves multiple genetic and epigenetic alterations, which result in oncogenic changes in gene expression. δ-Catenin (CTNND2) is overexpressed in cancer although the mechanisms of its upregulation are highly variable. Here we report that in prostate cancer the methylation of CpG islands in δ-catenin promoter was not a primary regulatory event. There was also no δ-catenin gene amplification. However, using Single-Strand onformation Polymorphism analysis, we observed the increased nucleotide changes in the 5'-untranslated region of δ-catenin gene in human prostate cancer. At least one such change (-9 G>A) is a true somatic point mutation associated with a high Gleason score, poorly differentiated prostatic adenocarcinoma. Laser capture microdissection coupled with PCR analyses detected the mutation only in cancerous but not in the adjacent benign prostatic tissues. Using chimeric genes encoding the luciferase reporter, we found that this mutation, but not a random mutation or a mutation that disrupts an upstream open reading frame, resulted in a remarkably higher expression and enzyme activity. This mutation did not affect transcriptional efficiency, suggesting that it promotes δ-catenin translation. This is the first report of δ-catenin gene mutation in cancer and supports the notion that multiple mechanisms contribute to its increased expression in carcinogenesis. Originally published ncogene, Vol. 28, No. 4, Jan 200

Gravity and Matters on a pure geometric thick polynomial f(R)f(R) brane

In this paper, the solutions of the pure geometric thick $f(R)$ brane are investigated. The formulation of $f(R)$ is chosen as $f(R)=\sum_{i=1}^{n}a_{i}R^{i}+\Lambda$. For the certain value of $n$, the brane solution can be calculated, and when $n=3$, $n=4$, and $n=10$, the thick brane solutions are presented. The solutions is stable under linear tensor fluctuation. The zero mode of gravity and scalar field can be localized on thick $f(R)$ branes naturally. The zero mode of vector field and left-chiral fermion can be localized on thick $f(R)$ branes by introducing the coupling with scalar curvature $R$ of spacetime, and the massive resonant modes can be quasilocalized on the brane with the large coupling coefficients.Comment: 22 pages, 18 figure

Physics perspectives of heavy-ion collisions at very high energy

Heavy-ion collisions at very high colliding energies are expected to produce a quark-gluon plasma (QGP) at the highest temperature obtainable in a laboratory setting. Experimental studies of these reactions can provide an unprecedented range of information on properties of the QGP at high temperatures. We report theoretical investigations of the physics perspectives of heavy-ion collisions at a future high-energy collider. These include initial parton production, collective expansion of the dense medium, jet quenching, heavy-quark transport, dissociation and regeneration of quarkonia, photon and dilepton production. We illustrate the potential of future experimental studies of the initial particle production and formation of QGP at the highest temperature to provide constraints on properties of strongly interaction matter.Comment: 35 pages in Latex, 29 figure

Neural networks impedance control of robots interacting with environments

In this paper, neural networks impedance control is proposed for robot-environment interaction. Iterative learning control is developed to make the robot dynamics follow a given target impedance model. To cope with the problem of unknown robot dynamics, neural networks are employed such that neither the robot structure nor the physical parameters are required for the control design. The stability and performance of the resulted closed-loop system are discussed through rigorous analysis and extensive remarks. The validity and feasibility of the proposed method are verified through simulation studies

The N-terminal Phosphodegron Targets TAZ/WWTR1 Protein for SCF β-TrCP -dependent Degradation in Response to Phosphatidylinositol 3-Kinase Inhibition

The Hippo tumor suppressor pathway plays a major role in development and organ size control, and its dysregulation contributes to tumorigenesis. TAZ (transcriptional co-activator with PDZ-binding motif; also known as WWTR1) is a transcription co-activator acting downstream of the Hippo pathway, and increased TAZ protein levels have been associated with human cancers, such as breast cancer. Previous studies have shown that TAZ is inhibited by large tumor suppressor (LATS)-dependent phosphorylation, leading to cytoplasmic retention and ubiquitin-dependent degradation. The LATS kinase, a core component of the Hippo pathway, phosphorylates the C-terminal phosphodegron in TAZ to promote its degradation. In this study, we have found that the N-terminal phosphodegron of TAZ also plays a role in TAZ protein level regulation, particularly in response to different status of cellular PI3K signaling. GSK3, which can be inhibited by high PI3K via AKT-dependent inhibitory phosphorylation, phosphorylates the N-terminal phosphodegron in TAZ, and the phosphorylated TAZ binds to β-TrCP subunit of the SCFβ-TrCP E3 ubiquitin ligase, thereby leading to TAZ ubiquitylation and degradation. We observed that the TAZ protein level is elevated in tumor cells with high PI3K signaling, such as in PTEN mutant cancer cells. This study provides a novel mechanism of TAZ regulation and suggests a role of TAZ in modulating tissue growth and tumor development in response to PI3K signaling

Genetic Single Nucleotide Polymorphisms (GSNPs) in the DNA Repair Genes and Hepatocellular Carcinoma Related to Aflatoxin B1 among Guangxiese Population

Aflatoxin B1 (AFB1) is an important environmental carcinogen for the development of hepatocellular carcinoma (HCC). HCC is a complex disease likely resulting from genetic single nucleotide polymorphisms (GSNPs) of multiple interacting genes and gene-environment interactions. Recent efforts have been made to analyze the associations between risk of this malignancy and GSNPs in genes involved in the repair of DNA damage induced by AFB1. Here, we reviewed the results of published case-control studies that have examined the effects of common alleles of all susceptible DNA repair genes, including XRCC1, XRCC3, XRCC4, XRCC7, XPC, and XPD, on risk of AFB1-related HCC among Guangxi population. Statistically significant differences in genotype frequencies found in case-control comparisons were rs25487, rs80309960, rs861539, rs7003908, rs28383151, rs3734091, rs13181, and rs2228001 polymorphism. The overall effects of these GNSPs were moderate in terms of relative risk, with ORs ranging from 2 to 10. Furthermore, some evidence of the interaction of GSNPs in DNA repair genes and AFB1 exposure modulate risk of this cancer was also found, although the results require confirmation with larger sample size studies

Association of gut microbiota and SCFAs with finishing weight of Diannan small ear pigs

Finishing weight is a key economic trait in the domestic pig industry. Evidence has linked the gut microbiota and SCFAs to health and production performance in pigs. Nevertheless, for Diannan small ear (DSE) pigs, a specific pig breed in China, the potential effect of gut microbiota and SCFAs on their finishing weight remains unclear. Herein, based on the data of the 16S ribosomal RNA gene and metagenomic sequencing analysis, we found that 13 OTUs could be potential biomarkers and 19 microbial species were associated with finishing weight. Among these, carbohydrate-decomposing bacteria of the families Streptococcaceae, Lactobacillaceae, and Prevotellaceae were positively related to finishing weight, whereas the microbial taxa associated with intestinal inflammation and damage exhibited opposite effects. In addition, interactions of these microbial species were found to be linked with finishing weight for the first time. Gut microbial functional annotation analysis indicated that CAZymes, such as glucosidase and glucanase could significantly affect finishing weight, given their roles in increasing nutrient absorption efficiency. Kyoto Encyclopedia of Genes and Genomes (KEGG) Orthologies (KOs) and KEGG pathways analysis indicated that glycolysis/gluconeogenesis, phosphotransferase system (PTS), secondary bile acid biosynthesis, ABC transporters, sulfur metabolism, and one carbon pool by folate could act as key factors in regulating finishing weight. Additionally, SCFA levels, especially acetate and butyrate, had pivotal impacts on finishing weight. Finishing weight-associated species Prevotella sp. RS2, Ruminococcus sp. AF31-14BH and Lactobacillus pontis showed positive associations with butyrate concentration, and Paraprevotella xylaniphila and Bacteroides sp. OF04-15BH were positively related to acetate level. Taken together, our study provides essential knowledge for manipulating gut microbiomes to improve finishing weight. The underlying mechanisms of how gut microbiome and SCFAs modulate pigs’ finishing weight required further elucidation