Edge Partitions of Optimal 22-plane and 33-plane Graphs

A topological graph is a graph drawn in the plane. A topological graph is $k$-plane, $k>0$, if each edge is crossed at most $k$ times. We study the problem of partitioning the edges of a $k$-plane graph such that each partite set forms a graph with a simpler structure. While this problem has been studied for $k=1$, we focus on optimal $2$-plane and $3$-plane graphs, which are $2$-plane and $3$-plane graphs with maximum density. We prove the following results. (i) It is not possible to partition the edges of a simple optimal $2$-plane graph into a $1$-plane graph and a forest, while (ii) an edge partition formed by a $1$-plane graph and two plane forests always exists and can be computed in linear time. (iii) We describe efficient algorithms to partition the edges of a simple optimal $2$-plane graph into a $1$-plane graph and a plane graph with maximum vertex degree $12$, or with maximum vertex degree $8$ if the optimal $2$-plane graph is such that its crossing-free edges form a graph with no separating triangles. (iv) We exhibit an infinite family of simple optimal $2$-plane graphs such that in any edge partition composed of a $1$-plane graph and a plane graph, the plane graph has maximum vertex degree at least $6$ and the $1$-plane graph has maximum vertex degree at least $12$. (v) We show that every optimal $3$-plane graph whose crossing-free edges form a biconnected graph can be decomposed, in linear time, into a $2$-plane graph and two plane forests

Anti-diabetic effects of emodin involved in the activation of PPAR gamma on high-fat diet-fed and low dose of streptozotocin-induced diabetic mice

Rheum palmatum unit has been widely applied in the clinical treatment of diabetes mellitus It has been found that emodin as the major bioactive component of R palmatum L exhibits the competency to activate peroxisomal proliferator-activated receptor-gamma (PPAR gamma) in vitro So the aim of this study was to evaluate the anti-diabetic effects of emodin through the activation of PPAR gamma on high-fat diet-fed and low dose of streptozotocin (STZ)-induced diabetic mice The diabetic mice were intraperitoneally injected with emodin for three weeks No changes of food consumption and the body weight in emodin-treated mice were monitored daily during the entire experiment At the end of experiment. the levels of blood glucose, triglyceride and total cholesterol in serum were significantly decreased after emodin treatment. However, serum high-density lipoprotein cholesterol (HDLc) concentration was significantly elevated The glucose tolerance and insulin sensitivity in emodin-treated group were significantly improved Furthermore, the results of quantitative RT-PCR analysis showed that emodin significantly elevated the mRNA expression level of PPAR gamma and regulated the mRNA expressions of LPL. FAT/CD36, resistin and FABPs (ap2) in liver and adipocyte tissues. No effects on the mRNA expressions of PPAR alpha and PPAR alpha-target genes were observed Taken together, the results suggested that the activation of PPAR gamma and the modulation of metabolism-related genes were likely involved in the anti-diabetic effects of emodin (C) 2009 Elsevier B V All rights reserve

Insufficient activity of MAPK pathway is a key monitor of Kidney-Yang Deficiency Syndrome.

OBJECTIVE: To explore the genetic characteristics and molecular regulator of Kidney-Yang Deficiency Syndrome (KDS). DESIGN: A typical KDS family was collected using a questionnaire of cold feeling and a 40-item scoring table of KDS based on Traditional Chinese Medicine (TCM), by single-blind method repeated annually over three years. Their transcriptomes were assayed by microarray and validated by RT-PCR and ELISA. Simultaneously, 10 healthy volunteers were recruited as controls and the same protocols were performed. RESULTS: This typical KDS family has 35 members, of whom 11 were evaluated as having severe KDS and 6 as having common KDS. Results of the cDNA microarray revealed that there were 420 genes/expressed sequence tags differentially expressed in KDS transcriptomes, indicating a global functional impairment in the mass-energy-information carrying network of KDS patients, involving energy metabolism, signal transduction, development, cell cycle, and immunity. Pathway analysis by gene set enrichment assay (GSEA) and other tools demonstrated that mitogenic activated protein kinase (MAPK) is among the most insufficiently activated pathways, while the oxidative phosphorylation and glycolysis/gluconeogenesis pathways, the two main pathways relevant to ATP synthesis, were among the most excessively activated pathways in KDS patients. Results of RT-PCR and ELISA confirmed the status of insufficient activity of the MAPK pathway. CONCLUSION: KDS patients undergo overall attenuated functions in the mass-energy-information carrying network. The marked low level of energy output in KDS may be primarily attributed to the insufficient activity of the MAPK pathway, which may be a key monitor for the abnormal energy metabolism and other impaired activities in KDS.published_or_final_versio

Glycogen Synthase Kinase (GSK) 3β phosphorylates and protects nuclear myosin 1c from proteasome-mediated degradation to activate rDNA transcription in early G1 cells

Nuclear myosin 1c (NM1) mediates RNA polymerase I (pol I) transcription activation and cell cycle progression by facilitating PCAF-mediated H3K9 acetylation, but the molecular mechanism by which NM1 is regulated remains unclear. Here, we report that at early G1 the glycogen synthase kinase (GSK) 3β phosphorylates and stabilizes NM1, allowing for NM1 association with the chromatin. Genomic analysis by ChIP-Seq showed that this mechanism occurs on the rDNA as active GSK3β selectively occupies the gene. ChIP assays and transmission electron microscopy in GSK3β-/- mouse embryonic fibroblasts indicated that at G1 rRNA synthesis is suppressed due to decreased H3K9 acetylation leading to a chromatin state incompatible with transcription. We found that GSK3β directly phosphorylates the endogenous NM1 on a single serine residue (Ser-1020) located within the NM1 C-terminus. In G1 this phosphorylation event stabilizes NM1 and prevents NM1 polyubiquitination by the E3 ligase UBR5 and proteasome-mediated degradation. We conclude that GSK3β-mediated phosphorylation of NM1 is required for pol I transcription activation

Search for new phenomena in final states with an energetic jet and large missing transverse momentum in pp collisions at √ s = 8 TeV with the ATLAS detector

Results of a search for new phenomena in final states with an energetic jet and large missing transverse momentum are reported. The search uses 20.3 fb−1 of √ s = 8 TeV data collected in 2012 with the ATLAS detector at the LHC. Events are required to have at least one jet with pT > 120 GeV and no leptons. Nine signal regions are considered with increasing missing transverse momentum requirements between Emiss T > 150 GeV and Emiss T > 700 GeV. Good agreement is observed between the number of events in data and Standard Model expectations. The results are translated into exclusion limits on models with either large extra spatial dimensions, pair production of weakly interacting dark matter candidates, or production of very light gravitinos in a gauge-mediated supersymmetric model. In addition, limits on the production of an invisibly decaying Higgs-like boson leading to similar topologies in the final state are presente

Inhibition of autophagy, lysosome and VCP function impairs stress granule assembly

Stress granules (SGs) are mRNA-protein aggregates induced during stress, which accumulate in many neurodegenerative diseases. Previously, the autophagy-lysosome pathway and valosin-containing protein (VCP), key players of the protein quality control (PQC), were shown to regulate SG degradation. This is consistent with the idea that PQC may survey and/or assist SG dynamics. However, despite these observations, it is currently unknown whether the PQC actively participates in SG assembly. Here, we describe that inhibition of autophagy, lysosomes and VCP causes defective SG formation after induction. Silencing the VCP co-factors UFD1L and PLAA, which degrade defective ribosomal products (DRIPs) and 60S ribosomes, also impaired SG assembly. Intriguingly, DRIPs and 60S, which are released from disassembling polysomes and are normally excluded from SGs, were significantly retained within SGs in cells with impaired autophagy, lysosome or VCP function. Our results suggest that deregulated autophagy, lysosomal or VCP activities, which occur in several neurodegenerative (VCP-associated) diseases, may alter SG morphology and composition

Small global-mean cooling due to volcanic radiative forcing

In both the observational record and atmosphere-ocean general circulation model (AOGCM) simulations of the last ∼∼ 150 years, short-lived negative radiative forcing due to volcanic aerosol, following explosive eruptions, causes sudden global-mean cooling of up to ∼∼ 0.3 K. This is about five times smaller than expected from the transient climate response parameter (TCRP, K of global-mean surface air temperature change per W m−2 of radiative forcing increase) evaluated under atmospheric CO2 concentration increasing at 1 % yr−1. Using the step model (Good et al. in Geophys Res Lett 38:L01703, 2011. doi:10.​1029/​2010GL045208), we confirm the previous finding (Held et al. in J Clim 23:2418–2427, 2010. doi:10.​1175/​2009JCLI3466.​1) that the main reason for the discrepancy is the damping of the response to short-lived forcing by the thermal inertia of the upper ocean. Although the step model includes this effect, it still overestimates the volcanic cooling simulated by AOGCMs by about 60 %. We show that this remaining discrepancy can be explained by the magnitude of the volcanic forcing, which may be smaller in AOGCMs (by 30 % for the HadCM3 AOGCM) than in off-line calculations that do not account for rapid cloud adjustment, and the climate sensitivity parameter, which may be smaller than for increasing CO2 (40 % smaller than for 4 × CO2 in HadCM3)

Improved measurement of the reactor antineutrino flux and spectrum at Daya Bay

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Advances in research on the use of biochar in soil for remediation: a review

Purpose: Soil contamination mainly from human activities remains a major environmental problem in the contemporary world. Significant work has been undertaken to position biochar as a readily-available material useful for the management of contaminants in various environmental media notably soil. Here, we review the increasing research on the use of biochar in soil for the remediation of some organic and inorganic contaminants.  Materials and methods: Bibliometric analysis was carried out within the past 10 years to determine the increasing trend in research related to biochar in soil for contaminant remediation. Five exemplar contaminants were reviewed in both laboratory and field-based studies. These included two inorganic (i.e., As and Pb) and three organic classes (i.e., sulfamethoxazole, atrazine, and PAHs). The contaminants were selected based on bibliometric data and as representatives of their various contaminant classes. For example, As and Pb are potentially toxic elements (anionic and cationic, respectively), while sulfamethoxazole, atrazine, and PAHs represent antibiotics, herbicides, and hydrocarbons, respectively.  Results and discussion: The interaction between biochar and contaminants in soil is largely driven by biochar precursor material and pyrolysis temperature as well as some characteristics of the contaminants such as octanol-water partition coefficient (KOW) and polarity. The structural and chemical characteristics of biochar in turn determine the major sorption mechanisms and define biochar’s suitability for contaminant sorption. Based on the reviewed literature, a soil treatment plan is suggested to guide the application of biochar in various soil types (paddy soils, brownfield, and mine soils) at different pH levels (4–5.5) and contaminant concentrations ( 50 mg kg−1).  Conclusions: Research on biochar has grown over the years with significant focus on its properties, and how these affect biochar’s ability to immobilize organic and inorganic contaminants in soil. Few of these studies have been field-based. More studies with greater focus on field-based soil remediation are therefore required to fully understand the behavior of biochar under natural circumstances. Other recommendations are made aimed at stimulating future research in areas where significant knowledge gaps exist