Character of frustration on magnetic correlation in doped Hubbard model

The magnetic correlation in the Hubbard model on a two-dimensional anisotropic triangular lattice is studied by using the determinant quantum Monte Carlo method. Around half filling, it is found that the increasing frustration $t'/t$ could change the wave vector of maximum spin correlation along ($\pi,\pi$)$\rightarrow$($\pi,\frac{5\pi}{6}$)$\rightarrow$($\frac{5\pi}{6},\frac{5\pi}{6}$)$\rightarrow$ ($\frac{2\pi}{3},\frac{2\pi}{3}$), indicating the frustration's remarkable effect on the magnetism. In the studied filling region =1.0-1.3, the doping behaves like some kinds of {\it{frustration}}, which destroys the $(\pi,\pi)$ AFM correlation quickly and push the magnetic order to a wide range of the $(\frac{2\pi}{3},\frac{2\pi}{3})$ $120^{\circ}$ order when the $t'/t$ is large enough. Our non-perturbative calculations reveal a rich magnetic phase diagram over both the frustration and electron doping.Comment: 6 pages, 7 figure

Light Deficiency Inhibits Growth by Affecting Photosynthesis Efficiency as well as JA and Ethylene Signaling in Endangered Plant Magnolia sinostellata

The endangered plant Magnolia sinostellata largely grows in the understory of forest and suffers light deficiency stress. It is generally recognized that the interaction between plant development and growth environment is intricate; however, the underlying molecular regulatory pathways by which light deficiency induced growth inhibition remain obscure. To understand the physiological and molecular mechanisms of plant response to shading caused light deficiency, we performed photosynthesis efficiency analysis and comparative transcriptome analysis in M. sinostellata leaves, which were subjected to shading treatments of different durations. Most of the parameters relevant to the photosynthesis systems were altered as the result of light deficiency treatment, which was also confirmed by the transcriptome analysis. Gene Ontology and KEGG pathway enrichment analyses illustrated that most of differential expression genes (DEGs) were enriched in photosynthesis-related pathways. Light deficiency may have accelerated leaf abscission by impacting the photosynthesis efficiency and hormone signaling. Further, shading could repress the expression of stress responsive transcription factors and R-genes, which confer disease resistance. This study provides valuable insight into light deficiency-induced molecular regulatory pathways in M. sinostellata and offers a theoretical basis for conservation and cultivation improvements of Magnolia and other endangered woody plants

Dialysate glucose response phenotypes during peritoneal equilibration test and their association with cardiovascular death : a cohort study

Different measures of rates of transfer of glucose during the peritoneal equilibrium test (PET), undertaken during peritoneal dialysis (PD) might provide additional information regarding a patient's risk of future cardiovascular mortality. This study aimed to characterize the heterogeneity of dialysate glucose (DG) response phenotypes during the PET and compare the cardiovascular mortality rates associated with the different phenotypes. Our cohort was derived from Henan peritoneal dialysis registry. A total of 3477 patients initiating PD in 2007 to 2014 had the DG measured at 0, 2-hour and 4-hour (D0, D2, and D4 respectively) during the PET for estimation of D2/D0 and D4/D0. Deaths mainly due to CVD within 2 years since the initiation of PD were defined as the outcome. Latent class mixed-effect models were fitted to identify distinct phenotypes of the DG response during the PET. Multivariable unconditional Logistic regression models with adjustment for cardiometabolic risk factors were used to compare the 2-year risk of cardiovascular mortality among patients in the different latent classes. Three distinct DG response phenotypes during the PET were identified. Those with consistently high D2/D0 and D4/D0 ratios had a 1.22 [95% confidence interval: 1.02, 1.35] excess risk of a cardiovascular death within 2 years of commencing PD compared with patients with the lowest D2/D0 ratio and decreased D4/D0 ratio after adjustment for cardiometabolic risk factors. Consistently elevated D2/D0 and D4/D0 ratios during the PET are associated with an increased risk of 2-year cardiovascular mortality independent of other cardiometabolic risk factors. In view of the potential bias due to unmeasured confounders (eg, Family history of cardiovascular diseases, and dietary patterns), this association should be further validated in other external cohorts

Microwave Photonic Imaging Radar with a Millimeter-level Resolution

Microwave photonic radars enable fast or even real-time high-resolution imaging thanks to its broad bandwidth. Nevertheless, the frequency range of the radars usually overlaps with other existed radio-frequency (RF) applications, and only a centimeter-level imaging resolution has been reported, making them insufficient for civilian applications. Here, we propose a microwave photonic imaging radar with a millimeter-level resolution by introducing a frequency-stepped chirp signal based on an optical frequency shifting loop. As compared with the conventional linear-frequency modulated (LFM) signal, the frequency-stepped chirp signal can bring the system excellent capability of anti-interference. In an experiment, a frequency-stepped chirp signal with a total bandwidth of 18.2 GHz (16.9 to 35.1 GHz) is generated. Postprocessing the radar echo, radar imaging with a two-dimensional imaging resolution of ~8.5 mm$\times$~8.3 mm is achieved. An auto-regressive algorithm is used to reconstruct the disturbed signal when a frequency interference exists, and the high-resolution imaging is sustained

A Novel Role of Dma1 in Regulating Forespore Membrane Assembly and Sporulation in Fission Yeast

By characterizing the fission yeast Dma1's function during meiosis, we revealed that Dma1 is required for spore formation, while it is dispensable for fidelity of nuclear divisions. We also found that Dma1 is functionally related to SIN pathway and meiosis-specific kinase Slk1 during sporulation

3-O-Caffeoylquinic acid in Periploca forrestii Schltr extract ameliorates collagen-induced arthritis by inducing IL17/IL23 cells in rats

Purpose: To study the therapeutic effect of 3-O-caffeoylquinic acid (3-O-CQA) from Periploca forrestii extract (PFE) on collagen-mediated arthritis (CIA) in rats, as well as the potential underlying mechanism of action. Methods: PFE and 3-O-CQA were successively and intragastrically administered to CIA rats. Paw swelling, arthritic scores and H & E staining were used to evaluate the therapeutic effect of 3-O-CQA. Moreover, to determine the effects of PFE and 3-O-CQA on fibroblast-resembling synoviocytes obtained from arthritic subjects (RAFLS), the viability of RAFLS cultured in vitro was measured with MMT, while apoptotic lesions were analyzed by flow cytometry. The levels of IL-6 in CIA and RAFLS were determined by enzyme-linked immunosorbent assay (ELISA), while quantitative reverse transcriptionpolymerase chain reaction (qRT-PCR) and immunoblotting were used to assess their mRNA and polypeptide levels, respectively. Results: PFE in 3-O-CQA ameliorated swelling and reduced arthritic scores in CIA rat model, and also decreased cytokine levels (p < 0.05). By decreasing mRNA and protein expressions, 3-O-CQA repressed the phosphorylation of STAT3 and JAK2 as well as the protein levels of IL-23 and RORγt (p < 0.05). Conclusion: The results of this study show that CIA and RAFLS are ameliorated in rats by 3-O-CQA in PFE through regulation of IL17/ IL23 and Th17 cells. Thus, 3-O-CQA affords a therapeutic strategy for the management of collagen-induced arthritis. Keywords: Arthriti; Periploca forrestii Schltr extract; 3-O-Caffeoylquinic acid; Interleukin (IL)-17; IL-23; Th17 cell

The Meq oncoprotein of Marek's disease virus interacts with p53 and inhibits its transcriptional and apoptotic activities

<p>Abstract</p> <p>Background</p> <p>Marek's disease virus (MDV) is an oncogenic herpesvirus, which causes malignant lymphoma in chickens. The Meq protein of MDV, which is expressed abundantly in MDV-infected cells and in Marek's disease (MD) tumor cells, functions as a transcriptional activator and has been proposed to play an important role in oncogenic transformation. Preliminary studies demonstrated that Meq is able to bind p53 <it>in vitro</it>, as demonstrated using a protein-binding assay. This observation prompted us to examine whether the interaction between Meq and p53 occurs in cells, and to investigate the biological significance of this interaction.</p> <p>Results</p> <p>We confirmed first that Meq interacted directly with p53 using a yeast two-hybrid assay and an immunoprecipitation assay, and we investigated the biological significance of this interaction subsequently. Exogenous expression of Meq resulted in the inhibition of p53-mediated transcriptional activity and apoptosis, as analyzed using a p53 luciferase reporter assay and a TUNEL assay. The inhibitory effect of Meq on transcriptional activity mediated by p53 was dependent on the physical interaction between these two proteins, because a Meq deletion mutant that lacked the p53-binding region lost the ability to inhibit p53-mediated transcriptional activity and apoptosis. The Meq variants L-Meq and S-Meq, but not VS-Meq and ∆Meq, which were expressed in MD tumor cells and MDV-infected cells, exerted an inhibitory effect on p53 transcriptional activity. In addition, ∆Meq was found to act as a negative regulator of Meq.</p> <p>Conclusions</p> <p>The Meq oncoprotein interacts directly with p53 and inhibits p53-mediated transcriptional activity and apoptosis. These findings provide valuable insight into the molecular basis for the function of Meq in MDV oncogenesis.</p

Immunoglobulin G Locus Events in Soft Tissue Sarcoma Cell Lines

Recently immunoglobulins (Igs) have been found to be expressed by cells other than B lymphocytes, including various human carcinoma cells. Sarcomas are derived from mesenchyme, and the knowledge about the occurrence of Ig production in sarcoma cells is very limited. Here we investigated the phenomenon of immunoglobulin G (IgG) expression and its molecular basis in 3 sarcoma cell lines. The mRNA transcripts of IgG heavy chain and kappa light chain were detected by RT-PCR. In addition, the expression of IgG proteins was confirmed by Western blot and immunofluorescence. Immuno-electron microscopy localized IgG to the cell membrane and rough endoplasmic reticulum. The essential enzymes required for gene rearrangement and class switch recombination, and IgG germ-line transcripts were also identified in these sarcoma cells. Chromatin immunoprecipitation results demonstrated histone H3 acetylation of both the recombination activating gene and Ig heavy chain regulatory elements. Collectively, these results confirmed IgG expression in sarcoma cells, the mechanism of which is very similar to that regulating IgG expression in B lymphocytes

Boosting the performance of single-atom catalysts via external electric field polarization

Single-atom catalysts represent a unique catalytic system with high atomic utilization and tunable reaction pathway. Despite current successes in their optimization and tailoring through structural and synthetic innovations, there is a lack of dynamic modulation approach for the single-atom catalysis. Inspired by the electrostatic interaction within specific natural enzymes, here we show the performance of model single-atom catalysts anchored on two-dimensional atomic crystals can be systematically and efficiently tuned by oriented external electric fields. Superior electrocatalytic performance have been achieved in single-atom catalysts under electrostatic modulations. Theoretical investigations suggest a universal “onsite electrostatic polarization” mechanism, in which electrostatic fields significantly polarize charge distributions at the single-atom sites and alter the kinetics of the rate determining steps, leading to boosted reaction performances. Such field-induced on-site polarization offers a unique strategy for simulating the catalytic processes in natural enzyme systems with quantitative, precise and dynamic external electric fields

Enhanced NFκB and AP-1 transcriptional activity associated with antiestrogen resistant breast cancer

BACKGROUND: Signaling pathways that converge on two different transcription factor complexes, NFκB and AP-1, have been identified in estrogen receptor (ER)-positive breast cancers resistant to the antiestrogen, tamoxifen. METHODS: Two cell line models of tamoxifen-resistant ER-positive breast cancer, MCF7/HER2 and BT474, showing increased AP-1 and NFκB DNA-binding and transcriptional activities, were studied to compare tamoxifen effects on NFκB and AP-1 regulated reporter genes relative to tamoxifen-sensitive MCF7 cells. The model cell lines were treated with the IKK inhibitor parthenolide (PA) or the proteasome inhibitor bortezomib (PS341), alone and in combination with tamoxifen. Expression microarray data available from 54 UCSF node-negative ER-positive breast cancer cases with known clinical outcome were used to search for potential genes signifying upregulated NFκB and AP-1 transcriptional activity in association with tamoxifen resistance. The association of these genes with patient outcome was further evaluated using node-negative ER-positive breast cancer cases identified from three other published data sets (Rotterdam, n = 209; Amsterdam, n = 68; Basel, n = 108), each having different patient age and adjuvant tamoxifen treatment characteristics. RESULTS: Doses of parthenolide and bortezomib capable of sensitizing the two endocrine resistant breast cancer models to tamoxifen were capable of suppressing NFκB and AP-1 regulated gene expression in combination with tamoxifen and also increased ER recruitment of the transcriptional co-repressor, NCoR. Transcript profiles from the UCSF breast cancer cases revealed three NFκB and AP-1 upregulated genes – cyclin D1, uPA and VEGF – capable of dichotomizing node-negative ER-positive cases into early and late relapsing subsets despite adjuvant tamoxfien therapy and most prognostic for younger age cases. Across the four independent sets of node-negative ER-positive breast cancer cases (UCSF, Rotterdam, Amsterdam, Basel), high expression of all three NFκB and AP-1 upregulated genes was associated with earliest metastatic relapse. CONCLUSION: Altogether, these findings implicate increased NFκB and AP-1 transcriptional responses with tamoxifen resistant breast cancer and early metastatic relapse, especially in younger patients. These findings also suggest that agents capable of preventing NFκB and AP-1 gene activation may prove useful in restoring the endocrine responsiveness of such high-risk ER-positive breast cancers