48 research outputs found

    Dose-response relation plots between carotenoids consumption and risk of PCa.

    No full text
    <p>(A) Dietary lycopene intake(mg/day) and risk of PCa; (B) Blood lycopene levels (ug/dl) and risk of PCa; (C) Dietary α-carotene intake(mg/day) and risk of PCa. These relationships were estimated by using random-effects metaregression. Dotted lines represent the 95% CIs for the fitted trend.</p

    Effect of Carotene and Lycopene on the Risk of Prostate Cancer: A Systematic Review and Dose-Response Meta-Analysis of Observational Studies

    No full text
    <div><p>Background</p><p>Many epidemiologic studies have investigated the association between carotenoids intake and risk of Prostate cancer (PCa). However, results have been inconclusive.</p><p>Methods</p><p>We conducted a systematic review and dose-response meta-analysis of dietary intake or blood concentrations of carotenoids in relation to PCa risk. We summarized the data from 34 eligible studies (10 cohort, 11 nested case-control and 13 case-control studies) and estimated summary Risk Ratios (RRs) and 95% confidence intervals (CIs) using random-effects models.</p><p>Results</p><p>Neither dietary β-carotene intake nor its blood levels was associated with reduced PCa risk. Dietary α-carotene intake and lycopene consumption (both dietary intake and its blood levels) were all associated with reduced risk of PCa (RR for dietary α-carotene intake: 0.87, 95%CI: 0.76–0.99; RR for dietary lycopene intake: 0.86, 95%CI: 0.75–0.98; RR for blood lycopene levels: 0.81, 95%CI: 0.69–0.96). However, neither blood α-carotene levels nor blood lycopene levels could reduce the risk of advanced PCa. Dose-response analysis indicated that risk of PCa was reduced by 2% per 0.2mg/day (95%CI: 0.96–0.99) increment of dietary α-carotene intake or 3% per 1mg/day (95%CI: 0.94–0.99) increment of dietary lycopene intake.</p><p>Conclusions</p><p>α-carotene and lycopene, but not β-carotene, were inversely associated with the risk of PCa. However, both α-carotene and lycopene could not lower the risk of advanced PCa.</p></div

    Pooled risks according to dietary carotenoids intake and its blood levels.

    No full text
    <p>Dietary intake of α-carotene, β-carotene, lycopene and PCa risk(left), blood levels of α-carotene, β-carotene, lycopene and PCa risk(right).</p

    Characteristics of included studies.

    No full text
    <p>Abbreviations: NCCS, nested case-control study; CCS, case-control study; SD, standard deviation; T, tertile; Q, quartile/quintile; BMI, body mass index; NSAIDs, non-steroidal anti-inflammatory drugs; FHPC, family history of prostate cancer; NR, not reported; NA, not accessible.</p><p><sup>a</sup>Derived from the slogan of a campaign, “Give us a CLUE to cancer.”</p><p><sup>b</sup>Indicated interquartile range(IQR).</p><p>Characteristics of included studies.</p

    Geochemical behaviours of chemical elements during subduction-zone metamorphism and geodynamic significance

    No full text
    <p>Seafloor subduction and subduction-zone metamorphism (SZM) are understood to be the very cause of both subduction-zone magmatism and mantle compositional heterogeneity. In this article, we compile geochemical data for blueschist and eclogite facies rocks from global palaeo-subduction-zones in the literature, including those from the Chinese Western Tianshan ultrahigh pressure (UHP) metamorphic belt. We synthesize our up-to-date understanding on how chemical elements behave and their controls during subduction-zone metamorphism. Although the compositional heterogeneity of metamorphic minerals from subducted rocks has been recently reported, we emphasize that the mineral compositional heterogeneity is controlled by elemental availability during mineral growth, which is affected by the protolith composition, the inherited composition of precursor minerals, and the competition with neighbouring growing minerals. In addition, given the likely effects of varying protolith compositions and metamorphic conditions on elemental behaviours, we classify meta-mafic rocks from global palaeo-subduction-zones with varying metamorphic conditions into groups in terms of their protolith compositions (i.e. ocean island basalt (OIB)-like, enriched mid-ocean ridge basalt (MORB)-like, normal [N]-MORB-like), and discuss geochemical behaviours of chemical elements within these co-genetic groups rather than simply accepting the conclusions in the literature. We also discuss the geochemical consequences of SZM with implications for chemical geodynamics, and propose with emphasis that: (1) the traditionally accepted ‘fluid flux induced-melting’ model for arc magmatism requires revision; and (2) the residual subducted ocean crust cannot be the major source material for OIB, although it can contribute to the deep mantle compositional heterogeneity. We also highlight some important questions and problems that need further investigations, e.g. complex subduction-zone geochemical processes, different contributions of seafloor subduction and resultant subduction of continental materials, and the representativeness of studied HP–UHP metamorphic rocks.</p

    Combined KEGG Pathway analysis of direct and functional E2A-PBX1 targets.

    No full text
    <p>The analysis was performed using Exploratory Gene Association Networks (EGAN) software tool. E2A-PBX1 direct (108 direct targets identified by ChIP-chip) and functional targets (122 significant differentially expressed genes between E2a-Pbx1 silenced samples and controls) and Pathways that might be regulated by them were visualized. Interfaces of direct and functional E2A-PBX1 targets are depicted. Magenta lines depict the connection of the genes to the direct target and/or functional target group; blue lines show the participation of the genes in KEGG pathways and brown lines show known interaction between genes connected.</p

    Identified ChIP-chip targets on expression array in E2A-PBX1 silenced vs control cells.

    No full text
    <p><b>A.</b> ChIP-chip analysis data and expression analysis data upon E2A-PBX1 silencing were combined to get an overview of the direct and functional targets of E2A-PBX1. siRNA to E2A-PBX1 was employed to silence E2A-PBX1. The MA plot depicts the expression array changes upon silencing E2A-PBX1. Genes are ordered on the x-axis on the basis of their expression in untreated 697 cells. The Y-axis displays the change in expression upon E2A-PBX1 silencing. Those genes that are direct hits of E2A-PBX1 by chromatin immunoprecipitation assays (108 genes) were plotted against the expression array changes upon silencing and are shown in red color and marked with a blue dot; grey dots indicate all other genes assessed by the array. <b>B.</b> Here we compare the changes in expression of the 108 E2A-PBX1 direct targets to the expression change of all the other genes (non-direct E2A-PBX1 targets) upon E2A-PBX1 silencing. The set of identified ChIP-chip targets show collective down-regulation trend in the E2A-PBX1 silenced samples compared to controls (p<1.63e-06).</p

    Expanded combined analysis of direct and functional E2A-PBX1 targets.

    No full text
    <p>The analysis was performed using the 102 direct targets identified by ChIP-chip analysis and the data set of the functional targets including the top 2000 genes up and down regulated after siRNA silencing of E2A-PBX1. Venn diagrams were generated and the interfaces of direct and functional E2A-PBX1 targets are depicted. 10 genes that were both direct targets and functionally down-regulated <b>(</b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0087602#pone-0087602-g005" target="_blank"><b>Figure 5A</b></a><b>)</b> and 10 that were both direct targets and functionally up-regulated <b>(</b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0087602#pone-0087602-g005" target="_blank"><b>Figure 5B</b></a><b>)</b> dependent on expression of E2A-PBX1 were identified. We are not able to address E2A-PBX1 as a functional repressor (for the 10 down regulated genes) or whether its depletion allowed accessibility to another transcriptional activator. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0087602#pone-0087602-g005" target="_blank"><b>Figure 5C</b></a> Selected direct and functional E2A-PBX1 targets are highly expressed in primary E2A-PBX1 leukemias. Pediatric Cancer Genome Project. <a href="http://www.pediatriccancergenomeproject.org/site/accessed" target="_blank">http://www.pediatriccancergenomeproject.org/site/accessed</a> 14 Oct 2013. The expression of four genes UGT2B15, ASNS, WNT16 and HK2, that were among the direct and functional E2A-PBX1 targets in primary leukemia’s are shown. The expression of these genes was analyzed in Hyperdiploid leukemia’s (H), in E2A-PBX1 leukemia’s (E), TEL-AML1 (T) leukemia’s and BCR-ABL1 (B) leukemia’s are shown. The analysis of expression was performed using the gene expression tool and data available at St. Jude Children’s Research Hospital – (Washington University).</p

    The 9p21 deletion is not always targeting CDKN2A.

    No full text
    <p>Copy number alterations in a group of 22 t(1;19)<sup>+</sup><i>E2A-PBX1</i> bone marrow samples are shown <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0087602#pone-0087602-g003" target="_blank"><b>Figure 3A</b></a>. Patient samples were subjected to hierarchical clustering analysis; we found the 9p21 deletion to exist in four of the 22 patients we have analyzed, with one patient exhibiting a homozygous deletion, white color refers to no changes, red to gain and blue to loss. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0087602#pone-0087602-g003" target="_blank"><b>Figure 3B</b></a>. Fine map of deletions in the 9p21 region showing the deletion endpoints among 8 patients. The commonly deleted region among 10 patients (with 45%, including 7 patients in this figure and the other 3 others with complete arm loss) is the interferon gene cluster telomeric to the <i>CDKN2A/B</i> locus.</p

    Swollen Ammoniated MoS<sub>2</sub> with 1T/2H Hybrid Phases for High-Rate Electrochemical Energy Storage

    No full text
    Because of its lamellar structure similar to that of graphite, molybdenum disulfide has been widely explored as a lithium-ion battery and supercapacitor electrode material, but its energy storage ability is strongly hindered by the poor electrical/ionic conductivity and transfer among the intrinsic lamellar structures. Herein we propose a novel swollen ammoniated MoS<sub>2</sub> with 1T/2H hybrid phases (MoS<sub>2</sub>-A), which possesses a high concentration of 1T phase and unique expanded lamellar structures, as a supercapacitor electrode material. The obtained MoS<sub>2</sub>-A reveals superior charge-storage performance with distinct pseudocapacitive behavior, including surface redox reaction and diffusive intercalation, and even when the scan speed is increased 100-fold from 1 to 100 mV s<sup>–1</sup>, the retention ratio of the specific capacitance can still reach 58.5%, demonstrating a superhigh rate capability. Moreover, this supercapacitor electrode also exhibits good cycling stability with a retention ratio of 95.4% after 2000 cycles. The outstanding electrochemical performance of MoS<sub>2</sub>-A should be ascribed to the existence of the metallic 1T phase, which favors high electrical conductivity, and the swollen lamellar structures possessing an enlarged interlayer space of 0.99 nm created by in situ intercalated species, facilitating the fast and reversible diffusive intercalation of electrolyte ions
    corecore