939 research outputs found

    CDK1-PDK1-PI3K/Akt signaling pathway regulates embryonic and induced pluripotency

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    Wild World of Wild Food Plants in Cambodia: The Utilization, Challenges, and Opportunities to Scaling up the Use of Wild Food Plants

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    Underexploited wild food plant (WFP) species have a high potential to contribute to nutritional and/or medicinal health, generate income, and sustain the environment. The objective of this study was to identify market-available WFP species and characterize their beneficial use and economic values in northwestern Cambodia. Two hundred seventy-five (275) retailers in Battambang and Siem Reap were interviewed to collect data on wild food plant species availability and their values. Thirty-four (34) plant species were identified as WFP species, including annual and perennial herbs, perennial shrubs, vines, and trees. Leave, shoots, stems, rhizomes, corms, flowers, and fruits were the parts of the plant used for cooked dishes. Most of the parts used (92.4%) were collected from the wild, while 7.6% were reported as cultivated. The plant species are high in vitamin A, C, a good source of minerals, and can be used as traditional medicine. To enhance health and alleviate the ‘hidden hunger’ of micronutrient malnutrition, Cambodia should promote the production and dietary incorporation of wild food plants rich in minerals and vitamins

    Rolling resistance contribution to a road pavement life cycle carbon footprint analysis

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    Purpose Although the impact of road pavement surface condition on rolling resistance has been included in the life cycle assessment (LCA) framework of several studies in the last years, there is still a high level of uncertainty concerning the methodological assumptions and the parameters that can affect the results. In order to adopt pavement carbon footprint/LCA as a decision-making tool, it is necessary to explore the impact of the chosen methods and assumptions on the LCA results. Methods This paper provides a review of the main models describing the impact of the pavement surface properties on vehicle fuel consumption and analyses the influence of the methodological assumptions related to the rolling resistance on the LCA results. It compares the CO2 emissions, calculated with two different rolling resistance models existing in literature, and performs a sensitivity test on some specific input variables (pavement deterioration rate, traffic growth, and emission factors/fuel efficiency improvement). Results and discussion The model used to calculate the impact of the pavement surface condition on fuel consumption significantly affects the LCA results. The pavement deterioration rate influences the calculation in both models, while traffic growth and fuel efficiency improvement have a limited impact on the vehicle CO2 emissions resulting from the pavement condition contribution to rolling resistance. Conclusions and recommendations Existing models linking pavement condition to rolling resistance and hence vehicle emissions are not broadly applicable to the use phase of road pavement LCA and further research is necessary before a widely-used methodology can be defined. The methods of modelling and the methodological assumptions need to be transparent in the analysis of the impact of the pavement surface condition on fuel consumption, in order to be interpreted by decision makers and implemented in an LCA framework. This will be necessary before product category rules (PCR) for pavement LCA can be extended to include the use phase

    Complement C1q Activates Tumor Suppressor WWOX to Induce Apoptosis in Prostate Cancer Cells

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    BACKGROUND:Tissue exudates contain low levels of serum complement proteins, and their regulatory effects on prostate cancer progression are largely unknown. We examined specific serum complement components in coordinating the activation of tumor suppressors p53 and WWOX (also named FOR or WOX1) and kinases ERK, JNK1 and STAT3 in human prostate DU145 cells. METHODOLOGY/PRINCIPAL FINDINGS:DU145 cells were cultured overnight in 1% normal human serum, or in human serum depleted of an indicated complement protein. Under complement C1q- or C6-free conditions, WOX1 and ERK were mainly present in the cytoplasm without phosphorylation, whereas phosphorylated JNK1 was greatly accumulated in the nuclei. Exogenous C1q rapidly restored the WOX1 activation (with Tyr33 phosphorylation) in less than 2 hr. Without serum complement C9, p53 became activated, and hyaluronan (HA) reversed the effect. Under C6-free conditions, HA induced activation of STAT3, an enhancer of metastasis. Notably, exogenous C1q significantly induced apoptosis of WOX1-overexpressing DU145 cells, but not vehicle-expressing cells. A dominant negative and Y33R mutant of WOX1 blocked the apoptotic effect. C1q did not enhance p53-mediated apoptosis. By total internal reflection fluorescence (TIRF) microscopy, it was determined that C1q destabilized adherence of WOX1-expressing DU145 cells by partial detaching and inducing formation of clustered microvilli for focal adhesion particularly in between cells. These cells then underwent shrinkage, membrane blebbing and death. Remarkably, as determined by immunostaining, benign prostatic hyperplasia and prostate cancer were shown to have a significantly reduced expression of tissue C1q, compared to age-matched normal prostate tissues. CONCLUSIONS/SIGNIFICANCE:We conclude that complement C1q may induce apoptosis of prostate cancer cells by activating WOX1 and destabilizing cell adhesion. Downregulation of C1q enhances prostate hyperplasia and cancerous formation due to failure of WOX1 activation

    Measuring and Comparing Party Ideology and Heterogeneity

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    Estimates of party ideological positions in Western Democracies yield useful party-level information, but lack the ability to provide insight into intraparty politics. In this paper, we generate comparable measures of latent individual policy positions from elite survey data which enable analysis of elite-level party ideology and heterogeneity. This approach has advantages over both expert surveys and approaches based on behavioral data, such as roll call voting and is directly relevant to the study of party cohesion. We generate a measure of elite positions for several European countries using a common space scaling approach and demonstrate its validity as a measure of party ideology. We then apply these data to determine the sources of party heterogeneity, focusing on the role of intraparty competition in electoral systems, nomination rules, and party goals. We find that policy-seeking parties and centralized party nomination rules reduce party heterogeneity. While intraparty competition has no effect, the presence of these electoral rules conditions the effect of district magnitude

    Evidence for an excess of B -> D(*) Tau Nu decays

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    Based on the full BaBar data sample, we report improved measurements of the ratios R(D(*)) = B(B -> D(*) Tau Nu)/B(B -> D(*) l Nu), where l is either e or mu. These ratios are sensitive to new physics contributions in the form of a charged Higgs boson. We measure R(D) = 0.440 +- 0.058 +- 0.042 and R(D*) = 0.332 +- 0.024 +- 0.018, which exceed the Standard Model expectations by 2.0 sigma and 2.7 sigma, respectively. Taken together, our results disagree with these expectations at the 3.4 sigma level. This excess cannot be explained by a charged Higgs boson in the type II two-Higgs-doublet model. We also report the observation of the decay B -> D Tau Nu, with a significance of 6.8 sigma.Comment: Expanded section on systematics, text corrections, improved the format of Figure 2 and included the effect of the change of the Tau polarization due to the charged Higg

    Search for the decay modes D^0 → e^+e^-, D^0 → μ^+μ^-, and D^0 → e^±μ∓

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    We present searches for the rare decay modes D^0→e^+e^-, D^0→μ^+μ^-, and D^0→e^±μ^∓ in continuum e^+e^-→cc events recorded by the BABAR detector in a data sample that corresponds to an integrated luminosity of 468  fb^(-1). These decays are highly Glashow–Iliopoulos–Maiani suppressed but may be enhanced in several extensions of the standard model. Our observed event yields are consistent with the expected backgrounds. An excess is seen in the D^0→μ^+μ^- channel, although the observed yield is consistent with an upward background fluctuation at the 5% level. Using the Feldman–Cousins method, we set the following 90% confidence level intervals on the branching fractions: B(D^0→e^+e^-)<1.7×10^(-7), B(D^0→μ^+μ^-) within [0.6,8.1]×10^(-7), and B(D^0→e^±μ^∓)<3.3×10^(-7)

    G protein-coupled receptor kinase 5 mediates Tazarotene-induced gene 1-induced growth suppression of human colon cancer cells

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    <p>Abstract</p> <p>Background</p> <p>Tazarotene-induced gene 1 (TIG1) is a retinoid-inducible type II tumour suppressor gene. The B isoform of TIG1 (TIG1B) inhibits growth and invasion of cancer cells. Expression of TIG1B is frequently downregulated in various cancer tissues; however, the expression and activities of the TIG1A isoform are yet to be reported. Therefore, this study investigated the effects of the TIG1A and TIG1B isoforms on cell growth and gene expression profiles using colon cancer cells.</p> <p>Methods</p> <p>TIG1A and TIG1B stable clones derived from HCT116 and SW620 colon cancer cells were established using the GeneSwitch system; TIG1 isoform expression was induced by mifepristone treatment. Cell growth was assessed using the WST-1 cell proliferation and colony formation assays. RNA interference was used to examine the TIG1 mediating changes in cell growth. Gene expression profiles were determined using microarray and validated using real-time polymerase chain reaction, and Western blot analyses.</p> <p>Results</p> <p>Both TIG1 isoforms were expressed at high levels in normal prostate and colon tissues and were downregulated in colon cancer cell lines. Both TIG1 isoforms significantly inhibited the growth of transiently transfected HCT116 cells and stably expressing TIG1A and TIG1B HCT116 and SW620 cells. Expression of 129 and 55 genes was altered upon induction of TIG1A and TIG1B expression, respectively, in stably expressing HCT116 cells. Of the genes analysed, 23 and 6 genes were upregulated and downregulated, respectively, in both TIG1A and TIG1B expressing cells. Upregulation of the G-protein-coupled receptor kinase 5 (GRK5) was confirmed using real-time polymerase chain reaction and Western blot analyses in both TIG1 stable cell lines. Silencing of TIG1A or GRK5 expression significantly decreased TIG1A-mediated cell growth suppression.</p> <p>Conclusions</p> <p>Expression of both TIG1 isoforms was observed in normal prostate and colon tissues and was downregulated in colon cancer cell lines. Both TIG1 isoforms suppressed cell growth and stimulated GRK5 expression in HCT116 and SW620 cells. Knockdown of GRK5 expression alleviated TIG1A-induced growth suppression of HCT116 cells, suggesting that GRK5 mediates cell growth suppression by TIG1A. Thus, TIG1 may participate in the downregulation of G-protein coupled signaling by upregulating GRK5 expression.</p

    Measurement of the branching fraction and CP content for the decay B(0) -> D(*+)D(*-)

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    This is the pre-print version of the Article. The official published version can be accessed from the links below. Copyright @ 2002 APS.We report a measurement of the branching fraction of the decay B0→D*+D*- and of the CP-odd component of its final state using the BABAR detector. With data corresponding to an integrated luminosity of 20.4  fb-1 collected at the Υ(4S) resonance during 1999–2000, we have reconstructed 38 candidate signal events in the mode B0→D*+D*- with an estimated background of 6.2±0.5 events. From these events, we determine the branching fraction to be B(B0→D*+D*-)=[8.3±1.6(stat)±1.2(syst)]×10-4. The measured CP-odd fraction of the final state is 0.22±0.18(stat)±0.03(syst).This work is supported by DOE and NSF (USA), NSERC (Canada), IHEP (China), CEA and CNRS-IN2P3 (France), BMBF (Germany), INFN (Italy), NFR (Norway), MIST (Russia), and PPARC (United Kingdom). Individuals have received support from the A.P. Sloan Foundation, Research Corporation, and Alexander von Humboldt Foundation
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