67 research outputs found

    Analisis Portofolio Optimal Dengan Single Index Model Untuk Meminimumkan Risiko Bagi Investor Di Bursa Efek Indonesia (Studi Pada Saham Indeks Kompas 100 Periode Februari 2010-juli 2014)

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    Investments can be made in the capital market, capital market instruments which are mostly attractive for investors is stock. Stock provides a return in the form of capital gains and dividends yield, not only noticing the return, investors need to pay attention to the investments risk. Unsystematis risk can be minimized by forming the optimal portfolio using one of the methods that is single index model. Study purpose is to knowing the stocks forming the optimal portfolio, the proportion of funds allocated to each stocks, the level of expectation return and risk.The method used in this research is descriptive research method with a quantitative approach. The samples used were 46 stocks in Kompas 100 Index, which meets the criteria for sampling. The results showed that 12 stocks of forming optimal portfolio, the stocks of which are UNVR, TRAM, MNCN, BHIT, JSMR, BMTR, GJTL, KLBF, AALI, CPIN, AKRA, and ASRI. Stock with highest proportion of funds is TRAM (23,52%), stock with lowest proportion of funds is AALI (0,62%). Portfolio which are formed will give return expectations by 3,05477% and carry the risk for about 0,1228%

    Hyperandrogen enhances apoptosis of human ovarian granulosa cells via up-regulation and demethylation of PDCD4

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    Apoptosis of granulosa cells (GCs) induced by hyperandrogen plays a key role in the pathogenesis of polycystic ovary syndrome (PCOS). However, the mechanism of androgen-induced apoptosis of GCs has not been clarified to date. Recent studies have reported that PDCD4 expression is higher in PCOS patients and might be a key factor in PCOS progression. In this study, we aimed to investigate the role of PDCD4 in regulating apoptosis of human GCs and whether hyperandrogen regulate PDCD4 expression through DNA methylation. Overexpression of PDCD4 in human ovarian granulosa cell line KGN cells promoted cells apoptosis. Meanwhile, expression of caspase-3 and caspase-9 were significantly elevated. High concentration of testosterone treatment resulted in up-regulation of PDCD4 and a significant increase of apoptosis in KGN cells. In addition, knockdown of PDCD4 in KGN cells treated with high concentration of testosterone abolished the hyperandrogen-induced apoptosis. Furthermore, high concentration of testosterone down-regulated DNMT1, DNMT3A and DNMT3B expression and the methylation level in the promoter region of PDCD4 was decreased. In conclusion, PDCD4 can promote apoptosis of human ovarian GCs. The mechanism of hyperandrogen-induced apoptosis may be mediated by PDCD4. Furthermore, the up-regulation of PDCD4 induced by hyperandrogen may through demethylation of its promoter regions.</p

    Improved Cyclability of Lithium–Oxygen Batteries by Synergistic Catalytic Effects of Two-Dimensional MoS<sub>2</sub> Nanosheets Anchored on Hollow Carbon Spheres

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    The design and development of high-efficient electrocatalysts plays a decisive role in improving the stability of lithium–oxygen (Li–O2) batteries. Here, two-dimensional (2D) MoS2 nanosheets anchored on hollow carbon spheres (MoS2/HCS) composites is designed and reported as promising cathode catalysts for Li–O2 batteries. The MoS2/HCS-based Li–O2 battery shows superior electrochemical performance, in terms of high capacity (4010 mA h g–1) and enhanced cycling performance (104 cycles). X-ray photoelectron spectroscopy (XPS) results reveal that the formation of Li2CO3 and other side products can be effectively alleviated when MoS2/HCS electrode is used as the cathode. On the basis of experimental studies, it is found that the synergistic effects, which originated from the superior catalytic property of MoS2 nanosheets and the good electrical conductivity of HCS with high surface area, is the main reason for performance improvement. The synergistic effects induced by the dispersed MoS2 nanosheets anchored on nanostructured HCS cathodes provide a promising strategy for developing catalysts of O2 electrode for Li–O2 batteries with excellent performance

    Image_2_IRF6 Is Directly Regulated by ZEB1 and ELF3, and Predicts a Favorable Prognosis in Gastric Cancer.TIF

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    Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes. However, its function in gastric cancer (GC) remains unknown to date. In this study, we found that the IRF6 expression was significantly downregulated in GC. And the decreased expression of IRF6 was clinically correlated with poor prognosis of GC. Moreover, loss-of-function and gain-of-function studies showed that IRF6 was negatively regulated by ZEB1 but positively regulated by ELF3. Additionally, transcription factor ZEB1 and ELF3 could directly bind on IRF6 promoter, which suggested that transcription factor IRF6 is transcriptionally regulated by ZEB1 and ELF3. Nevertheless, we found that IRF6 expression was negatively related to its promoter methylation in TCGA stomach cancer cohorts. The downregulation of IRF6 in GC might be due to the overexpression of ZEB1 and the DNA methylation of IRF6 promoter.</p

    Image_1_IRF6 Is Directly Regulated by ZEB1 and ELF3, and Predicts a Favorable Prognosis in Gastric Cancer.TIF

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    Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes. However, its function in gastric cancer (GC) remains unknown to date. In this study, we found that the IRF6 expression was significantly downregulated in GC. And the decreased expression of IRF6 was clinically correlated with poor prognosis of GC. Moreover, loss-of-function and gain-of-function studies showed that IRF6 was negatively regulated by ZEB1 but positively regulated by ELF3. Additionally, transcription factor ZEB1 and ELF3 could directly bind on IRF6 promoter, which suggested that transcription factor IRF6 is transcriptionally regulated by ZEB1 and ELF3. Nevertheless, we found that IRF6 expression was negatively related to its promoter methylation in TCGA stomach cancer cohorts. The downregulation of IRF6 in GC might be due to the overexpression of ZEB1 and the DNA methylation of IRF6 promoter.</p

    Image_3_IRF6 Is Directly Regulated by ZEB1 and ELF3, and Predicts a Favorable Prognosis in Gastric Cancer.TIF

    No full text
    Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes. However, its function in gastric cancer (GC) remains unknown to date. In this study, we found that the IRF6 expression was significantly downregulated in GC. And the decreased expression of IRF6 was clinically correlated with poor prognosis of GC. Moreover, loss-of-function and gain-of-function studies showed that IRF6 was negatively regulated by ZEB1 but positively regulated by ELF3. Additionally, transcription factor ZEB1 and ELF3 could directly bind on IRF6 promoter, which suggested that transcription factor IRF6 is transcriptionally regulated by ZEB1 and ELF3. Nevertheless, we found that IRF6 expression was negatively related to its promoter methylation in TCGA stomach cancer cohorts. The downregulation of IRF6 in GC might be due to the overexpression of ZEB1 and the DNA methylation of IRF6 promoter.</p
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