| 1. |
- Weinstein, John N., et al.
(författare)
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The cancer genome atlas pan-cancer analysis project
- 2013
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 45:10, s. 1113-1120
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Forskningsöversikt (refereegranskat)abstract
- The Cancer Genome Atlas (TCGA) Research Network has profiled and analyzed large numbers of human tumors to discover molecular aberrations at the DNA, RNA, protein and epigenetic levels. The resulting rich data provide a major opportunity to develop an integrated picture of commonalities, differences and emergent themes across tumor lineages. The Pan-Cancer initiative compares the first 12 tumor types profiled by TCGA. Analysis of the molecular aberrations and their functional roles across tumor types will teach us how to extend therapies effective in one cancer type to others with a similar genomic profile. © 2013 Nature America, Inc. All rights reserved.
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| 2. |
- Shen, Xiantao, et al.
(författare)
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Molecular imprinting for removing highly toxic organic pollutants
- 2012
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Ingår i: Chemical Communications. - : Royal Society of Chemistry (RSC). - 1364-548X. ; 48:6, s. 788-798
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Tidskriftsartikel (refereegranskat)abstract
- Molecular imprinting technology allows synthesis of polymers with specific recognition ability towards target pollutants, which show potential to selectively remove Highly Toxic Organic Pollutants (HTOPs) in the presence of common organic matrices that are thousands of times more abundant than the targets. This feature article summarizes the current development of molecular imprinting for removing HTOPs from polluted water, with a special emphasis on the application of molecularly imprinted polymers to improve the efficiency of photocatalytic and biological degradation of HTOPs in wastewater.
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| 3. |
- Terenius, Olle, et al.
(författare)
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RNA interference in Lepidoptera : An overview of successful and unsuccessful studies and implications for experimental design
- 2011
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Ingår i: Journal of insect physiology. - : Elsevier BV. - 0022-1910 .- 1879-1611. ; 57:2, s. 231-245
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Tidskriftsartikel (refereegranskat)abstract
- Gene silencing through RNA interference (RNAi) has revolutionized the study of gene function, particularly in non-model insects. However, in Lepidoptera (moths and butterflies) RNAi has many times proven to be difficult to achieve. Most of the negative results have been anecdotal and the positive experiments have not been collected in such a way that they are possible to analyze. In this review, we have collected detailed data from more than 150 experiments including all to date published and many unpublished experiments. Despite a large variation in the data, trends that are found are that RNAi is particularly successful in the family Saturniidae and in genes involved in immunity. On the contrary, gene expression in epidermal tissues seems to be most difficult to silence. In addition, gene silencing by feeding dsRNA requires high concentrations for success. Possible causes for the variability of success in RNAi experiments in Lepidoptera are discussed. The review also points to a need to further investigate the mechanism of RNAi in lepidopteran insects and its possible connection to the innate immune response. Our general understanding of RNAi in Lepidoptera will be further aided in the future as our public database at http://insectacentral.org/RNAi will continue to gather information on RNAi experiments.
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| 4. |
- Wang, Daqin, et al.
(författare)
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A periodic review lot sizing problem with random yields, disruptions and inventory capacity
- 2014
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Ingår i: International Journal of Production Economics. - : Elsevier. - 0925-5273 .- 1873-7579. ; 155, s. 330-339
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Forskningsöversikt (refereegranskat)abstract
- This paper examines a periodic-reviewed lot sizing problem with random yields, disruptions and limited inventory capacity. To characterise the continuous production, an additive random yield model is considered rather than a multiplicative one. Disruptions cause breakdowns to production. Inventory capacity is included since the production has to be shut down when the inventory buffer is full. Both disruptions and shutdowns lead to a start-up cost and a stochastic lead time to recover the production. These compound factors of uncertainty are encountered in practical planning decisions in process industries. We review the existing random yield models, which are then compared with the additive model. With a linear production cost, the additive model has an order-up-to policy to be optimal. Disruptions deteriorate the expected actual production quantity and the fill-rate dramatically, even though the optimal order-up-to level increases compared with the cases of no disruption. Considering inventory capacity makes the problem to be a non-convex dynamic programming problem. Numerical analysis shows that the performance is dramatically deteriorated when the inventory capacity is rather tight, which indicates the importance of selecting a proper inventory capacity to reduce the negative impacts and avoid redundant investment on capacity. Moreover, the start-up cost plays an important role in determining the level of inventory capacity.
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| 5. |
- Zhu, Wuyang, et al.
(författare)
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Interaction of E2 glycoprotein with heparan sulfate is crucial for cellular infection of Sindbis virus
- 2010
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Ingår i: PLoS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 5:3, s. e9656-
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Tidskriftsartikel (refereegranskat)abstract
- Cell culture-adapted strains of Sindbis virus (SINV) initially attach to cells by the ability to interact with heparan sulfate (HS) through selective mutation for positively charged amino acid (aa) scattered in E2 glycoprotein (W. B. Klimstra, K. D. Ryman, and R. E. Johnston, J. Virol. 72: 7357-7366, 1998). Here we have further confirmed that interaction of E2 protein with HS is crucial for cellular infection of SINV based on the reverse genetic system of XJ-160 virus, a Sindbis-like virus (SINLV). Both SINV YN87448 and SINLV XJ-160 displayed similar infectivity on BHK-21, Vero, or C6/36 cells, but XJ-160 failed to infect mouse embryonic fibroblast (MEF) cells. The molecular mechanisms underlying the selective infectivity of XJ-160 were approached by substituting the E1, E2, or both genes of XJ-160 with that of YN87448, and the chimeric virus was denominated as XJ-160/E1, XJ-160/E2, or XJ-160/E1E2, respectively. In contrast to the parental XJ-160, all chimeric viruses became infectious to wild-type MEF cells (MEF-wt). While MEF-Ext(-/-) cells, producing shortened HS chains, were resistant not only to XJ-160, but also to YN87448 as well as the chimeric viruses, indicating that the inability of XJ-160 to infect MEF-wt cells likely due to its incompetent discrimination of cellular HS. Treatment with heparin or HS-degrading enzyme resulted in a substantial decrease in plaque formation by YN87448, XJ-160/E2, and XJ-160/E1E2, but had marginal effect on XJ-160 and XJ-160/E1, suggesting that E2 glycoprotein from YN87448 plays a more important role than does E1 in mediating cellular HS-related cell infection. In addition, the peptide containing 145-150 aa from E2 gene of YN87448 specifically bound to heparin, while the corresponding peptide from the E2 gene of XJ-160 essentially showed no binding to heparin. As a new dataset, these results clearly confirm an essential role of E2 glycoprotein, especially the domain of 145-150 aa, in SINV cellular infection through the interaction with HS.
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