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  • Nagurney, Anna, et al. (författare)
  • Pharmaceutical supply chain networks with outsourcing under price and quality competition
  • 2013
  • Ingår i: International Transactions in Operational Research. - 0969-6016. ; 20:6, s. 859-888
  • Tidskriftsartikel (refereegranskat)abstract
    • In this paper, we present a pharmaceutical supply chain network model with outsourcing under price and quality competition, in both equilibrium and dynamic versions. We consider a pharmaceutical firm that is engaged in determining the optimal pharmaceutical flows associated with its supply chain network activities in the form of manufacturing and distribution. In addition to multimarket demand satisfaction, the pharmaceutical firm seeks to minimize its total cost, with the associated function also capturing the firm's weighted disrepute cost caused by possible quality issues associated with the contractors. Simultaneously, the contractors, who compete with one another noncooperatively in prices in the manner of Bertrand, and in quality, seek to secure manufacturing and distribution of the pharmaceutical product from the pharmaceutical firm. This game theory model allows for the determination of the optimal pharmaceutical product flows associated with the supply chain in-house and outsourcing network activities and provides the pharmaceutical firm with its optimal make-or-buy decisions and the optimal contractor selections. We state the governing equilibrium conditions and derive the equivalent variational inequality formulation. We then propose dynamic adjustment processes for the evolution of the product flows, the quality levels, and the prices, along with stability analysis results. The algorithm yields a discretization of the continuous-time adjustment processes. We present convergence results and compute solutions to numerical examples to illustrate the generality and applicability of the framework.
  • Nagurney, Anna, et al. (författare)
  • Spatial price equilibrium with information asymmetry in quality and minimum quality standards
  • 2014
  • Ingår i: International Journal of Production Economics. - 0925-5273. ; 158, s. 300-313
  • Tidskriftsartikel (refereegranskat)abstract
    • A spatial price equilibrium model with information asymmetry in quality is developed in both static and dynamic versions. Producers at the supply markets are aware of the quality of their products, whereas consumers, located at the demand markets, are aware only of the average quality of the products that are shipped to their demand markets. Minimum quality standards are also captured in order to assess the impacts of such policy interventions. We establish qualitative results, in the form of existence, uniqueness, and stability analysis. An algorithm is proposed, along with a convergence proof. It is then utilized to compute solutions to a spectrum of spatial price equilibrium numerical examples in order to explore the impacts of information asymmetry under different scenarios. The numerical examples, which are of quite general functional forms, reveal that, as the number of supply markets increases, the "anonymizing" effect leads to a decrease in the average quality. On the other hand, as the number of demand markets increases, the pressure to improve quality increases, and the average quality increases. Finally, we demonstrate that, after the imposition of minimum quality standards, the average quality at the demand markets increases and the prices also increase. (C) 2014 Elsevier B.V. All rights reserved.
  • Nauta, Ake L., et al. (författare)
  • Permafrost collapse after shrub removal shifts tundra ecosystem to a methane source
  • 2015
  • Ingår i: Nature Climate Change. - Nature Research. - 1758-678X. ; 5:1, s. 67-70
  • Tidskriftsartikel (refereegranskat)abstract
    • Arctic tundra ecosystems are warming almost twice as fast as the global average. Permafrost thaw and the resulting release of greenhouse gases from decomposing soil organic carbon have the potential to accelerate climate warming. In recent decades, Arctic tundra ecosystems have changed rapidly, including expansion of woody vegetation, in response to changing climate conditions. How such vegetation changes contribute to stabilization or destabilization of the permafrost is unknown. Here we present six years of field observations in a shrub removal experiment at a Siberian tundra site. Removing the shrub part of the vegetation initiated thawing of ice-rich permafrost, resulting in collapse of the originally elevated shrub patches into waterlogged depressions within five years. This thaw pond development shifted the plots from a methane sink into a methane source. The results of our field experiment demonstrate the importance of the vegetation cover for protection of the massive carbon reservoirs stored in the permafrost and illustrate the strong vulnerability of these tundra ecosystems to perturbations. If permafrost thawing can more frequently trigger such local permafrost collapse, methane-emitting wet depressions could become more abundant in the lowland tundra landscape, at the cost of permafrost-stabilizing low shrub vegetation.
  • Nehme, Ralda, et al. (författare)
  • Combining NGN2 Programming with Developmental Patterning Generates Human Excitatory Neurons with NMDAR-Mediated Synaptic Transmission
  • 2018
  • Ingår i: Cell reports. - Cell Press. - 2211-1247 .- 2211-1247. ; 23:8, s. 2509-2523
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Transcription factor programming of pluripotent stem cells (PSCs) has emerged as an approach to generate human neurons for disease modeling. However, programming schemes produce a variety of cell types, and those neurons that are made often retain an immature phenotype, which limits their utility in modeling neuronal processes, including synaptic transmission. We report that combining NGN2 programming with SMAD and WNT inhibition generates human patterned induced neurons (hpiNs). Single-cell analyses showed that hpiN cultures contained cells along a developmental continuum, ranging from poorly differentiated neuronal progenitors to well-differentiated, excitatory glutamatergic neurons. The most differentiated neurons could be identified using a CAMK2A::GFP reporter gene and exhibited greater functionality, including NMDAR-mediated synaptic transmission. We conclude that utilizing single-cell and reporter gene approaches for selecting successfully programmed cells for study will greatly enhance the utility of hpiNs and other programmed neuronal populations in the modeling of nervous system disorders.</p>
  • Nemeth, Zsuzsanna, et al. (författare)
  • Heme oxygenase-1 in macrophages controls prostate cancer progression.
  • 2015
  • Ingår i: Oncotarget. - Impact Journals, LLC. - 1949-2553. ; 6:32, s. 33675-33688
  • Tidskriftsartikel (refereegranskat)abstract
    • Innate immune cells strongly influence cancer growth and progression via multiple mechanisms including regulation of epithelial to mesenchymal transition (EMT). In this study, we investigated whether expression of the metabolic gene, heme oxygenase-1 (HO-1) in tumor microenvironment imparts significant effects on prostate cancer progression. We showed that HO-1 is expressed in MARCO-positive macrophages in prostate cancer (PCa) xenografts and human prostate cancers. We demonstrated that macrophage specific (LyzM-Cre) conditional deletion of HO-1 suppressed growth of PC3 xenografts in vivo and delayed progression of prostate intraepithelial neoplasia (PIN) in TRAMP mice. However, initiation and progression of cancer xenografts in the presence of macrophages lacking HO-1 resulted in loss of E-cadherin, a known marker of poor prognosis as well as EMT. Application of CO, a product of HO-1 catalysis, increased levels of E-cadherin in the adherens junctions between cancer cells. We further showed that HO-1-driven expression of E-cadherin in cancer cells cultured in the presence of macrophages is dependent on mitochondrial activity of cancer cells. In summary, these data suggest that HO-1-derived CO from tumor-associated macrophages influences, in part, E-cadherin expression and thus tumor initiation and progression.
  • Nicholson, George, et al. (författare)
  • A genome-wide metabolic QTL analysis in Europeans implicates two loci shaped by recent positive selection
  • 2011
  • Ingår i: PLoS genetics. - 1553-7404. ; 7:9, s. e1002270
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>We have performed a metabolite quantitative trait locus (mQTL) study of the <sup>1</sup>H nuclear magnetic resonance spectroscopy (<sup>1</sup>H NMR) metabolome in humans, building on recent targeted knowledge of genetic drivers of metabolic regulation. Urine and plasma samples were collected from two cohorts of individuals of European descent, with one cohort comprised of female twins donating samples longitudinally. Sample metabolite concentrations were quantified by <sup>1</sup>H NMR and tested for association with genome-wide single-nucleotide polymorphisms (SNPs). Four metabolites' concentrations exhibited significant, replicable association with SNP variation (8.6×10<sup>−11</sup>&lt;<em>p</em>&lt;2.8×10<sup>−23</sup>). Three of these—trimethylamine, 3-amino-isobutyrate, and an <em>N</em>-acetylated compound—were measured in urine. The other—dimethylamine—was measured in plasma. Trimethylamine and dimethylamine mapped to a single genetic region (hence we report a total of three implicated genomic regions). Two of the three hit regions lie within haplotype blocks (at 2p13.1 and 10q24.2) that carry the genetic signature of strong, recent, positive selection in European populations. Genes <em>NAT8</em> and <em>PYROXD2</em>, both with relatively uncharacterized functional roles, are good candidates for mediating the corresponding mQTL associations. The study's longitudinal twin design allowed detailed variance-components analysis of the sources of population variation in metabolite levels. The mQTLs explained 40%–64% of biological population variation in the corresponding metabolites' concentrations. These effect sizes are stronger than those reported in a recent, targeted mQTL study of metabolites in serum using the targeted-metabolomics Biocrates platform. By re-analysing our plasma samples using the Biocrates platform, we replicated the mQTL findings of the previous study and discovered a previously uncharacterized yet substantial familial component of variation in metabolite levels in addition to the heritability contribution from the corresponding mQTL effects.</p>
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