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Karel Van Acker - One of the best experts on this subject based on the ideXlab platform.

  • downcycling versus recycling of construction and demolition waste combining lca and lcc to support sustainable policy making
    Waste Management, 2018
    Co-Authors: Andrea Di Maria, Johan Eyckmans, Karel Van Acker
    Abstract:

    Urgent solutions are needed in Europe to deal with construction and demolition waste (CDW). EU policy has contributed to significantly reducing the amount of CDW going to landfill, but most of the effort has been put in downcycling practices. Therefore, further policies are needed to stimulate high-quality recycling of CDW. The present paper presents a combined life cycle assessment (LCA) and life cycle costing (LCC) methodologies to analyse the environmental and the economic drivers in four alternative CDW end-of-life scenarios in the region of Flanders, in Belgium. The four analysed alternatives are (i) landfilling, (ii) downcycling, (iii) advanced recycling and (iv) recycling after selective demolition. LCA results show that landiflling is the scenario having the highest environmental impacts in terms of person equivalent (PE), followed by downcycling and recycling (-36%) and recycling after selective demolition (-59%). The decrease in environmental impacts is mostly due to the avoided landfilling of CDW and the recovery of materials from selective demolition. LCC results indicate that landfilling is the scenario bearing the highest total economic costs. This is due to the high landfill tax in Flanders. The recycling after selective demolition bears the second highest cost. The increase of high-quality CDW recycling can significantly reduce the overall environmental impact of the system. Implementing a high landfill tax, increasing the gate fee to the recycling plant, and boosting the sales price of recycled aggregates are the most effective drivers to facilitate a transition towards a more sustainable CDW management system. The paper demonstrates that the combined LCA and LCC results can highlight the environmental and economic drivers in CDW management. The results of the combined analysis can help policymakers to promote the aspects contributing to sustainability and to limit the ones creating a barrier.

  • bridging the gap between lca lcc and cba as sustainability assessment tools
    Environmental Impact Assessment Review, 2014
    Co-Authors: Rob Hoogmartens, Karel Van Acker, Steven Van Passel, Maarten Dubois
    Abstract:

    Abstract Increasing interest in sustainability has led to the development of sustainability assessment tools such as Life Cycle Analysis (LCA), Life Cycle Costing (LCC) and Cost–Benefit Analysis (CBA). Due to methodological disparity of these three tools, conflicting assessment results generate confusion for many policy and business decisions. In order to interpret and integrate assessment results, the paper provides a framework that clarifies the connections and coherence between the included assessment methodologies. Building on this framework, the paper further focuses on key aspects to adapt any of the methodologies to full sustainability assessments. Aspects dealt with in the review are for example the reported metrics, the scope, data requirements, discounting, product- or project-related and approaches with respect to scarcity and labor requirements. In addition to these key aspects, the review shows that important connections exist: (i) the three tools can cope with social inequality, (ii) processes such as valuation techniques for LCC and CBA are common, (iii) Environmental Impact Assessment (EIA) is used as input in both LCA and CBA and (iv) LCA can be used in parallel with LCC. Furthermore, the most integrated sustainability approach combines elements of LCA and LCC to achieve the Life Cycle Sustainability Assessment (LCSA). The key aspects and the connections referred to in the review are illustrated with a case study on the treatment of end-of-life automotive glass.

Arthur Weiss - One of the best experts on this subject based on the ideXlab platform.

  • Lck promotes zap70 dependent lat phosphorylation by bridging zap70 to lat
    Nature Immunology, 2018
    Co-Authors: Wanlin Lo, Neel H Shah, Nagib Ahsan, Veronika Horkova, Ondrej Stepanek, Arthur R Salomon, John Kuriyan, Arthur Weiss
    Abstract:

    T cell–antigen receptor (TCR) signaling requires the sequential activities of the kinases Lck and Zap70. Upon TCR stimulation, Lck phosphorylates the TCR, thus leading to the recruitment, phosphorylation, and activation of Zap70. Lck binds and stabilizes phosho-Zap70 by using its SH2 domain, and Zap70 phosphorylates the critical adaptors LAT and SLP76, which coordinate downstream signaling. It is unclear whether phosphorylation of these adaptors occurs through passive diffusion or active recruitment. We report the discovery of a conserved proline-rich motif in LAT that mediates efficient LAT phosphorylation. Lck associates with this motif via its SH3 domain, and with phospho-Zap70 via its SH2 domain, thereby acting as a molecular bridge that facilitates the colocalization of Zap70 and LAT. Elimination of this proline-rich motif compromises TCR signaling and T cell development. These results demonstrate the remarkable multifunctionality of Lck, wherein each of its domains has evolved to orchestrate a distinct step in TCR signaling. TCR signaling initiates a signaling cascade involving the kinases Lck and Zap70 and the adaptor LAT. Weiss and colleagues discover a proline-rich motif in LAT, which facilitates interactions among Lck, LAT and Zap70 for efficient TCR signaling.

  • differential contribution of Lck and fyn protein tyrosine kinases to intraepithelial lymphocyte development
    European Journal of Immunology, 1997
    Co-Authors: Stephanie T Page, Arthur Weiss, Nicolai S C Van Oers, Roger M Perlmutter, Ann M Pullen
    Abstract:

    The developmental stages and the role of protein tyrosine kinases (PTK) in the maturation of CD3+CD8 alpha alpha+ intraepithelial lymphocytes (IEL) have not been extensively characterized. However, comparisons of thymic and extrathymic T cell development indicate that these processes involve some distinct signaling and selection events. We used mice deficient in Lck, Fyn, or both Lck and Fyn to analyze the role that these src-family PTK play in IEL development. In contrast to thymocyte development, we found that all IEL subsets develop in mice deficient for either kinase alone. However, Lck-/- animals exhibited reduced numbers of TcR alphabeta+ CD8alpha alpha+ IEL, indicating that Lck is important in the development of these cells. Mice which lack both Lck and Fyn fail to generate TcR alphabeta+ IEL, suggesting that signaling through the preTcR, mediated by Lck and, to a lesser extent Fyn, is required for maturation of all TcR alphabeta+ IEL lineages. Interestingly, a small population of TcR gammadelta+ CD8 alpha alpha+ cells are apparent in Lck-/-fyn-/- animals, demonstrating that TcR alphabeta+ CD8 alpha alpha+ and TcR gammadelta+ CD8alpha alpha+ IEL have distinct PTK requirements for their development or expansion. CD3-CD8alpha- CD44+ and CD3-CD8alpha alpha+ CD16/32+ B220+ cells comprise the majority of IEL in both Lck-/- fyn-/- and rag -/- mice, while they are poorly represented in wildtype controls. Comparison of the cell surface phenotype of these putative precursor IEL in Lck-/- fyn-/- and rag-/- animals suggests that IEL maturation in these animals is arrested at an equivalent developmental stage. Overall, the data presented demonstrate that signals mediated by Lck or Fyn direct TcR alphabeta+ CD8alpha alpha+ IEL maturation but are dispensable for the development of TcR gammadelta+ CD8 alpha alpha+ IEL.

  • genetic evidence for the involvement of the Lck tyrosine kinase in signal transduction through the t cell antigen receptor
    Cell, 1992
    Co-Authors: David B Straus, Arthur Weiss
    Abstract:

    Abstract Signaling through the T cell antigen receptor (TCR) results both in rapid increases in tyrosine phosphorylation on a number of proteins and in the activation of the phosphatidylinositol pathway. It is not clear how stimulation of the TCR leads to these signaling events. Mutants of the Jurkat T cell line have been previously isolated that fail to show increases in calcium following receptor stimulation. Analysis of one of these mutants, JCaM1, which is defective in the induction of tyrosine phosphorylation, revealed a defect in the expression of functional Lck tyrosine kinase. The lack of Lck activity was caused in part by a splicing defect. Expression of the Lck cDNA in JCaM1 restores the ability of the cell to respond to TCR stimulation. These results indicate that Lck is required for normal signal transduction through the TCR.

Yutaka Takata - One of the best experts on this subject based on the ideXlab platform.

  • lack of cholecystokinin a receptor enhanced gallstone formation a study in cck a receptor gene knockout mice
    Digestive Diseases and Sciences, 2003
    Co-Authors: Norikazu Sato, Kyoko Miyasaka, Shinji Suzuki, Takako Kawanami, Yuki Yoshida, Soichi Takiguchi, Tetsuo Noda, Yutaka Takata
    Abstract:

    The etiology of gallstones is multifactorial, with interactions between genes and the environment. We generated cholecystokinin (CCK) -A receptor (R)-deficient (-/-) mice and found that CCK did not produce gallbladder contraction in CCK-AR(-/-) mice. The purpose of this study was to identify the role of CCK-AR on gallstone formation. Age-matched CCK-AR gene (+/+) and (-/-) progenies were used. Sludge and gallstone formation, as well as plasma cholesterol levels, were measured at 12 and 24 months of age. Sludge and gallstone formation were significantly higher in CCK-AR(-/-) mice than in CCK-AR(+/+) mice at 12 and 24 months of age, although these were not different between 12 and 24 months of age. The plasma cholesterol levels, daily food intake, and body weight were not significantly different between CCK-AR(+/+) and (-/-) mice. Sludge and gallstone formation were not observed at 6 months of age. In conclusion, deteriorated gallbladder contraction due to a lack of CCK-AR favored gallstone formation after the middle age of life.

  • anxiety related behaviors in cholecystokinin a b and ab receptor gene knockout mice in the plus maze
    Neuroscience Letters, 2002
    Co-Authors: Kyoko Miyasaka, Minoru Ohta, Setsuko Kanai, Aki Nagata, Toshimitsu Matsui, Yuki Yoshida, Soichi Takiguchi, Tetsuo Noda, Satoru Kobayashi, Yutaka Takata
    Abstract:

    Abstract Cholecystokinin (CCK)-A receptor (AR) and B receptor (BR) share highly amino acid sequence homology and overlap in their tissue distribution. We examined the anxiety-related behavior of CCK-AR, CCK-BR, and CCK-ARBR gene knockout (−/−) mice in the elevated plus-maze. CCK-AR(−/−) mice showed a significantly higher frequency of open-arm entries than wild-type and CCK-BR(−/−) mice, whereas the percentage open-arm entry values in CCK-AR(−/−) mice did not differ from those in wild-type mice. Thus, this increased frequency in open-arm entries for CCK-AR(−/−) mice was interpreted to be due to an increase in locomotor activity, rather than to a reduction in anxiety. By contrast, CCK-BR(−/−) mice showed significantly lower percentage open-arm entry values and spent significantly less time in the open- arms than wild-type and CCK-AR(−/−) mice. We therefore conclude that a lack of CCK-BR increases the anxiety-related behavior of the mouse in the elevated plus- maze.

Mark Harris - One of the best experts on this subject based on the ideXlab platform.

  • the hepatitis c virus ns5a protein binds to members of the src family of tyrosine kinases and regulates kinase activity
    Journal of General Virology, 2004
    Co-Authors: Andrew Macdonald, Katherine Crowder, Andrew Street, Christopher Mccormick, Mark Harris
    Abstract:

    The hepatitis C virus (HCV) non-structural NS5A protein has been shown to associate with a variety of cellular signalling proteins. Of particular interest is the observation that a highly conserved C-terminal polyproline motif in NS5A was able to interact with the Src-homology 3 (SH3) domains of the adaptor protein Grb2. As it has previously been shown that specific polyproline motifs can interact with a range of SH3 domains, we investigated whether NS5A was capable of interacting with other SH3 domain-containing proteins. We show here that NS5A interacts with the SH3 domains of members of the Src family of tyrosine kinases: a combination of in vitro binding assays and co-immunoprecipitation experiments revealed an interaction between NS5A and Hck, Lck, Lyn and Fyn, but interestingly not Src itself. Mutational analysis confirmed that the polyproline motif responsible for binding to Grb2 also bound to the SH3 domains of Hck, Lck, Lyn and Fyn. Furthermore, a previously unidentified polyproline motif, adjacent to the first motif, was also able to mediate binding to the SH3 domain of Lyn. Using transient transfections and Huh-7 cells harbouring a persistently replicating subgenomic HCV replicon we demonstrate that NS5A bound to native Src-family kinases in vivo and differentially modulated kinase activity, inhibiting Hck, Lck and Lyn but activating Fyn. Lastly, we show that signalling pathways controlled by Src-family kinases are modulated in replicon cells. We conclude that the interactions between NS5A and Src-family kinases are physiologically relevant and may play a role in either virus replication or pathogenesis.

  • The Human Immunodeficiency Virus Type 1 NEF Protein Binds the Src-Related Tyrosine Kinase Lck SH2 Domain Through a Novel Phosphotyrosine Independent Mechanism
    Virology, 1998
    Co-Authors: Helene Dutartre, Mark Harris, Daniel Olive, Yves Collette
    Abstract:

    Primate lentiviruses encode for an unique nef gene with an essential function in both viral replication and pathogenicity in the host. The molecular basis for this function remains however poorly defined. Several Nef-binding cellular proteins are thought to be instrumental in its function. Indeed, Nef contains a proline-rich motif implicated in the binding to the Src-like tyrosine kinase Hck and also to a Ser/Thr kinase of molecular weight 62 kDa. The disruption of this motif affects the binding to both these kinases as well as viral replication. Whereas Hck is expressed in the myeloid lineage and hence may account for the nef function in infected monocytes, we and others have reported previously that Nef also interacts with the T-lymphocyte Src-kinase Lck, leading to specific cell signaling impairment. This interaction occurs through the binding of Nef to both Lck SH2 and SH3 domains. Both the proline motif and phosphorylation of Nef on tyrosine residue were proposed to account for these interactions. Here, we investigate the mechanism of Lck SH2 binding by HIV-1 Nef. Using recombinant fusion proteins to precipitate lysates, we show that although SH2 binding is dependent on phosphorylation events, it occurs in a tyrosine independent manner because it requires neither tyrosine residues in Nef nor the phosphotyrosine binding pocket from the Lck SH2 domain, hence suggesting a role for a phosphoserine or a phosphothreonine residue. Further, we show that Hck SH2 does not interact with Nef, indicating that Hck SH3 binding is sufficient for Nef binding, whereas Lck SH2 cooperate together with SH3 to allow Nef binding to a level similar to Hck SH3. Together, our results establish different mechanisms for Hck and Lck binding by HIV-1 Nef protein, and identify a novel mechanism for Src-like tyrosine kinase targeting by a viral protein.

Kyoko Miyasaka - One of the best experts on this subject based on the ideXlab platform.

  • lack of cholecystokinin a receptor enhanced gallstone formation a study in cck a receptor gene knockout mice
    Digestive Diseases and Sciences, 2003
    Co-Authors: Norikazu Sato, Kyoko Miyasaka, Shinji Suzuki, Takako Kawanami, Yuki Yoshida, Soichi Takiguchi, Tetsuo Noda, Yutaka Takata
    Abstract:

    The etiology of gallstones is multifactorial, with interactions between genes and the environment. We generated cholecystokinin (CCK) -A receptor (R)-deficient (-/-) mice and found that CCK did not produce gallbladder contraction in CCK-AR(-/-) mice. The purpose of this study was to identify the role of CCK-AR on gallstone formation. Age-matched CCK-AR gene (+/+) and (-/-) progenies were used. Sludge and gallstone formation, as well as plasma cholesterol levels, were measured at 12 and 24 months of age. Sludge and gallstone formation were significantly higher in CCK-AR(-/-) mice than in CCK-AR(+/+) mice at 12 and 24 months of age, although these were not different between 12 and 24 months of age. The plasma cholesterol levels, daily food intake, and body weight were not significantly different between CCK-AR(+/+) and (-/-) mice. Sludge and gallstone formation were not observed at 6 months of age. In conclusion, deteriorated gallbladder contraction due to a lack of CCK-AR favored gallstone formation after the middle age of life.

  • anxiety related behaviors in cholecystokinin a b and ab receptor gene knockout mice in the plus maze
    Neuroscience Letters, 2002
    Co-Authors: Kyoko Miyasaka, Minoru Ohta, Setsuko Kanai, Aki Nagata, Toshimitsu Matsui, Yuki Yoshida, Soichi Takiguchi, Tetsuo Noda, Satoru Kobayashi, Yutaka Takata
    Abstract:

    Abstract Cholecystokinin (CCK)-A receptor (AR) and B receptor (BR) share highly amino acid sequence homology and overlap in their tissue distribution. We examined the anxiety-related behavior of CCK-AR, CCK-BR, and CCK-ARBR gene knockout (−/−) mice in the elevated plus-maze. CCK-AR(−/−) mice showed a significantly higher frequency of open-arm entries than wild-type and CCK-BR(−/−) mice, whereas the percentage open-arm entry values in CCK-AR(−/−) mice did not differ from those in wild-type mice. Thus, this increased frequency in open-arm entries for CCK-AR(−/−) mice was interpreted to be due to an increase in locomotor activity, rather than to a reduction in anxiety. By contrast, CCK-BR(−/−) mice showed significantly lower percentage open-arm entry values and spent significantly less time in the open- arms than wild-type and CCK-AR(−/−) mice. We therefore conclude that a lack of CCK-BR increases the anxiety-related behavior of the mouse in the elevated plus- maze.

  • lack of satiety effect of cholecystokinin cck in a new rat model not expressing the cck a receptor gene
    Neuroscience Letters, 1994
    Co-Authors: Kyoko Miyasaka, Takako Kawanami, Akira Kono, S Kanai, Akihiro Funakoshi
    Abstract:

    Abstract This work expands recent observations that Otsuka Long-Evans Tokushima Fatty (OLETF) rats show little or no pancreatic expression of the cholecystokinin (CCK)-A receptor gene. We examined whether the CCK-A and -B receptor genes were expressed in the brain (hypothalamus) of OLETF rats in comparison with control (Long-Evans Tokushima Otsuka = LET) rats. CCK-A receptor mRNA was detected in the hypothalamus of LETO rats but not OLETF rats. The CCK-B receptor gene was expressed in the hypothalamus in both strains. Cerebroventricular administration of CCK-8 sulfate inhibited daily food intake in LETO rats, but not in OLETF rats. These results show that in OLETF rats the absence of CCK-A receptor gene expression in the hypothalamus results in hyperphagia because of lack of satiety.