资源检索作业4

（四）利用英文全文数据库——Elsevier 进行文献信息检索示例1、检索课题名称：高效能并行计算机体系结构研究2、课题分析：中文关键词：1 高效能2 并行计算机体系英文关键词：（1）high potency（2）collateral computer system3、选择检索工具：Elsevier 数据库4、构建检索策略：high potencyandcollateralcomputer system5、简述检索过程:选定在Elsevier 中期刊、图书、文摘数据库等全部文献资源中检索1989 年以后的关于高性能并行计算机系统的相关文献。

利用确定的检索策略，文献全文（含文献题目、摘要、关键词）中检索，检到576 篇相关文献；在文献题目、摘要和关键词中检索，检索到0篇相关文献；在文献关键词中检索到134 篇相关文献；在文献题目中检索到0篇相关文献。

6、整理检索结果：从以上文献中选择出3条切题文献1Aging impairs collateral sprouting of nociceptive axons in the ratReceived 13 November 2007; revised 25 March 2008; accepted 29 March 2008. Available online 21 May 2008.Abstract：Sprouting of uninjured nociceptive axons was examined in young adult, middle aged and aged rats. Axon sprouting from the spared sural nerve, both into adjacent denervated skin and into end-to-side coapted nerve graft, was significantly higher in young rats than in aged rats. Cross-transplantations of the end-to-side coapted nerve grafts between young and aged rats demonstrated that axon sprouting from young recipient nerves into aged donor nerve grafts was significantly deteriorated, whereas the axon sprouting from aged recipient nerves into young donor nerve grafts was not statistically significantly affected. The levels of laminin polypeptides in peripheral nerves were 50–100% higher in young adult than in aged rats. However, the levels of peripherin, NGF isoforms and TrkA in skin, peripheral nerves and DRG, respectively, were not significantly reduced in aged rats. Therefore, impaired sprouting of nociceptive axons in aged rats is due rather to the alterations in peripheral neural pathways, than to the limited sprouting capacity of aged sensory neurons. Decreased levels of extracellular matrix components might be important in this respect.Keywords: Collateral sprouting; Dorsal root ganglion; End-to-side nerve coaptation; Laminin; NGF; Pain; Peripheral nerve; Peripherin; Sensory neurons; TrkA; Western blot analysis2A NMDA receptor glycine site partial agonist, GLYX-13, simultaneously enhances LTP and reduces LTD at Schaffer collateral–CA1 synapses in hippocampusThis article is not included in your organization's subscription. However, you may be able to access this article under your organization's agreement with Elsevier.Xiao-lei Zhanga, John A. Sullivana, Joseph R. Moskalb and Patric K. Stantona, c, ,aDepartment of Cell Biology & Anatomy, New York Medical College, Basic Sciences Building, Room 217, Valhalla, NY 10595, USAbThe Falk Center for Molecular Therapeutics, Department of Biomedical Engineering, McCormickSchool of Engineering and Applied Sciences, Northwestern University, Evanston, IL 60201, USA cDepartment of Neurology, New York Medical College, Valhalla, NY 10595, USAReceived 13 June 2008; revised 18 July 2008; accepted 4 August 2008. Available online 29 August 2008.Abstract：N-methyl-d-aspartate glutamate receptors (NMDARs) are a key route for Ca2+ influx into neurons important to both activity-dependent synaptic plasticity and, when uncontrolled, triggering events that cause neuronal degeneration and death. Among regulatory binding sites on the NMDAR complex is a glycine binding site, distinct from the glutamate binding site, which must be co-activated for NMDAR channel opening. We developed a novel glycine site partial agonist, GLYX-13, which is both nootropic and neuroprotective in vivo. Here, we assessed the effects of GLYX-13 on long-term synaptic plasticity and NMDAR transmission at Schaffer collateral–CA1 synapses in hippocampal slices in vitro. GLYX-13 simultaneously enhanced the magnitude of long-term potentiation (LTP) of synaptic transmission, while reducing long-term depression (LTD). GLYX-13 reduced NMDA receptor-mediated synaptic currents in CA1 pyramidal neurons evoked by low frequency Schaffer collateral stimulation, but enhanced NMDAR currents during high frequency bursts of activity, and these actions were occluded by a saturating concentration of the glycine site agonist d-serine. Direct two-photon imaging of Schaffer collateral burst-evoked increases in [Ca2+] in individual dendritic spines revealed that GLYX-13 selectively enhanced burst-induced NMDAR-dependent spine Ca2+ influx. Examining the rate of MK-801 block of synaptic versus extrasynaptic NMDAR-gated channels revealed that GLYX-13 selectively enhanced activation of burst-driven extrasynaptic NMDARs, with an action that was blocked by the NR2B-selective NMDAR antagonist ifenprodil. Our data suggest that GLYX-13 may have unique therapeutic potential as a learning and memory enhancer because of its ability to simultaneously enhance LTP and suppress LTD.Keywords: Glutamate receptor; Learning; Memory; N-methyl-d-aspartate receptor; Partial agonist; Glycine; Synaptic plasticity3Isodomoic acids A and C exhibit low KA receptor affinity and reduced in vitro potency relative to domoic acid in region CA1 of rat hippocampusP.M. Sawanta, B.A. Wearea, P.T. Hollandb, A.I. Selwoodb, K.L. Kingc, C.M. Mikulskic, G.J. Doucettec, D.O. Mountfortb and D.S. Kerra, ,aDepartment of Pharmacology and Toxicology, University of Otago School of Medical Sciences, P.O. Box 913, Dunedin, New ZealandbBiotoxins Section, Cawthron Institute, Nelson, New ZealandcMarineBiotoxins Program, National Oceanic and Atmospheric Administration, Center for Coastal Environmental Health and Biomolecular Research, Charleston, SC, USAReceived 12 February 2007; revised 16 May 2007; accepted 29 May 2007. Available online 8 June 2007.Abstract：Several natural isomers of the seizurogenic neurotoxin domoic acid (DA) have been found to occur at up to mg/kg levels in shellfish. The aim of the current study was to assess the neurotoxic potency of isodomoic acids A and C (Iso-A and Iso-C), recently isolated from commercial shellfish. Hippocampal slices were obtained from young adult rats and maintained in a tissue recordingchamber. Synaptically evoked population spikes were recorded in region CA1 before and after exposure to DA or its isomers. Both Iso-A and Iso-C produced transient neuronal hyperexcitability followed by a dose-dependent suppression of population spikes, but were, respectively, 4- and 20-fold less potent than DA (spike area: EC50 DA=237 nM; Iso-A=939 nM; Iso-C=4.6 μM). In the hippocampus, DA preconditioning induces tolerance to subsequent DA toxicity. However, in the present study neither Iso-A nor Iso-C were effective as preconditioning agents. Competitive binding studies using homomeric GluR6 kainate (kainic acid, KA) receptors showed the affinity of Iso-A to be 40-fold lower than DA (Ki DA=3.35 nM; Iso-A=130 nM). Together with earlier work showing Iso-C affinity at GluR6 receptors to be 240-fold lower than DA, our results suggest that neuroexcitatory effects of Iso-A in CA1 may involve both α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and KA receptors, while Iso-C likely involves the activation of AMPA receptors alone.Keywords: Domoic acid; Isodomoic acid A; Isodomoic acid C; KA receptor affinity; Hippocampal slice; In vitro preconditioning6、全文摘录选择一篇：一、篇名Isodomoic acids A and C exhibit low KA receptor affinityand reduced in vitro potency relative to domoic acid in regionCA1 of rat hippocampus二、著者P.M. Sawanta, B.A. Wearea, P.T. Hollandb, A.I. Selwoodb, K.L. Kingc,C.M. Mikulskic, G.J. Doucettec,D.O. Mountfortb, D.S. Kerra,三、著者机构aDepartment of Pharmacology and Toxicology, University of Otago School of Medical Sciences, P.O. Box 913, Dunedin, New ZealandbBiotoxins Section, Cawthron Institute, Nelson, New ZealandcMarineBiotoxins Program, National Oceanic and Atmospheric Administration, Center for Coastal Environmental Health and BiomolecularResearch, Charleston, SC, USAReceived 12 February 2007; received in revised form 16 May 2007; accepted 29 May 2007 Available online 8 June 2007四、文摘AbstractSeveral natural isomers of the seizurogenic neurotoxin domoic acid (DA) have been found to occur at up to mg/kg levels inshellfish. The aim of the current study was to assess the neurotoxic potency of isodomoic acids A and C (Iso-A and Iso-C),recently isolated from commercial shellfish. Hippocampal slices were obtained from young adult rats and maintained in a tissuerecording chamber. Synaptically evoked population spikes were recorded in region CA1 before and after exposure to DA or itsisomers. Both Iso-A and Iso-C produced transient neuronal hyperexcitability followed by a dose-dependent suppression ofpopulation spikes, but were, respectively, 4- and 20-fold less potent than DA (spike area: EC50 DA ¼ 237nM; Iso-A ¼ 939nM;Iso-C ¼ 4.6 mM). In the hippocampus, DA preconditioning induces tolerance to subsequent DA toxicity. However, in thepresent study neither Iso-A nor Iso-C were effective as preconditioning agents. Competitivebinding studies using homomericGluR6 kainate (kainic acid, KA) receptors showed the affinity of Iso-A to be 40-fold lower than DA (Ki DA ¼ 3.35nM; Iso-A ¼ 130 nM). Together with earlier work showing Iso-C affinity at GluR6 receptors to be 240-fold lower than DA, our resultssuggest that neuroexcitatory effects of Iso-A in CA1 may involve both a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate(AMPA) and KA receptors, while Iso-C likely involves the activation of AMPA receptors alone.r 2007 Elsevier Ltd. All rights reserved五、关键词Keywords: Domoic acid; Isodomoic acid A; Isodomoic acid C; KA receptor affinity; Hippocampal slice; In vitro preconditioning六、正文1. Introduction and objectives （首段）Domoic acid (DA) is a potent agonist of a-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) and kainic acid (KA)-sensitive ionotropicglutamate receptors (Lerma et al., 1993; Tasker et al., 1996; Larm et al., 1997; HampsonandManolo, 1998; Crawford et al., 2000; Sari and Kerr,2001; Jakobsen et al., 2002; Qiu and Curra´ s-Collazo, 2006; Qiu et al., 2006) and has been identified as a causative agent in cases of animal andhuman poisoning (Perl et al., 1990; Teitelbuamet al., 1990; Lefebvre et al., 1999; Scholin et al.,2000; Gulland et al., 2002). Acutely, activation ofAMPA/KA receptors by DA producesneuronaldepolarization, hyperexcitability and severe generalizedmotor seizures, which are particularly robust inaged animals (Hesp et al., 2004a). In addition, DAcan produce substantial excitotoxic lesions of thehippocampus and related limbic circuits, and hasbeen associated with lasting neurological deficitsincluding chronic epileptiform activity and amnesiain humans (Perl et al., 1990; Cendes et al., 1995).（末段）Supported by the NZ Foundation for Research,Science and Technology as a subcontract to the Cawthron Institute, PGSF Contract CAW X0201.We are grateful to Dr. Fran Wolber and Linley Fray, Institute of Food, Nutrition and HumanHealth, Massey University, New Zealand, for their help and the use of their facilities during thedevelopment of the affinity-binding assay for domoic acid.七、参考文献References[1] Campbell, A.V., McKinnon, K.L., Whitehead, R.F., Skrabal,S.A., Kieber, R.J., Wright, J.L.C., 2004. Transformation andphotodegradation of domoic acid in seawater. In: Steidinger,K.A., Landsberg, J.H., Tomas, C.R., Vargo, G.A. (Eds.),Harmful Algae 2002. Florida Fish and Wildlife ConservationCommission, Florida Institute of Oceanography, and IntergovernmentalOceanographic Commission of UNESCO,Paris, pp. 150–152[2]Cendes, F., Andermann, F., Carpenter, S., Zatorre, R.J.,Cashman, N.R., 1995. Temporal lobe epilepsy caused bydomoic acid intoxication: evidence for glutamate receptormediatedexcitotoxicity in humans. Ann. Neurol. 37,123–126[3]Clayden, J., Read, B., Hebditch, K.R., 2005. Chemistry ofdomoic acid, isodomoic acids, and their analogues. Tetrahedron 61, 5713–5724······。