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Träfflista för sökning "WFRF:(Lu J.) srt2:(2000-2004)"

Sökning: WFRF:(Lu J.) > (2000-2004)

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1.
  • Lockwood, M, et al. (författare)
  • Coordinated Cluster and ground-based instrument observations of transient changes in the magnetopause boundary layer during an interval of predominantly northward IMF : relation to reconnection pulses and FTE signatures
  • 2001
  • Ingår i: Annales Geophysicae. - : Copernicus GmbH. - 0992-7689 .- 1432-0576. ; 19:10-12, s. 1613-1640
  • Forskningsöversikt (refereegranskat)abstract
    • We study a series of transient entries into the low-latitude boundary layer (LLBL) of all four Cluster spacecraft during an outbound pass through the mid-afternoon magnetopause ([X(GSM), Y(GSM), Z(GSM)] approximate to [2, 7, 9] R(E)). The events take place during an interval of northward IMF, as seen in the data from the ACE satellite and lagged by a propagation delay of 75 min that is well-defined by two separate studies: (1) the magnetospheric variations prior to the northward turning (Lockwood et al., 2001, this issue) and (2) the field clock angle seen by Cluster after it had emerged into the magnetosheath (Opgenoorth et al., 2001, this issue). With an additional lag of 16.5 min, the transient LLBL events cor-relate well with swings of the IMF clock angle (in GSM) to near 90degrees. Most of this additional lag is explained by ground-based observations, which reveal signatures of transient reconnection in the pre-noon sector that then take 10-15 min to propagate eastward to 15 MLT, where they are observed by Cluster. The eastward phase speed of these signatures agrees very well with the motion deduced by the cross-correlation of the signatures seen on the four Cluster spacecraft. The evidence that these events are reconnection pulses includes: transient erosion of the noon 630 nm (cusp/cleft) aurora to lower latitudes; transient and travelling enhancements of the flow into the polar cap, imaged by the AMIE technique; and poleward-moving events moving into the polar cap, seen by the EISCAT Svalbard Radar (ESR). A pass of the DMSP-F15 satellite reveals that the open field lines near noon have been opened for some time: the more recently opened field lines were found closer to dusk where the flow transient and the poleward-moving event intersected the satellite pass. The events at Cluster have ion and electron characteristics predicted and observed by Lockwood and Hapgood (1998) for a Flux Transfer Event (FTE), with allowance for magnetospheric ion reflection at Alfvenic disturbances in the magnetopause reconnection layer. Like FTEs, the events are about 1 R(E) in their direction of motion and show a rise in the magnetic field strength, but unlike FTEs, in general, they show no pressure excess in their core and hence, no characteristic bipolar signature in the boundary-normal component. However, most of the events were observed when the magnetic field was southward, i.e. on the edge of the interior magnetic cusp, or when the field was parallel to the magnetic equatorial plane. Only when the satellite begins to emerge from the exterior boundary (when the field was northward), do the events start to show a pressure excess in their core and the consequent bipolar signature. We identify the events as the first observations of FTEs at middle altitudes.
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2.
  • Twigger, S, et al. (författare)
  • Rat Genome Database : A comparative genomics platform for rat mouse and human.
  • 2001
  • Ingår i: Journal of Molecular Medicine. - : Springer. - 0946-2716 .- 1432-1440. ; , s. B30-
  • Konferensbidrag (refereegranskat)abstract
    • The Rat Genome Database (RGD) is a NIH funded project who’s stated mission is “to collect, consolidate, and integrate data generated from ongoing rat genetic and genomic research efforts and make these data widely available to the scientific community.” In a collaboration between the Medical College of Wisconsin, the Jackson Lab, the National Center for Biotechnology and Information and the Genetics Lundberg Laboratory, Gothenburg, Sweden, RGD has been created to meet these stated aims. The primary focus of RGD is to aid Rat researchers in their work studying the rat as a model organism for human disease. To support these studies we have integrated a large amount of rat genetic and genomic resources in RGD and these are constantly being expanded through ongoing literature curation. One of the major features of RGD version 1.1, released in January of this year, is incorporation of QTL data to facilitate physiological genomics studies relating disease with the genome. In addition, a dynamic sequence-based homology tool is in final testing which will enable Rat, Mouse and Human researchers to view mapped genes and sequences and their locations in the other two organisms. We hope to release this tool in the second quarter of 2001. This will facilitate the application of results in one species to experiments in another species. In collaboration with the Mouse Genome Database and NCBI, close links are being created between RGD and MGD, LocusLink and UniGene to increase access to each set of data. To support its other general functions RGD has a variety of tools available for the rat researcher, plus ones that are equally useful to researchers working in other organisms and a sampling of these tools will be presented. Thus RGD is not only a valuable resource for those working with the rat but also for researchers in other model organisms wishing to harness the existing genetic and physiological data available in the rat to complement their own work.
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  • Scherer, SW, et al. (författare)
  • Human chromosome 7: DNA sequence and biology
  • 2003
  • Ingår i: Science (New York, N.Y.). - : American Association for the Advancement of Science (AAAS). - 1095-9203 .- 0036-8075. ; 300:5620, s. 767-772
  • Tidskriftsartikel (refereegranskat)abstract
    • DNA sequence and annotation of the entire human chromosome 7, encompassing nearly 158 million nucleotides of DNA and 1917 gene structures, are presented. To generate a higher order description, additional structural features such as imprinted genes, fragile sites, and segmental duplications were integrated at the level of the DNA sequence with medical genetic data, including 440 chromosome rearrangement breakpoints associated with disease. This approach enabled the discovery of candidate genes for developmental diseases including autism.
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9.
  • Baeckström, Dan, 1956, et al. (författare)
  • Activation of the alpha2beta1 integrin prevents c-erbB2-induced scattering and apoptosis of human mammary epithelial cells in collagen.
  • 2000
  • Ingår i: Oncogene. - : Springer Science and Business Media LLC. - 0950-9232 .- 1476-5594. ; 19:40, s. 4592-603
  • Tidskriftsartikel (refereegranskat)abstract
    • Constitutive overexpression of c-erbB2 in the mammary epithelial cell line MTSV1-7 has been shown to result in epithelial-mesenchymal conversion, anchorage-independent growth and loss of organized morphogenesis in collagen. To elucidate the events leading to this drastic change, MTSV1-7 cells and its subclone HB2 (which shows a more strictly epithelial phenotype) were transfected with the hybrid trk-neu receptor consisting of the extracellular domain of the trkA nerve growth factor (NGF) receptor and the transmembrane and cytoplasmic domains of c-erbB2 (neu). In cells expressing this construct, c-erbB2 homodimerization can be mimicked by addition of NGF. In trk-neu transfectants of HB2 cells, modest expression led to increased cell proliferation upon NGF treatment. When clones with higher expression levels were grown in collagen, NGF instead induced cell scattering, diminished viability and dramatically increased apoptosis. Interestingly, both the dissociation of colonies and loss of cell viability could be completely reversed by treatment of the cells with antibodies that activate the adhesive capacity of the alpha2beta1 integrin. Long-term NGF treatment of high-expressing transfectants generated fibroblastic clones displaying a reduced expression of integrin alpha2 and E-cadherin, and extensive apoptosis in collagen. These results, which indicate that strong c-erbB2 signalling may lead to downregulation and/or inactivation of the alpha2beta1 integrin, promoting apoptosis in collagen, provide one possible explanation to the increased apoptosis frequently seen in early tumour development.
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