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  • 1
    In: Journal of Cognitive Neuroscience, MIT Press, Vol. 14, No. 6 ( 2002-08-15), p. 922-937
    Abstract: The aim of this study was to identify the neuroanatomical basis of the retrieval of people's names. Lesion data showed that patients with language-dominant temporal lobectomy had impairments in their ability to retrieve familiar and newly learned people's names, whereas patients with language-nondominant temporal lobectomy had difficulty retrieving newly learned people's names. Functional magnetic resonance imaging experiments revealed activations in the left temporal polar region during the retrieval of familiar and newly learned people's names, and in the right superior temporal and bilateral prefrontal cortices during the retrieval of newly learned information from face cues. These data provide new evidence that the left anterior temporal region is crucial for the retrieval of people's names irrespective of their familiarity and that the right superior temporal and bilateral prefrontal areas are crucial for the process of associating newly learned people's faces and names.
    Type of Medium: Online Resource
    ISSN: 0898-929X , 1530-8898
    Language: English
    Publisher: MIT Press
    Publication Date: 2002
    SSG: 5,2
    SSG: 7,11
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  • 2
    Online Resource
    Online Resource
    Proceedings of the National Academy of Sciences ; 2004
    In:  Proceedings of the National Academy of Sciences Vol. 101, No. 24 ( 2004-06-15), p. 8981-8986
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 101, No. 24 ( 2004-06-15), p. 8981-8986
    Abstract: IFN regulatory factors (IRFs) are a family of transcription factors that play an essential role in the homeostasis and function of immune systems. Recent studies indicated that IRF-8 is critical for the development of CD11b low CD8α + conventional dendritic cells (DCs) and plasmacytoid DCs. Here we show that IRF-4 is important for CD11b high CD8α – conventional DCs. The development of CD11b high DCs from bone marrow of IRF-4 –/– mice was severely impaired in two culture systems supplemented with either GM-CSF or Flt3-ligand. In the IRF-4 –/– spleen, the number of CD4 + CD8α – DCs, a major subset of CD11b high DCs, was severely reduced. IRF-4 and IRF-8 were expressed in the majority of CD11b high CD4 + CD8α – DCs and CD11b low CD8α + DCs, respectively, in a mutually exclusive manner. These results imply that IRF-4 and IRF-8 selectively play critical roles in the development of the DC subsets that express them.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
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    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2004
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    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 3
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 300, No. 5621 ( 2003-05-09), p. 958-961
    Abstract: We have performed an in situ test of the iron limitation hypothesis in the subarctic North Pacific Ocean. A single enrichment of dissolved iron caused a large increase in phytoplankton standing stock and decreases in macronutrients and dissolved carbon dioxide. The dominant phytoplankton species shifted after the iron addition from pennate diatoms to a centric diatom, Chaetoceros debilis , that showed a very high growth rate, 2.6 doublings per day. We conclude that the bioavailability of iron regulates the magnitude of the phytoplankton biomass and the key phytoplankton species that determine the biogeochemical sensitivity to iron supply of high-nitrate, low-chlorophyll waters.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
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    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2003
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    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 4
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 22, No. 1 ( 2002-01-01), p. 82-92
    Abstract: The physical interaction between the presynaptic vesicle release complex and the large cytoplasmic region linking domains II and III of N-type (Ca v 2.2) calcium channel α 1 B subunits is considered to be of fundamental importance for efficient neurotransmission. By PCR analysis of human brain cDNA libraries and IMR32 cell mRNA, we have isolated novel N-type channel variants, termed Ca v 2.2-Δ1 and Δ2, which lack large parts of the domain II–III linker region, including the synaptic protein interaction site. They appear to be widely expressed across the human CNS as indicated by RNase protection assays. When expressed in tsA-201 cells, both novel variants formed barium-permeable channels with voltage dependences and kinetics for activation that were similar to those observed with the full-length channel. All three channel types exhibited the hallmarks of prepulse facilitation, which interestingly occurred independently of G-protein βγ subunits. By contrast, the voltage dependence of steady-state inactivation seen with both Δ1 and Δ2 channels was shifted toward more depolarized potentials, and recovery from inactivation of Δ1 and Δ2 channels occurred more rapidly than that of the full-length channel. Moreover, the Δ1 channel was dramatically less sensitive to both ω-conotoxin MVIIA and GVIA than either the Δ2 variant or the full-length construct. Finally, the domain II–III linker region of neither variant was able to effectively bind syntaxin in vitro . These results suggest that the structure of the II–III linker region is an important determinant of N-type channel function and pharmacology. The lack of syntaxin binding hints at a unique physiological function of these channels.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2002
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 5
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 99, No. 24 ( 2002-11-26), p. 15794-15799
    Abstract: Plants have a unique transdifferentiation mechanism by which differentiated cells can initiate a new program of differentiation. We used a comprehensive analysis of gene expression in an in vitro zinnia ( Zinnia elegans L.) culture model system to gather fundamental information about the gene regulation underlying the transdifferentiation of plant cells. In this model, photosynthetic mesophyll cells isolated from zinnia leaves transdifferentiate into xylem cells in a morphogenic process characterized by features such as secondary-wall formation and programmed cell death. More than 8,000 zinnia cDNA clones were isolated from an equalized cDNA library prepared from cultured cells transdifferentiating into xylem cells. Microarray analysis using these cDNAs revealed several types of unique gene regulation patterns, including: the transient expression of a set of genes during cell isolation, presumably induced by wounding; a rapid reduction in the expression of photosynthetic genes and the rapid induction of protein synthesis-associated genes during the first stage; the preferential induction of auxin-related genes during the subsequent stage; and the transient induction of genes closely associated with particular morphogenetic events, including cell-wall formation and degradation and programmed cell death during the final stage. This analysis also revealed a number of previously uncharacterized genes encoding proteins that function in signal transduction, such as protein kinases and transcription factors that are expressed in a stage-specific manner. These findings provide new clues to the molecular mechanisms of both plant transdifferentiation and wood formation.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
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    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2002
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Proceedings of the National Academy of Sciences ; 2004
    In:  Proceedings of the National Academy of Sciences Vol. 101, No. 13 ( 2004-03-30), p. 4690-4694
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 101, No. 13 ( 2004-03-30), p. 4690-4694
    Abstract: Mutations in the WNK4 gene cause pseudohypoaldosteronism type II (PHAII), an autosomal-dominant disorder of hyperkalemia and hypertension. The target molecules of this putative kinase and the molecular mechanisms by which the mutations cause the phenotypes are currently unknown. Although recent reports found that expression of WNK4 in Xenopus oocytes causes inhibition of the thiazide-sensitive NaCl cotransporter and the renal K channel ROMK, there may be additional targets of WNK4. For example, an increase in paracellular chloride permeability has been postulated to be a mediator of PHAII pathogenesis, a possibility supported by the localization of WNK4 at tight junctions in vivo . To determine the validity of this hypothesis, we measured transepithelial Na and Cl permeability in Madin-Darby canine kidney II cells stably expressing wild-type or a pathogenic mutant of WNK4. We found that transepithelial paracellular Cl permeability was increased in cells expressing a disease-causing mutant WNK4 (D564A) but that Na permeability was decreased slightly. Furthermore, WNK4 bound and phosphorylated claudins 1-4, major tight-junction membrane proteins known to be involved in the regulation of paracellular ion permeability. The increases in phosphorylation of claudins were greater in cells expressing the mutant WNK4 than in cells expressing wild-type protein. These results clearly indicate that the pathogenic WNK4 mutant possesses a gain-of-function activity and that the claudins may be important molecular targets of WNK4 kinase. The increased paracellular “chloride shunt” caused by the mutant WNK4 could be the pathogenic mechanism of PHAII.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2004
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Proceedings of the National Academy of Sciences ; 2003
    In:  Proceedings of the National Academy of Sciences Vol. 100, No. 9 ( 2003-04-29), p. 5034-5039
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 100, No. 9 ( 2003-04-29), p. 5034-5039
    Abstract: Glucagon-like peptide (GLP) 1 is produced through posttranslational processing of proglucagon and acts as a regulator of various homeostatic events. Among its analogs, however, the function of GLP-1-(1–37), synthesized in small amounts in the pancreas, has been unclear. Here, we find that GLP-1-(1–37) induces insulin production in developing and, to a lesser extent, adult intestinal epithelial cells in vitro and in vivo , a process mediated by up-regulation of the Notch-related gene ngn3 and its downstream targets, which are involved in pancreatic endocrine differentiation. These cells became responsive to glucose challenge in vitro and reverse insulin-dependent diabetes after implantation into diabetic mice. Our findings suggest that efficient induction of insulin production in intestinal epithelial cells by GLP-1-(1–37) could represent a new therapeutic approach to diabetes mellitus.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2003
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Location Call Number Limitation Availability
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