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  • English  (4)
  • 2005-2009  (4)
  • Linguistics  (4)
  • 1
    Online Resource
    Online Resource
    Proceedings of the National Academy of Sciences ; 2008
    In:  Proceedings of the National Academy of Sciences Vol. 105, No. 6 ( 2008-02-12), p. 2076-2081
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 105, No. 6 ( 2008-02-12), p. 2076-2081
    Abstract: Acquisition of additional genetic and/or epigenetic abnormalities other than the BCR / ABL fusion gene is believed to cause disease progression in chronic myeloid leukemia (CML) from chronic phase to blast crisis (BC). To gain insights into the underlying mechanisms of progression to BC, we screened DNA samples from CML patients during blast transformation for mutations in a number of transcription factor genes that are critical for myeloid–lymphoid development. In 85 cases of CML blast transformation, we identified two new mutations in the coding region of GATA-2 , a negative regulator of hematopoietic stem/progenitor cell differentiation. A L359V substitution within zinc finger domain (ZF) 2 of GATA-2 was found in eight cases with myelomonoblastic features, whereas an in-frame deletion of 6 aa (Δ341–346) spanning the C-terminal border of ZF1 was detected in one patient at myeloid BC with eosinophilia. Further studies indicated that L359V not only increased transactivation activity of GATA-2 but also enhanced its inhibitory effects on the activity of PU.1, a major regulator of myelopoiesis. Consistent with the myelomonoblastic features of CML transformation with the GATA-2 L359V mutant, transduction of the GATA-2 L359V mutant into HL-60 cells or BCR / ABL -harboring murine cells disturbed myelomonocytic differentiation/proliferation in vitro and in vivo , respectively. These data strongly suggest that GATA-2 mutations may play a role in acute myeloid transformation in a subset of CML patients.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2008
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 2
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 106, No. 9 ( 2009-03-03), p. 3342-3347
    Abstract: All- trans retinoic acid (ATRA)/arsenic trioxide (ATO) combination-based therapy has benefitted newly diagnosed acute promyelocytic leukemia (APL) in short-term studies, but the long-term efficacy and safety remained unclear. From April 2001, we have followed 85 patients administrated ATRA/ATO with a median follow-up of 70 months. Eighty patients (94.1%) entered complete remission (CR). Kaplan–Meier estimates of the 5-year event-free survival (EFS) and overall survival (OS) for all patients were 89.2% ± 3.4% and 91.7% ± 3.0%, respectively, and the 5-year relapse-free survival (RFS) and OS for patients who achieved CR ( n = 80) were 94.8% ± 2.5% and 97.4% ± 1.8%, respectively. Upon ATRA/ATO, prognosis was not influenced by initial white blood cell count, distinct PML-RAR α types, or FLT3 mutations. The toxicity profile was mild and reversible. No secondary carcinoma was observed, and 24 months after the last dose of ATRA/ATO, patients had urine arsenic concentrations well below the safety limit. These results demonstrate the high efficacy and minimal toxicity of ATRA/ATO treatment for newly diagnosed APL in long-term follow-up, suggesting a potential frontline therapy for de novo APL.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2009
    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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  • 3
    Online Resource
    Online Resource
    MIT Press ; 2008
    In:  Journal of Cognitive Neuroscience Vol. 20, No. 5 ( 2008-05-01), p. 816-827
    In: Journal of Cognitive Neuroscience, MIT Press, Vol. 20, No. 5 ( 2008-05-01), p. 816-827
    Abstract: To explore the temporal features and underlying brain structures of self-referential processing, participants were shown examples of Chinese handwriting, half of which were their own and the other half belonged to others, and asked to judge whether the handwriting was their own. In Experiment 1, the task was to categorize the handwriting by pressing the correct key as quickly as possible. In Experiment 2, after the participants recognized the stimuli, they were required to gaze at the handwriting for 3000 msec before making a response rather than responding immediately after stimulus onset. The results showed prominent differences in event-related potentials elicited by own and other handwriting conditions in the 200–500 msec and 1000–2000 msec time windows. Dipole analyses of the difference waves, own minus other, were conducted in both of these time windows. There were two dipoles in the 200–500 msec time window localized to the medial-temporal lobe and the anterior cingulate cortex (ACC), and MTL activation preceded ACC activation. Only one dipole at the posterior cingulate cortex was fitted to the 1000–2000 msec time window. These structures were activated sequentially in a temporal course, which provides evidence that the cortex middle structures potentially form a specific self-related processing unit, which is involved in processing various aspects of the self.
    Type of Medium: Online Resource
    ISSN: 0898-929X , 1530-8898
    Language: English
    Publisher: MIT Press
    Publication Date: 2008
    SSG: 5,2
    SSG: 7,11
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  • 4
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 28, No. 48 ( 2008-11-26), p. 12815-12819
    Abstract: Nectin-like 1 (Necl-1) is a neural-specific cell adhesion molecule that is expressed in both the CNS and PNS. Previous in vitro studies suggested that Necl-1 expression is essential for the axon-glial interaction and myelin sheath formation in the PNS. To investigate the in vivo role of Necl-1 in axonal myelination of the developing nervous system, we generated the Necl-1 mutant mice by replacing axons 2–5 with the LacZ reporter gene. Expression studies revealed that Necl-1 is exclusively expressed by neurons in the CNS. Disruption of Necl-1 resulted in developmental delay of axonal myelination in the optic nerve and spinal cord, suggesting that Necl-1 plays an important role in the initial axon-oligodendrocyte recognition and adhesion in CNS myelination.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2008
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
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