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        Breeding for Heat Tolerance Rice Based on Marker-Assisted Backcrosing in Vietnam

        Nguyen Thi Lang,Pham Thi Thu Ha,Pham Cong Tru,Tran Bao Toan,Bui Chi Buu,조영찬 한국육종학회 2015 Plant Breeding and Biotechnology Vol.3 No.3

        A total of six markers RM3586 and RM160 on chromosome 3 and RM3735, RM3471, RM3687 and RM3536 on chromosome 4 were used to select promising lines in backcrossing populations for heat tolerance at flowering stage in rice. Fifty lines selected in BC3F2, BC4F1, and BC4F2 and parents were planted in 2013, and 2014 dry seasons at the CLRRI field under natural heat stress and greenhouse to evaluate heat tolerance at the reproductive period. Heat tolerance scoring under field condition was based on percentage of unfilled grains. All selected lines exhibited their homozygous alleles with two heat tolerance germplasm N22 or Dular in QTL loci. Twelve lines harboring homozygous alleles to QTL loci RM3586 on chromosome 3 and RM3735 on chromosome 4, respectively were selected and evaluated to agronomic traits and yield potential. Four lines BC4-1-10-1 from OM5930/N22//4 *OM5930, BC4-5-8 from OM5930/Dular//4*OM5930, BC4-5-9-4 from AS996/N22//4*AS996, and BC4-6-3 from AS996/Dular//4 *AS996, respectively were finally selected to would be for regional adaptable test in Central Coast of Vietnam under heat stress condition to release to rice farmers.

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        Corticotropin-releasing Factor (CRF) and Urocortin Promote the Survival of Cultured Cerebellar GABAergic Neurons Through the Type 1 CRF Receptor

        Jae Sun Choi,Thao Thi Hien Pham,Yoon Jin Jang,Bao Chi Bui,이봉희,주경민,Choong Ik Cha,이경훈 대한의학회 2006 Journal of Korean medical science Vol.21 No.3

        Corticotropin releasing factor (CRF) is known to be involved in the stress response and in some degenerative brain disorders. In addition, CRF has a role as a neuro-modulator in adult cerebellar circuits. Data from developmental studies suggest a putative role for CRF as a trophic factor during cerebellar development. In this study, we investigated the trophic role for CRF family of peptides by culturing cerebellar neurons in the presence of CRF, urocortin or urocortin II. Primary cell cultures of cerebella from embryonic day 18 mice were established, and cells were treated for either 1, 5 or 9 days with Basal Medium Eagles complete medium alone or com-plete medium with 1 M CRF, urocortin, or urocortin II. The number of GABA-pos-itive neurons in each treatment condition was counted at each culture age for moni-toring the changes in neuronal survival. Treatment with 1 M CRF or 1 M urocortin increased the survival of GABAergic neurons at 6 days in vitro and 10 days in vitro, and this survival promoting effect was abolished by treatment with astressin in the presence of those peptides. Based on these data, we suggest that CRF or urocortin has a trophic role promoting the survival of cerebellar GABAergic neurons in cul-tures.

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        Cellular localization of the full-length isoform of the type 2 corticotropin releasing factor receptor in the postnatal mouse cerebellar cortex

        Lee, Kyung-Hoon,Bishop, Georgia A.,Tian, Jin Bin,Jang, Yoon-Jin,Bui, Bao Chi,Nguyen, Truong Le Xuan,Ahn, Jee-Yin,King, James S. Liss 2007 Journal of neuroscience research Vol.85 No.9

        <P>Corticotropin releasing factor (CRF) and its cognate receptors, defined as Type 1 and Type 2 have been localized within the cerebellum. The Type 2 CRF receptor (CRF-R2) is known to have both a full length (CRF-R2α) and a truncated (CRF-R2α-tr) isoform. A recent study documented CRF-R2α primarily in Bergann glia and astrocytes, as well as in populations of Purkinje cells in the adult cerebellum. The goal of the present study is to determine if CRF-R2α is present in the postnatal cerebellum, and if so to describe its cellular distribution. RT-PCR data showed that CRF-R2α is expressed in the mouse cerebellum from birth through postnatal day 21. Between birth and P14, CRF-R2α-immunoreactivity was localized within the somata of Purkinje cells, and migrating GABAergic interneurons. GFAP-immunoreactive astrocytes, including Bergmann glia, also expressed CRF-R2α-immunoreactivity from P3-P14. There is a change, however, in CRF-R2α immunolabeling within neurons as the cerebellum matures. Compared to its expression in the adult cerebellum, Purkinje cells, and GABAergic interneurons showed more extensive CRF-R2α immunolabeling during early postnatal development. We postulate that CRF-R2α could be involved in developmental events related to the survival and differentiation of Purkinje cells and GABAergic neurons, whereas in the adult, this isoform of the CRF receptor family is likely involved in modulating Bergmann glia that have been shown to play a role in regulating the synaptic environment around Purkinje neurons. © 2007 Wiley-Liss, Inc.</P>

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        SCN1A Gene Mutation and Adaptive Functioning in 18 Vietnamese Children with Dravet Syndrome

        Thi Thu Hang Do,Diem My Vu,Thi Thuy Kieu Huynh,Thi Khanh Van Le,손은화,Thieu Mai Thao Le,Huu Hao Ha,Chi Bao Bui 대한신경과학회 2017 Journal of Clinical Neurology Vol.13 No.1

        Background and Purpose Dravet syndrome is a rare and severe type of epilepsy in infants. The heterogeneity in the overall intellectual disability that these patients suffer from has been attributed to differences in genetic background and epilepsy severity. Methods Eighteen Vietnamese children diagnosed with Dravet syndrome were included in this study. SCN1A variants were screened by direct sequencing and multiplex ligation-dependent probe amplification. Adaptive functioning was assessed in all patients using the Vietnamese version of the Vineland Adaptive Behavior Scales, and the results were analyzed relative to the SCN1A variants and epilepsy severity. Results We identified 13 pathogenic or likely pathogenic variants, including 6 that have not been reported previously. We found no correlations between the presence or type of SCN1A variants and the level of adaptive functioning impairment or severity of epilepsy. Only two of nine patients aged at least 5 years had an adaptive functioning score higher than 50. Both of these patients had a low frequency of convulsive seizures and no history of status epilepticus or prolonged seizures. The remaining seven had very low adaptive functioning scores (39 or less) despite the variability in the severity of their epilepsy confirming the involvement of factors other than the severity of epilepsy in determining the developmental outcome. Conclusions Our study expands the spectrum of known SCN1A variants and confirms the current understanding of the role of the genetic background and epilepsy severity in determining the developmental outcome of Dravet syndrome patients.

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