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      • 인삼 선발계통의 지역적응성 검정

        Bong Jae Seong,Sun Ick Kim,Ka Soon Lee,Moo Geun Jee,Su Dong Kim,A Reum Kwon,Hyun Ho Kim1,Young Chang Kim 한국약용작물학회 2017 한국약용작물학술대회 발표집 Vol.2017 No.05

        Background : For cultivation of varieties of ginseng, the pure line selection method, which is to select the best among those cultivated in farms for pedigree breeding, replicated yield trials and regional adaptation trials before registering as a new variety, is widely used. Although there are 25 registered varieties of ginseng in Korea, the quality of ginseng is declining together with the amount of harvest being decreased by 15 - 20% due to the heat injuries and diseases from the warming & abnormal climate. Thus, the needs for development of disaster-resistant varieties with better chances of surviving through high temperature, salts and disease are increasing. Therefore, this study is to cultivate disaster-resistant varieties among those selected for their disaster tolerance and salt tolerance through regional adaptation trials. Methods and Results : As a result of examining the growth characteristics of the selected 2 - 5 year old varieties used in the study, among the 5-year old crops, Goryeo 4 and Eumseong 5 showed superior growth in both above and below aerial parts, and among the 4-year old crops, Eumseong 11 and Cheonryang showed superior growth while the growth in the below aerial parts were satisfactory in the order of Cheonryang > Eumseong 10 > Eumseong 11 > Eumseong 9. Among the 3-year old crops, the most superior growth in both above and below aerial parts was observed in Eumseong 14 with the weight of the below aerial part, root diameter and taproot length at 13.8 g, 11.8 ㎝ and 6.2 ㎝ respectively. Among the 2-year old crops, Eumseong 10 showed the most superior growth in both above and below aerial parts. Conclusion : Based on the above results, Goryeo 4 and Eumseong 5 among the 5-year old crops, Eumseong 11 among the 4-year old crops, Eumseong 14 among the 3-year old crops and Eumseon 10 among the 2-year old crops showed the most superior growth among the selected varieties. The growth characteristics of both above and below aerial parts in each year will continuously be monitored.

      • KCI등재

        The Presence of Urinary Ketones according to Metabolic Status and Obesity

        Kim Bo-Reum,Seo Jeong Woo,Kim Sang Man,Kim Kyu-Nam,주남석 대한의학회 2020 Journal of Korean medical science Vol.35 No.31

        Background: Recently, new concepts about obesity and normal weight subtypes with metabolic conditions are rising and ketone bodies are emerging as a significant indicator of metabolic health. This study aimed to find a relationship between ketonuria and those subtypes. Methods: The data of 19,036 subjects were analyzed in this cross-sectional study (2013–2017 Korea National Health and Nutrition Examination Survey, KNHANES). Based on body mass index and adult treatment panel III with modification of waist circumference, individuals were categorized into 4 groups: metabolically healthy normal weight (MHNW), metabolically healthy obese (MHO), metabolically unhealthy normal weight (MUNW), and metabolically unhealthy obese (MUO). Individuals were divided into 2 groups, positive and negative ketonuria groups, and the metabolic parameters were compared. Results: The metabolic indicators of the positive ketonuria group showed better results than those of the negative ketonuria group and the MHNW group showed the highest proportion of positive ketonuria. The MHNW group showed higher urinary ketones than the MUO group (odds ratio [OR], 0.391; 95% confidence interval [CI], 0.254–0.601) in men. In women, OR of having ketonuria was 0.698 (95% CI, 0.486–1.002) in the MHO group and 0.467 (95% CI, 0.226–0.966) in the MUNW group compared to the MHNW group, respectively. Conclusion: Compared to the MHNW group, the MUO group showed lower presence of ketonuria in men, and tendency to have less ketonuria in women.

      • NEDD4L limits cAMP signaling through ubiquitination of CREB‐regulated transcription coactivator 3

        Kim, Yo‐,Han,Yoo, Hanju,Hong, A‐,Reum,Kwon, Minseo,Kang, Sang‐,Wook,Kim, Kyunggon,Song, Youngsup Federation of American Society for Experimental Bi 2018 The FASEB Journal Vol.32 No.7

        <P>The transcription factor cAMP-responsive element-binding protein (CREB) is involved in a variety of physiologic processes. Although its activity appears to be largely correlated with its phosphorylation status, cAMP-mediated dephosphorylation and the subsequent nuclear migration of the CREB-regulated transcription factors (CRTCs) are required to stimulate CREB transcriptional activity. Among the 3 identified mammalian homologs of CRTCs, CRTC3 has been shown to be expressed predominantly in adipose tissues in response to catecholamine signals that regulate lipid metabolism. Here, we show that prolonged cAMP signaling down-regulates CRTC3 in a proteasome-dependent manner and that neural precursor cell-expressed developmentally down-regulated gene 4-like (NEDD4L), a specific ubiquitin ligase for CRTC3, is responsible for this process. By recognizing the PY motif of CRTC3, NEDD4L interacts with CRTC3 and promotes its polyubiquitination. Interaction between NEDD4L and CRTC3 is further boosted by cAMP signaling, and this enhanced interaction appears to be dependent on the cAMP-mediated phosphorylation of NEDD4L at the Ser448 site. Furthermore, we show that food withdrawal stimulates NEDD4L phosphorylation in mice, which then show a decrease of adipose tissue CRTC3 protein levels. Together, these results suggest that NEDD4L plays a key role in the feedback regulation of cAMP signaling by limiting CRTC3 protein levels.Kim, Y.-H., Yoo, H., Hong, A.-R., Kwon, M., Kang, S.-W., Kim, K., Song, Y. NEDD4L limits cAMP signaling through ubiquitination of CREB-regulated transcription coactivator 3.</P>

      • Observation of Olefin/Paraffin Selectivity in Azo Compound and Its Application into a Metal-Organic Framework

        Kim, Seo-Yul,Yoon, Tae-Ung,Kang, Jo Hong,Kim, Ah-Reum,Kim, Tea-Hoon,Kim, Seung-Ik,Park, Wanje,Kim, Ki Chul,Bae, Youn-Sang American Chemical Society 2018 ACS APPLIED MATERIALS & INTERFACES Vol.10 No.32

        <P>Olefin/paraffin separation is an important and challenging issue because the two molecules have similar physicochemical properties. Although a couple of olefin adsorbents have been developed by introducing inorganic nanoparticles into metal-organic frameworks (MOFs), there has been no study on the development of an olefin adsorbent by introducing a certain organic functional group into a MOF. In this study, we posited that azo compounds could offer olefin/paraffin selectivity. We have revealed using first-principles calculations that the simplest aromatic azo compound (azobenzene, Azob) has an unusual propylene/propane selectivity due to special electrostatic interactions between Azob and propylene molecules. On the basis of this interesting discovery, we have synthesized a novel propylene adsorbent, MIL-101(Cr)_DAA, by grafting 4,4′-diaminoazobenzene (DAA) into open metal sites in a mesoporous MIL-101(Cr). Remarkably, MIL-101(Cr)_DAA exhibited enhanced propylene/propane selectivity as well as considerably higher propylene heat of adsorption compared to pristine MIL-101(Cr) while maintaining the high working capacity of MIL-101(Cr). This clearly indicates that azo compounds when introduced into MOFs can provide propylene selectivity. Moreover, MIL-101(Cr)_DAA showed good C<SUB>3</SUB>H<SUB>6</SUB>/C<SUB>3</SUB>H<SUB>8</SUB> separation and easy regeneration performances from packed-bed breakthrough experiments and retained its propylene adsorption capacity even after exposure to air for 12 h. As far as we know, this is the first study that improves the olefin selectivity of MOF by postsynthetically introducing an organic functional group.</P> [FIG OMISSION]</BR>

      • Facile loading of Cu(I) in MIL-100(Fe) through redox-active Fe(II) sites and remarkable propylene/propane separation performance

        Kim, Ah-Reum,Yoon, Tae-Ung,Kim, Eun-Jung,Yoon, Jung Woon,Kim, Seo-Yul,Yoon, Ji Woong,Hwang, Young Kyu,Chang, Jong-San,Bae, Youn-Sang Elsevier 2018 Chemical engineering journal Vol.331 No.-

        <P><B>Abstract</B></P> <P>A novel Cu(I) loading method, which includes the reduction of CuCl<SUB>2</SUB> to CuCl without an external reducing agent and high-temperature calcination, was developed using the redox properties of coordinatively unsaturated Fe(II) sites in MIL-100(Fe). The successful loading of Cu(I) ions and their redox-couple reactions are supported by various methods such as TEM/EDS, XPS, PXRD, and ICP-AES techniques, as well as N<SUB>2</SUB> adsorption isotherms at 77K. Compared to Cu loaded into isostructural MIL-100(Al) devoid of redox active sites, Cu(I)-loaded MIL-100(Fe) exhibits higher C<SUB>3</SUB>H<SUB>6</SUB>/C<SUB>3</SUB>H<SUB>8</SUB> selectivity and superior air stability. This indicates that the Fe(II) sites in MIL-100(Fe) act as antioxidants that protect the resultant Cu(I) species, as well as reducing agents for CuCl<SUB>2</SUB>. Remarkably, in the typical pressure-swing adsorption (PSA) range (1–5bar), the Cu(I)-loaded MIL-100(Fe) exhibits a large C<SUB>3</SUB>H<SUB>6</SUB> working capacity as well as very high C<SUB>3</SUB>H<SUB>6</SUB>/C<SUB>3</SUB>H<SUB>8</SUB> selectivities that are superior to those of the benchmark adsorbents, zeolite-13X and HKUST-1. Moreover, this material is easily regenerated under mild conditions and exhibits good separation performance under dynamic mixed-flow conditions. This facile method for loading Cu(I) can be applied to other adsorbents containing redox-active sites.</P> <P><B>Highlights</B></P> <P> <UL> <LI> A novel Cu(I) loading method was developed by utilizing the redox-active Fe(II) sites in MIL-100(Fe). </LI> <LI> Fe(II) sites in MIL-100(Fe) act as antioxidants that protect the resultant Cu(I) species. </LI> <LI> Cu(0.6)@MIL-100(Fe) is superior to benchmark adsorbents considering both C<SUB>3</SUB>H<SUB>6</SUB> selectivity and working capacity. </LI> <LI> Cu(0.6)@MIL-100(Fe) exhibits good separation and easy regeneration performance under mixed-flow conditions. </LI> </UL> </P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>

      • Acupuncture suppresses kainic acid-induced neuronal death and inflammatory events in mouse hippocampus

        Kim, Seung-Tae,Doo, Ah-Reum,Kim, Seung-Nam,Kim, Song-Yi,Kim, Yoon Young,Kim, Jang-Hyun,Lee, Hyejung,Yin, Chang Shik,Park, Hi-Joon Springer-Verlag 2012 JOURNAL OF PHYSIOLOGICAL SCIENCES Vol.62 No.5

        <P>The administration of kainic acid (KA) causes seizures and produces neurodegeneration in hippocampal CA3 pyramidal cells. The present study investigated a possible role of acupuncture in reducing hippocampal cell death and inflammatory events, using a mouse model of kainic acid-induced epilepsy. Male C57BL/6 mice received acupuncture treatments at acupoint HT8 or in the tail area bilaterally once a day for 2?days and again immediately after an intraperitoneal injection of KA (30?mg/kg). HT8 is located on the palmar surface of the forelimbs, between the fourth and fifth metacarpal bones. Twenty-four hours after the KA injection, neuronal cell survival, the activations of microglia and astrocytes, and mRNA expression of two proinflammatory cytokines, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), were measured in the hippocampus. Acupuncture stimulation at HT8, but not in the tail area, significantly reduced the KA-induced seizure, neuron death, microglial and astrocyte activations, and IL-1β mRNA expression in the hippocampus. The acupuncture stimulation also decreased the mRNA expression of TNF-α, but it was not significant. These results indicate that acupuncture at HT8 can inhibit hippocampal cell death and suppress KA-induced inflammatory events, suggesting a possible role for acupuncture in the treatment of epilepsy.</P>

      • Identifying <i>SYNE1</i> ataxia and extending the mutational spectrum in Korea

        Kim, Ji Sun,Kim, Ah Reum,Youn, Jinyoung,Lee, Chung,Kim, Nam-Soon,Park, Woong-Yang,Park, Jong Kyu,Kim, Nayoung K.D.,Cho, Jin Whan Elsevier 2019 Parkinsonism & related disorders Vol.58 No.-

        <P><B>Abstract</B></P> <P><B>Introduction</B></P> <P>Recent advances in next generation sequencing technologies have uncovered the genetic background of various diseases. The mutations in the <I>SYNE1</I> gene was previously identified as a potential cause of pure cerebellar ataxia. Although autosomal recessive ataxias are slightly more frequent than autosomal dominant forms worldwide, autosomal recessive forms are extremely rare in Korea. In this study, we aimed to identify <I>SYNE1-</I>associated ataxia by whole exome sequencing in a Korean sample, and to review the prevalence of <I>SYNE1</I> in non-French-Canadians.</P> <P><B>Methods</B></P> <P>Patients with suspected cerebellar ataxia who visited movement disorders clinic from March 2014 to December 2017 were clinically screened. After excluding cases with acquired causes and common genetic causes in Korea, including spinocerebellar ataxia and dentatorubral-pallidoluysian atrophy, 63 undiagnosed subjects were screened for <I>SYNE1</I> mutations by next generation sequencing methods.</P> <P><B>Results</B></P> <P>We identified four novel mutations (one splicing, one truncating, and two missense mutations) distributed throughout the <I>SYNE1</I> gene in two patients. The phenotype was mainly pure cerebellar ataxia in both cases. However, axonal neuropathy, mild frontal dysfunction, and autonomic dysfunction were also revealed. The age of disease onset was relatively late and the disease course was only mildly progressive.</P> <P><B>Conclusion</B></P> <P>Our results indicate that <I>SYNE1</I> mutations are not an uncommon cause of recessive ataxia with additional clinical features in the Korean population. The results of this study should alert neurologists to request <I>SYNE1</I> testing to aid the diagnosis of undetermined adult-onset ataxia in Korean patients.</P> <P><B>Highlights</B></P> <P> <UL> <LI> <I>SYNE1</I> mutation is not uncommon outside the French-Canadian founder population. </LI> <LI> We identified 4 novel mutations distributed throughout the <I>SYNE1</I> gene in 2 patients. </LI> <LI> Phenotype was mainly pure ataxia in Korean <I>SYNE1</I> ataxia. </LI> <LI> Axonal neuropathy and mild cognitive impairment was also shown in <I>SYNE1</I> ataxia. </LI> </UL> </P>

      • Differential disruption of autoinhibition and defect in assembly of cytoskeleton during cell division decide the fate of human <i>DIAPH1</i>-related cytoskeletopathy

        Kim, Bong Jik,Ueyama, Takehiko,Miyoshi, Takushi,Lee, Seungmin,Han, Jin Hee,Park, Hye-Rim,Kim, Ah Reum,Oh, Jayoung,Kim, Min Young,Kang, Yong Seok,Oh, Doo Yi,Yun, Jiwon,Hwang, Sang Mee,Kim, Nayoung K D BMJ Publishing Group Ltd 2019 Journal of medical genetics Vol.56 No.12

        <P><B>Background</B></P><P>Diaphanous-related formin 1 (DIA1), which assembles the unbranched actin microfilament and microtubule cytoskeleton, is encoded by <I>DIAPH1</I>. Constitutive activation by the disruption of autoinhibitory interactions between the N-terminal diaphanous inhibitory domain (DID) and C-terminal diaphanous autoregulatory domain (DAD) dysregulates DIA1, resulting in both hearing loss and blood cell abnormalities.</P><P><B>Methods and results</B></P><P>Here, we report the first constitutively active mutant in the DID (p.A265S) of humans with only hearing loss and not blood cell abnormality through whole exome sequencing. The previously reported DAD mutants and our DID mutant (p.A265S) shared the finding of diminished autoinhibitory interaction, abnormally upregulated actin polymerisation activity and increased localisations at the plasma membrane. However, the obvious defect in the DIA1-driven assembly of cytoskeleton ‘during cell division’ was only from the DAD mutants, not from p.A265S, which did not show any blood cell abnormality. We also evaluated the five DID mutants in the hydrophobic pocket since four of these five additional mutants were predicted to critically disrupt interaction between the DID and DAD. These additional pathogenic DID mutants revealed varying degrees of defect in the DIA1-driven cytoskeleton assembly, including nearly normal phenotype during cell division as well as obvious impaired autoinhibition, again coinciding with our key observation in DIA1 mutant (p.A265S) in the DID.</P><P><B>Conclusion</B></P><P>Here, we report the first mutant in the DID of humans with only hearing loss. The differential cell biological phenotypes of DIA1 during cell division appear to be potential determinants of the clinical severity of <I>DIAPH1-</I>related cytoskeletopathy in humans.</P>

      • SCISCIESCOPUS

        Unraveling of Enigmatic Hearing-Impaired <i>GJB2</i> Single Heterozygotes by Massive Parallel Sequencing: DFNB1 or Not?

        Kim, So Young,Kim, Ah Reum,Kim, Nayoung K. D.,Lee, Chung,Kim, Min Young,Jeon, Eun-Hee,Park, Woong-Yang,Choi, Byung Yoon,Xie., Maohua Williams & Wilkins Co 2016 Medicine Vol.95 No.14

        <▼1><P>Supplemental Digital Content is available in the text</P></▼1><▼2><P><B>Abstract</B></P><P>The molecular etiology of nonsyndromic sensorineural hearing loss (SNHL) in subjects with only one detectable autosomal recessive <I>GJB2</I> mutation is unclear. Here, we report <I>GJB2</I> single heterozygotes with various final genetic diagnoses and suggest appropriate diagnostic strategies. A total of 160 subjects with SNHL without phenotypic markers were screened for <I>GJB2</I> mutations. Single-nucleotide variants or structural variations within the DFNB1 locus or in other deafness genes were examined by Sanger sequencing, breakpoint PCR, and targeted exome sequencing (TES) of 129 deafness genes. We identified 27 subjects with two mutations and 10 subjects with only one detectable mutation in <I>GJB2.</I> The detection rate of the single <I>GJB2</I> mutation among the 160 SNHL subjects in the present study (6.25%) was higher than 2.58% in normal hearing controls in Korean. The DFNB1 was clearly excluded as a molecular etiology in four (40%) subjects: other recessive deafness genes (N = 3) accounted for SNHL and the causative gene for the other non-DFNB1 subject (N = 1) was not identified. The etiology of additional two subjects was potentially explained by digenic etiology (N = 2) of <I>GJB2</I> with <I>MITF</I> and <I>GJB3</I>, respectively. The contribution of the single <I>GJB2</I> mutation in the four remaining subjects is unclear. Comprehensive diagnostic testing including TES is prerequisite for understanding <I>GJB2</I> single heterozygotes.</P></▼2>

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