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      • KCI등재

        통합심리치료의 인지분화훈련이 정신분열병 환자의 기초 인지기능에 미치는 영향

        이희상,현명호,조현상,이연희,김태용,장순아,노규식,정기립,이만홍,유계준 大韓神經精神醫學會 1998 신경정신의학 Vol.37 No.5

        연구목적 : 정신분열별 환자들을 대상으로 통합심리치료의 소프로그램인 인지분화훈련을 실시하여 실행기능, 개념형성능력, 언어능력 및 추론력에 대한 훈련이 보다 더 하위단계의 인지기능인 주의력, 기억력, 반응시간 등을 호전시킬 수 있는 지를 알아보고자 하였다. 연구방법 : DSM-IV상 정신분열병으로 진단된 24명의 입원환자를 무작위로 양분하여 한 군은 인지분화훈련군으로 다른 한 군은 대조군으로 나누었다. 훈련군은 4주동안 1주일에 3회(매회 60분간)로 총 12회의 통합심리치료의 인지분화훈련을 받았으며 대조군은 동일한 시간동안 정신건강교육을 받았다. 훈련전후에 훈련군과 대조군을 대상으로 개정판 Wechsler 기억검사로 주의집중력, 장·단기 기억력을 측정하였고 Vienna test system중 결정반응시간검사로 반응시간, 반응결정시간, 반응운동시간을 평가하였다. 연구결과 : 1) 주의집중력에서는 훈련군과 대조군사이에 집단간 효과, 집단내 효과 및 상호작용 효과가 없었다. 2) 단기기억력에서는 훈련군과 대조군사이에 집단내 효과는 있었으나(F(1,24)=10.46. p〈.05). 집단간 효과, 상호작용 효과는 없었다. 3) 장기기억력에서는 훈련군과 대조군사이에 집단내 효과는 있었으나(F(1,24)=15.09. p〈.05). 집단간 효과, 상호작용 효과는 없었다. 4) 반응시간에서는 상호작용 효과(F(1,24)=5.18, p〈.05)가 있었다. 5) 반응운동시간에서는 집단간 효과, 집단내 효과 및 상호작용 효과가 없었다. 6) 반응결정시간에서는 상호작용 효과(F(1.24)=6.00, p〈.05)가 있었다. 결 론 : 통합심리치료의 인지분화훈련은 정신분열병 환자에서 하위단계의 인지기능 중 반응시간(특히 반응결정시간)을 단축시키는 효과가 있었다. Objectives : The purpose of this study was to investigate the effects of cognitive differentiation training of Integrated Psychological Therapy(a training program of executive function, concept formation, language, and abstraction) on micro-level cognitive function such as attention, memory and reaction time in patients time in patients with schizophrenia. Methods : Twenty-four inpatients diagnosed as schizophrenia using DSM-IV were randomly assigned to 2 groups. The training group went through a total of 12 sessions of cognitive differentiation training for 4 weeks. The control group received psychoeducation program during the same period. Wechsler Memory Scale-Revised and Decision-Reaction Timer of Vienna Test System were administered to all patients, both before and after the training program. Results : 1) In the attention and concentration scores of Wechsler Memory Scale-Revised, between group, within group and interaction effects of training were not significant. 2) In the short-term memory scores of Wechsler Memory Scale-Revised, within group effect of training was significant(F(1,24)=10.46, p〈0.05), but the between group and interaction effects did not reach significance. 3) In the long-term memory scores of Wechsler Memory Scale-Revised, within group effect of training was significant(F(1,24)=15.09, p〈0.05), but the between group and interaction effects did not reach significance. 4) In the reaction time scores of Decision-Reaction Timer, interaction effect of training was significant(F(1,24)=5.18, p〈0.05). 5) In the motor time scores of Decision-Reaction Timer, between group, within group and interaction effects of training were not significant. 6) In the decision time scores of Decision-Reaction Timer, interaction effect of training was significant(F(1,24)=6.00, p〈0.05). Conclusion : Our findings suggest that cognitive differentiation training of Integrated Psycho-logical Therapy is partly effective on improving micro-level cognitive functions such as reaction time(especially, decision time) in patents with schizophrenia.

      • 초산모의 분만유형과 모성관련지식에 관한 연구

        김혜란,노진아,손은정,이명아,김증임 순천향대학교 교수학습개발센터 2004 Journal of Soonchunhyang Medical Science Vol.10 No.3

        Purpose: This study was to know primipara's general characteristics, delivery type, delivery characteristics, maternity related knowledge level, and relation of delivery type and maternity related knowledge level. Method: This is a survey. Subjects were sixty primiparas who had admitted to a pediatric outpatient clinic at general hospital in Seoul. Subject's age was ranged from 15 to 44 and it was lapsed 10 weeks after delivery of their first baby. Maternity related knowledge level was measured by "primipara's maternity related knowledge level". Data was nalyzed using frequency. percentage, mean, standard deviation, ANOVA, t-test by SPSS 11.0. Result: Relation of delivery type and maternity related knowledge in primipary did not show a statistically significant. But the relation of natural delivery and maternity related knowledge in primipara was a littlehig than that of caesarean section. Conclusion: There is no significant diference of maternity related knowledge between natural delivery and caesarean section. We suggest for randomized clinical trials with a larger sample size.

      • SCIEKCI등재

        Alpha-linolenic acid regulates amyloid precursor protein processing by mitogen-activated protein kinase pathway and neuronal apoptosis in amyloid beta-induced SH-SY5Y neuronal cells

        Lee, Ah Young,Lee, Myoung-Hee,Lee, Sanghyun,Cho, Eun Ju The Korean Society for Applied Biological Chemistr 2018 Applied Biological Chemistry (Appl Biol Chem) Vol.61 No.1

        Alpha-linolenic acid (ALA), which is an omega-3 fatty acid from plant oils, has been reported to have beneficial effects on human brain health. However, the protective effect of ALA and its mechanism of action against amyloid beta ($A{\beta}$)-mediated neurotoxicity, neuronal apoptosis and amyloid precursor protein (APP) processing are unclear. To investigate the neuroprotective effect of ALA, we treated $A{\beta}_{25-35}$-induced SH-SY5Y cells with ALA (1, 2.5, 5 and $25{\mu}g/mL$). In our results, $A{\beta}_{25-35}$-induced neuronal cell loss was observed, whereas ALA significantly increased the cell viability and decreased lactate dehydrogenase release. In addition, over-production of reactive oxygen species caused by $A{\beta}_{25-35}$ was attenuated by treatment with ALA, and these inhibitory activities were mediated by regulation of the mitogen-activated protein kinase signaling pathway. Furthermore, our data shows that $A{\beta}_{25-35}$ cause an increase in protein expression of APP-C-terminal fragment ${\beta}$, ${\beta}-site$ APP-cleaving enzyme and presenilin-1 in SH-SY5Y cells, while ALA significantly down-regulated the expression of those amyloidogenic APP processing-related proteins. In addition, we confirmed that ALA enhanced ${\alpha}$-secretase activity by up-regulating the protein levels of A distintegrin and metalloprotease 10 and tumor necrosis factor-${\alpha}$-converting enzyme, indicating that ALA could promote non-amyloidogenic signaling pathways. ALA also significantly attenuated $A{\beta}_{25-35}$-induced neuronal apoptosis by up-regulation of the Bcl-2/Bax ratio. These findings suggest that ALA may be a beneficial agent for promoting prevention of Alzheimer's disease.

      • SCIESCOPUSKCI등재

        The Neuro-Protective Effect of the Methanolic Extract of Perilla frutescens var. japonica and Rosmarinic Acid against H<sub>2</sub>O<sub>2</sub>-Induced Oxidative Stress in C6 Glial Cells

        Lee, Ah Young,Wu, Ting Ting,Hwang, Bo Ra,Lee, Jaemin,Lee, Myoung-Hee,Lee, Sanghyun,Cho, Eun Ju The Korean Society of Applied Pharmacology 2016 Biomolecules & Therapeutics(구 응용약물학회지) Vol.24 No.3

        Neurodegenerative diseases are often associated with oxidative damage in neuronal cells. This study was conducted to investigate the neuro-protective effect of methanolic (MeOH) extract of Perilla frutescens var. japonica and its one of the major compounds, rosmarinic acid, under oxidative stress induced by hydrogen peroxide ($H_2O_2$) in C6 glial cells. Exposure of C6 glial cells to $H_2O_2$ enhanced oxidative damage as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and thiobarbituric acid-reactive substance assays. The MeOH extract and rosmarinic acid prevented oxidative stress by increasing cell viability and inhibiting cellular lipid peroxidation. In addition, the MeOH extract and rosmarinic acid reduced $H_2O_2-indcued$ expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the transcriptional level. Moreover, iNOS and COX-2 protein expression was down-regulated in $H_2O_2-indcued$ C6 glial cells treated with the MeOH extract and rosmarinic acid. These findings suggest that P. frutescens var. japonica and rosmarinic acid could prevent the progression of neurodegenerative diseases through attenuation of neuronal oxidative stress.

      • SCIESCOPUSKCI등재

        Perilla frutescens var. japonica and rosmarinic acid improve amyloid-β<SUB>25-35</SUB> induced impairment of cognition and memory function

        Ah Young Lee,Bo Ra Hwang,Myoung Hee Lee,Sanghyun Lee,Eun Ju Cho 대한지역사회영양학회 2016 Nutrition Research and Practice Vol.10 No.3

        BACKGROUND/OBJECTIVES: The accumulation of amyloid-β (Aβ) in the brain is a hallmark of Alzheimer’s disease (AD) and plays a key role in cognitive dysfunction. Perilla frutescens var. japonica extract (PFE) and its major compound, rosmarinic acid (RA), have shown antioxidant and anti-inflammatory activities. We investigated whether administration of PFE and RA contributes to cognitive improvement in an Aβ25-35-injected mouse model. MATERIALS/METHODS: Male ICR mice were intracerebroventricularly injected with aggregated Aβ25-35 to induce AD. Aβ25-35-injected mice were fed PFE (50 mg/kg/day) or RA (0.25 mg/kg/day) for 14 days and examined for learning and memory ability through the T-maze, object recognition, and Morris water maze test. RESULTS: Our present study demonstrated that PFE and RA administration significantly enhanced cognition function and object discrimination, which were impaired by Aβ25-35, in the T-maze and object recognition tests, respectively. In addition, oral administration of PFE and RA decreased the time to reach the platform and increased the number of crossings over the removed platform when compared with the Aβ25-35-induced control group in the Morris water maze test. Furthermore, PFE and RA significantly decreased the levels of nitric oxide (NO) and malondialdehyde (MDA) in the brain, kidney, and liver. In particular, PFE markedly attenuated oxidative stress by inhibiting production of NO and MDA in the Aβ25-35-injected mouse brain. CONCLUSIONS: These results suggest that PFE and its active compound RA have beneficial effects on cognitive improvement and may help prevent AD induced by Aβ.

      • Age-dependent decreases in insulin-like growth factor-I and its receptor expressions in the gerbil olfactory bulb

        Lee, Tae-Kyeong,Chen, Bai Hui,Lee, Jae-Chul,Shin, Myoung Cheol,Cho, Jun Hwi,Lee, Hyang-Ah,Choi, Jung Hoon,Hwang, In Koo,Kang, Il Jun,Ahn, Ji Hyeon,Park, Joon Ha,Choi, Soo Young,Won, Moo-Ho SPANDIDOS PUBLICATIONS 2018 MOLECULAR MEDICINE REPORTS Vol.17 No.6

        <P>Insulin-like growth factor-I (IGF-I) is a multifunctional protein present in the central nervous system. A number of previous studies have revealed alterations in IGF-I and its receptor (IGF-IR) expression in various regions of the brain. However, there are few reports on age-dependent alterations in IGF-I and IGF-IR expressions in the olfactory bulb, which contains the secondary neurons of the olfactory system. The present study examined the cellular morphology in the olfactory bulb by using cresyl violet (CV) staining at postnatal month (PM) 3 in the young group, PM 6 in the adult group and PM 24 in the aged group in gerbils. In addition, detailed examinations were performed of the protein levels and immunoreactivities of IGF-I and IGF-IR in the olfactory bulb in each group. There were no significant changes in the cellular morphology between the three groups. The protein levels and immunoreactivities of the IGF-I and IGF-IR were the highest in the young group and they decreased with age. He protein levels and immunoreactivities of the IGF-I and IGF-IR were the lowest in the aged group. In brief, our results indicate that IGF-I and IGF-IR expressions are strong in young olfactory bulbs and significantly reduced in aged olfactory bulbs. In conclusion, subsequent decreases in IGF-I and IGF-IR expression with age may be associated with olfactory decline. Further studies are required to investigate the roles of IFG-I and IGF-IR in disorders of the olfactory system.</P>

      • Tumor necrosis factor receptor 2 is required for ischemic preconditioning-mediated neuroprotection in the hippocampus following a subsequent longer transient cerebral ischemia

        Lee, Jae-Chul,Park, Chan Woo,Shin, Myoung Cheol,Cho, Jun Hwi,Lee, Hyang-Ah,Kim, Young-Myeong,Park, Joon Ha,Ahn, Ji Hyeon,Cho, Jeong Hwi,Tae, Hyun-Jin,Hwang, In Koo,Lee, Tae-Kyeong,Won, Moo-Ho,Kang, Il Elsevier 2018 Neurochemistry International Vol.118 No.-

        <P><B>Abstract</B></P> <P>Tumor Necrosis Factor-α (TNF-α) is a proinflammatory cytokine implicated in neuronal damage in response to cerebral ischemia. Ischemic preconditioning (IPC) provides neuroprotection against a subsequent severer or longer transient ischemia by ischemic tolerance. Here, we focused on the role of TNF-α in IPC-mediated neuroprotection against neuronal death following a subsequent longer transient cerebral ischemia (TCI). Gerbils used in this study were randomly assigned to eight groups; sham group, TCI operated group, IPC plus (+) sham group, IPC + TCI operated group, sham + etanercept (an inhibitor of TNF-a) group, TCI + etanercept group, IPC + sham + etanercept group, and IPC + TCI + etanercept group. IPC was induced by a 2-min sublethal transient ischemia, which was operated 1 day prior to a longer (5-min) TCI. A significant death of neurons was found in the stratum pyramidale (SP) in the CA1 area (CA1) of the hippocampus 5 days after TCI; however, IPC protected SP neurons from TCI. We found that TNF-α immunoreactivity was significantly increased in CA1 pyramidal neurons in the TCI and IPC + TCI groups compared to the sham group. TNF-R1 expression in CA1 pyramidal neurons of the TCI group was also increased 1 and 2 days after TCI; however, in the IPC + TCI group, TNF-R1 expression was significantly lower than that in the TCI group. On the other hand, we did not detect TNF-R2 immunoreactivity in CA1 pyramidal neurons 1 and 2 days after TCI; meanwhile, in the IPC + TCI group, TNF-R2 expression was significantly increased compared to TNF-R2 expression at 1 and 2 days after TCI. In addition, in this group, TNF-R2 was newly expressed in pericytes, which are important cells in the blood brain barrier, from 1 day after TCI. When we treated etanercept to the IPC + TCI group, IPC-induced neuroprotection was significantly weakened. In brief, this study indicates that IPC confers neuroprotection against TCI by TNF-α signaling through TNF-R2 and suggests that the enhancement of TNF-R2 expression by IPC may be a legitimate strategy for a therapeutic intervention of TCI.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Ischemic preconditioning (IPC) protects CA1 pyramidal neurons from ischemic damage. </LI> <LI> IPC attenuates TNF-α and TNF-R1 expressions in ischemic CA1 pyramidal neurons. </LI> <LI> IPC increases TNF-R2 expressions in pericytes in CA1 area after ischemic insult. </LI> <LI> IPC-mediated neuroprotective effect is reversed by etanercept (an inhibitor of TNF-a) treatment. </LI> </UL> </P>

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