• Title/Summary/Keyword: Korean medicine complex treatment

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COMPARATIVE STUDY OF BEHAVIOR AND COGNITIVE FUNCTION BY ADMINISTRATION OF METHYLPHENIDATE AND IMIPRAMINE IN ATTENTION DEFICIT-HYPERACTIVITY DISORDER (Methylphenidate와 Imipramine투여에 따른 주의력 결핍${\cdot}$과잉운동장애 환아의 행동 및 인지기능 변화에 대한 연구)

  • Ahn, D.H;Hong, K.E;Oh, K.J;Shin, M.S;Yoo, B.C;Chung, K.M
    • Journal of the Korean Academy of Child and Adolescent Psychiatry
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    • v.3 no.1
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    • pp.26-45
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    • 1992
  • This study presents the behavioral and cognitive changes by administration of methylphenidate(MPH) and imipramine(IMI) for the treatment of attention-deficit hyperactivity disorder(ADHD) in $5_{1/2}{\sim}12$ years old children referred to child psychiatric clinics. Behavioral changes are assessed with parent's and teacher's ratings. Drug effects on attention. short-term memory, and impulsivity are evaluated with psychological tests in laboratory. The changes were assessed twice in a 8-week periods. The data were analyzed seperately for 15 subjects each drug using repeated measured analysis of variance(ANOVA). The findings indicates that behavioral and cognitive impairments are improved by both drugs, but impulsivity is not. And MPH is superior to IMI on the improvement of attentional problem ; especially the findings indicates important differences between simple task and complex. perceptual-search task. These data confirm the effectiveness of MPH for treatment of ADHD, also raise questions regarding assessment method of attention and impulsivity as fell as importance of impulsivity in ADHD.

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The Proteasome Inhibitor MG132 Sensitizes Lung Cancer Cells to TRAIL-induced Apoptosis by Inhibiting NF-κ Activation (폐암세포주에서 NFκ 활성 억제를 통한 Proteasome 억제제 MG132의 TRAIL-유도성 Apoptosis 감작 효과)

  • Seo, Pil Won;Lee, Kye Young
    • Tuberculosis and Respiratory Diseases
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    • v.65 no.6
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    • pp.476-486
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    • 2008
  • Background: TRAIL (TNF-related apoptosis inducing ligand) is a newly identified member of the TNF gene family which appears to have tumor-selective cytotoxicity due to the distinct decoy receptor system. TRAIL has direct access to caspase machinery and induces apoptosis regardless of p53 phenotype. Therefore, TRAIL has a therapeutic potential in lung cancer which frequently harbors p53 mutation in more than 50% of cases. However, it was shown that TRAIL also could activates $NF-{\kappa}B$ in some cell lines which might inhibit TRAIL-induced apoptosis. This study was designed to investigate whether TRAIL can activate $NF-{\kappa}B$ in lung cancer cell lines relatively resistant to TRAIL-induced apoptosis and inhibition of $NF-{\kappa}B$ activation using proteasome inhibitor MG132 which blocks $I{\kappa}B{\alpha}$ degradation can sensitize lung cancer cells to TRAIL-induced apoptosis. Methods: A549 (wt p53) and NCI-H1299 (null p53) lung cancer cells were used and cell viability test was done by MTT assay. Apoptosis was confirmed with Annexin V assay followed by FACS analysis. To study $NF-{\kappa}B$-dependent transcriptional activation, a luciferase reporter gene assay was used after making A549 and NCI-H1299 cells stably transfected with IgG ${\kappa}-NF-{\kappa}B$ luciferase construct. To investigate DNA binding of $NF-{\kappa}B$ activated by TRAIL, electromobility shift assay was used and supershift assay was done using anti-p65 antibody. Western blot was done for the study of $I{\kappa}B{\alpha}$ degradation. Results: A549 and NCI-H1299 cells were relatively resistant to TRAIL-induced apoptosis showing only 20~30% cell death even at the concentration 100 ng/ml, but MG132 ($3{\mu}M$) pre-treatment 1 hour prior to TRAIL addition greatly increased cell death more than 80%. Luciferase assay showed TRAIL-induced $NF-{\kappa}B$ transcriptional activity in both cell lines. Electromobility shift assay demonstrated DNA binding complex of $NF-{\kappa}B$ activated by TRAIL and supershift with p65 antibody. $I{\kappa}B{\alpha}$ degradation was proven by western blot. MG132 completely blocked both TRAIL-induced $NF-{\kappa}B$ dependent luciferase activity and DNA binding of $NF-{\kappa}B$. Conclusion: This results suggest that inhibition of $NF-{\kappa}B$ can be a potentially useful strategy to enhance TRAIL-induced tumor cell killing in lung cancer.

Proteome analysis of storage roots of two sweet potato cultivars with contrasting low temperature tolerance during storage (저온 저장 감수성 및 저항성 고구마 품종에서 저온 반응성 단백질체 연구)

  • Kim, Yun-Hee;Ji, Chang Yoon;Kim, Ho Soo;Chung, Jung-Sung;Choi, Sung Hwan;Kwak, Sang-Soo;Lee, Jeung Joo
    • Journal of Plant Biotechnology
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    • v.49 no.2
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    • pp.118-123
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    • 2022
  • To obtain information on the molecular mechanism underlying the low temperature tolerance of sweet potato [Ipomoea batatas (L.) Lam], the proteome expressed in the sweet potato cultivar Xushu 15-1 with high cold storage tolerance and in the cultivar Xushu 15-4 with low cold storage tolerance was analyzed using 2-D and MALDI-TOF/TOF analyses. Compared with the control (without cold treatment), four protein spots were newly expressed in Xushu 15-1. The expression level of one protein spot was higher in Xushu 15-4 than in Xushu 15-1. Spot 2, which was newly expressed in Xushu 15-1, was identified as sporamin. Assessment of the change in protein expression levels over 8 weeks in the storage roots of the two cultivars treated at 4℃ revealed no significant difference in the expression levels in Xushu 15-1 over time. However, in Xushu 15-4, the expression level of one protein spot increased, while those of four spots decreased. Of the proteins with reduced expression levels, spots 7 and 8 were identified as actin and spots 9 and 10 were identified as fructokinase-like proteins. The present results are expected to enhance the understanding of the complex mechanism underlying the low temperature tolerance of sweet potatoes during storage and can be used to identify candidate genes for the development of new varieties of sweet potatoes with improved low temperature tolerance during cold storage in the future.