• Journal of Ginseng Research
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• v.31 no.1
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• pp.51-53
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• 2007

Ginseng shows protective and trophic effects in neurodegenerative diseases in experimental models, and showed cognitive improvement in normal population. To investigate the efficacy of ginseng in patients with Alzheimer's disease, patients, who met NINDS-ADRDA criteria for AD were studied Subjects were randomly assigned to ginseng group and control group, and ginseng group was treated with Korean white ginseng powder (4.5 g/day) for 12 weeks. Efficacy variables included changes in mini-mental status exam (MMSE) and cognitive subscales of Alzheimer's disease assessment scale (ADAS-cog) at 4 weeks and 12 weeks. Baseline MMSE and ADAS scores showed no difference between the two groups. Results showed that ginseng improved ADAS-cog compared to the control group at 12 weeks (p<0.05). MMSE was also increased by ginseng treatment compared to the control at 12 weeks (p<0.01). This study suggests the symptomatic efficacy of ginseng in patients with Alzheimer's disease.

• BMB Reports
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• v.41 no.2
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• pp.146-152
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• 2008

In the presence of NGF, PC12 cells extend neuronal processes, cease cell division, become electrically excitable, and undergo several biochemical changes that are detectable in developing sympathetic neurons. We investigated the expression pattern of the apoptosis-related genes at each stage of neuronal differentiation using a cDNA microarray containing 320 apoptosis-related rat genes. By comparing the expression patterns through time-series analysis, we identified candidate genes that appear to regulate neuronal differentiation. Among the candidate genes, HO2 was selected by real-time PCR and Western blot analysis. To identify the roles of selected genes in the stages of neuronal differentiation, transfection of HO2 siRNA in PC12 cells was performed. Down-regulation of HO2 expression causes a reduction in neuronal differentiation in PC12 cells. Our results suggest that the HO2 gene could be related to the regulation of neuronal differentiation levels.

• The Korean Publising Journal, Monthly
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• s.336
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• pp.12-12
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• 2003

• Nuclear industry
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• v.12 no.12 s.118
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• pp.37-40
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• 1992

• 한국전자현미경학회:학술대회논문집
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• 1997.05a
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• pp.12-12
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• 1997

• Vending industry
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• v.10 no.2
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• pp.12-12
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• 2010

• Journal of Korean Electronics
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• v.21 no.12
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• pp.98-100
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• 2001

• Monthly Duck's Village
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• s.246
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• pp.12-12
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• 2023

• Journal of Microbiology and Biotechnology
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• v.12 no.1
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• pp.106-113
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• 2002

One-hundred and twenty-four trimethoprim-resistant Shigella sonnei isolates extracted in Korea during the last two decades were investigated for their epidemiological relationship and mechanisms of resistance to trimethoprim. The S. sonnei isolates were distributed into two groups by three different epidemiological tools: biotyping, antibiogram, and pulsed-field gel electrophoresis. One group contained the isolates from the 1980s and the other group included the isolates from the 1990s. The geometric mean MICs of trimethoprim in S. sonnei isolates from the 1980s and 1990s were found to be $672.9{\mu}g/ml\;and\;>2,048{\mu}g/ml$, respectively. Trimethoprim resistance was associated with dfrA5, dfrA12, and dfrA13 genes in the isolates from the 1980s, dfrA1, dfrA5, and dfrA12 in the isolates from 1991, and dfrA1 and dfrA12 in the isolates from 1992 to 1999. The dfrA1 gene was located downstream of the intI2 gene in Tn7, which was located on chromosome. Some dfrA12 genes were found as gene cassettes in the class 1 integron. The dfrA5 and dfrA13 genes were located on conjugative plasmids. These results suggested that a clonal change occurred in S. sonnei isolates in Korea during the last two decades and that dfr genes located on different transposable genetic elements had gradually changed.

• The Journal of Korean Medicine
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• v.18 no.1
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• pp.385-398
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• 1997

The location and local arrangement of motor, sensory neurons within brain stem, nodose ganglia, spinal ganglia and sympathetic ganglia projecting to rat's kidney and meridian point BL 23, GB 25 were investigated by HRP immunohistochemical methods following injection of 5% WGA-HRP into left kidney and meridian point BL 23, GB 25. Following injection of WGA-HRP into left kidney, anterogradely labelled sensory neurons were founded within either nodose ganglia and spinal ganglia. The sensory neurons innervating rat's left kidney were observed within spinal ganglia $T_{7}{\sim}L_3$. Sympathetic motor neurons innervating rat's left kidney were labelled within left suprarenal ganglia, either celiac ganglia, superior mesenteric ganglia, and sympathetic chain ganglia $T_{1}{\sim}L_3$. Sympathetic chain ganglia were concentrated in $T_{12}{\sim}L_1$. The sensory neurons innervating rat's meridian point BL 23 were founded within spinal ganglia $T_{2}{\sim}L_2$. They were numerous in spinal in ganglia $T_{10}{\sim}T_{12}$. Sympathetic motor neurons innervating rat's meridian point BL 23 were observed in suprarenal ganglia and greater splanchnic trunk, sympathetic chain ganglia from $T_1$ to $L_3$. They were concentrated in $T_{12}{\sim}L_3$. The sensory neurons innervating rat's meridian point GB 25 were labelled within spinal ganglia $T_{6}{\sim}T_{13}$. They were numerous in from T10 to $T_{12}$. Sympathetic motor neurons innervating rat's meridian point GB 25 were labelled within greater splanchnic trunk and sympathetic chain ganglia $T_{12}{\sim}L_3$. They were concentrated in $T_{13}{\sim}L_1$. This results neuroanatomically imply that the location of rat's motor and sensory neurons innervating meridian point BL 23 and GB 25 were closely related that of innervating kidney.