• Journal of Web Engineering
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• v.14 no.19
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• pp.4103-4118
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• 2022

The physiological or dietary advantages of germinated grains have been the subject of numerous discussions over the past decade. Around 23 million tons of oats are consumed globally, making up a sizeable portion of the global grain market. Oat seedlings contain more protein, beta-glucan, free amino acids, and phenolic compounds than seeds. The progressive neurodegenerative disorder of Alzheimer's is accompanied by worsening memory and cognitive function. A key indicator of this disorder is the unusual buildup of amyloid-beta protein (or Aβ) in human brains. In this context, oat seedling extract (OSE) has been identified as a new therapeutic candidate for AD, due to its antioxidant activity and AD-specific mechanism of action. This study directly investigated how OSE affected AD and its impacts by examining the cognitive function and exploring the inflammatory response mechanism. The dried oat seedlings were grounded finely with a grinder, inserted with 50% fermented ethanol 10 times (w/v), and extracted by stirring for 10 h at 45 ℃. After filtering the extract by 0.22 um filter, some of it was used for UHPLC analysis. The results indicated that the treatment with OSE protects against Aβ25-35-induced cytotoxicity in BV2 cells. Tg-5Xfad AD mice had strong deposition of Aβ throughout their brains, while WT mice did not exhibit any such deposition within their brains. A drastic reduction was observed in terms of numbers, as well as the size, of Aβ plaques within Tg-5Xfad AD mice exposed to OSE. This study indicated OSE's neuroprotective impacts against neurodegeneration, synaptic dysfunction, and neuroinflammation induced by amyloid-beta. Our results suggest that OSE acts as a neuroprotective agent to combat AD-specific apoptotic cell death, neuroinflammation, amyloid-beta accumulation, as well as synaptic dysfunction in AD mice's brains. Furthermore, the study indicated that OSE treatment affects JNK/ERK/p38 MAPK signaling, with considerable inhibition in p-JNK, p-p38, and p-ERK levels seen in the brain of OSE-treated Tg-5Xfad AD mice.

• 대한핵의학회:학술대회논문집
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• 1995.05a
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• pp.222-222
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• 1995

• Proceedings of the Zoological Society Korea Conference
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• 1994.10a
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• pp.164.2-164
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• 1994

No Abstract, See Full Text

• Proceedings of the Zoological Society Korea Conference
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• 1994.10a
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• pp.164.1-164
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• 1994

No Abstract, See Full Text

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.151.2-152
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• 2000

• Proceedings of the Zoological Society Korea Conference
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• 2003.08a
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• pp.165.2-165
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• 2003

No Abstract, See Full Text

• Proceedings of the KSMRM Conference
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• 2001.11a
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• pp.112-112
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• 2001

Purpose： We developed the software for diffusion tensor imaging and evaluated its feasibility in norm brains. Method： Five normal volunteers, aged from 25 to 29 years, were examined on a 1.5 T MR system. the diffusion tensor pulse sequence used a SE-EPI with 6 diffusion gradie directions of (1, 1, 0), (-1, 1,0), (1, 0, 1), (-1, 0, 1), (0, 1, 1), (0, 1, -1) and also with no diffusion gradient. A b-factor of 500 sec/mm2 was used. Measurement parameter were as follows； TR/TE=10000 ms/99 ms, FOV=240 mm, matrix=128$\times$128, slice thickness/gap=6 mm/0 mm, bandwidth=91 kHz and the number of total slices=20. Four repeated axial diffusion images were averaged for diffusion tensor imaging. A total scan 11 of 4 min 30 sec was used. Six full diffusion tensor components of Dxx, Dyy, Dzz, Dxy, Dxz and Dyz were obtained using two-point linear regression model from 7 diffusion-weight images at each pixel and fractional anisotropy and lattice index images was estimated fr their eigenvectors and eigenvalues. Our program was written on a platform of IDL. W evaluated the qualities of fractional anisotropy and lattice index images of normal brains a knew whether our software for diffusion tensor imaging may be feasible.

• The Journal of Korean Society of Virology
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• v.28 no.2
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• pp.183-192
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• 1998

DNA methylation degree in the several murine brain and liver genes of different ages and after scrapie infection have been examined by using methylation-sensitive restriction endonuclease digestion. We found that the methylation of c-fos and c-myc in the brain and liver was increased during the late fetal to one month postnatal developmental periods. However, those of the SGP-2, $S100{\beta}$, APP950, PrP, and APLP1 genes were decreased at the same periods. The comparison of the DNA methylation patterns between scrapie infected brains and controls demonstrated there is no significant difference in methylation degree of scrapie-infected brains. These observations indicate that DNA methylation might be importantly related to the aging process. The scrapie-infected murine brain was not significantly developed more senescent than the same age-controls did.

• The Journal of Korean Medicine
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• v.24 no.2
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• pp.204-212
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• 2003

Current therapy for acute ischemic stroke is highly focused on neuroprotective agents, and many herbal medicines have been challenged for experimental models. The aim of this study is to investigate whether Angelicae gigantis Radix can protect nerve cells against ischemic neural damage of middle cerebral artery occlusion (MCAO) in rats' brains. Rats were treated with Angelicae gigantis Radix immediately after 2 hours of MCAO for 7 days. On the 7th day, the brains of the rats were sliced through the hippocampus and dyedby c-Fos immunohistochemistry stain and cresyl violet stain for microscopic examination. The number of viable neurons and c-Fos immunoreactive cells in CA1 regions was counted. MCAO caused significant decrease in density of neurons and c-Fos immunoreactive cells compared to those of sham-operated rats. Administration of Angelicae gigantis Radix significantly elevated MCAO-induced decrease in density of neurons and c-Fos immunoreactive cells. These results suggest that the neuroprotective effect of Angelicae gigantis Radix against focal cerebral ischemia is related to c-Fos gene expression. Thus, these findings indicate that Angelicae gigantis Radix can be used for treatment and prevention of cerebral ischemia.

• Biomolecules & Therapeutics
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• v.22 no.3
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• pp.232-238
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• 2014

Alzheimer's disease (AD) is the most common neurodegenerative disease without known ways to cure. A key neuropathologic manifestation of the disease is extracellular deposition of beta-amyloid peptide (Ab). Specific mechanisms underlying the development of the disease have not yet been fully understood. In this study, we investigated effects of 4-O-methylhonokiol on memory dysfunction in APP/PS1 double transgenic mice. 4-O-methylhonokiol (1 mg/kg for 3 month) significantly reduced deficit in learning and memory of the transgenic mice, as determined by the Morris water maze test and step-through passive avoidance test. Our biochemical analysis suggested that 4-O-methylhonokiol ameliorated $A{\beta}$ accumulation in the cortex and hippocampus via reduction in beta-site APP-cleaving enzyme 1 expression. In addition, 4-O-methylhonokiol attenuated lipid peroxidation and elevated glutathione peroxidase activity in the double transgenic mice brains. Thus, suppressive effects of 4-O-methylhonokiol on $A{\beta}$ generation and oxidative stress in the brains of transgenic mice may be responsible for the enhancement in cognitive function. These results suggest that the natural compound has potential to intervene memory deficit and progressive neurodegeneration in AD patients.