• Journal of Genetic Medicine
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• v.18 no.2
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• pp.75-82
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• 2021

Speech and language functions are highly cognitive and human-specific features. The underlying causes of normal speech and language function are believed to reside in the human brain. Developmental persistent stuttering, a speech and language disorder, has been regarded as the most challenging disorder in determining genetic causes because of the high percentage of spontaneous recovery in stutters. This mysterious characteristic hinders speech pathologists from discriminating recovered stutters from completely normal individuals. Over the last several decades, several genetic approaches have been used to identify the genetic causes of stuttering, and remarkable progress has been made in genome-wide linkage analysis followed by gene sequencing. So far, four genes, namely GNPTAB, GNPTG, NAGPA, and AP4E1, are known to cause stuttering. Furthermore, thegeneration of mouse models of stuttering and morphometry analysis has created new ways for researchers to identify brain regions that participate in human speech function and to understand the neuropathology of stuttering. In this review, we aimed to investigate previous progress, challenges, and future perspectives in understanding the genetics and neuropathology underlying persistent developmental stuttering.

• BMB Reports
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• v.49 no.11
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• pp.629-634
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• 2016

Transmembrane and coiled-coil domain family 3 (TMCC3) has been reported to be expressed in the human brain; however, its function is still unknown. Here, we found that expression of TMCC3 is higher in human whole brain, testis and spinal cord compared to other human tissues. TMCC3 was expressed in mouse developing hind brain, lung, kidney and somites, with strongest expression in the mesenchyme of developing tongue. By expression of recombinant TMCC3 and its deletion mutants, we found that TMCC3 proteins self-assemble to oligomerize. Immunostaining and confocal microscopy data revealed that TMCC3 proteins are localized in endoplasmic reticulum through transmembrane domains. Based on immunoprecipitation and mass spectroscopy data, TMCC3 proteins associate with TMCC3 and 14-3-3 proteins. This supports the idea that TMCC3 proteins form oligomers and that 14-3-3 may be involved in the function of TMCC3. Taken together, these results may be useful for better understanding of uncharacterized function of TMCC3.

• Natural Product Sciences
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• v.26 no.3
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• pp.221-229
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• 2020

This study was undertaken to investigate the protective effect of rice bran oil (RBO) on amyloid β protein (Aβ) (25-35)-induced memory impairment and brain damage in an ICR mouse model. Memory impairment was produced by intracerebroventricular microinjection of 15 nmol Aβ (25-35) and assessed using the passive avoidance test. Treatment with RBO at 0.1, 0.5, or 1 mL/kg (p.o. daily for 8 days) protected against Aβ (25-35)-induced memory impairment. Furthermore, Aβ (25-35)-induced decreases in glutathione and increases in lipid peroxidation and cholinesterase activity in brain tissue were inhibited by RBO, and Aβ (25-35)-induced increases of phosphorylated mitogen-activated protein kinases (MAPKs) and inflammatory factors, and changes in the levels of apoptosis-related proteins were significantly inhibited by RBO. Furthermore, Aβ (25-35) suppressed the PI3K/Akt pathway and the phosphorylation of CREB, but increased phosphorylation of tau (p-tau) in mice brain; these effects were significantly inhibited by administration of RBO. These results suggest that RBO inhibits Aβ (25-35)-induced memory impairment by inducing anti-apoptotic and anti-inflammatory effects, promoting PI3K/Akt/CREB signaling, and thus, inhibiting p-tau formation.

• Korean Journal of Clinical Laboratory Science
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• v.47 no.1
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• pp.51-58
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• 2015

Ethanol has long been implicated in triggering apoptotic neurodegeneration. Alcohol also may indirectly harm the fetus by imparing the mother's physiology. We examined the effects of ethanol on immature brain of mice. Three-weeks-old female ICR strain mice daily intraperitoneally injected with ethanol at the concentration of 4 and 20% in saline for 0, 6, and 24 hours and 1 and 4 weeks. The mice were weighted and sacrificed, and the brains were ectomized for the present histological, immunohistochemical and TUNEL assays. Based on the histologic hematoxylin and eosin stain, immunohistochemical expression of glutamate receptor protein and neuronal cell adhesion molecule (NCAM) were evaluated. The cerebral cortex of the ethanol-treated group showed few typical symptoms of apoptosis such as chromosome condensation and disintegration of the cell bodies. TUNEL staining revealed DNA fragmentation in the 6 and 24 hours. This results demonstrated that acute ethanol administration causes neuronal cell death. I found that either glutamate receptor inhibition or activation could induce cerebellar degeneration as ethanol effect. Neuronal death also can be induced by excess activity of certain neurotransmitter, including glutamate. Neurons must establish cell-to-cell contact during growth and development in order to survive, migrate to their final destination, and develop appropriate connections with neighboring cell. Purkinje cell in cerebellar are especially vulnerable to the cell death and degeneration. After ethanol treatment in cerebellar, NCAM had decreased by 4 weeks. This result suggest that apoptosis seems to be involved in the slow elimination of neuron and cerebellar degeneration.

• Food Science and Biotechnology
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• v.14 no.6
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• pp.788-792
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• 2005

The effect of docosahexaenoic acid (DHA) on maze-learning ability in aged mice was investigated. Aged mice fed a diet deficient in n-3 fatty acid received a semi-purified diet of 0.5, 1 and 2% DHA-ethyl ester (DHA-EE) for 4 months. Maze-learning ability was assessed at 3 months after the start of the experiment. The time required to reach the maze exit and the number of times that a mouse strayed into blind alleys in the maze were measured in 3 trials conducted at 4-day intervals. The time was significantly less in the DHA-EE 0.5% and DHA-EE 2% groups than in the control group (p<0.05). The number of times mice strayed into blind alleys in the maze was significantly lower in the DHA-EE 2% group than in the control group (p<0.05). Mice fed DHA showed increased DHA and decreased level of arachidonic acid (AA) in the brain. These results suggest that the intake of a 2% DHA diet improves learning ability in aged mice, which is associated with a higher DHA content in the brain.

• YAKHAK HOEJI
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• v.35 no.6
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• pp.522-529
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• 1991

The purpose of this research is to evaluate effects of chloramphenicol, phenobarbital and progesterone on damage of DNA, RNA and protein which was induced by dimethylnitrosamine. $N,N-Di[^{14}C]$ methyl-nitrosamine (DMN) was used as a damaging agent and levels of DNA, RNA and protein damage in liver, brain and pancreas were compared with a control group. Pretreatment of mice with chloramphenicol increased protein damage in pancreas two times more than the control level. Liver RNA damage was increased up to 5.8 times and brain DNA damage up to 6.95 times by treatment of phenobarbital but brain RNA damage was decreased significantly down to 21% of the control group. The damage of liver RNA was significantly decreased by treatment of progesterone, although liver protein damage, pancreas RNA damage and pancreas protein damage were increased.

• Proceedings of the Korean Society of Medical Physics Conference
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• 2006.08a
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• pp.29-29
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• 2006

• Proceedings of the PSK Conference
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• 2000.04a
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• pp.106.2-107
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• 2000

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.256.1-256.1
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• 2003

As a part of our ongoing research to discover novel monamine oxidase (MAO) inhibitors of plant origin, we found that a MeOH extract from the whole plant of Cayratia japonica (Vitaceae) strongly inhibited the MAO activity in mouse brain. The EtOAc-soluble fraction was. therefore, subjected to the bioactivity-guided fractionations to isolate the active compounds. (omitted)

• Journal of Oriental Neuropsychiatry
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• v.10 no.2
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• pp.71-83
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• 1999

This study was to investigate the effects of SUNGSIMJIHWANGTANG(SSJHT) on the blood and brain tissues of aged rats. For the experiment, the aged rats were divided into three groups : Non treated group(NC), distilled water fed group(PC), SSJHT fed group(SSJHT). Each group was fed for ten days before administration of scopolamine. Then, we injected scopolamine intraperitoneally to PC and SSJHT group for 5 days. We observed the changes of their blood cell(WBC, RBC, platelet), blood serum(BUN, creatinine, glucose, uric acid), erythrocyte hemolysis, and the activities of cholinesterase and measured the amounts of malondialdehyde in the serum, catalase, and SOD in the brain tissue. The main results of this investigation are as follows. 1. In respect of the number of WBC, SSJHT group exhibited significant increase in comparison with PC. 2. In respect of the amount of creatinine and uric acid in the blood serum, SSJHT group exhibited significant decrease in comparison with PC. 3. In respect of erythrocyte hemolysis, SSJHT group exhibited significant suppression in comparison with PC. 4. In respect of the activity of cholinesterase in the serum, SSJHT group exhibited significant activation in comparison with PC. 5. In respect of the amounts of malondialdehyde in the serum, SSJHT group exhibited significant decrease in comparison with PC. 6. In respect of the activity of catalase in brain tissue, SSJHT group didn't exhibit significant change in comparison with PC. 7. In respect of the activity of SOD in brain tissue, SSJHT group exhibited significant activation in comparison with PC. As a result of this study, SSJHT is expected to have antiaging effect by suppressing the formation of free radicals, the accumulation of antioxidants and further study needs to be carried on about SSJHT.