• PNF and Movement
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• v.5 no.1
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• pp.57-66
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• 2007

This review discusses the development of muscle receptors, in particular, that of muscle sensory neurons and monosynaptic stretch reflex circuit. The development of muscle sensory neurons and monosynaptic stretch reflex requires a series of steps including expression of neurotrophic transcriptional factors and their receptor. The monosynaptic stretch reflex circuit is unique neuronal circuit system, and highly precise synaptic connection systems. Thus, coordination of sensory-motor function in muscle receptors depend on the expression of distinct classes of molecular cues, and on the formation of selective synaptic connections between sensory-motor neurons and their target muscle. Recent neurotrophic and transcription factor expression studies have expanded our knowledge on how muscle sensory neuron is formed, and how sensory-motor system is developed.

• Journal of Neurogastroenterology and Motility
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• v.26 no.1
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• pp.106-116
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• 2020

Background/Aims Emerging evidence shows that the mechanism of irritable bowel syndrome (IBS) is associated with neurotrophic factors and tight junction proteins (TJPs). It is known that there are sex differences in the pathophysiology of IBS. The aim of the present study is to determine expression levels of neurotrophic factors, TJPs, and cytokines according to IBS subtype and sex. Methods From 59 IBS (33 IBS-constipation, 21 IBS-diarrhea, and 5 IBS-mixed) and 36 control patients, colonic mucosa mRNA expression levels of transient receptor potential vanilloid-1 (TRPV1), nerve growth factor (NGF), glial cell-derived neurotrophic factor (GDNF), and various TJPs were assessed by real-time polymerase chain reaction. Western blot was performed to determine levels of zonular occludens-1 (ZO-1). Serum levels of cytokines were measured by enzyme-linked immunosorbent assay. Results TRPV1, GDNF, and NGF mRNA levels were significantly increased in those with IBS-constipation compared to those in controls (all P < 0.05). However, they showed no significant difference between those with IBS-diarrhea and controls. Expression level of TRPV1 correlated with that of GDNF (r = 0.741, P < 0.001) and NGF (r = 0.935, P < 0.001). ZO-1 RNA expression levels were lower (P = 0.021) in female IBS-diarrhea than those in controls, although they showed no significant differences between male IBS-diarrhea and controls. Serum IL-1β levels in female IBS were significantly higher than those of male IBS, especially in IBS-constipation (P < 0.001). Conclusion Our results suggest that neurotrophic factors and IL-1β are closely related to IBS-constipation and that decrease of ZO-1 is an important factor in female with IBS-diarrhea.

• Proceedings of the Ginseng society Conference
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• 1998.06a
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• pp.21-30
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• 1998

Ginseng root has been considered to prevent neuronal degeneration associated with brain ischemia, but experimental proof in support of this speculation is limited. Moreover, few studies have compared the neuroprotective actions of ginseng ingredients with those of peptide growth factors and cytokines isf vivo. Using a gerbil forebrain ischemia model, we demonstrated that the oral administration of red ginseng powder before an ischemic insult prevents delayed neuronal death in the hippocampal CAI field and that a neuroprotective molecule within red ginseng powder is ginsenoside Rbl. The neurotrophic effect of ginsenoside Rbl, when examined in the gerbil ischemia model and in neuronal cultures was as potent as or more potent than the effects of epidermal growth factor, ciliary neurotrophic factor, erythropoietin, prosaposin, interleukin-6 and interleukin-3. Besides the protection of hippocampal CAI neurons against brain ischemia/repercussion injuries, ginsenoside Rbl was shown to prevent place navigation disability, cortical infarction and secondary thalamic degeneration in stroke-prone spontaneous hypertensive rats with permanent occlusion of the unilateral middle cerebral artery distal to the striate branches. These findings may validate the empirical use of ginseng root for the treatment of cerebrovascular diseases

• BMB Reports
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• v.44 no.6
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• pp.421-421
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• 2011

• Toxicological Research
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• v.24 no.4
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• pp.245-251
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• 2008

Dietary restriction (DR) is the most efficacious intervention for retarding the deleterious effects of aging. DR increases longevity, decreases the occurrence and severity of age-related diseases, and retards the physiological decline associated with aging. The beneficial effects of DR have been mostly studied in non-neuronal tissues. However, several studies have showed that DR attenuate neuronal loss after several different insults including exposure to kainate, ischemia, and MPTP. Moreover, administration of the non-metabolizable glucose analog 2-deoxy-D-glucose (2DG) could mimic the neuroprotective effect of DR in rodent, presumably by limiting glucose availability at the cellular level. Based on the studies of chemically induced DR, it has been proposed that the mechanism whereby DR and 2DG protect neurons is largely mediated by stress response proteins such as HSP70 and GRP78 which are increased in neurons of rats and mice fed a DR regimen. In addition, DR, as mild metabolic stress, could lead to the increased activity in neuronal circuits and thus induce expression of neurotrophic factors. Interestingly, such increased neuronal activities also enhance neurogenesis in the brains of adult rodents. In this review, we focus on what is known regarding molecular mechanisms of the protective role of DR in neurodegenerative diseases and aging process. Also, we propose that DR is a mild cellular stress that stimulates production of neurotrophic factors, which are major regulators of neuronal survival, as well as neurogenesis in adult brain.

• Journal of the Korean Applied Science and Technology
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• v.35 no.2
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• pp.412-422
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• 2018

The purpose of this study was to investigate effects of 12-weeks aerobic exercise and taekwondo exercise on brain wave activation and brain-derived neurotrophic factors in undergraduate male students. Twenty four male subjects participated in this study. They were separated into a Control group(CG; n=8), Aerobic training group (ATG; n=8) and Taekwondo training group(TTG; n=8). ATG and TTG participated in Aerobic exercise training and Taekwondo exercise training for 12 weeks, 50~80 minutes per day, 3 times a week at 60~80% HRR respectively. All data were analyzed by repeated measures two-way ANOVA. As a result, there were no significant differences in the body composition and brain activation in all groups. However BDNF increased significantly after 12 weeks in the aerobic training groups(ATG). It is suggest that 12 weeks of regular Taekwondo exercise training did not statistically affect brain activation and neurotrophic factors in undergraduate students.

• Journal of Korean Biological Nursing Science
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• v.4 no.1
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• pp.101-112
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• 2002

Peripheral nerve injury results in plastic changes in the dorsal ganglia (DRG) and spinal cord, and is often complicated with neuropathic pain. The mechanisms underlying these changes are not known, but these changes seem to be most likely related to the neurotrophic factors. This study investigated the effects of mechanical peripheral nerve injury on expression of brain-derived neurotrophic factor(BDNF) in the DRG and spinal cord in rats. 1) Bennett model and Chung model groups showed significantly increased percentage of small, medium and large BDNF-immunoreactive neurons in the ipsilateral $L_4$ DRG compared with those in the contralateral side at 1 and 2 weeks of the injury. 2) In the ipsilateral $L_5$ DRG of the Chung model, percentage of medium and large BDNF-immunoreactive neurons increased significantly at 1 week, whereas that of large BDNF-immunoreactive neurons decreased at 2 week when compared with those in the contralateral side. The intensity of immunoreactivity of each neuron was lower in the ipsilateral than in the contralateral DRG. 3) In the spinal cord, the Bennett and Chung model groups showed a markedly increased BDNF-immunoreactivity in axonal fibers of both superficial and deeper laminae. The present study demonstrates that peripheral nerve injury in neuropathic models altered the BDNF expression in the DRG and spinal cord. This may suggest important roles of BDNF in sensory abnormalities after nerve injury and in protecting the large-sized neurons in the damaged DRG.

• Korean Journal of Biological Psychiatry
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• v.12 no.2
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• pp.216-220
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• 2005

Background:Brain-derived neurotrophic factor(BDNF) genes are thought to be important factors in some personality traits. The goal of this study was to determine the role of these genes in personality traits. Method:The participants included 170 healthy adults with no history of psychiatric disorders and other physical illnesses for the last 6 months. All participants were tested by the Temperament and Character Inventory (TCI). BDNF Val64Met gene polymorphisms were analyzed with PCR(Polymerase Chain Reaction). Differences on TCI dimensions and sub-scales among groups were examined with ANOVA. Result:There was a significant correlation between BDNF Val64Met and Persistence(PS)(p=0.036) in female subjects, but none with the other TCI dimensions. A post-hoc comparison revealed significant a difference between Val/Val and Met/Met (p=0.031). Conclusion:Our study suggests that the BDNF Val64Met gene polymorphism is associated with persistence in Korean female subjects, but the small number of subjects limits generalization of our results. Further studies with a larger number of homogenous subjects are needed to confirm whether the BDNF gene is related to personality traits.

• Korean Journal of Biological Psychiatry
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• v.11 no.2
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• pp.104-109
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• 2004

Objectives:Abnormalities in neurotrophic factors that regulate neuronal development and synaptic plasticity are often implicated as some causes of schizophrenia. In previous studies, researchers reported that brain and serum BDNF levels underwent similar changes during maturation and aging processes in rats. They also found a positive correlation between serum and cortical BDNF levels. In this study, we investigated whether the serum levels of BDNF in Korean schizophrenic patients would be different from those of healthy controls. Methods:Using an ELISA kit, serum BDNF levels were assessed in schizophrenic group(N=49) and control group(N=50). Results:Serum BDNF levels in the schizophrenic group($36.29{\pm}19.78$ng/ml) were significantly higher than those in control group($22.4{\pm}14.4$ng/ml). The BDNF levels did not correlate with duration of treatment, age or daily dose of antipsychotics in patients with schizophrenia. Conclusions:This result suggests that schizophrenia is characterized by high serum BDNF levels and supports the hypothesis of neurotrophic factor involvement in psychotic disorder. Serum BDNF level is likely to be one of the possible biological markers for schizophrenia.

• Clinical and Experimental Reproductive Medicine
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• v.31 no.1
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• pp.19-27
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• 2004

Objective: This study was to examine the in vitro neural cell differentiation patterns of human embryonic stem (hES) cells following treatment of various neurotrophic factors [basic fibroblast growth factor (bFGF), retinoic acid (RA), brain derived neurotrophic factor (BDNF) and transforming growth factor (TGF)-$\alpha$], particulary in dopaminergic neuron formation. Methods: The hES cells were induced to differentiate by bFGF and RA. Group I) In bFGF induction method, embryoid bodies (EBs, for 4 days) derived from hES were plated onto gelatin dish, selected for 8 days in ITSFn medium and expanded at the presence of bFGF (10 ng/ml) for another 6 days followed by a final differentiation in N2 medium for 7, 14 and 21 days. Group II) For RA induction, EBs were exposed of RA ($10^{-6}M$) for 4 days and allowed to differentiate in N2 medium for 7, 14 and 21 days. Group III) To examine the effects of additional neurotrophic factors, bFGF or RA induced cells were exposed to either BDNF (10 ng/ml) or TGF-$\alpha$ (10 ng/ml) during the 21 days of final differentiation. Neuron differentiation and dopamine secretion were examined by indirect immunocytochemistry and HPLC, respectively. Results: The bFGF or RA treated hES cells were resulted in similar neural cell differentiation patterns at the terminal differentiation stage, specifically, 75% neurons and 11% glial cells. Additionally, treatment of hES cells with BDNF or TGF-$\alpha$ during the terminal differentiation stage led to significantly increased tyrosine hydroxylase (TH) expression of a dopaminergic neuron marker, compared to control (p<0.05). In contrast, no effect was observed on the rate of mature neuron (NF-200) or glutamic acid decarboxylase-positive neurons. Immunocytochemistry and HPLC analyses revealed the higher levels of TH expression (20.3%) and dopamine secretion (265.5 $\pm$ 62.8 pmol/mg) in bFGF and TGF-sequentially treated hES cells than those in $\alpha$ RA or BDNF treated hES cells. Conclusion: These results indicate that the generation of dopamine secretory neurons from in vitro differentiated hES cells can be improved by TGF-$\alpha$ addition in the bFGF induction protocol.