• Molecules and Cells
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• v.24 no.3
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• pp.338-342
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• 2007

Spinocerebellar ataxias (SCAs) are caused by expansion of (CAG)n triplet repeats. These repeats occur as polymorphic forms in general population; however, beyond a threshold size they become pathogenic. The sizes and distributions of repeats at the SCA1, SCA2, SCA3, SCA7 and DRPLA loci were assessed by molecular analysis of 124 unrelated ataxia patients and 44 controls, and the association of larger normal (LN) alleles with disease prevalence was evaluated. Triplet repeat expansions in the disease range were detected in 8% (10/124) of the cases, with the majority having expansion at the SCA1 locus. Normal allele ranges in the cohort studied were similar to the Caucasian and North Indian populations but differed from the Korean and Japanese populations at various loci. The percentage of individuals with LN alleles at the SCA1 and SCA2 loci was higher than reported in Indians, Japanese and Caucasians. LN alleles showed a good correlation with the incidence of SCA1, indicating that SCA1 is the most prevalent ataxia in our population. The majority of cases with clinical symptoms of SCA could not be diagnosed by established CAG repeat criteria, suggesting that there may be an alternative basis for disease pathogenesis: (i) Repeats lower than the normal range may also result in abnormal phenotypes (ii) LN alleles at different loci in the same individual may contribute to symptoms (iii) Exogenous factors may play a role in triggering disease symptoms in individuals with LN alleles (iv) Triplet repeats may reach the disease range in the brain but not in the blood.

• Journal of Life Science
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• v.19 no.4
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• pp.449-456
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• 2009

Murine Neuro-2a (N2a) cells have been widely used for the investigation of neuronal differentiation, trophic interaction and neurotoxic effects of various compounds and their associated mechanisms. N2a cells have many genomic variations such as gains or losses in DNA copy number, similar to other neuroblastoma cells, and no systematic or high-resolution studies of their genome-wide chromosomal aberrations have been reported. Presently, we conducted a systematic genome-wide determination of chromosomal aberrations in N2a cells using a high-throughput, oligonucleotide array-based comparative genomic hybridization (oaCGH) technique. A hidden Markov Model was employed to assign each genomic oligonucleotide to a DNA copy number state: double loss, single loss, normal, gain, double gain and amplification. Unlike most neuroblastoma cells, Mycn amplification was not observed in N2a cells. In addition, these cells showed gain only in the neuron-derived neurotrophic factor (NF), while other neurotrophic factors such as glial line-derived NF and brain-derived NF presented normal copy numbers. Chromosomes 4, 8, 10, 11 and 15 displayed more than 1000 aberrational oligonucleotides, while chromosomes 3, 17, 18 and 19 displayed less than 20. The largest region of gain was located on chromosome 8 and its size was no less than 26.7 Mb (Chr8:8427841-35162415), while chromosome 4 had the longest region of single deletion, with a size of 15.1 Mb (Chr4:73265785-88374165).

• Journal of Acupuncture Research
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• v.29 no.2
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• pp.73-88
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• 2012

Objectives : The purpose of this study is to research the effects of acupuncturing $BL_{67}$ and $LI_1$ and determine the mechanism of action of acupuncturing $BL_{67}$ and $LI_1$ by measuring the changes of regional cerebral blood flow(rCBF) and mean arterial blood pressure(MABP) in normal rats and ischemic rats. Method : This study researched the effects of acupuncturing $BL_{67}$ and $LI_1$ on the change of rCBF and MABP. To determine the mechanism of action of acupuncturing $BL_{67}$ and $LI_1$, pretreatment with indomethacine and methylene blue was done. Result : 1. Acupuncturing $BL_{67}$ and $LI_1$ significantly increased rCBF and acupuncturing $BL_{67}$ and $LI_1$ induced increase of rCBF was significantly inhibited by pretreatment with indomethacin(1 mg/kg, i.p.), an inhibitor of cyclooxygenase, and methylene blue(10 ${\mu}g$/kg, i.p.), an inhibitor of guanylate cyclase. 2. Acupuncturing $BL_{67}$ and $LI_1$ decreased MABP and there was no significantly change of decrease of MABP on acupuncturing $BL_{67}$ and $LI_1$ by pretreatment with indomethacin and methylene blue. 3. These result suggested that acupuncturing $BL_{67}$ and $LI_1$ might significantly increase rCBF by dilating arterial diameter and mechanism of acupuncturing $BL_{67}$ and $LI_1$ might be mediated by cyclooxygenase and guanylate cyclase. 4. The rCBF was significantly and stably increased by acupuncturing $BL_{67}$ and $LI_1$ during the period of cerebral reperfusion in cerebral ischemic rats, which contrasted with the rapid and marked increase in the control group. Pretreatment with methylene blue significantly decreased rCBF by acupuncturing $BL_{67}$ and $LI_1$ during the period of ischemic state, increased rCBF during the period of cerebral reperfusion. These results suggested that the mechanism of acupuncturing $BL_{67}$ and $LI_1$ might be mediated by guanylate cyclase. Conclusion : Acupuncturing $BL_{67}$ and $LI_1$ can increase rCBF in normal state, and improve stability of rCBF in ischemic state. In addition, we suggested that mechanisms related with acupuncturing $BL_{67}$ and $LI_1$ was more involved in the guanylate cyclase pathway.

• Journal of Digital Convergence
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• v.14 no.10
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• pp.521-534
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• 2016

This study examined the neurophysiological mechanisms of exercise deprivation by investigating differences in emotion changes and EEG prefrontal asymmetry in relation with exercise. Twenty male undergraduate university students in the 23-27 age range, amateur marathon runners, were selected as the participants (n=20) and divided into one of two experimental conditions at random: (1) exercise deprivation group (n=10), and (2) non-exercise deprivation group (n=10). PANAS-X measurement and EEG measurement from F3 and F4 scalp sites were performed at pre-test, 3 days after exercise deprivation, and 5 days after exercise deprivation. Results revealed that participants of EDG significantly decreased a positive effect after exercise deprivation on EEG and self-reported measures, and showed an increased negative effect after exercise deprivation on self-reported measures. In contrast, participants of NEDG significantly increased positive feelings after exercise and showed a decreased negative effect after exercise on EEG and self-reported measures. Our results showed that exercise deprivation increasing negative emotion after exercise deprivation. The findings of this study suggest that EEG frontal brain asymmetry can be used as diagnosing method for exercise deprivation.

• The Journal of Internal Korean Medicine
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• v.23 no.2
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• pp.181-190
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• 2002

The water extract of Omija-tang(OMJT) has been traditionally used for treatment of ischemic heart and brain damage in oriental medicine. However, little is known about the mechanism by which the water extract of OMJT protects cells from such damage. Therefore, this study was conducted to investigate the protective mechanisms of OMJT on $H_2O_2$-induced toxicity in H9c2 cardiomyoblast cells. Treatment of $H_2O_2$ markedly induced death of H9c2 cardiomyoblast cells in a dose-dependent manner. The characteristics of $H_2O_2$-induced death of H9c2 showed apparent apoptotic features, such as DNA fragmentation. However, OMJT significantly reduced both $H_2O_2$-induced cell death and chromatin fragmentation. The decrease of Bcl-XL expression by $H_2O_2$ was inhibited by OMJT. In addition, the increase of Bcl-XS and Bax expression were also inhibited by OMJT. In particular, Fas expression, which is generally recognized as cell death inducing signal by Fas/FasL interaction, was markedly increased by $H_2O_2$ in a time-dependent manner, whereas this increase was completely prevented by OMJT. The combined treatment of OMJT and $H_2O_2$ in H9c2 cells also reduced activation of caspase-9 and caspase-3 like protease. Taken together, this study indicates that the protective effects of the water extract of OMJT against oxidative damage may be mediated by the modulation of BcI-XL/S and Bax expression by way of the regulation of mitochondrial membrane potential and caspase cascades.

• Korean Journal of Psychosomatic Medicine
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• v.9 no.1
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• pp.81-92
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• 2001

Stress has been linked to the pathophysiology and pathogenesis of various psychiatric illnesses. Over the past few years, our understanding of the brain and neuroendocrine systems that are linked to stress responses has increased enormously. This article reviews a series of animal and human studies to understand what are the central pathways by which stress is perceived, processed, and transduced into a neuroendocrine response. We focus on the limbic-hypothalamic-pituitary-adrenal(LHPA) axis and several neurotransmitter systems such as norepinephrine, CRF, serotonin, acetylcholine, and dopamine. LHPA stress circuit is a complex system with multiple control mechanisms which are altered in pathological states. CRF and related peptides in the central nervous system appear to enhance behavioral responses to stressors. Norepinephrine systems are also activated by stressors and cause the release of catecholamines from the autonomic nervous system. CRF-norepinephrine interaction makes a feed-forward system which may be important for an organism to mobilize not only the pituitary system but also the central nervous system, in response to environmental challenges. The interactions among several neurotransmitters and endocrine systems appear to play key roles in mediating various behavioral and psychological stress responses involving abnormal responses to stressors such as anxiety and affective disorders.

• The Korean Journal of Pharmacology
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• v.30 no.1
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• pp.101-109
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• 1994

Pharmacological characterization of GS 283, a tetrahydroisoquinoline derivative has been elucidated using rat thoracic aorta, guinea pig tenea coli and rabbit mesentery artery in vitro. GS 283 showed calcium antagonistic action in vascular smooth muscle, since high $K^+-induced$ contraction was concentration dependently inhibited. GS 283 also inhibited the contraction induced by ${\alpha}_1$ receptor activation. Vasodilating action of GS 283 was not modified by the propranolol, indicating that GS 283 has no ${\beta}$ receptor stimulatory action. Simultaneous measurement of intracellular calcium change and muscle tension indicated that the inhibitory effect of GS 283 was accompanied by the increase in tissue fluorescence. This increment was not due to fura 2 fluorescence but to endogenous pyridine nucleotide, suggesting that GS 283 has an effect to inhibit mitochondrial function. GS 283 had an inhibitory action on cyclic AMP and GMP-dependent phosphodiesterases from rat brain with Ki values of 2.5 and 6.7 mM. From these findings we concluded that GS 283 has multiple action such as the inhibition of cyclic nucleotide-dependent phosphodiesterases, blocking of calcium channel as well as inhibition of mitochondrial function which are responsible for vasodilatation.

• The Korean Journal of Pharmacology
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• v.30 no.3
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• pp.343-349
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• 1994

A number of neurological syndromes(e.g. tardive dyskinesia) are developed as a consequence of chronic treatment with neuroleptics or antipsychotic agents. Despite the long and succesful use of phenothiazine derivatives and related agents in the treatment of certain states of mental disease, the mechanisms of these drugs are still poorly understood. One current hypothesis from extensive reviews is that these compounds might significantly interfere with the cyclic nucleotide system in brain (Levin and Weiss, 1977; Nowicki et al., 1991; Haley et al., 1992). Nitric oxide (NO), one of an interesting messenger molecule and aberrant transmitter, is believed to play a important role in biological functions of cyclic nucleotides in nervous system. It has been reported that calcium-dependent NO synthesis in endothelial cytosol is mediated by calmodulin which is supposed to be tightly related to pharmacological actions of antipsychotic agents. In the present study, the effect of several antipsychotic agents on the activity of NO synthesis and formation of cyclic GMP were investigated. These agents inhibited both the formation of $[^3H]L-citrulline$ and that of $[^3H]cyclic$ GMP by concentration-dependent manner, and their inhibiting patterns are so similar to that of calmodulin antagonist.

• 한국HCI학회:학술대회논문집
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• 2008.02b
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• pp.651-655
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• 2008

It provides a three-dimensional virtual experience consisting of information presented to and perceived by the senses of the user. Recently, the advent of a virtual avatar, which mimics the appearance and behavior of humans, enable that the virtual reality (VR) can provide not only a virtual space but also a virtual society to be interact with a virtual avatar which represents humans. But, it is impossible that the user directly interacts with the VE in previous studies, though direct interactions occur in real social relationship. Therefore, In this study, we know that the cognition about a avatar when the user directly interacts with the virtual avatar in the VE. In order to investigate this purpose, we performed a fMRI study using VE that a avatar accept or reject the user's offer when the user offer his (or her) hand to a avatar. In result of questionnaire about the user's feeling by avatar's action, the user feels about avatar's acceptance action that the avatar acts positively and suitably. In contrast the user feels about avatar's rejective action that the avatar acts negatively and disapprovingly. In result of fMRI analysis, the primary visual area, the visual association area, the SMA, the premotor area, the cerebellum and etc, activate in common with the other avatar's acceptance action and rejective action. The results show that the subject recognizes not only avatars as social objects but also avatar's action as socially meaningful action. In other words, it is possible to transfer social context and emotion through avatar's action.

• Journal of Ginseng Research
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• v.28 no.2
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• pp.120-126
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• 2004

Glial cells such as astrocytes and microglial cells are the main source of proinflammatory cytokines and nitric oxide(NO) in the central nervous system, which exert neuroimmune and inflammatory functions and other various neurobiologic effects. Though Panax ginseng C.A. Meyer has been known to strengthen the body's defence mechanisms and also to maintain the homeostasis in the central nervous system, the effects of Panax ginseng on the production of immune and inflammatory mediators have not been studied well in the brain. Therefore, this study was designed to study the effects of ginseng saponins on the production of proinflammatory cytokines and NO in the primary cultures of mixed glial cells. White ginseng saponin, 200-500 $\mu$g/ml, showed significant cytotoxicity after 72 hrs and increased TNF-$\alpha$, IL-$\beta$, and NO production. Lower doses of 50-100 $\mu\textrm{g}$/ml showed little cytotoxicity until 72 hrs and also increased the production of TNF-$\alpha$, IL-1$\beta$, and NO. Triple immune staining showed that white ginseng saponin, 200$\mu\textrm{g}$/ml for 72 ks, induced stellation of astrocytes and iNOS expression exclusively in microglial cells. Taken together, the white ginseng saponin increased the production of proinflammatory cytokines such as TNF-$\alpha$ and IL-1$\beta$, and induced iNOS expression and NO production in mixed glial cell cultures, which may be ascribed to the enhancement of central immune responses and the regulation of inflammatory reactions by Panax ginseng.