• Proceedings of the PSK Conference
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• 2003.10b
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• pp.123.2-123.2
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• 2003

The cellular mechanisms by which excess exposure to the excitatory neurotransmitter glutamate can produce neuronal injury are unknown. In this study, we found that glutamate induced cell death at IC (50) of 100 microM on the cultured human SH-SY5Y neuroblastoma cells. It has been hypothesized that glutamate excitotoxicity is related with the elevation of calcium (Ca) levels. To determine the dependence of glutamate neurotoxicity on Ca environment, extracellular (EDTA) and intracellular (BAPTA/AM) chelator were used. (omitted)

• Analytical Science and Technology
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• v.23 no.1
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• pp.60-67
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• 2010

A sensitive competitive heterogeneous bioluminescence immunoassay for serotonin was developed using photoprotein, aequorin as a label for the first time with the optimal assay conditions; especially, serotoninavidin conjugate was prepared by Mannich reaction and the synthetic process of serotonin-avidin conjugate was optimized by controlling the initial molar ratios of serotonin, formaldehyde and avidin (1:12,000:25). The developed bioluminescence immunoassay for serotonin showed good sensitivity (LOD of 0.68 ng/mL) with wide area of dynamic range ($5.0{\times}10^{-10}\;M\sim5.0{\times}10^{-7}\;M$). (cf. the range for serotonin in human blood serum is $151{\pm}45\;ng$/mL). In addition, cross-reactivity studies demonstrated that 5-methoxytryptamine showed some cross-reactivity (28.0%), whereas 3-methylindole, melatonin and 5-hydroxylindole-3-acetic acid showed no crossreactivity, and good recoveries were obtained in serum. Thus, this developed method provides a good tool to monitor serotonin in serum.

• Journal of Korean Physical Therapy Science
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• v.9 no.2
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• pp.159-170
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• 2002

Parkinson's disease(PD) is a progressive neurodegenerative disease that affects the functioning of the basal ganglia, a brain area that contributes to the control of movement. The disease is caused by the death of nerve cells in the brain that produce dopamine, a chemical messenger. The cells affected usually produce a neurotransmitter(a chemical that transmits nerver impulses) called dopamine, which acts with acetylcholine, another neurotransmitter, to fine-tune muscle control. In Parkinson's disease, the level of dopamine relative to acetylcholine is reduced, adversely affecting muscle control. When the supply of dopamine is depleted, the function of the basal ganglia is disrupted and its ability to control movement-deteriorates. The result is that PD patients experience moderate rigidity, difficulty in initiating movements and slowness in executing them, and a rhythmical tremor at rest. Although the cause of Parkinson's disease is not known, genetic factors may be involved. About 3 in 10 people with the disorder have an affected family member. About 1 in 100 people over the age of 60 in the US have Parkinson's disease. And Parkinson's disease is slightly more common in men. The course of the disease is variable, but drags may be the best effective in treating the symptoms and improving quality of life. But, The doctor may arrange physical therapy to help with physical mobility problems. It is important to continue to exercise and take care of your general health. Try to take a walk each day. Stretching exercises can help you maintain your strength and mobility. So, This papers will serve about the information of PD for clinical physical therapist. Finally, The aim of review is increasing approach method and technique for PD patients by the view of physical therapy.

• Journal of Korean Ophthalmic Optics Society
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• v.19 no.3
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• pp.413-418
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• 2014

Purpose: The objective of this study was analyzing the distribution of the excitatory neurotransmitter glutamate receptor to investigate the function in the retina of the greater horseshoe bat. Methods: After retinal tissues of adult greater horseshoe bat were cut into $40{\mu}m$ vertical sections, standard immuno-cytochemical techniques was applied for analysis. Immunofluorescence images were obtained using the Bio-Rad MRC 1024 laser scanning confocal microscope. Results: AMPA (GluR1-4), Kainate (GluR5-7, KA1-2) and NMDA (1, 2A, 2B) mainly distributed in the inner plexiform layer and outer plexiform layer. KA1 receptors have existed not only plexiform layer but also ganglion cell layer. Conclusions: The greater horseshoe bat has same neuron and neurotransmitter to mammalian retina. These findings suggest that bat has a functional retina for visual analysis.

• The Journal of Korean Academy of Orthopedic Manual Physical Therapy
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• v.8 no.2
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• pp.73-87
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• 2002

Parkinson's disease(PD) is a progressive neurodegenerative disease that affects the functioning of the basal ganglia, a brain area that contributes to the control of movement. The disease is caused by the death of nerve cells in the brain that produce dopamine, a chemical messenger. The cells affected usually produce a neurotransmitter(a chemical that transmits nerver impulses) called dopamine, which acts with acetylcholine, another neurotransmitter, to fine-tune muscle control. In Parkinson's disease, the level of dopamine relative to acetylcholine is reduced, adversely affecting muscle control. When the supply of dopamine is depleted, the function of the basal ganglia is disrupted and its ability to control movement deteriorates. The result is that PD patients experience moderate rigidity, difficulty in initiating movements and slowness in executing them, and a rhythmical tremor at rest. Although the cause of Parkinson's disease is not known, genetic factors may be involved. About 3 in 10 people with the disorder have an affected family member. About 1 in 100 people over the age of 60 in the US have Parkinson's disease. And Parkinson's disease is slightly more common in men. The course of the disease is variable, but drugs may be the best effective in treating the symptoms and improving quality of life. But, The doctor may arrange physical therapy to help with physical mobility problems. It is important to continue to exercise and take care of your general health. Try to take a walk each day. Stretching exercises can help you maintain your strength and mobility. So, This papers will serve about the information of PD for clinical physical therapist. Finally, The aim of review is increasing approach method and technique for PD patients by the view of physical therapy.

• Clinical and Experimental Reproductive Medicine
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• v.41 no.2
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• pp.62-67
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• 2014

Objective: The objective of this study was to investigate whether there was a correlation between catechol-o-methyltransferase (COMT) gene polymorphism, which is believed to play a role in the etiology of psychotic disorders, and premenstrual syndrome (PMS). Methods: Fifty-three women with regular menstrual cycles, aged between 18 and 46 years and diagnosed with PMS according to the American Congress of Obstetrics and Gynecology criteria were included in this study as the study group, and 53 healthy women having no health problems were selected as the controls. Venous blood was collected from all patients included in the study and kept at $-18^{\circ}C$ prior to analysis. Results: There was no significant difference between the groups in terms of demographic features such as age, body mass index, number of pregnancies, parity, and number of children. No statistically significant difference was observed in terms of COMT gene polymorphism (p=0.61) between women in the PMS and the control groups. However, a significant difference was found between arthralgia, which is an indicator of PMS, and low-enzyme activity COMT gene (Met/Met) polymorphism (p=0.04). Conclusion: These results suggested that there was no significant relationship between PMS and COMT gene polymorphism. Since we could not find a direct correlation between the COMT gene polymorphism and PMS, further studies including alternative neurotransmitter pathways are needed to find an effective treatment for this disease.

• Journal of Genetic Medicine
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• v.6 no.2
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• pp.170-174
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• 2009

Tetrahydrobiopterin ($BH_4$) deficiency is caused by mutations in genes encoding enzymes involved in the synthesis and regeneration of $BH_4$. The condition is usually accompanied by hyperphenylalaninemia (HPA) and deficiency of neurotransmitter precursors L-dopa and 5-hydroxytryptophan. $BH_4$ deficiency is much rarer than classical phenylketonuria. Dihydropteridine reductase (DHPR) deficiency, an autosomal recessive genetic disorder, is a cause of malignant hyperphenylalaninemia due to $BH_4$ deficiency. When left untreated, DHPR deficiency leads to neurologic deterioration at the age of 4 or 5 months, including psychomotor retardation, tonicity disorders, drowsiness, irritability, abnormal movements, hyperthermia, hypersalivation, and difficulty swallowing. Treatment of DHPR deficiency should be initiated as early as possible with $BH_4$ supplementation and replacement of the neurotransmitter precursors L-dopa and 5-hydroxytryptophan. We report the first case of DHPR deficiency in Korea, a child diagnosed at 9 years of age by genetic testing.

• Journal of Microbiology and Biotechnology
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• v.30 no.11
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• pp.1626-1639
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• 2020

In Caenorhabditis elegans, SHN-1 is the homologue of SHANK, a scaffolding protein. In this study, we determined the molecular basis for SHN-1/SHANK in the regulation of innate immune response to fungal infection. Mutation of shn-1 increased the susceptibility to Candida albicans infection and suppressed the innate immune response. After C. albicans infection for 6, 12, or 24 h, both transcriptional expression of shn-1 and SHN-1::GFP expression were increased, implying that the activated SHN-1 may mediate a protection mechanism for C. elegans against the adverse effects from fungal infection. SHN-1 acted in both the neurons and the intestine to regulate the innate immune response to fungal infection. In the neurons, GLR-1, an AMPA ionotropic glutamate receptor, was identified as the downstream target in the regulation of innate immune response to fungal infection. GLR-1 further positively affected the function of SER-7-mediated serotonin signaling and antagonized the function of DAT-1-mediated dopamine signaling in the regulation of innate immune response to fungal infection. Our study suggests the novel function of SHN-1/SHANK in the regulation of innate immune response to fungal infection. Moreover, our results also denote the crucial role of neurotransmitter signals in mediating the function of SHN-1/SHANK in regulating innate immune response to fungal infection.

• Journal of Korean Society of Occupational and Environmental Hygiene
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• v.21 no.2
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• pp.82-89
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• 2011

Methylcyclohexane is frequently used in industrial sites (2,592tons/year) as rubber adhesives, ink, paint thinners, organic solvents, and so on. However, there are limited data on the toxic evaluation of methylcyclohexane. This study aims to predict the hazards and neurological effects of methylcyclohexane using SD rats in order to prevent health disorders of workers. The OECD Guideline for Testing of Chemicals (OECD, 2001) was used as a reference during the tests. For 13 weeks (once a day, five days per week) 0, 10, 100 and 1,000mg/kg/day of methylcyclohexane was injected to SD rats to observe any changes in the body or organ weight, hematology, histopathology, mobility, blood pressure, and neurotransmitter. As a result, some male and female SD rats injected with 1,000mg/kg/day of methylcyclohexane died. On the other hand, surviving rats showed significant changes such as hematological changes involving the decrease in the number of red blood corpuscles, and the decrease or increase in the weight of the lungs, kidneys, spleens, and livers (p< 0.05, p<0.01). Also histopathological lesions were observed in the hearts and kidneys. In the test for the effect on the nervous system, SD rats injected with 100mg/kg/day of methylcyclohexane had higher blood pressure levels compared to the control group. However, no abnormal effects was observed in the mobility, serotonin, neurotransmitter, and the biopsy of the brain and coronary arteries. The study results revealed that the livers, hearts, and kidneys were affected by methylcyclohexane. The absolute toxic dose of methylcyclohexane is 1,000mg/kg/day, NOAEL is 100 mg/kg/day, and it is not a toxic substance to the nervous system.

• Journal of the Korean society of biological therapies in psychiatry
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• v.24 no.3
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• pp.129-141
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• 2018

Suicide is a behavior that is intended to cause death by itself and requires medical treatment, resulting in suicidal attempt or completion. Suicide causes loss of life, damages the body, costs a lot of medical expenses, and causes families to fall into sorrow and suffering therefore this suicide is a huge loss to family and society. There have been attempts to reduce and prevent suicide by understanding the mechanism of suicide. The mechanism of suicide can be thought of as psychological mechanism and biological mechanism. In the past, if we considered the psychological and biological mechanisms separately, the development of neuroscience now connects and integrates these two. Psychological factors affect biological factors and biological temperaments also affect perception or thinking about the situation and increase psychological vulnerability. Distant factors in suicidal behavior-such as childhood adversity and family and genetic predisposition-increase the lifetime risk of suicide. They alter the response to stress and other processes through changes in gene expression and regulation of emotional and behavioral characteristics. Distant factors affect the biological system and consequently changes in these systems can increase the risk of suicide. In other words, the distal factor does not directly induce suicidal behavior but rather acts indirectly through developmental or mediating factors. These mediating factors are impulsive aggressive and anxious trait, and chronic use of substances. The mechanism of this disorder is the abnormality of the serotonin system and the abnormality of the lipid level. Proximal factors are associated with the onset of suicide events and include changes in the major neurotransmitter systems, inflammatory changes, and dysfunction of glial cells in the brain. A series of studies, including a variety of research methods and postmortem and in-vivo imaging studies, show the impairment of the serotonergic neurotransmitter system and hypothalamic-pituitary-adrenal axis stress response system for suicidal behavior. These disorders lead to suicidal behavior due to difficulty in cognitive control of mood, pessimism, reactive aggression, abnormality in problem solving abilities, excessive response to negative social signals, severe emotional distress, and cognitive dysregulation of suicidal ideation.