• Journal of Chest Surgery
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• v.43 no.4
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• pp.345-355
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• 2010

Background: Extracellular and intracellular pH ($pH_o$ and $pH_i$), which can be changed in various pathological conditions such as hypoxia, affects vascular contractility. To elucidate the mechanism to alter vascular contractility by pH, the effects of pH on reactivity to vasocontracting agents, intracellular $Ca^{2+}$ influx, and $Ca^{2+}$ sensitivity in vascular smooth muscle were examined. Material and Method: Isometric contractions in rat superior mesenteric arteries (SMA) were observed. Intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) was recorded by microfluorometer using Fura-2/acetoxylmethyl ester in muscle cells. $pH_o$ was increased from 7.4 to 7.8 or decreased to 6.9 or 6.4. $pH_i$ was decreased by applying $NH_4^+$ or propionic acid or modulated by changing $pH_o$ after increasing membrane permeability using $\beta$-escin. Result: Decreases in $pH_o$ from 7.4 to 6.9 or 6.4 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the right and significantly increased half maximal effective concentration (EC50) to NE or SE. Increase in $pH_o$ from 7.4 to 7.8 shifted concentration-response curve by norepinephrine (NE) or serotonin (SE) to the left and significantly reduced EC50 to NE or SE. NE increased $[Ca^{2+}]_i$ in cultured smooth muscle cells from SMA and the increased $[Ca^{2+}]_i$ was reduced by decreases in $pH_o$. NE-induced contraction was inhibited by $NH_4^+$, whereas the resting tension was increased by $NH_4^+$ or propionic acid. When the cell membrane of SMA was permeabilized using ${\beta}$-escin, SMA was contracted by increasing extracellular $Ca^{2+}$ concentration from 0 to $10{\mu}M$ and the magnitude of contraction was decreased by a decrease in $pH_o$ and vice versa. Conclusion: From these results, it can be concluded that a decrease in $pH_o$ might inhibit vascular contraction by reducing the reactivity of vascular smooth muscle to vasoactive agents, $Ca^{2+}$ influx and the sensitivity of vascular smooth muscle to $Ca^{2+}$.

• Korean Journal of Psychosomatic Medicine
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• v.28 no.1
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• pp.72-80
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• 2020

Objectives : The aim of this study was to compare the effect of Selective Serotonin Reuptake Inhibitor (SSRI) and Serotonin Norepinephrine Reuptake Inhibitor (SNRI) for mood symptoms, pain, and somatic symptoms in elderly depression patients with pain and somatic symptoms. Methods : This study is a prospective open-label study conducted by a single institution. A total of 43 subjects diagnosed with major depressive disorder under the DSM-5 diagnostic criteria participated in this study (average age: 72.53, 58.1% women). The subjects were classified as SSRI and SNRI groups. Depressive symptoms, pain, and somatic symptoms were evaluated by Korean version of the Hamilton Depression Rating Scale (K-HDRS), visual analogue scale (VAS) and Patient Health Questionnare-15 (PHQ-15) respectively at baseline and six weeks later. Two-way repeated-measure ANOVA was performed to analyze changes in the KHDRS, VAS, and PHQ-15 scores. Results : In the SSRI and SNRI groups, K-HDRS, VAS, and PHQ-15 all showed significant improvement after 6 weeks compared to each baseline values. There were no differences in therapeutic effect between the two groups. Conclusions : We found that SSRI and SNRI both improved somatic symptoms and pain in elderly depression patients. The results of this study are thought to help select antidepressants when administering medication to elderly depression patients who complain pain and somatic symptoms. Further research is needed on the longterm effects of the SSRI and SNRI.

• Tuberculosis and Respiratory Diseases
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• v.55 no.5
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• pp.506-515
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• 2003

Background : A decreased level of serum arginine vasopressin(AVP) and an increased sensitivity to an exogenous AVP is expected in patients with septic shock who often require a high infusion rate of catecholamines. The goal of the study was to determine whether an exogenous AVP infusion to the patients with septic shock would achieve a significant decrement in infusion rate of catecholamine vasopressors while maintaining hemodynamic stability and adequate urine output. Method : Eight patients with septic shock who require a high infusion rate of norepinephrine had received a trial of 4-hour AVP infusion with simultaneous titration of norepinephrine. Hemodynamic parameters and urine output were monitored during the AVP infusion and the monitoring continued up to 4 hours after the AVP infusion had stopped. Results : Mean arterial pressure showed no significant changes during the study period(p=0.197). Norepinephrine infusion rate significantly decreased with concurrent AVP administration(p=0.001). However, beneficial effects had disappeared after the AVP infusion was stopped. In addition, hourly urine output showed no significant changes throughout the trials(p=0.093). Conclusion : Concurrent AVP infusion achieved the catecholamine vasopressor sparing effect in the septic shock patients, but there was no evidence of the improvement of renal function. Further study may be indicated to determine whether AVP infusion would provide an organ-protective effect to the septic shock patients.

• Journal of the Korean Academy of Child and Adolescent Psychiatry
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• v.16 no.2
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• pp.160-172
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• 2005

Attention-Deficit/Hyperactivity Disorder(ADHD) is the most common neurodevelopmental disorder in child psychiatry. The etiology or ADHD is not completely understood, but involved in genetical and/or neurocognitive deficits. This article reviews the current state of the literature pertaining to the neurodevelopmental aspects of ADHD. Although the neurodevelopment of ADHD remains unclear, emerging evidence documents its genetic and neurobiologic underpinnings. A pathophysiology of ADHD has not been fully characterized, although genetic, neurobiologic, neuroimaging, and neuropsychological studies of ADHD consistently implicates dysfunction in the fronto-subcortical network and abnormality in the dopaminergic and noradnergic systems. Furthermore some suggests that the timing of aberrant brain development in ADHD could be in early gestation and genetic and/or early environmental influences on brain development in ADHD are fixed, nonprogressive. Although many studies provide evidences for the important or psychosocial or environmental adversities in ADHD, they may be not specific predictors of ADHD but nonspecific triggers of an underlying predisposition or modifiers of the course of disorder.

• The Korean Journal of Physiology
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• v.24 no.1
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• pp.91-102
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• 1990

The effects of extracellular $Ca^{2+}$ and various $Ca^{2+}$ antagonists on endothelium-dependent relaxation to acetylcholine were studied in the isolated rabbit thoracic aorta in order to elucidate the control mechanism of endothelium derived relaxing factor (EDRF) release. Endothelium was removed from aortic strips by gentle rubbing with cotton ball. The effect of hemoglobin on basal tension was also observed with hemolysate. The results obtained were as follows: 1) Endothelium-dependent relaxation (EDR) to acetylcholine (ACh) showed biphasic pattern; the initial rapid relaxation phase and the late slow relaxation phase. 2) With the depletion of the extracellular $Ca^{2+}$, EDR was gradually suppressed, especially the late slow relaxation. 3) Verapamil, nifedipine, $Mn^{2+}$ and $Cd^{2+}$ had not any effect on EDR, while $La^{3+}$ and $Co^{2+}$ suppressed EDR completely. 4) The resting tension of the strips with rubbed endothelium was not altered by the addition of hemoglobin. That of the strips with intact endothelium, however, was enhanced and EDR to ACh was completely blocked From these results, we suggest that extracellular $Ca^{2+}$ is necessary for ACh-induced slow relaxation while $Ca^{2+}$ antagonists have not any effect on EDR.

• Science of Emotion and Sensibility
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• v.10 no.2
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• pp.243-252
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• 2007

Anti-depressant and anti-anxiety effects of Saccharomyces cerevisiae extract and its hydrolyzed fraction. The purpose of the present study was to examine the effect of Saccharomyces cerevisiae extract (SCE) and its hydrolyzed fraction (SCE-40) on depression and anxiety-related behaviors in mice. Actions of SCE and SCE-40 on serotonin, norepinephrine and GABAergic systems in the rat cerebral cortex membranes were also examined. SCE and SCE-40 significantly reduced the immobility time in the forced swimming and tail suspension test in mice. Duration time of the open arms in the elevated plus maze test was significantly increased in the SCE and SCE-40-treated groups, compared with the saline-treated control group. SCE and its fraction SCE-40 significantly inhibited serotonin and norepinephrine transporter and GABA receptor binding, compared to the saline-treated group. In addition, serotonin and norepinephrine reuptake were significantly suppressed by SCE and SCE-40. These results demonstrate that SCE and SCE-40 produce anti-depressant and anti-anxiety effects through enhancing central serotonin, norepinephrine and GABAergic transmissions. These results suggest that SCE and SCE-40 as functional food might prove to be an effective antidepressant and anti-anxiety agent.

• Journal of Chest Surgery
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• v.42 no.5
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• pp.588-596
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• 2009

Background: To clarify the effect of hypoxia on vascular contractility, we tried to show whether hypoxia induced the release of endothelium-derived relaxing factor (EDRF) and the nature of the underlying mechanism for this release. Material and Method: Isometric contractions were observed in rabbit aorta, and the released EDRF from the rabbit aorta was bioassayed by using rabbit denuded carotid artery. The intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) in the cultured rabbit aortic endothelial cells was recorded by a microfluorimeter with using Fura-2/AM. Hypoxia was evoked to the blood vessels or endothelial cells by eliminating the $O_2$ in the aerating gases in the external solution. Chemical hypoxia was evoked by applying deoxyglucose or $CN^-$. Result: Hypoxia relaxed the precontracted rabbit thoracic aorta that had its endothelium, and the magnitude of the relaxation was gradually increased by repetitive bouts of hypoxia. In contrast, hypoxia-induced relaxation was not evoked in the aorta that was denuded of endothelium. In a bioassay experiment, hypoxia released endothelium-derived relaxing factor (EDRF) and the release was inhibited by L-NAME or the $K^+$ channel blocker tetraethylammonium (TEA). In the cultured endothelial cells, hypoxia augmented the ATP-induced increase of the intracellular $Ca^{2+}$ concentration ($[Ca^{2+}]_i$) and this increase was inhibited by TEA. Furthermore, chemical hypoxia also increased the $Ca^{2+}$ influx. Conclusion: From these results, it can be concluded that hypoxia might induce the release of NO from rabbit aortic endothelial cells by increasing $[[Ca^{2+}]_i$.