• The Korean Journal of Nuclear Medicine
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• v.39 no.6
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• pp.438-444
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• 2005

Purpose: Anhedonia has been proposed to be the result of a basic neurophysiologic dysfunction and a vulnerability marker that precede and contribute to the liability of developing schizophrenia. We hypothesized that anhedonia, as a construct reflecting the decreased capacity to experience pleasure, should be associated with decreased positive hedonic affect trait. This study examined the relationship between anhedonia and positive hedonic affect trait and searched for the brain legions which correlate with anhedonia in normal subjects. Materials and Methods: Using $^{18}F$-FDG PET scan, we investigated the brain activity of twenty one subjects during resting state. Questionnaires were administrated after the scan in order to assess the self-rated individual differences in physical/social anhedonia and positive/negative affect traits. Results: Negative correlation between physical anhedonia score and positive affect trait score was significant (Pearson coefficient =-0.440, p<0.05). The subjects physical and social anhedonia scores showed positive correlation with metabolic rates in the cerebellum and negative correlation with metabolic rates in the inferior temporal gyrus and middie frontal gyrus. In addition, the positive affect trait score positively correlated with various areas, most prominent with the inferior temporal gyrus. Conclusion: These results suggest that neural substrates, such as the inferior temporal gyrus and prefrontal-cerebellar circuit, which dysfunction has been proposed to be involved with the cognitive deficits of schizophrenia, may also play a significant role in the liability of affective deficits like anhedonia.

• Tuberculosis and Respiratory Diseases
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• v.43 no.4
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• pp.547-557
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• 1996

Background : An excessive accumulation of neutrophils in lung tissue has been known to play an important role in mediating the tissue injury among the adult respiratory distress syndrome, idiopathic pulmonary fibrosis and cystic fibrosis by releasing toxic oxygen radicals and proteolytic enzymes. Therefore, it is important to understand a possible mechanism of neutrophil accumulation in lung tissue. In many species, exposure to hyperoxic stimuli can cause changes of lung tissues very similar to human adult respiratory distress syndrome and neutrophils are also functioning as the main effector cells in hyperoxic lung injury. The purpose of the present study was to examine whether neutrophils function as a key effector cell and to study the nature of possible neutrophil chemotactic factors found in bronchoalveolar lavage fluid from the hyperoxia exposed rats. Methods : We exposed the rats to the more than 95% oxygen for 24, 48, 60 arid 72 hours and bronchoalveolar lavage(BAL) was performed. Neutrophil chemotactic activity was measured from the BAT- fluid of each experimental groups. We also evaluated the molecular weight of neutrophil chemotactic tractors using fast performance liquid chromatography and characterized the substances by dialyzer membrane and heat treatment. Results : 1) The neutrophil proportions in bronchoalveolar lavage fluid began to rise from 48 hours after oxygen exposure, and continued to be significantly increased with exposure times. 2) chemotactic index for neutrophils in lung lavages from rats exposed to hyperoxia was significantly higher in 48 hours group than in control group, and was significantly increased with exposure time. 3) No deaths occured until after 48 hours of exposure. However, mortality rates were increased to 33.3 % in 60 hours group and 81.3 % in 72 fours group. 4) Gel filtration using fast performance liquid chromatography disclosed two peaks of neutrophil chemotactic activity in molecular weight of 104,000 and 12,000 daltons. 5) Chemotactic indices of bronchoalveolar lavage fluid were significantly deceased when bronchoalveolar lavage fluid was treated with heat ($56^{\circ}C$ for 30 min or $100^{\circ}C$ for 10 min) or dialyzed (dialyzer membrane molecular weight cut off : 12,000 daltons). Conclusion : These results suggested that the generation of neutrophil chemotactic factor and subsequent neutrophil influx into the lungs are playing an important roles in hyperoxia-induced acute lung injury. Neutrophil chemotactic factor in the lung lavage fluids consisted of several distinct components having different molecular weight and different physical characteristics.

• Korean Journal of Fisheries and Aquatic Sciences
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• v.33 no.2
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• pp.87-92
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• 2000

This study was designed to investigate the effects og $10{\%},\;20{\%}\;and\;40{\%}$-addition of functional brown algae (FBA)-noodles on oxygen radicals and their scavenger enzymes in liver of Sprague-Dawley(SD) male rats. Hydroxyl radicals$({\cdot}OH)$ formations were significantly inhibited$(20{\~}35{\%}\;and\;12{\~}20{\%})$ in liver mitochondria and microsomes of rats administered $0{\%},\;20{\%}\;and\;40{\%}$ FBA-noodles compared with that of control group. Significant differences in $H_2O_2$ formations of liver microsome in these FBA-noodles fed groups could not be obtained, but superoxide-radical $(O_2^({\cdot}-))$ formations of liver cytosol resulted in a significant decrease about $10{\%}\;in\;20{\%}\;and\;40{\%}$ FBA-noodles compared with control group. Mn-SOD activities in liver mitochondria were significanlty increased $(10{\~}15{\%})$ in the groups fed $10{\%},\;20{\%}\;and\;40{\%}$ FBA-noodles, while a group administered $40{\%}$ FBA-noodle only resulted In a significant increases $(about 12{\%})$ in Mn-SOD activity of liver microsomes compared with control group. Cu, Zn-SOD activities in liver cytosol were significantly increased $(10{\~}20{\%})\;in\;10{\%},\;20{\%}\;and\;40{\%}$ FEA-noodles compared with control group. Administration of $10{\%},\;20{\%}\;and\;40{\%}$ FBA-noodles resulted in a marked increases$(20{\~}40{\%})$ in liver cytosolic glutathione peroxidase (GSHPx) compared with control group. Significant differences in lipid peroxide (LPO) levels of mitochondria and microsomes in $10{\%}$ FBA-noodle could not be obtained, while LPO levels of $20{\%} and 40{\%}$ FBA-noodles were significantly inhibited about $10{\%}$ in mitochondria and microsomes compared with control group. These results suggest that these FBA-noodles may play a desirable role in attenuating an oxygen radical formations and increasing a scavenger enzymes activity by some brown algae (Undaria pinnatifida) components.

• Molecules and Cells
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• v.27 no.5
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• pp.591-599
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• 2009

Nicotinic acetylcholine receptors (nAChRs) play important roles in nervous system functions and are involved in a variety of diseases. We previously demonstrated that ginsenosides, the active ingredients of Panax ginseng, inhibit subsets of nAChR channel currents, but not ${\alpha}7$, expressed in Xenopus laevis oocytes. Mutation of the highly conserved Leu247 to Thr247 in the transmembrane domain 2 (TM2) channel pore region of ${\alpha}7$ nAChR induces alterations in channel gating properties and converts ${\alpha}7$ nAChR antagonists into agonists. In the present study, we assessed how point mutations in the Leu247 residue leading to various amino acids affect 20(S)-ginsenoside $Rg_3$ ($Rg_3$) activity against the ${\alpha}7$ nAChR. Mutation of L247 to L247A, L247D, L247E, L247I, L247S, and L247T, but not L247K, rendered mutant receptors sensitive to $Rg_3$. We further characterized $Rg_3$ regulation of L247T receptors. We found that $Rg_3$ inhibition of mutant ${\alpha}7$ nAChR channel currents was reversible and concentration-dependent. $Rg_3$ inhibition was strongly voltage-dependent and noncompetitive manner. These results indicate that the interaction between $Rg_3$ and mutant receptors might differ from its interaction with the wild-type receptor. To identify differences in $Rg_3$ interactions between wild-type and L247T receptors, we utilized docked modeling. This modeling revealed that $Rg_3$ forms hydrogen bonds with amino acids, such as Ser240 of subunit I and Thr244 of subunit II and V at the channel pore, whereas $Rg_3$ localizes at the interface of the two wild-type receptor subunits. These results indicate that mutation of Leu247 to Thr247 induces conformational changes in the wild-type receptor and provides a binding pocket for $Rg_3$ at the channel pore.