• Anxiety and mood
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• v.11 no.1
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• pp.33-37
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• 2015

Objective : Impaired response inhibition has been suggested to play an important role in the pathophysiology of obsessive-compulsive disorder (OCD). The aim of this study was to evaluate the response inhibition in patients with OCD, by using the Go/NoGo paradigm, and to better understand its associations with clinical symptoms. Methods : The participants included 63 OCD patients and 80 healthy volunteers matched in age and sex. response inhibition was evaluated using computerized Go/NoGo task, in which their commission error rates, omission error rates, and mean response times were measured. The severity of clinical symptoms in the OCD patients was assessed using Montgomery-Asberg Depression Scale and Yale-Brown Obsessive Compulsive Scale. Result : OCD patients showed significantly impaired inhibition and higher omission errors rates despite their slower response time, compared to normal controls. Clinical symptoms were not correlated with commission errors and omission errors. Conclusion : The present results indicate that impairment in response inhibition may play a critical role in the pathophysiology of OCD as a trait. These findings suggest that deficit of response inhibition may contribute to developing and maintaining clinical symptoms such as compelling need to repeat certain actions in patients with OCD.

• Journal of Audiology & Otology
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• v.24 no.3
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• pp.149-156
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• 2020

Background and Objectives: The gap prepulse inhibition of the acoustic startle response has been used to screen tinnitus in an animal model. Here, we examined changes in the auditory late response under various conditions of gap prepulse inhibition. Subjects and Methods: We recruited 19 healthy adults (5 males, 14 females) and their auditory late responses were recorded after various stimuli with or without gap prepulsing. The N1 and P2 responses were selected for analysis. The gap prepulse inhibition was estimated to determine the optimal auditory late response in the gap prepulse paradigm. Results: We found that the gap per se generated a response that was very similar to the response elicited by sound stimuli. This critically affected the gap associated with the maximal inhibition of the stimulus response. Among the various gap-stimulus intervals (GSIs) between the gap and principal stimulus, the GSI of 150 ms maximally inhibited the response. However, after zero padding was used to minimize artifacts after a P2 response to a gap stimulus, the differences among the GSIs disappeared. Conclusions: Overall, the data suggest that both the prepulse inhibition and the gap per se should be considered when using the gap prepulse paradigm to assess tinnitus in humans.

• Korean Journal of Audiology
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• v.24 no.3
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• pp.149-156
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• 2020

Background and Objectives: The gap prepulse inhibition of the acoustic startle response has been used to screen tinnitus in an animal model. Here, we examined changes in the auditory late response under various conditions of gap prepulse inhibition. Subjects and Methods: We recruited 19 healthy adults (5 males, 14 females) and their auditory late responses were recorded after various stimuli with or without gap prepulsing. The N1 and P2 responses were selected for analysis. The gap prepulse inhibition was estimated to determine the optimal auditory late response in the gap prepulse paradigm. Results: We found that the gap per se generated a response that was very similar to the response elicited by sound stimuli. This critically affected the gap associated with the maximal inhibition of the stimulus response. Among the various gap-stimulus intervals (GSIs) between the gap and principal stimulus, the GSI of 150 ms maximally inhibited the response. However, after zero padding was used to minimize artifacts after a P2 response to a gap stimulus, the differences among the GSIs disappeared. Conclusions: Overall, the data suggest that both the prepulse inhibition and the gap per se should be considered when using the gap prepulse paradigm to assess tinnitus in humans.

• The Journal of Korean Physical Therapy
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• v.32 no.2
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• pp.70-74
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• 2020

Purpose: This study examined whether 1) the motor inhibition response as cognitive-behavioral component is learning though a stop signal task using stop-signal paradigm, and 2) whether there is a difference in the learning degree according to imagery training and actual practice training. Methods: Twenty young adults (males: 9, females: 11) volunteered to participate in this study, and were divided randomly into motor imagery training (IT, n=10) and practice training (PT, n=10) groups. The PT group performed an actual practice stop-signal task, while the IT group performed imagery training, which showed a stop-signal task on a monitor of a personal computer. The non-signal reaction time and stop-signal reaction time of both groups were assessed during the stop-signal task. Results: In the non-signal reaction time, there were no significant intra-group and inter-group differences between pre- and post-intervention in both groups (p>0.05). The stop-signal reaction time showed a significant difference in the PT group in the intra-group analysis (p<0.05). On the other hand, there was no significant intra-group difference in the IT group and inter-group difference between pre- and post-intervention (p>0.05). Conclusion: These results showed that the motor inhibition response could be learned through a stop-signal task. Moreover, these findings suggest that actual practice is a more effective method for learning the motor inhibition response.

• Korean Journal of Veterinary Research
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• v.28 no.1
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• pp.29-36
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• 1988

To examine the selectivity of verapamil, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor rsponses, effects of verapamil on alpha-adrenoceptor agonist-induced pressor responses were investigated in urethane-anesthetized rabbits, spinal rabbits, rats and pithed rats. To evaluate the effects of verapamil on each pressor response induced by norepinephrine, phenylephrine and clonidine, these agonists were previously injected into a ear vein, and then same procedures were performed 1~2 min after treatment with intravenous verapamil. The results are summarized as follows: 1. Intravenous verapamil produced dose-dependent depressor response in rabbits and rats. 2. Pressor responses to intravenous norepinephrine($10{\mu}g/kg$) and phenylphrine($30{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 3. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$), phenylephrine($20{\mu}g/kg$) and clonidine ($300{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. 4. Pressor responses to intravenous norepinephrine($3{\mu}g/kg$) and phenylephrine($10{\mu}g/kg$) were inhibited by pretreatment with intravenous verapairlil in rats and no difference was noted between the degree of both inhibitions of the pressor response by verapamil. 5. Pressor responses to intravenous norepinephrine ($3{\mu}g/kg$), phenylephrine($30{\mu}g/kg$) and clonidine($100{\mu}g/kg$) were inhibited by pretreatment with intravenous verapamil in pithed rats. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by verapamil. The inhibition of clonidine-induced pressor response by verapamil was more prominent than that of norepinephrine- or phenylephrine-induced pressor response. These results suggest that verapamil significantly inhibits both pressor responses mediated by alpha-1 and alpha-2 adrenoceptors and the inhibition is greater in alpha-2 adrenoceptor-induced response than in alpha-1 adrenoceptor-induced one, and calcium channel takes part in the process of the pressor response mediated by alpha-1 adrenoceptors as well as alpha-2 adrenoceptors.

• Animal cells and systems
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• v.4 no.4
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• pp.337-340
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• 2000

The photosynthetic and stomatal responses of several woody plants (Powlonia coreana, Firmiana simplex, Quercus acutissima Q. variabilis and Q. serrata) to SO$_2$ were investigated in order to understand their ecophysiological tolerance to $SO_2$ Of the plants, P, coreana showed the largest reduction in its photosynthesis in response to exposure of 0.4 ppm $SO_2$ for 20 h. Fumigation of 0.7 ppm $SO_2$ for 20 h caused complete leaf necrosis of P. coreana and f simplex, which made them unavailable for the measurement of photosynthesis. Q. variabilis exhibited the smallest reduction in photosynthesis following exposure of 0.7 ppm $SO_2$ for 20 h. Both stomatal- and non-stomatal inhibition of the plants by $SO_2$ were determined according to equations by lkeda et at. (1992). When exposed to 0.4 ppm $SO_2$ for 20 h, F. simplex and P. coreana showed the lowest stomatal and non-stomatal inhibition, respectively, while Q. variabilis and Q. serrata exhibited the lowest stomatal and non-stomatal inhibition, respectively, in response to 0.7 ppm $SO_2$ for 20 h. The data are discussed with regard to resistance mechanisms of other plants to $SO_2$ exposure and implications for restoration of declined Korean forests.

• BMB Reports
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• v.50 no.11
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• pp.539-545
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• 2017

The Integrated Stress Response (ISR) refers to a signaling pathway initiated by stress-activated $eIF2{\alpha}$ kinases. Once activated, the pathway causes attenuation of global mRNA translation while also paradoxically inducing stress response gene expression. A detailed analysis of this pathway has helped us better understand how stressed cells coordinate gene expression at translational and transcriptional levels. The translational attenuation associated with this pathway has been largely attributed to the phosphorylation of the translational initiation factor $eIF2{\alpha}$. However, independent studies are now pointing to a second translational regulation step involving a downstream ISR target, 4E-BP, in the inhibition of eIF4E and specifically cap-dependent translation. The activation of 4E-BP is consistent with previous reports implicating the roles of 4E-BP resistant, Internal Ribosome Entry Site (IRES) dependent translation in ISR active cells. In this review, we provide an overview of the translation inhibition mechanisms engaged by the ISR and how they impact the translation of stress response genes.

• Journal of the Korean Home Economics Association
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• v.36 no.4
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• pp.19-34
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• 1998

The purpose of this study was to examine early emotionality and mothering and fathering antecedents of inhibition of children at age 3 years in a sample of 100 children(51 boys; 49 girls). In order to assess child's behavioral inhibition and mothering, the behaviors of each child-mother dyad was videotaped in a structured lab situation. Data on Fathering behavior were gathered through questionnaires. 2X2ANOVA, Hierachical Regression Analyses and Fisher's Z test were conducted for the statistical analyses. The main results were as follows; 1) Only small portion of the variance in subsequent inhibition could be explained by early emotionality(i.e.negative, positive, and the interaction of both emotionality). 2) High negativity coupled with low positivity in infancy predicted high inhibition especially for girls. 3) In general, sensitive mothering and appropriateness of mothers' response were related to child's low inhibition, while parental intrusiveness and negative affect increased child's inhibition. 4) Mothering appeared more influential in the case of children who showed low positivity during infancy. The importance of distinguishing positive and negative emotionality in infancy and studying parental behavior to predict child's inhibition were discussed.

• The Journal of Korean Medicine
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• v.24 no.4
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• pp.82-86
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• 2003

Objective : To examine the inhibition of 5-Hydroxytryptamine(5-HT) induced vasocontraction of the water extract of Acanthopanax senticosus Harms roots (ASR) on rat thoracic Aorta and mesenteric artery with and without endothelium. Methods : Segments of thoracic aorta and mesenteric artery obtained from rats immediately after delivery were mounted in organ baths superfused on a polygraph. Results : We found that the thoracic aorta segments responded to the water extract of ASR with a dose-dependent and concentration-dependent vasorelaxation. 5-HT produced a concentration-dependent contraction of the thoracic aorta and mesenteric artery. At high concentrations of ASR, the inhibition responses were 93.7% (Jang-su), 93.5% (Heok-ryong-kang-sung), 92.8% (Mt. Back-doo), and 83.5% (Yeon-byun) of the maximum 5-HT induced contraction. At high concentrations of ASR, the relaxational response at thoracic aorta and mesenteric artery wi1h endothelium were 95.2% and 94.6%; without endothelium were 93.5% and 92.5% of 1he maximum 5-HT induced contraction. Conclusions : In conclusion, the effect of water extract of ASR had potent inhibition at 5-HT and the effect of ASR in isolated thoracic aorta and mesenteric artery showed dose-dependent inhibition but endothelium-independent response.

• Korean Journal of Veterinary Research
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• v.28 no.1
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• pp.23-28
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• 1988

To examine the selectivity of diltiazem, used in the cardiovascular diseases, on alpha-1 and alpha-2 adrenoceptor-induced pressor responses, effect of diltiazem on alpha-adrenocepter agonist-induced pressor responses were investigated in urethane-anesthetized rabbits and spinal rabbits. The results are summarized as follows: 1. Intravenous diltiazem(10, 30, 100, 300, $1000{\mu}g/kg$) produced dose-dependent depressor response in rabbits. 2. Pressor responses to intravenous norepinephrine($10{\mu}g/kg$) and phenylephrine ($30{\mu}g/kg$) were inhibited by pretreatment with intravenous diltiazem in rabbits and no difference was noted between the degree of both inhibitions of the pressor response by diltiazem. 3. Presser responses to intravenous norepinephrine ($3{\mu}g/kg$), phenylephrine ($20{\mu}g/kg$) and clonidine ($300{\mu}g/kg$) were inhibited by pretreatment with intravenous diltiazem in spinal rabbits. No difference was noted between the inhibition of norepinephrine-induced pressor response and that of phenylephrine-induced pressor response by diltiazem. The inhibition of clonidine-induced pressor response by diltiazem was slightly prominent than that of norepinephrine- or phenylephrine-induced pressor response. These results suggest that diltiazem significantly inhibits both pressor responses mediated by alpha-1 and alpha-2 adrenoceptors.