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Search Results: 1 - 10 of 102 matches for " Yukihiko Shirayama "
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Neural Activation by Milnacipran and Memory Extinction  [PDF]
Hisahito Ishida, Masaaki Iwata, Yukihiko Shirayama, Katsumasa Muneoka
Journal of Behavioral and Brain Science (JBBS) , 2012, DOI: 10.4236/jbbs.2012.22016
Abstract: Background: Among neurotransmitter influencing memory formation, the noradrenergic system has been recognized as an important system. Memory formation involves various regions including the prefrontal cortex, hippocampus, amygdala and septum. Method: We investigated the effects of milnacipran on passive avoidance task and evaluated Fos counting in the prefrontal cortex, hippocampus, septum, amygdala and nucleus accumbens. Results: The milnacipran-treated rats (20 mg/kg, 4 days) showed a significant decrease in the number of Fos-immunoreactive cells in the infralimbic portion of prefrontal cortex, the shell portion of nucleus accumbens and the CA1 region of hippocampus, but a significant increase in the Fos counts in the lateral septum with no changes in the Fos counts in the striatum and amygdala. The milnacipran-treated rats showed amelioration in memory extinction (although not statistically significant), but not in memory acquisition and consolidation in the passive avoidance test. Conclusion: The differential activation of the brain regions might be possible sites for ameliorating memory extinction as well as antidepressant effects.
Rate of social anxiety disorder, its comorbidity with depression and paroxetine effects in outpatients in Japan  [PDF]
Yukihiko Shirayama, Michio Takahashi, Masatoshi Suzuki, Atsushi Kimura, Koichi Sato
Open Journal of Psychiatry (OJPsych) , 2013, DOI: 10.4236/ojpsych.2013.31A015
Abstract: The prevalence of persons with social anxiety disorder (SAD) in Japan remains unknown. This study examined 293 patients with age between 20 and 60 at first visit on the outpatient clinic of psychiatry by the section of social phobia of M.I.N.I. and DSM-IV. After that, 10 patients with both SAD out of 16 patients (trial recruited) completed 12 weeks of treatment with paroxetine. Among 63 patients with 4 points and 40 patients with 3 points on the M.I.N.I., 21 patients (33%) and 16 patients (40%) were diagnosed as SAD on DSM-IV criteria, respectively. Together, 37 patients (12.6%) were diagnosed as SAD out of the 293 outpatients. Among 37 patients with SAD, 23 patients (62%) had comorbid depression. As for 10 patients after treatment with paroxetine, 8 patients improved from the point of recovery of depression (HAM-D scores below 10), whereas only 4 patients improved from the point of recovery of social phobia (L-SAS scores below 30). Three points as well as 4 points on the M.I.N.I. is meaningful for the diagnosis of SAD. For a while, paroxetine exerted less beneficial effects on SAD rather than on depression.
Effects of etizolam and ethyl loflazepate on the P300 event-related potential in healthy subjects
Goro Fukami, Tasuku Hashimoto, Yukihiko Shirayama, Tadashi Hasegawa, Hiroyuki Watanabe, Mihisa Fujisaki, Kenji Hashimoto, Masaomi Iyo
Annals of General Psychiatry , 2010, DOI: 10.1186/1744-859x-9-37
Abstract: Healthy people were administered etizolam and ethyl loflazepate acutely and subchronically (14 days). The auditory P300 event-related potential and the neuropsychological batteries described below were employed to assess the effects of drugs on cognition. The P300 event-related potential was recorded before and after drug treatments. The digit symbol test, trail making test, digit span test and verbal paired associates test were administered to examine mental slowing and memory functioning.Acute administration of drugs caused prolongation in P300 latency and reduction in P300 amplitude. Etizolam caused a statistically significant prolongation in P300 latency compared to ethyl loflazepate. Furthermore, subchronic administration of etizolam, but not ethyl loflazepate, still caused a weak prolongation in P300 latency. In contrast, neuropsychological tests showed no difference.The results indicate that acute administration of ethyl loflazepate induces less effect on P300 latency than etizolam.Benzodiazepines have anxiolytic, sedative, anticonvulsant and myorelaxant properties, and have been widely prescribed in various clinical settings. These compounds, however, also induce adverse effects such as oversedation, cognitive impairment, motor impairment and withdrawal. These adverse effects may be partly associated with the elimination half-life (EH) of the compounds from the body; that is, long-term use of the compounds with a short elimination rate may induce withdrawal syndromes, whereas accumulation-related effects of a long elimination rate may include oversedation, cognitive dysfunction and motor impairment [1-4].It has been observed previously that cognitive impairment induced by benzodiazepines may go unnoticed while profoundly disturbing social activity [5]. Therefore, it is clinically very important to take note of the cognitive effects of benzodiazepines. In order to assess the effects of benzodiazepines on cognition, the event-related potential (ERP), P300, may
Personality Traits as Risk Factors for Treatment-Resistant Depression
Michio Takahashi, Yukihiko Shirayama, Katsumasa Muneoka, Masatoshi Suzuki, Koichi Sato, Kenji Hashimoto
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0063756
Abstract: Background The clinical outcome of antidepressant treatment in patients with major depressive disorder (MDD) is thought to be associated with personality traits. A number of studies suggest that depressed patients show high harm avoidance, low self-directedness and cooperativeness, as measured on the Temperament and Character Inventory (TCI). However, the psychology of these patients is not well documented. Methods Psychological evaluation using Cloninger’s TCI, was performed on treatment-resistant MDD patients (n = 35), remission MDD patients (n = 31), and age- and gender-matched healthy controls (n = 174). Results Treatment-resistant patients demonstrated high scores for harm avoidance, and low scores for reward dependence, self-directedness, and cooperativeness using the TCI, compared with healthy controls and remission patients. Interestingly, patients in remission continued to show significantly high scores for harm avoidance, but not other traits in the TCI compared with controls. Moreover, there was a significant negative correlation between reward dependence and harm avoidance in the treatment-resistant depression cohort, which was absent in the control and remitted depression groups. Conclusions This study suggests that low reward dependence and to a lesser extent, low cooperativeness in the TCI may be risk factors for treatment-resistant depression.
Low Openness on the Revised NEO Personality Inventory as a Risk Factor for Treatment-Resistant Depression
Michio Takahashi, Yukihiko Shirayama, Katsumasa Muneoka, Masatoshi Suzuki, Koichi Sato, Kenji Hashimoto
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0071964
Abstract: Background Recently, we reported that low reward dependence, and to a lesser extent, low cooperativeness in the Temperature and Character Inventory (TCI) may be risk factors for treatment-resistant depression. Here, we analyzed additional psychological traits in these patients. Methods We administered Costa and McCrae's five-factor model personality inventory, NEO Personality Inventory-Revised (NEO-PI-R), to antidepressant-treatment resistant depressed patients (n = 35), remitted depressed patients (n = 27), and healthy controls (n = 66). We also evaluated the relationships between scores on NEO and TCI, using the same cohort of patients with treatment-resistant depression, as our previous study. Results Patients with treatment-resistant depression showed high scores for neuroticism, low scores for extraversion, openness and conscientiousness, without changes in agreeableness, on the NEO. However, patients in remitted depression showed no significant scores on NEO. Patients with treatment-resistant depression and low openness on NEO showed positive relationships with reward dependence and cooperativeness on the TCI. Conclusions Many studies have reported that depressed patients show high neuroticism, low extraversion and low conscientiousness on the NEO. Our study highlights low openness on the NEO, as a risk mediator in treatment-resistant depression. This newly identified trait should be included as a risk factor in treatment-resistant depression.
Control Pathways from the Subcortical Limbic Structures to the Trigeminal Motor System in the Lower Brainstem: A Hodological Review  [PDF]
Yukihiko Yasui
Neuroscience & Medicine (NM) , 2015, DOI: 10.4236/nm.2015.61005
Abstract:
The organization of the emotion-related somatic motor behavior, including jaw movements, is governed not only by the cortical limbic system but also by the subcortical limbic system including the amygdala and hypothalamus. GABAergic neurons in the central amygdaloid nucleus (CeA) and glutamatergic neurons in the posterior lateral hypothalamus (PLH) exert inhibitory and excitatory influences, respectively, upon premotor neurons for the motor trigeminal nucleus (Vm) in the parvicellular reticular formation (RFp) of the medulla oblongata. The CeA also has an inhibitory influence on non-dopaminergic (probably GABAergic) neurons in the retrorubral field of the midbrain that send their axons to the RFp. Furthermore, the CeA and lateral hypothalamus including the PLH may also modulate Vm neurons via projections to the mesencephalic trigeminal nucleus which contains the cell bodies of primary afferent neurons conveying inputs from the masticatory muscle spindles or the periodontal ligament receptors to jaw closing motoneurons within the Vm. These pathways from the subcortical limbic structures to the trigeminal motor system in the lower brainstem underlie the regulation of emotional jaw movements.
Time Series Forecasting with Multiple Deep Learners: Selection from a Bayesian Network  [PDF]
Shusuke Kobayashi, Susumu Shirayama
Journal of Data Analysis and Information Processing (JDAIP) , 2017, DOI: 10.4236/jdaip.2017.53009
Abstract: Considering the recent developments in deep learning, it has become increasingly important to verify what methods are valid for the prediction of multivariate time-series data. In this study, we propose a novel method of time-series prediction employing multiple deep learners combined with a Bayesian network where training data is divided into clusters using K-means clustering. We decided how many clusters are the best for K-means with the Bayesian information criteria. Depending on each cluster, the multiple deep learners are trained. We used three types of deep learners: deep neural network (DNN), recurrent neural network (RNN), and long short-term memory (LSTM). A naive Bayes classifier is used to determine which deep learner is in charge of predicting a particular time-series. Our proposed method will be applied to a set of financial time-series data, the Nikkei Average Stock price, to assess the accuracy of the predictions made. Compared with the conventional method of employing a single deep learner to acquire all the data, it is demonstrated by our proposed method that F-value and accuracy are improved.
Negative Correlation between Brain Glutathione Level and Negative Symptoms in Schizophrenia: A 3T 1H-MRS Study
Daisuke Matsuzawa, Takayuki Obata, Yukihiko Shirayama, Hiroi Nonaka, Yoko Kanazawa, Eiji Yoshitome, Junichi Takanashi, Tsuyoshi Matsuda, Eiji Shimizu, Hiroo Ikehira, Masaomi Iyo, Kenji Hashimoto
PLOS ONE , 2008, DOI: 10.1371/journal.pone.0001944
Abstract: Background Glutathione (GSH), a major intracellular antioxidant, plays a role in NMDA receptor-mediated neurotransmission, which is involved in the pathophysiology of schizophrenia. In the present study, we aimed to investigate whether GSH levels are altered in the posterior medial frontal cortex of schizophrenic patients. Furthermore, we examined correlations between GSH levels and clinical variables in patients. Methods and Findings Twenty schizophrenia patients and 16 age- and gender-matched normal controls were enrolled to examine the levels of GSH in the posterior medial frontal cortex by using 3T SIGNA EXCITE 1H-MRS with the spectral editing technique, MEGA-PRESS. Clinical variables of patients were assessed by the Global Assessment of Functioning (GAF), Scale for the Assessment of Negative Symptoms (SANS), Brief Psychiatric Rating Scale (BPRS), Drug-Induced Extra-Pyramidal Symptoms Scale (DIEPSS), and five cognitive performance tests (Word Fluency Test, Stroop Test, Trail Making Test, Wisconsin Card Sorting Test and Digit Span Distractibility Test). Levels of GSH in the posterior medial frontal cortex of schizophrenic patients were not different from those of normal controls. However, we found a significant negative correlation between GSH levels and the severity of negative symptoms (SANS total score and negative symptom subscore on BPRS) in patients. There were no correlations between brain GSH levels and scores on any cognitive performance test except Trail Making Test part A. Conclusion These results suggest that GSH levels in the posterior medial frontal cortex may be related to negative symptoms in schizophrenic patients. Therefore, agents that increase GSH levels in the brain could be potential therapeutic drugs for negative symptoms in schizophrenia.
A randomised, double-blind, placebo-controlled trial of tropisetron in patients with schizophrenia
Akihiro Shiina, Yukihiko Shirayama, Tomihisa Niitsu, Tasuku Hashimoto, Taisuke Yoshida, Tadashi Hasegawa, Tadashi Haraguchi, Nobuhisa Kanahara, Tetsuya Shiraishi, Mihisa Fujisaki, Goro Fukami, Michiko Nakazato, Masaomi Iyo, Kenji Hashimoto
Annals of General Psychiatry , 2010, DOI: 10.1186/1744-859x-9-27
Abstract: A randomised, placebo-controlled trial of tropisetron in patients with schizophrenia was performed. A total of 40 patients with chronic schizophrenia who had taken risperidone (2 to 6 mg/day) were enrolled. Subjects were randomly assigned to a fixed titration of tropisetron (n = 20, 10 mg/day) or placebo (n = 20) in an 8-week double-blind trial. Auditory sensory gating P50 deficits and Quality of Life Scale (QLS), Cambridge Neuropsychological Test Automated Battery (CANTAB), and Positive and Negative Syndrome Scale (PANSS) scores were measured.In all, 33 patients completed the trial. Tropisetron was well tolerated. Administration of tropisetron, but not placebo, significantly improved auditory sensory gating P50 deficits in non-smoking patients with schizophrenia. The score on the rapid visual information processing (sustained visual attention) task of CANTAB was significantly improved by tropisetron treatment. Total and subscale scores of PANSS were not changed by this trial. QLS scores in the all patients, but not non-smoking patients, were significantly improved by tropisetron trial.This first randomised, double-blind, placebo-controlled trial supports the safety and efficacy of adjunctive tropisetron for treatment of cognitive deficits in schizophrenia.Cognitive deficits in schizophrenia are frequently severe and strongly correlated with decreased functional outcome and quality of life (QOL) [1-5]. Atypical antipsychotics have been shown to provide an improvement in several domains of cognitive function, especially working memory, executive function, and attention [2,6]. However, many patients, even if they are medicated with atypical antipsychotics, fail to recover from cognitive deficits, resulting in a failure of their reintegration into society.Several lines of evidence suggest that the α7 subtype of the nicotinic acetylcholine receptors (α7 nAChRs) plays an important role in the mechanism of auditory P50 gating deficits of schizophrenia, and that α7 nAChR a
Role of Atrial Fibrillation Threshold Evaluation on Guiding Treatment
Takeshi Shirayama
Indian Pacing and Electrophysiology Journal , 2003,
Abstract: Atrial fibrillation could be induced reproducibly by 50Hz rapid stimulation which was given through systolic and early diastolic phase of atrial excitation. Duration of atrial fibrillation induced in this way was roughly dependent on the current amplitude of the stimulation. The minimum current that could induce long-lasting atrial fibrillation (30sec in the clinical setting, 2sec in the rabbit or rat model) was defined as atrial fibrillation threshold (AFT). AFT was larger in patients who had history of atrial fibrillation than those who did not. Anti-arrhythmic drugs raised AFT by various degrees both in experimental and clinical cases. Long-term efficacy of a drug could be predicted in a patient, measuring how much the drug increased AFT (cut-off point = 5mA increase). AFT is a useful marker to evaluate atrial vulnerability and to guide pharmacological treatment of atrial fibrillation.
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