• Title/Summary/Keyword: Brain activation

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Pupil Size Variability as an Index of Autonomic Activity - from the Experiments of Posture, Sleepiness and Cognitive Task (자율신경활성도의 지표로서의 동공크기 변이율 -자세변화, 졸음, 인지과제 실험으로부터)

  • Lee, Jeung-Chan;Kim, Ji-Eun;Park, Kyung-Mo
    • Journal of Biomedical Engineering Research
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    • v.28 no.1
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    • pp.55-65
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    • 2007
  • This paper sought to investigate pupil size variability, pupil size parameters in terms of time domain and frequency domain, the autonomic activity change induced by posture change, degree of sleepiness and cognitive task (math task). With a specially designed pupil image acquisition system in the dark room, these three kinds of experiments were performed to induce a dominant state of sympathetic or parasympathetic activation. Electrocardiogram and pupil size were measured in all the experiments. Based on three experiments, we calculated heart rate variability. In the pupil size analysis, we calculated the mean and standard deviation of pupil size (in time domain), and proposed several frequency bands that exhibit different autonomic activation between different sessions. The results indicate that in terms of heart rate variability, posture change exhibited significant differences but not between sleepiness level, or between cognitive task. Pupil sizes differed only during the postures. And we found some frequency bands that correlated with autonomic activation in each experiment. While heart rate variability reflects posture change that need cardiac control, pupil size variability reflects not only posture induced autonomic activation but sleepiness and cognitive load, which is processed in the brain, in time and frequency domain parameter.

A Comprasion of the Activation of Mirror Neurons Induced by Action Observation between Simple and Complex Hand Movement

  • Lee, Mi Young;Kim, Ju Sang
    • The Journal of Korean Physical Therapy
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    • v.31 no.3
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    • pp.157-160
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    • 2019
  • Purpose: We compared the activation pattern of the mirror neurons (MN) between two types of hand movement according to action observation using functional MRI. Methods: Twelve right-handed healthy subjects (5 male and 7 female, mean age $21.92{\pm}2.02years$) participated in the experiment. During fMRI scanning, subjects underwent two different stimuli on the screen: 1) video clips showing repeated grasping and releasing of the ball via simple hand movement (SHM), and (2) video clips showing an actor performing a Purdue Pegboard test via complex hand movement (CHM). paired t-test in statistical parametric mapping (SPM) was used to compare the activation differences between the two types of hand movement. Results: CHM as compared with the SHM produced a higher blood oxygen level dependent (BOLD) signal response in the right superior frontal gyrus, left inferior and superior parietal lobules, and lingual gyrus. However, no greater BOLD signal response was found by SHM compared with CHM (FWE corrected, p<0.05). Conclusion: Our findings provided that the activation patterns for observation of SHM and CHM are different. CHM also elicited boarder or stronger activations in the brain, including inferior parietal lobule called the MN region.

Identification of a Novel Function of Extract of Gingko biloba (EGb 761®) as a Regulator of PYY Secretion and FFA4 Activation

  • Kim, Hye Young;Kim, Kyong
    • Natural Product Sciences
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    • v.25 no.2
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    • pp.165-171
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    • 2019
  • Although the functions of a standardized extract of Gingko biloba leaves (EGb $761^{(R)}$) has been reported with regard to neurobiological properties, no attention has been paid to the impact of EGb $761^{(R)}$ on the neuronal regulation of energy homeostasis. To evaluate the hypothesis that EGb $761^{(R)}$ affect the secretion of peptide tyrosine tyrosine (PYY) and the activation of free fatty acid receptor 4 (FFA4), which are involved in the neuronal circuitries that control energy homeostasis by inducing the transfer of information about the influx of energy to the brain, we examined whether EGb $761^{(R)}$ can stimulate PYY secretion in the enteroendocrine NCI-H716 cells and if EGb $761^{(R)}$ can activate FFA4 in FFA4-expressing cells. In NCI-H716 cells, EGb $761^{(R)}$ stimulated PYY secretion and the EGb $761^{(R)}$-induced PYY secretion was involved in the increase in intracellular $Ca^{2+}$ concentration and the activation of FFA4. Furthermore, in FFA4-expressing cells, EGb $761^{(R)}$ activated FFA4. These results suggest that EGb $761^{(R)}$ may affect the control of energy homeostasis via the regulation of PYY secretion and FFA4 activation.

Silibinin Inhibits Osteoclast Differentiation Mediated by TNF Family Members

  • Kim, Jung Ha;Kim, Kabsun;Jin, Hye Mi;Song, Insun;Youn, Bang Ung;Lee, Junwon;Kim, Nacksung
    • Molecules and Cells
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    • v.28 no.3
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    • pp.201-207
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    • 2009
  • Silibinin is a polyphenolic flavonoid compound isolated from milk thistle (Silybum marianum), with known hepatoprotective, anticarcinogenic, and antioxidant effects. Herein, we show that silibinin inhibits receptor activator of $NF-{\kappa}B$ ligand (RANKL)-induced osteoclastogenesis from RAW264.7 cells as well as from bone marrow-derived monocyte/macrophage cells in a dose-dependent manner. Silibinin has no effect on the expression of RANKL or the soluble RANKL decoy receptor osteoprotegerin (OPG) in osteoblasts. However, we demonstrate that silibinin can block the activation of $NF-{\kappa}B$, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and extracellular signal-regulated kinase (ERK) in osteoclast precursors in response to RANKL. Furthermore, silibinin attenuates the induction of nuclear factor of activated T cells (NFAT) c1 and osteoclast-associated receptor (OSCAR) expression during RANKL-induced osteoclastogenesis. We demonstrate that silibinin can inhibit $TNF-{\alpha}$-induced osteoclastogenesis as well as the expression of NFATc1 and OSCAR. Taken together, our results indicate that silibinin has the potential to inhibit osteoclast formation by attenuating the downstream signaling cascades associated with RANKL and $TNF-{\alpha}$.

Extracranial systemic antitumor response through the abscopal effect induced by brain radiation in a patient with metastatic melanoma

  • D'Andrea, Mark A.;Reddy, G.K.
    • Radiation Oncology Journal
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    • v.37 no.4
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    • pp.302-308
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    • 2019
  • The abscopal effect is a term that has been used to describe the phenomenon in which localized radiation therapy treatment of a tumor lesion triggers a spontaneous regression of metastatic lesion(s) at a non-irradiated distant site(s). Radiation therapy induced abscopal effects are believed to be mediated by activation and stimulation of the immune system. However, due to the brain's distinctive immune microenvironment, extracranial abscopal responses following cranial radiation therapy have rarely been reported. In this report, we describe the case of 42-year-old female patient with metastatic melanoma who experienced an abscopal response following her cranial radiation therapy for her brain metastasis. The patient initially presented with a stage III melanoma of the right upper skin of her back. Approximately 5 years after her diagnosis, the patient developed a large metastatic lesion in her upper right pectoral region of her chest wall and axilla. Since the patient's tumor was positive for BRAF and MEK, targeted therapy with dabrafenib and trametinib was initiated. However, the patient experienced central nervous system (CNS) symptoms of headache and disequilibrium and developed brain metastases prior to the start of targeted therapy. The patient received radiation therapy to a dose of 30 Gy delivered in 15 fractions to her brain lesions while the patient was on dabrafenib and trametinib therapy. The patient's CNS metastases improved significantly within weeks of her therapy. The patient's non-irradiated large extracranial chest mass and axilla mass also shrank substantially demonstrating the abscopal effect during her CNS radiation therapy. Following radiation therapy of her residual chest lesions, the patient was disease free clinically and her CNS lesions had regressed. However, when the radiation therapy ended and the patient continued her targeted therapy alone, recurrence outside of her previously treated fields was noted. The disease recurrence could be due to the possibility of developing BRAF resistance clones to the BRAF targeted therapy. The patient died eventually due to wide spread systemic disease recurrence despite targeted therapy.

The Role of Corticotropin-Releasing Factor and Urocortin in Brain Mechanisms Controlling Feed Intake of Sheep

  • Sunagawa, K.;Weisiger, R.S.;McKinley, M.J.;Purcell, B.S.;Thomson, C.;Burns, P.L.
    • Asian-Australasian Journal of Animal Sciences
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    • v.13 no.11
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    • pp.1529-1535
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    • 2000
  • The aim of the present study was to determine whether brain corticotropin-releasing factor (CRF) and a new peptide, urocortin (UCN) have a direct action in brain mechanisms controlling feed, water and salt intake in sheep. We gave a continuous intracerebroventricular (ICV) infusion of the peptide at a small dose of $5{\mu}g/0.2ml/hr$ for 98.5 hrs from day 1 to day 5 in sheep not exposed to stress. Feed and water intake during ICV infusion of CRF or UCN decreased significantly compared to those during artificial cerebrospinal fluid (CSF) infusion. NaCl intake during infusion of CRF or UCN was the same as that during CSF infusion. Mean carotid arterial blood pressure (MAP) and heart rate during ICV infusion of CRF or UCN were not significantly different from that during CSF infusion. On the other hand, the plasma glucose concentration during ICV infusion of CRF or UCN tended to be higher than that during CSF infusion. These observations indicate that decreased feed intake induced by CRF and UCN infusion is not mediated by the activation of both the pituitary-adrenal axis and the sympathetic nervous system. The results suggested that brain CRF and UCN act directly in brain mechanisms controlling ingestive behavior to decrease feed and water intake, but do not alter salt intake in sheep.

Immunohistochemical localization of PLC in rat brain after chronic ECS

  • Hey suk Ihm;You, Je-Kyung;Ryu, Jae-Ryun;Shin, Chan-Young;Ko, Kwang-Ho
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1998.11a
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    • pp.197-197
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    • 1998
  • Chronic electroconvulsive shock(ECS) was shown to Increase phosphatidylinositol-4,5-bisphosphate(PIP$_2$) breakdown and the activity of PLC with the accumulation of inositol-1,4,5-triphosphate(IP3). The purpose of the present study was to determine the effect of ECS on the expression of phospholipase C(PLC) isotypes in rat brain. Two groups of animals were prepared: sham and ECS treated groups. Rats in ECS treated groups received maximal ECS(70mA, 0.5second, 60㎐) by constant current stimulator through ear-clip to induce tonic extension seizures for 12 consecutive days. The expression of PLC isotypes in rat brain was determined by immunohistochemical procedure using sagital section of rat brain. The immunoreactivity of PLC${\beta}$1 was observed in corpus striatum, hippocampus, thalamus and that of PLC${\gamma}$1 in corpus striatum, hippocampus, thalamus, frontal cortex, parietooccipital cortex, limbic forebrain, pons, medulla, superior colliculus, inferior colliculus, rest of midbrain. The amount of PLC was analyzed by Western blot using antibodies against PLC${\beta}$1 and PLC${\gamma}$1. Chronic ECS reduced the immunoreactivity of PLC${\beta}$1 in corpus striatum, hippocampus, thalamus but had little effect on PLC${\gamma}$1. To quantify this change, quantitative Western blot using antibodies against PLC${\beta}$1 and PLC${\gamma}$1 was conducted. The immunoreactivity of PLC${\beta}$1 in ECS treated rat whole brain was decreased by 40 % in cytosolic fraction and 26 % in membrane fraction. This different effect of ECS on PLC isotypes may results from the difference of their activation mechanisms and the different effects of ECS on them. The results from the present study suggest that chronic ECS primalily affects neurotransmitter receptors related IP$_3$ signaling in rat brain.

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A Study of Correlation between Big 5 Personality Traits and SRQ of Brain Quotient (Big 5 성격특성과 뇌기능 분석지수(BQ)의 자기조절지수 (Self Regulation Quotient)와의 상관관계 연구)

  • Im, Giyong;Park, Hee-Rae;Choi, Nam-Sook;Park, Pyong-Woon
    • Journal of the Korea Academia-Industrial cooperation Society
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    • v.16 no.6
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    • pp.3760-3768
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    • 2015
  • This study was to examine the correlation of Personality and EEG. Personality test and EEG of the 40 team leader of a business enterprise were carried out at the same time and the correlation of test results were analyzed. Personality test was done by Big 5 and brain waves were measured by 2-Channel EEG System at Fp1 and Fp2. The analysis showed a positive correlation between the Big 5 agreeableness and SRQ(Self Regulation Quotient) relaxation status which is related with alpha rhythm, and showed a negative correlation between the Big 5 openness and SRQ concentration status which is related with low_beta rhythm. It means that the personality is closely correlated with human brain cortex activation and can be checked by brainwave analysis.

Aluminum Nanoparticles Induce ERK and p38MAPK Activation in Rat Brain

  • Kwon, Jung-Taek;Seo, Gyun-Baek;Jo, Eunhye;Lee, Mimi;Kim, Hyun-Mi;Shim, Ilseob;Lee, Byung-Woo;Yoon, Byung-Il;Kim, Pilje;Choi, Kyunghee
    • Toxicological Research
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    • v.29 no.3
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    • pp.181-185
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    • 2013
  • Aluminum nanoparticles (Al-NPs) are one of the most widely used nanomaterial in cosmetics and medical materials. For this reason, Al-NP exposure is very likely to occur via inhalation in the environment and the workplace. Nevertheless, little is known about the mechanism of Al-NP neurotoxicity via inhalation exposure. In this study, we investigated the effect AL-NPs on the brain. Rats were exposed to Al-NPs by nasal instillation at 1 mg/kg body weight (low exposure group), 20 mg/kg body weight (moderate exposure group), and 40 mg/kg body weight (high exposure group), for a total of 3 times, with a 24-hr interval after each exposure. Inductively coupled plasma mass spectrometry (ICP-MS) analysis indicated that the presence of aluminum was increased in a dose-dependent manner in the olfactory bulb (OFB) and the brain. In microarray analysis, the regulation of mitogen-activated protein kinases (MAPK) activity (GO: 0043405), including Ptprc, P2rx7, Map2k4, Trib3, Trib1, and Fgd4 was significantly over-expressed in the treated mice than in the controls (p = 0.0027). Moreover, Al-NPs induced the activation of ERK1 and p38 MAPK protein expression in the brain, but did not alter the protein expression of JNK, when compared to the control. These data demonstrate that the nasal exposure of Al-NPs can permeate the brain via the olfactory bulb and modulate the gene and protein expression of MAPK and its activity.

Abnormal Behavior Controlled via GPR56 Expression in Microglia (미세아교세포에서 GPR56 발현에 의한 이상 행동)

  • Hyunju Kim
    • Journal of Life Science
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    • v.33 no.6
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    • pp.455-462
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    • 2023
  • During pregnancy, maternal immune activation (MIA) from infection increases the risk of neurodevelopmental diseases, including schizophrenia and autism spectrum disorders. MIA induced by polyinosinic-polycytidylic acid (poly (I:C)) and lipopolysaccharide (LPS) in animal experiments has led to offspring with abnormal behaviors and brain development. In addition, it has recently been reported that microglia, which reside in the brain and function as immune cells, play an important role in behavioral abnormalities and brain development in MIA-induced offspring. However, the underlying mechanism remains unclear. In this study, we investigated whether microglia-specific inhibition of GPR56, a member of the G protein-coupled receptor (GPCR) family, causes behavioral abnormalities in brain development. First, MIA induction did not affect the microglia population, but when examining the expression of microglial GRP56 in MIA-induced fetuses, GPR56 expression was inhibited between embryonic days 14.5 (E14.5) and E18.5 regardless of sex. Furthermore, microglial GPR56-suppressed mice showed abnormal behaviors in the MIA-induced offspring, including sociability deficits, repetitive behavioral patterns, and increased anxiety levels. Although abnormal cortical development such as that in the MIA-induced offspring were not observed in the microglial GPR56-suppressed mice, their brain activity was observed through c-fos staining. These results suggest that microglia-specific GPR56 deficiency may cause abnormal behaviors and could be used as a biomarker for the diagnosis and/or as a therapeutic target of behavioral deficits in MIA offspring.