• The Korean Journal of Physiology and Pharmacology
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• 제20권3호
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• pp.229-236
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• 2016

Resveratrol (RSV) may provide numerous protective effects against chronic inflammatory diseases. Due to local hypoxia and hypertonicity, the renal medulla is subject to extreme oxidative stress, and aldehyde products formed during lipid peroxidation, such as 4-hydroxy-2-hexenal (HHE), might be responsible for tubular injury. This study aimed at investigating the effects of RSV on renal and its signaling mechanisms. While HHE treatment resulted in decreased expression of Sirt1, AQP2, and nuclear factor erythroid 2-related factor 2 (Nrf2), mouse cortical collecting duct cells (M1) cells treated with HHE exhibited increased activation of p38 MAPK, extracellular signal regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and increased expression of NOX4, $p47^{phox}$, Kelch ECH associating protein 1 (Keap1) and COX2. HHE treatment also induced $NF-{\kappa}B$ activation by promoting $I{\kappa}B-{\alpha}$ degradation. Meanwhile, the observed increases in nuclear $NF-{\kappa}B$, NOX4, $p47^{phox}$, and COX2 expression were attenuated by treatment with Bay 117082, N-acetyl-l-cysteine (NAC), or RSV. Our findings indicate that RSV inhibits the expression of inflammatory proteins and the production of reactive oxygen species in M1 cells by inhibiting $NF-{\kappa}B$ activation.

• 한국발생생물학회지:발생과생식
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• 제24권4호
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• pp.297-306
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• 2020

Repetitive changes in the intracellular calcium concentration ([Ca²⁺]i) triggers egg activation, including cortical granule exocytosis, resumption of second meiosis, block to polyspermy, and initiating embryonic development. [Ca²⁺]i oscillations that continue for several hours, are required for the early events of egg activation and possibly connected to further development to the blastocyst stage. The sources of Ca²⁺ ion elevation during [Ca²⁺]i oscillations are Ca²⁺ release from endoplasmic reticulum through inositol 1,4,5 tri-phosphate receptor and Ca²⁺ ion influx through Ca²⁺ channel on the plasma membrane. Ca²⁺ channels have been characterized into voltage-dependent Ca²⁺ channels (VDCCs), ligand-gated Ca²⁺ channel, and leak-channel. VDCCs expressed on muscle cell or neuron is specified into L, T, N, P, Q, and R type VDCs by their activation threshold or their sensitivity to peptide toxins isolated from cone snails and spiders. The present study was aimed to investigate the localization pattern of N and P/Q type voltage-dependent calcium channels in mouse eggs and the role in fertilization. [Ca²⁺]i oscillation was observed in a Ca²⁺ contained medium with sperm factor or adenophostin A injection but disappeared in Ca²⁺ free medium. Ca²⁺ influx was decreased by Lat A. N-VDCC specific inhibitor, ω-Conotoxin CVIIA induced abnormal [Ca²⁺]i oscillation profiles in SrCl₂ treatment. N or P/Q type VDC were distributed on the plasma membrane in cortical cluster form, not in the cytoplasm. Ca²⁺ influx is essential for [Ca²⁺]i oscillation during mammalian fertilization. This Ca²⁺ influx might be controlled through the N or P/Q type VDCCs. Abnormal VDCCs expression of eggs could be tested in fertilization failure or low fertilization eggs in subfertility women.

• Korean Journal of Acupuncture
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• 제35권4호
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• pp.187-202
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• 2018

Objectives : Non-invasive transcranial electrical stimulation is one of therapeutic interventions to change in neural excitability of the cortex. Transcranial electro-acupuncture (TEA) can modulate brain functions through changes in cortical excitability as a model of non-invasive transcranial electrical stimulation. Some composites of fermented Scutellaria baicalenis (FSB) can activate intercellular signaling pathways for activation of brain-derived neurotrophic factor that is critical for formation of neural plasticity in stroke patients. This study was aimed at evaluation of combinatory treatment of TEA and FSB on behavior recovery and cortical neural excitability in rodent focal stroke model. Methods : Focal ischemic stroke was induced by photothrombotic injury to the motor cortex of adult rats. Application of TEA with 20 Hz and $200{\mu}A$ in combination with daily oral treatment of FBS was given to stroke animals for 3 weeks. Motor recovery was evaluated by rotating bean test and ladder working test. Electrical activity of cortical pyramidal neurons of stroke model was evaluated by using multi-channel extracellular recording technique and thallium autometallography. Results : Compared with control stroke group who did not receive any treatment, Combination of TEA and FSB treatment resulted in more rapid recovery of forelimb movement following focal stroke. This combination treatment also elicited increase in spontaneous firing rate of putative pyramidal neurons. Furthermore expression of metabolic marker for neural excitability was upregulated in peri-infract area under thallium autometallography. Conclusions : These results suggest that combination treatment of TEA and FSB can be a possible remedy for motor recovery in focal stroke.

• 생물정신의학
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• 제12권1호
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• pp.32-41
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• 2005

Objective:Impaired processing of working memory is one of the cognitive deficits seen in patients with schizophrenia. This aimed at corroborating the differences in the brain activities involved in the process of working memory between patients with schizophrenia and the control subjects. Method:Fourteen patients with schizophrenia and 12 healthy volunteers were recruited in this study. Functional magnetic resonance imaging(fMRI) was used to assess cortical activities during the performance of a 2-back visual working memory paradigm using the Korean alphabet as mnemonic content. Results:Group analysis revealed that left lateral prefrontal cortex and right parietal lobule showed decreased cortical activities in the patient group. On the other hand, an increased activation in left superior and middle frontal gyrus, left middle temporal gyrus, right cuneus, both occipital lobes, right fusiform gyrus and right cingulate gyrus. The activation in left anterior lobe and both declive of cerebellum was also increased. Conclusions:This study showed a decreased activation in left lateral prefrontal and right parietal neural networks from the patient group and confirmed the earlier findings on the impaired working memory of patients with schizophrenia using fMRI investigation. The regions implicated in our study suggest an abnormal functioning of the fronto-parietal cortical areas that are critical to the information processing stream, which might be correspondent to common pathophysiology rather than a common etiology in schizophrenia.

• The Journal of Korean Physical Therapy
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• 제15권3호
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• pp.295-345
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• 2003

This study investigated activation of cerebral cortex in patients with hemiplegia that was caused by neural damage. Key-point control movement therapy of Bobath was performed for 9 weeks in 3 subjects with hemiplegia and fMRI was used to compare and analyze activated degree of cerebral cortex in these subjects. fMRI was conducted using the blood oxygen level-dependent(BOLD) technique at 3.0T MR scanner with a standard head coil. The motor activation task consisted of finger flexion-extension exercise in six cycles(one half-cycles = 8 scans = $3\;sec{\times}\;8\;=\;24\;sec$). Subjects performed this task according to visual stimulus that sign of right hand or left hand twinkled(500ms on, 500ms off). After mapping activation of cerebral motor cortex on hand motor function, below results were obtained. 1. Activation decreased in primary motor area, whereas it increased in supplementary motor area and visual association area(p<.001). 2. Activation was observed in bilateral medial frontal gyrus, middle frontal gyrus of left cerebrum, inferior frontal gyrus, inter-hemispheric, fusiform gyrus of right cerebrum, superior parietal lobule of parietal lobe and precuneus in subjedt 1, parahippocampal gyrus of limbic lobe and cingulate gyrus in subject 2, and inferior frontal gyrus of right frontal lobe, middle frontal gyrus, and inferior parietal lobule of left cerebrum in subject 3 (p<.001). 3. Activation cluster extended in declive of right cellebellum posterior lobe in subject 1, culmen of anterior lobe and declive of posterior lobe in subject 2, and dentate gyrus of anterior lobe, culmen and tuber of posterior lobe in subject 3 (p<.001). In conclusion, these data showed that Key-point control movement therapy of Bobath after stroke affect cerebral cortex activation by increasing efficiency of cortical networks. Therefore mapping of brain neural network activation is useful for plasticity and reorganization of cerebral cortex and cortico-spinal tract of motor recovery mechanisms after stroke.

• The Korean Journal of Physiology and Pharmacology
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• 제21권2호
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• pp.179-188
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• 2017

With the explosive increase in exposure to radiofrequency electromagnetic fields (RF-EMF) emitted by mobile phones, public concerns have grown over the last few decades with regard to the potential effects of EMF exposure on the nervous system in the brain. Many researchers have suggested that RF-EMFs can effect diverse neuronal alterations in the brain, thereby affecting neuronal functions as well as behavior. Previously, we showed that long-term exposure to 835 MHz RF-EMF induces autophagy in the mice brain. In this study, we explore whether shortterm exposure to RF-EMF leads to the autophagy pathway in the cerebral cortex and brainstem at 835 MHz with a specific absorption rate (SAR) of 4.0 W/kg for 4 weeks. Increased levels of autophagy genes and proteins such as LC3B-II and Beclin1 were demonstrated and the accumulation of autophagosomes and autolysosomes was observed in cortical neurons whereas apoptosis pathways were up-regulated in the brainstem but not in the cortex following 4 weeks of RF exposure. Taken together, the present study indicates that monthly exposure to RF-EMF induces autophagy in the cerebral cortex and suggests that autophagic degradation in cortical neurons against a stress of 835 MHz RF during 4 weeks could correspond to adaptation to the RF stress environment. However, activation of apoptosis rather than autophagy in the brainstem is suggesting the differential responses to the RF-EMF stresses in the brain system.

• The Korean Journal of Physiology and Pharmacology
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• 제3권1호
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• pp.93-100
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• 1999

The present study was designed to assess the roles of $PLA_2$ activation and arachidonic acid (AA) metabolites in hypoxia-induced renal cell injury. Hypoxia increased LDH release in a dose-dependent manner in rabbit renal cortical slices, and this increase was significant after 20-min hypoxia. The hypoxia-induced LDH release was prevented by amino acids, glycine and alanine, and extracellular acidosis (pH 6.0). Buffering intracellular $Ca^{2+}$ by a chelator, but not omission of $Ca^{2+}$ in the medium produced a significant reduction in hypoxia-induced LDH release. The effect of hypoxia was blocked by $PLA_2$ inhibitors, mepacrine, butacaine, and dibucaine. A similar effect was observed by a 85-kD $cPLA_2$ inhibitor $AACOCF_3.$ AA increased hypoxia-induced LDH release, and albumin, a fatty acid absorbent, prevented the LDH release, suggesting that free fatty acids are involved in hypoxia-induced cell injury. These results suggest that $PLA_2$ activation and its metabolic products play important roles in pathogenesis of hypoxia-induced cell injury in rabbit renal cortical slices.

• BMB Reports
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• 제48권7호
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• pp.369-370
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• 2015

Actin dynamics is critical for the formation and sustainment of the immunological synapse (IS) during T cell interaction with antigen-presenting cells (APC). Thus, many actin regulating proteins are involved in spatial and temporal actin remodeling at the IS. However, little is known whether or how actin stabilizing protein controls IS and the consequent T cell functions. TAGLN2 − an actin-binding protein predominantly expressed in T cells − displays a novel function to stabilize cortical F-actin, thereby augmenting F-actin contents at the IS, and acquiring leukocyte function-associated antigen-1 activation following T cell activation. TAGLN2 also competes with cofilin to protect F-actin in vitro and in vivo. During cytotoxic T cell interaction with cancer cells, the expression level of TAGLN2 at the IS correlates with the T cell adhesion to target cancer cells and production of lytic granules such as granzyme B and perforin, thus expressing cytotoxic T cell function. These findings identify a novel function for TAGLN2 as an actin stabilizing protein that is essential for stable immunological synapse formation, thereby regulating T cell immunity. [BMB Reports 2015; 48(7): 369-370]

• 한국산학기술학회논문지
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• 제16권3호
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• pp.1707-1714
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• 2015

본 연구는 사건관련 fMRI를 이용하여 언어 내 및 언어 간 그림명명 과제를 수행하는 동안 모국어와 외래어 명사관련 피질 활성화 영역을 비교해 보고, 특히 외래어의 활성화 패턴이 모국어에 동조되는지를 알아보았다. 아울러 과제수행 언어가 정해지지 않은 임의적 언어전환 조건에 관여하는 활성화 영역도 연구대상이었다. 실험결과, 한 가지 수행언어만으로 제한되는 과제에서는 모국어 및 외래어 모두 좌측 하전두회(LIFG) 활성화가 일어났으나 모국어의 활성화 정도가 더 컸으며, 특히 외래어 명명 시 모국어와의 활성화 강도는 약화된 반면 영역분포는 유사한 결과를 얻었다. 이는 외래어가, 외국어가 아닌 모국어에 동조되었음을 시사한다 하겠다. 마지막으로 언어전환 조건에서의 실험에서는 좌측 하전두피질 외에 우측 중전두피 질이 관여함을 발견함으로써 실험수준이 아닌 일상수준의 다언어 사용에 있어, 의식이전의 언어 간 부호전환에 관여하는 우반구의 상대적인 기여와 역할을 시사하는 결과를 얻었다.

• The Korean Journal of Physiology and Pharmacology
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• 제13권6호
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• pp.461-467
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• 2009

The auditory cortex (A1) encodes the acquired significance of sound for the perception and interpretation of sound. Nitric oxide (NO) is a gas molecule with free radical properties that functions as a transmitter molecule and can alter neural activity without direct synaptic connections. We used whole-cell recordings under voltage clamp to investigate the effect of NO on spontaneous GABAergic synaptic transmission in mechanically isolated rat auditory cortical neurons preserving functional presynaptic nerve terminals. GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) in the A1 were completely blocked by bicuculline. The NO donor, S-nitroso-N-acetylpenicillamine (SNAP), reduced the GABAergic sIPSC frequency without affecting the mean current amplitude. The SNAP-induced inhibition of sIPSC frequency was mimicked by 8-bromoguanosine cyclic 3',5'-monophosphate, a membrane permeable cyclic-GMP analogue, and blocked by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a specific NO scavenger. Blockade of presynaptic $K^+$ channels by 4-aminopyridine, a $K^+$ channel blocker, increased the frequencies of GABAergic sIPSCs, but did not affect the inhibitory effects of SNAP. However, blocking of presynaptic $Ca^{2+}$ channels by $Cd^{2+}$, a general voltage-dependent $Ca^{2+}$ channel blocker, decreased the frequencies of GABAergic sIPSCs, and blocked SNAP-induced reduction of sIPSC frequency. These findings suggest that NO inhibits spontaneous GABA release by activation of cGMP-dependent signaling and inhibition of presynaptic $Ca^{2+}$ channels in the presynaptic nerve terminals of A1 neurons.