• The Journal of Korean Academy of Orthopedic Manual Physical Therapy
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• v.10 no.2
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• pp.5-32
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• 2004

We have studied the effect and application of CST which is the function and disease of the autonomic nerve system based on recovery of flexibleness of the autonomic nerve. CST purpose to keep sustenance of human body by recovering joints have limitation of mobility and controlling autonomic nerve system by diminution tense of the sympathetic nerve. CST makes well flowing of CSF by pressure the fourth ventricle of the brain or relaxation of soft tissues of the base of a cranial bone. There is no result of studies about CST in Korea yet. It will bring a benefit if it prove the effect of CST in countries depend on drugs way high such as Korea. It needs positive approach and definite research for the improvement.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.1
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• pp.27-37
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• 2020

Neuroinflammation is an important process underlying a wide variety of neurodegenerative diseases. Carvacrol (CAR) is a phenolic monoterpene commonly used as a food additive due to its antibacterial properties, but it has also been shown to exhibit strong antioxidative, anti-inflammatory, and neuroprotective effects. Here, we sought to investigate the effects of CAR on inflammation in the hippocampus and prefrontal cortex, as well as the molecular mechanisms underlying these effects. In our study, lipopolysaccharide was injected into the lateral ventricle of rats to induce memory impairment and neuroinflammation. Daily administration of CAR (25, 50, and 100 mg/kg) for 21 days improved recognition, discrimination, and memory impairments relative to untreated controls. CAR administration significantly attenuated expression of several inflammatory factors in the brain, including interleukin-1β, tumor necrosis factor-α, and cyclooxygenase-2. In addition, CAR significantly increased expression of brain-derived neurotrophic factor (BDNF) mRNA, and decreased expression of Toll-like receptor 4 (TLR4) mRNA. Taken together, these results show that CAR can improve memory impairment caused by neuroinflammation. This cognitive enhancement is due to the anti-inflammatory effects of CAR medicated by its regulation of BDNF and TLR4. Thus, CAR has significant potential as an inhibitor of memory degeneration in neurodegenerative diseases.

• Journal of Veterinary Clinics
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• v.33 no.3
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• pp.168-171
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• 2016

Signalment: An 8-month-old female Alaskan malamute was presented for progressive cluster seizure disorder. Results: There were no abnormalities on neurological examination, survey radiographs, or blood analysis. Magnetic resonance (MR) imaging and computed tomography revealed extension of the olfactory bulb and frontal lobe into the nasal cavity. They also confirmed abnormal anatomy of the nasal turbinates within the rostral part of the nasal cavity and the absence of a cribriform plate. On T2-weighted and fluid-attenuated inversion recovery images, the herniated brain showed heterogeneous and hyperintense signals consistent with intraparenchymal edema. Transverse MR images showed brain herniation into the right frontal cavity and an asymmetrical lateral ventricle because of a left midline shift. On contrast-enhanced MR images, the protruding brain parenchyma was mildly enhanced. Ethmoidal encephalocele was suspected as the final diagnosis. Despite symptomatic treatment, the dog continued to exhibit seizures and was euthanized. Clinical relevance: Ethmoidal encephalocele is a rare disease in dogs. However, it could be considered as a cause of seizure in young dogs.

• Journal of Industrial Convergence
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• v.17 no.4
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• pp.39-43
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• 2019

Mouse embryonic stem cell could show an substitutional materials of cells of neuron differentiation, positively increasing their effectiveness in the treatment of nervous symptom. We examined that mouse embryonic stem cells (mESCs) can be induced to undergo neuronal differentiation. After neuronal induction, the phenotype of mESCs changed towards neuronal morphology and mESCs were injected into the lateral ventricle of the experimental animal brain. Transplanted cells migrated to various parts of the brain and ischemic brain injury by middle cerebral artery occlusion (MCAO) increased their migration to the injured cortex. Intracerebral grafting of mESCs mostly improve sensory and motor nervous system of neurological injury in focal cerebral rats.

• Animal cells and systems
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• v.16 no.4
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• pp.302-312
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• 2012

The purpose of this study was to examine whether Phellodendri Cortex extract (PCE) could improve learning and memory impairments caused by lipopolysaccharide (LPS)-induced inflammation in the rat brain. The effect of PCE on modulating pro-inflammatory mediators in the hippocampus and its underlying mechanism were investigated. Injection of LPS into the lateral ventricle caused acute regional inflammation and subsequent deficits in spatial learning ability in the rats. Daily administration of PCE (50, 100, and 200 mg/kg, i.p.) for 21 days markedly improved the LPS-induced learning and memory disabilities in the Morris water maze and passive avoidance test. PCE administration significantly decreased the expression of pro-inflammatory mediators such as tumor necrosis factor-${\alpha}$, interleukin-$1{\beta}$, and cyclooxygenase-2 mRNA in the hippocampus, as assessed by RT-PCR analysis and immunohistochemistry. Together, these findings suggest that PCE significantly attenuated LPS-induced spatial cognitive impairment through inhibiting the expression of pro-inflammatory mediators in the rat brain. These results suggested that PCE may be effective in preventing or slowing the development of neurological disorders, including Alzheimer's disease, by improving cognitive and memory function because of its anti-inflammation activity in the brain.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.04a
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• pp.212-212
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• 1996

Effects of ginseng total saponin(GTS) on changes in the glutamatergic nervous system induced by AF64A were studied in rats. Rats were pretreated with the infusion of AF64A (3mM) into lateral ventricle and were posttreated with GTS (50mg/kg, j.p) for 1 week. Twenty four hrs after the last administration, rats were sacrified and each brain resions was dissected ; striatum, hippocampus and frontal cortex. At each brain regions, total glutamate and other amino acids levels, [$^3$H]MK801 binding sites and glutamine synthetase activity were measured using HPLC-ECD, ligand binding assay and enzyme activity assay, respectively. The AF64-induced increase in the levels of total glutamate in hippocampus were significantly decreased by the administration of GTS. Furthermore, that compared with saline and GTS was decreased in striatum. The levels of total GABA compared with saline and GTS were declined in frontal cortex. Moreover, the AF64A-induced decrease in the levels of total taurine were significantly increased by the administration of GTS to extents of normal states. The numbers of [$^3$H]MK801 binding sites were differently affected in brain resiojns ; the decrease in hippocampus and no change in both striatum and frontal cortex, Glutamine synthetase activity was significantly increased in hippocampus. In comparision with saline and GTS, that was significantly decreased in striatum These results suggest that GTS may adjust the levels of glutamate, GABA and taurine constantly and may induce increase of glutamine synthetase activity declined.

• Journal of Korean Neurosurgical Society
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• v.66 no.4
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• pp.400-408
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• 2023

Objective : Nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2) is a crucial factor for the survival of neuron. The role of NMNAT2 in damage following traumatic brain injury (TBI) remains unknown. This study was designed to investigate the role of NMNAT2 in TBI-induced neuronal degeneration and neurological deficits in rats. Methods : The TBI model was established in Sprague-Dawley rats by a weight-dropping method. Real-time polymerase chain reaction, western blot, immunofluorescence, Fluoro-Jade C staining, and neurological score analyses were carried out. Results : NMNAT2 mRNA and protein levels were increased in the injured-side cortex at 6 hours and peaked 12 hours after TBI. Knocking down NMNAT2 with an injection of small interfering RNA in lateral ventricle significantly exacerbated neuronal degeneration and neurological deficits after TBI, which were accompanied by increased expression of BCL-2-associated X protein (Bax). Conclusion : NMNAT2 expression is increased and NMNAT2 exhibits neuroprotective activity in the early stages after TBI, and Bax signaling pathway may be involved in the process. Thus, NMNAT2 is likely to be an important target to prevent secondary damage following TBI.

• Journal of Chest Surgery
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• v.40 no.9
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• pp.593-599
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• 2007

Background: The correlation between levels of brain natriuretic peptide (BNP) and the effect of pulmonary resection on the right ventricle of the heart is not yet widely known. This study aims to assess the relationship between the change in hemodynamic values of the right ventricle and increased BNP levels as a compensatory mechanism for right heart failure following pulmonary resection and to evaluate the role of the BNP level as an index of right heart failure after pulmonary resection. Material and Method: In 12 non small cell lung cancer patients that had received a lobectomy or pnemonectomy, the level of NT-proBNP was measured using the immunochemical method (Elecsys $1010^{(R)}$, Roche, Germany) which was compared with hemodynamic variables determined through the use of a Swan-Garz catheter prior to and following the surgery. Echocardiography was performed prior to and following the surgery, to measure changes in right ventricular and left ventricular pressures. For statistical analysis, the Wilcoxon rank sum test and linear regression analysis were conducted using SPSSWIN (version, 11.5). Result: The level of postoperative NT-proBNP (pg/mL) significantly increased for 6 hours, then for 1 day, 2 days, 3 days and 7 days after the surgery (p=0.003, 0.002, 0.002, 0.006, 0.004). Of the hemodynamic variables measured using the Swan-Ganz catheter, the mean pulmonary artery pressure after the surgery when compared with the pressure prior to surgery significantly increased at 0 hours, 6 hours, then 1 day, 2 days, and 3 days after the surgery (p=0.002, 0,002, 0.006, 0.007, 0.008). The right ventricular pressure significantly increased at 0 hours, 6 hours, then 1 day, and 3 days after the surgery (p=0.000, 0.009, 0.044, 0.032). The pulmonary vascular resistance index [pulmonary vascular resistance index=(mean pulmonary artery pressure-mean pulmonary capillary wedge pressure)/cardiac output index] significantly increased at 6 hours, then 2 days after the surgery (p=0.008, 0.028). When a regression analysis was conducted for changes in the mean pulmonary artery pressure and NT-proBNP levels after the surgery, significance was evident after 6 hours (r=0.602, p=0.038) and there was no significance thereafter. Echocardiography displayed no significant changes after the surgery. Conclusion: There was a significant correlation between changes in the mean pulmonary artery pressure and the NT-proBNP level 6 hours after a pulmonary resection. Therefore, it can be concluded that changes in NT-proBNP level after a pulmonary resection can serve as an index that reflects early hemodynamic changes in the right ventricle after a pulmonary resection.

• Journal of Korean Neurosurgical Society
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• v.29 no.2
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• pp.249-254
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• 2000

Objective : As a minimally invasive strategy, endoscopic technique was introduced for removal of the traumatic intracerebral hematoma. Material and Method : A 54-year-old man with three-day history of seizure and progressive mental deterioration after traffic accident was presented. Computerized Tomography(CT) of the brain showed a huge intracerebral hematoma on the right frontal lobe and ventricle. The operation was performed via right frontal superolateral keyhole with 2cm eyebrow skin incision. Using 0-degree and 30-degree angled lens 4mm rigid endoscopes, nearly all of the hematoma was evacuated under the direct endoscopic visualization and a ventricular catheter was exactly placed into the frontal horn of the right lateral ventricle at the end of procedure. Results : The seizure was discontinued and neurological status had been improved during postoperative periods. Postoperative CT demonstrated that most of the hematoma was removed and the ventricular drainge tube was exactly placed in the right foramen of Monro. Conclusion : With endoscopic technique, the authors successfully evacuated traumatic intracerebral hematoma and exactly placed the ventricular drainage catheter under direct visualization. This technique may be considered as an another option for removal of traumatic intracerebral hematoma.

• The Korean Journal of Pharmacology
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• v.18 no.1
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• pp.11-16
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• 1982

This study was carried out in order to clarify whether the cardiovascular effect of prostaglandin(PG) $F_{2{\alpha}}$ might be centrally mediated. In unrestrained conscious rat, $PGF_{2{\alpha}}$ was administered into the lateral ventricle. The mechanism of action was also studied by observing the interaction with several adrenergic antagonists injected subcutaneously, Indomethacin was administered into lateral ventricle to investigate the role of endogenous $PGF_{2{\alpha}}$ on the central regulation of cardiovascular system. The results were as follows: 1) The intraventricular injection of $PGF_{2{\alpha}}$ produced an increase in blood pressure and heart rate. 2) The pretreatment with phenoxybenzamine (2 mg/g, s.c.) inhited pressor, but not heart rate responses to the intraventricular injection of $PGF_{2{\alpha}}$ $(2{\mu}g/kg)$. 3) The pretreatment with propranolol (1 mg/kg, s.c.) inhibited tachycardia, but not pressor responses to the intraventricular injection of $PGF_{2{\alpha}}(2{\mu}g/kg)$. 4) The intraventricular injection of indomethacin $(40{\mu}g/kg)$ could not induce significant changes in blood preesure and heart rate. 5) The result indicates that intraventricular injection of $PGF_{2{\alpha}}$ produces pressor and tachycardia responses in the unanesthetized rat, and it is mediated primarily by centrally increased sympathetic outflow. But the endogenous $PGF_{2{\alpha}}$ synthetized in the brain seems to play minor role in the direct regulation of cardiovascular system.