• Journal of Korean Neurosurgical Society
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• 제64권1호
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• pp.4-12
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• 2021

Spinal metastases can present with varying degrees of mechanical instability. The Spinal Instability Neoplastic Score (SINS) was developed as a tool to assess spinal neoplastic-related instability while helping to guide referrals among oncology specialists. Some previous papers suggested that the SINS was accurate and reliable, while others disagreed with this opinion. We performed a systematic review regarding the SINS to evaluate its accuracy and precision in predicting vertebral compression fractures (VCFs). The 21 included studies investigated a total of 2118 patients. Thirteen studies dealt with the accuracy of SINS to predict post-radiotherapy VCFs, and eight dealt with the precision. Among 13 studies, 11 agreed that the SINS categories showed statistically significant accuracy in predicting VCF. Among eight studies, body collapse was effective for predicting VCFs in six studies, and alignment and bone lesion in two studies. Location has no statistical significance in predicting VCFs in any of the eight studies. The precision of SINS categories was substantial to excellent in six of eight studies. Among the six components of the SINS, the majority of the included studies reported that location showed near perfect agreement; body collapse, alignment, and posterolateral involvement showed moderate agreement; and bone lesion showed fair agreement. Bone lesion showed significant accuracy in predicting VCFs in half of eight studies, but displayed fair reliability in five of seven studies. Although location was indicated as having near perfect reliability, the component showed no accuracy for predicting VCFs in any of the studies and deleting or modifying the item needs to be considered. The SINS system may be accurate and reliable in predicting the occurrence of post-radiotherapy VCFs for spinal metastasis. Some components seem to be substantially weak and need to be revised.

• Journal of Ginseng Research
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• 제45권2호
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• pp.264-272
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• 2021

Background: Gintonin is a ginseng-derived exogenous G-protein-coupled lysophosphatidic acid (LPA) receptor ligand, which exhibits in vitro and in vivo functions against Alzheimer disease (AD) through lysophosphatidic acid 1/3 receptors. A recent study demonstrated that systemic treatment with gintonin enhances paracellular permeability of the blood-brain barrier (BBB) through the LPA1/3 receptor. However, little is known about whether gintonin can enhance brain delivery of donepezil (DPZ) (Aricept), which is a representative cognition-improving drug used in AD clinics. In the present study, we examined whether systemic administration of gintonin can stimulate brain delivery of DPZ. Methods: We administered gintonin and DPZ alone or coadministered gintonin with DPZ intravenously or orally to rats. Then we collected the cerebral spinal fluid (CSF) and serum and determined the DPZ concentration through liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. Results: Intravenous, but not oral, coadministration of gintonin with DPZ increased the CSF concentration of DPZ in a concentration- and time-dependent manner. Gintonin-mediated enhancement of brain delivery of DPZ was blocked by Ki16425, a LPA1/3 receptor antagonist. Coadministration of vascular endothelial growth factor (VEGF) + gintonin with DPZ similarly increased CSF DPZ concentration. However, gintonin-mediated enhancement of brain delivery of DPZ was blocked by axitinip, a VEGF receptor antagonist. Mannitol, a BBB disrupting agent that increases the BBB permeability, enhanced gintonin-mediated enhancement of brain delivery of DPZ. Conclusions: We found that intravenous, but not oral, coadministration of gintonin facilitates brain delivery of DPZ from plasma via LPA1/3 and VEGF receptors. Gintonin is a potential candidate as a ginseng-derived novel agent for the brain delivery of DPZ for treatment of patients with AD.

• Journal of Ginseng Research
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• 제45권3호
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• pp.390-400
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• 2021

Background: We recently showed that gintonin, an active ginseng ingredient, exhibits antibrain neurodegenerative disease effects including multiple target mechanisms such as antioxidative stress and antiinflammation via the lysophosphatidic acid (LPA) receptors. Amyotrophic lateral sclerosis (ALS) is a spinal disease characterized by neurodegenerative changes in motor neurons with subsequent skeletal muscle paralysis and death. However, pathophysiological mechanisms of ALS are still elusive, and therapeutic drugs have not yet been developed. We investigate the putative alleviating effects of gintonin in ALS. Methods: The G93A-SOD1 transgenic mouse ALS model was used. Gintonin (50 or 100 mg/kg/day, p.o.) administration started from week seven. We performed histological analyses, immunoblot assays, and behavioral tests. Results: Gintonin extended mouse survival and relieved motor dysfunctions. Histological analyses of spinal cords revealed that gintonin increased the survival of motor neurons, expression of brain-derived neurotrophic factors, choline acetyltransferase, NeuN, and Nissl bodies compared with the vehicle control. Gintonin attenuated elevated spinal NAD(P) quinone oxidoreductase 1 expression and decreased oxidative stress-related ferritin, ionized calcium-binding adapter molecule 1-immunoreactive microglia, S100β-immunoreactive astrocyte, and Olig2-immunoreactive oligodendrocytes compared with the control vehicle. Interestingly, we found that the spinal LPA1 receptor level was decreased, whereas gintonin treatment restored decreased LPA1 receptor expression levels in the G93A-SOD1 transgenic mouse, thereby attenuating neurological symptoms and histological deficits. Conclusion: Gintonin-mediated symptomatic improvements of ALS might be associated with the attenuations of neuronal loss and oxidative stress via the spinal LPA1 receptor regulations. The present results suggest that the spinal LPA1 receptor is engaged in ALS, and gintonin may be useful for relieving ALS symptoms.

• Journal of Ginseng Research
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• 제45권3호
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• pp.401-407
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• 2021

Background: Gintonin is an exogenous ginseng-derived G-protein-coupled lysophosphatidic acid (LPA) receptor ligand. LPA induces in vitro morphological changes and migration through neuronal LPA1 receptor. Recently, we reported that systemic administration of gintonin increases blood-brain barrier (BBB) permeability via the paracellular pathway and its binding to brain neurons. However, little is known about the influences of gintonin on in vivo neuron morphology and migration in the brain. Materials and methods: We examined the effects of gintonin on in vitro migration and morphology using primary hippocampal neural precursor cells (hNPC) and in vivo effects of gintonin on adult brain neurons using real time microscopic analysis and immunohistochemical analysis to observe the morphological and locational changes induced by gintonin treatment. Results: We found that treating hNPCs with gintonin induced morphological changes with a cell rounding following cell aggregation and return to individual neurons with time relapses. However, the in vitro effects of gintonin on hNPCs were blocked by the LPA1/3 receptor antagonist, Ki16425, and Rho kinase inhibitor, Y27632. We also examined the in vivo effects of gintonin on the morphological changes and migration of neurons in adult mouse brains using anti-NeuN and -neurofilament H antibodies. We found that acute intravenous administration of gintonin induced morphological and migrational changes in brain neurons. Gintonin induced some migrations of neurons with shortened neurofilament H in the cortex. The in vivo effects of gintonin were also blocked by Ki16425. Conclusion: The present report raises the possibility that gintonin could enter the brain and exert its influences on the migration and morphology of adult mouse brain neurons and possibly explains the therapeutic effects of neurological diseases behind the gintonin administration.

• 동의신경정신과학회지
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• 제32권1호
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• pp.1-11
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• 2021

Objectives: To investigate the prevalence of acute stress disorder (ASD) and post-traumatic stress disorder (PTSD) in patients with traffic injuries. In addition, PTSD patients was classified using 'pattern identification for jing ji and zheng chong'. Methods: Questionnaires such as the primary care PTSD screen for DSM-5(PC-PTSD-5), Korean version of PTSD checklist-5 (PCL-5-K), and the instrument of pattern identification for jing ji and zheng chong were conducted on 195 patients within 3 days to 1 year after traffic accidents. Patients were recruited from six medical institutions. Collected data were used to determine the prevalence of acute stress disorder and post-traumatic stress disorder. Results: On PC-PTSD-5, the prevalence was 39.1% for ASD and 50% for PTSD. On PCL-5-K, the prevalence was 20.4% for ASD and 29.3% for PTSD. Satisfying both PC-PTSD-5 and PCL-5-K, the prevalence was 18.2% for ASD and 25.8% for PTSD. As a result of pattern identification for jing ji and zheng chong, 'weakness of heart and gall bladder type' accounted for the highest proportions in both ASD and PTSD groups. Conclusions: In this study, the prevalence was 39.1% for ASD and 50% for PTSD by PC-PTSD-5. Satisfying both PC-PTSD-5 and PCL-5-K, the prevalence was 18.2% for ASD and 25.8% for PTSD. Further large-scale prospective studies are needed to analyze the prevalence of ASD and PTSD, the rate of progression from ASD to PTSD, and the type of pattern identification.

• 인지과학
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• 제33권1호
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• pp.23-50
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• 2022

출처기억은 사물에 대한 일화기억 경험의 맥락을 표상하는 중요 인지기제이다. 출처기억에 대한 그 동안의 연구는 일상의 일화기억과 밀접한 뇌신경, 행동학적 중요 연구들의 기초가 되어 왔고, 특히 집행기능이나 연합기제와 같은 인지기제를 강조하여 왔다. 본 연구에서는 계량서지학적 방법론을 통해 1989년에서 2020년 사이 출간된 출처기억 연구논문들을 분석하였고 핵심어 공동출현 연결네트워크와 저자 인용 연결망을 기반으로 출처기억 연구의 발전 흐름에 대한 깊이 있는 개관을 제시한다. 계량서지학적 분석을 통해 출처기억 연구의 추세를 확인한 결과, 2010년을 기준으로 이전 연구들에서는 출처기억의 인지적 기제와 관련한 개별 특성을 살핀 반면, 최근의 연구들은 뇌신경영역 간 연결성 특징 분석을 통한 임상적 특징연구를 비롯해 사회신경과학적 주제에 이르는 영향을 탐색하였다. 핵심어 연결성 분석을 통해 노화, 집행기능이 주요 핵심 주제어로서 연구되었음을 확인하였고, 최근 아동발달심리학과 메타기억 등의 관점에서 연구되는 추세로 나아가고 있음을 보았다. 관련된 출처기억의 이론과 연구모델을 기반으로 심리과학분야 내외에서 인지적 향상의 발달과 관련된 연구가 지속될 가능성을 제안하였다.

• 생명과학회지
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• 제32권1호
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• pp.70-77
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• 2022

현대사회에서 내분비계 교란물질(Endocrine Disrupting Chemicals)은 다양한 질환을 유발하는 원인 물질로 잘 알려져 있다. 내분비계 교란물질은 플라스틱병 및 용기, 세제, 금속 식품 캔 라이너, 난연제, 식품, 장난감, 화장품 및 살충제를 비롯한 많은 상업용 제품에서 발견된다. 내분비계 교란물질은 호르몬의 작용을 모방하여 인체 내 뇌하수체, 갑상샘, 부신, 난소 등을 포함한 내분비계를 교란해 생식 기능의 저하, 저티록신 혈증 및 암까지 유발할 수 있는 물질로 사료되고 있다. 최근, 신경과학 분야에서 내분비계 교란물질과 신경 질환과의 연관성에 대한 연구가 활발히 진행되고 있으며, 내분비계 교란물질은 신경세포의 증식, 발달, 분화에 부정적인 영향을 미쳐 자폐증, 주의력 결핍 장애를 포함한 신경 발달장애질환과 파킨슨병, 알츠하이머병과 같은 퇴행성 뇌질환을 유발한다는 연구결과가 발표되었다. 하지만 전 세계적으로 내분비계 교란물질은 인간 생활에 편리함을 제공한다는 이유로 계속 사용되고 있다. 이에 각국의 정부에서는 내분비계 교란물질의 노출을 최소화하기 위한 적절한 규제 및 정책 수립이 필요하며, 내분비계 교란물질이 인체에 미치는 정확한 기전 이해가 절실히 필요한 실정이다. 특히, 내분비계 교란물질이 신경계에 미치는 영향에 대한 정확한 기전 연구가 필요하며 전 세계적으로 이들 연구가 활발히 이루어져야 한다고 사료된다.

• 한국엔터테인먼트산업학회논문지
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• 제15권8호
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• pp.255-267
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• 2021

본 연구의 목적은 스마트도구를 활용한 플립드 러닝 수업 설계 모형을 개발하고 그 타당성을 검증함으로써 체계적이고 효과적인 기초의학 교육을 위한 기초자료를 제시함에 있다. 이를 위해 본 연구에서는 문헌고찰을 바탕으로 모형 시안을 개발하였으며, 전문가 검토 및 현장 적용을 통해 그 타당성을 검증하였다. 본 연구에서는 스마트 도구를 활용한 플립드러닝 수업 설계 모형으로서 RECIPE (R: Ready, E: Establish a Plan, C: Create and Connect Media, I: Into the Classroom, P: Process-focused Assessment, E: Evaluation) 모델을 개발하였다. 이 모델은 플립드 러닝을 설계하는 각각의 단계에서 적합한 스마트도구를 적용함으로서 학습효과를 제고시키는 모델이다. 2019년 1학기 해부학 및 신경과학 강의 개발에 본 모델을 적용한 결과 학생들의 흥미와 만족도가 높게 나타난 결과를 토대로 기초의학 분야에서의 특화된 모델로서 제안하는 바이다. 따라서 본 연구에서 개발한 RECIPE 모델은 여러 기초의학 관련 수업에 적용 가능하며, 이에 기초한 플립드 러닝 수업 설계를 통해 학생들의 기초의학에 대한 이해를 도모할 수 있을 것으로 기대한다.

• 정신신체의학
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• 제30권2호
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• pp.55-65
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• 2022

공감적 존재인 Homo Empathicus로서의 인간들이 살아가는 세상임에도 불구하고, 실제로 우리 사회는 집단간의 분열과 갈등이 끊이지 않고 있다. 인간의 공감 반응은 타자의 정의로움에 민감하여, 타인의 정의로움 여부에 따라 타인의 고통에 공감 반응을 보이기도 하고 쾌감을 느끼기도 한다. 그러나, 타자에 대한 우리의 공감 반응은 항상 정의로운 것은 아니며, 내집단 편향성이라는 내재적 한계를 가지고 있다. 즉, 자신과 같은 집단이나 범주에 속하는 사람인지 아닌지에 따라, 우리는 스스로 의식하지도 못한 채 타인의 고통에 편향적으로 공감하기도 하고, 편향적으로 쾌감을 느끼기도 한다. 최근의 정보통신기술 발전은, 내집단 관련 SNS혹은 내집단 매체에 대한 편향적 접근을 용이하게 하며, 이를 통해 집단과 관련한 보다 편향된 의미론적 정보 네트워크의 구축을 심화시킨다. 이러한 현상들은 공감의 내재적 한계 속성들과 상호작용하여 더욱 편향된 내집단 공감 및 내집단 활동을 하게 하는 악순환의 고리를 형성함으로써 분열과 대립을 가속화할 수 있다. 저자는 공감의 신경 기전에 대한 이해를 통해 공감의 속성과 한계를 고찰해보고, 신경과학적 관점에서 공감과 정의의 관련성을 탐색해봄으로써, 분열과 갈등의 현대 사회를 기존의 사회과학적 시각과는 다른 차원에서 조명해보고자 하였다.

• 한국동물생명공학회지
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• 제37권4호
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• pp.292-297
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• 2022

Direct injection of CRISPR/Cas9 into zygotes enables the production of genetically modified nonhuman primates (NHPs) essential for modeling specific human diseases, such as Usher syndrome, and for developing novel therapeutic strategies. Usher syndrome is a rare genetic disease that causes loss of hearing, retinal degeneration, and problems with balance, and is attributed to a mutation in MYO7A, a gene that encodes an uncommon myosin motor protein expressed in the inner ear and retinal photoreceptors. To produce an Usher syndrome type 1B (USH1B) rhesus macaque model, we disrupted the MYO7A gene in developing zygotes. Identification of appropriately edited MYO7A embryos for knockout embryo transfer requires sequence analysis of material recovered from a trophectoderm (TE) cell biopsy. However, the TE biopsy procedure is labor intensive and could adversely impact embryo development. Recent studies have reported using cell-free DNA (cfDNA) from embryo culture media to detect aneuploid embryos in human in vitro fertilization (IVF) clinics. The cfDNA is released from the embryo during cell division or cell death, suggesting that cfDNA may be a viable resource for sequence analysis. Moreover, cfDNA collection is not invasive to the embryo and does not require special tools or expertise. We hypothesized that selection of appropriate edited embryos could be performed by analyzing cfDNA for MYO7A editing in embryo culture medium, and that this method would be advantageous for the subsequent generation of genetically modified NHPs. The purpose of this experiment is to determine whether cfDNA can be used to identify the target gene mutation of CRISPR/Cas9 injected embryos. In this study, we were able to obtain and utilize cfDNA to confirm the mutagenesis of MYO7A, but the method will require further optimization to obtain better accuracy before it can replace the TE biopsy approach.