Policy Directions & Tasks for the Human Resource Development in Education

본 연구에서는 교육인적자원 개발의 성패를 좌우한다고 볼 수 있는 핵심세력인 1) 교원, 2) 학교행정가, 3) 교육전문직, 4) 일반행정직, 5) 대학교수, 6) 대학행정직 등 교육 분야의 주요 핵심 인력을 대상으로 인적자원 개발·관리의 현황과 문제, 그리고 개선방안을 탐색하였다. 구체적으로 말해, 교육인적자원 개발·관리의 주요과정인 1) 양성, 2) 개발, 3) 활용, 4) 유지 등의 측면에서 우리나라 교육인적자원개발의 현황 및 문제점, 그리고 앞으로의 개선 방향 및 과제 등을 모색함으로써 우리나라 교육분야 인적자원 정책개발과 방향 설정에 시사점을 제공해 보고자 하였다.Ⅰ. 연구의 개요 1 1. 연구 필요성 및 목적 1 2. 연구의 내용과 범위 2 3. 연구방법 3 Ⅱ. 초·중등 교사의 확보와 개발 5 1. 서 설 5 2. 교사의 확보, 개발의 현황 5 3. 교사의 확보, 개발의 문제점 17 4. 주요국의 교사 양성 27 5. 교사의 확보, 개발의 발전방향 28 6. 소 결 34 Ⅲ. 대학교원의 확보와 개발 35 1. 서 설 35 2. 교수요원 인적자원 개발 35 3. 현황 및 문제점 38 4. 주요국의 대학 교원 45 5. 발전 방향 및 과제 52 6. 소 결 57 Ⅳ. 학교행정가의 확보와 개발 59 1. 서 설 59 2. 학교행정가 확보 및 개발의 현황과 문제점 60 3. 주요국의 학교행정가 양성 및 개발 67 4. 학교행정가의 양성 및 개발 방향 74 5. 소 결 80 Ⅴ. 교육전문직의 확보와 개발 85 1. 서 설 85 2. 교육전문직의 역할과 업무 87 3. 교육전문직의 자질과 자격 92 4. 주요국의 교육전문직 95 5. 교육전문직의 인력관리 현황 및 문제점 101 6. 교육전문직의 확보와 개발을 위한 방향 및 과제 109 7. 소 결 116 Ⅵ. 대학행정직의 확보와 개발 117 1. 서 설 117 2. 대학행정관리직의 현황 및 문제점 118 3. 주요국의 대학행정직 122 4. 대학행정관리 혁신을 위한 기반조성 128 5. 대학행정관리자의 자격과 핵심역량의 개발과제 134 6. 소 결 137 Ⅶ. 교육행정직의 확보와 개발 139 1. 서 설 139 2. 교육행정직의 개념과 규모 140 3. 현황 142 4. 주요 문제점 153 5. 교육행정직 인적자원개발 정책방향과 과제 156 6. 소 결 160 Ⅷ. 결론 및 제언 161 참고문헌 16

A Study on The Infra Construction of National Human Resource Development

21세기 국가 전략사업의 일환으로 국가인적자원의 개발의 인프라 구축을 위해서는 인적자원개발과 관련한 제반 사항들이 종합적으로 재검토되어야 한다. 이를 위해서는 교육행정체제에 대한 전면적인 진단과 분석이 요구되며, 교원개발체제의 새로운 구축, 국가인적자원개발을 위한 정부 부처간 조정과 협력을 비롯한 관련 법령의 재정비가 요청되며, 아울러 국가인적자원개발을 위한 투자와 재원의 우선 순위가 시급히 재검토되어야 한다. 따라서, 본 연구는 이와 같은 각각의 과제에 대한 대안들이 구안하고 제시함으로써 국가인적자원개발의 전략 수립과 추진을 위한 기초적인 정보와 자료를 제공하는 데 주안점을 두고자 한다.Recently the government came up with the National Human Resources Development(NHRD) policy. The South Korean government has adopted the NHRD as an essential project. Because the efficient training and use of the NHR upgrade the quality of life and national competitiveness. That is to say, it is the NHRD that can develop human potentiality and ability throughout the social system. It is imperative to establish the social infra system that would play a role in the training, placement and use of the NHR in the future for its efficient operation . Until now, studies on the NHRD have been limited to specific scholars or organizations. More profound researches and studies have to be prevailed for improving the NHRD. In this paper, in order to clear the way of developing human resources, we have taken five issues: 1) the construction of educational administration system, 2) the establishment of teacher training system, 3) the adjustment and cooperation among the government organizations, 4) the investigation of laws and regulations related to the NHRD and 5) the investment and the financial resource for the NHRD. First, we study the educational administration system at the level of the central government and the local government respectively. Nationally, we study the educational administration structure of the central government and locally, do we focus on the interrelationship with the central one. In addition, we went over the drive system of local government's NHRD policy. Second, in order to establish the teacher training system, considering the educational contents of teachers and their human resource, we suggested the establishment of the teacher evaluation system, the enforcement of the teacher's licence test, the enactment of standard curriculum for the teacher training, practice education enforcement as institution of the probationary period, and the change of the performance-oriented research study. Third, through the adjustment and cooperation among the government organizations, the government can make the best use of the NHRD policy. Overlapped policies must be adjusted to one organization and, if necessary, intense cooperation between the organizations also ought to be made. On the basis of this adjustment and cooperation, we study four fields : 1) connecting job training to related work, 2) training professional human resources and supporting R&D in national strategic field, 3) developing woman resources and their application on the field . 4) developing vulnerable youths and physically challenged peoplen To achieve these purposes, our research shows that the government need to make a use of internet, publicize the importance of the NHRD, share the information of the NHR with people, reorganize the government, revaluate the NHRD policy regularly, and maximize the autonomy of the private sector. Fourth, we investigate laws and regulations related to the NHRD and propose some solutions. We study the Education Basic Law (the legislation of basic articles about job education, the problem of religion education in primary and secondary school), the Primary and Secondary Education Law(the enactment of various school systems, government designed textbook, controversial point and assignment of the merger and abolition of the schools), the Higher Education law, the Life-long Education and Training Law and so on . Last, we study the necessary investment and the financial resource for the NHRD, the priority and the method for the investment. The priority of the investment is to finance basic social utilities and database on information society, higher quality human resources, and the undeveloped areas and lower class for the purpose of unifying the society. In addition, there are two methods in the NHRD for the government. One is to invest directly and the other is to compensate private sector investment which needs to examined seriously. For Infra construction for the NHRD, we have studied five fields, analysed the situation, and produced the alternatives. However, these tasks too serious to be reached independently further. Anyway there are enough reasons the government must invest the manpower and human resources to develop the national competitiveness and the quality of life.연구요약 Ⅰ. 서 론 1 1. 연구의 필요성 및 목적 1 2. 연구내용 및 방법 4 3. 연구의 범위와 한계 5 Ⅱ. 국가인적자원개발을 위한 교육행정체제의 구축 7 1. 인적자원개발의 개념과 의미 7 2. 국가인적자원개발을 위한 인프라 구축 과제 16 3. 국가인적자원개발을 위한 교육행정체제 구축 19 Ⅲ. 국가인적자원개발을 위한 교원개발체제의 구축 29 1. 교원개발을 위한 모형과 기준 29 2. 인적자원개발 관점에서의 교원개발체제 구축방안 33 Ⅳ. 국가인적자원개발을 위한 정부 부처간 조정과 협력 43 1. 문제 인식 43 2. 분석의 준거와 대상 46 3. 실태 분석 결과 48 4. 정부부처간 조정과 협력을 위한 과제 59 Ⅴ. 국가인적자원 개발을 위한 관련 법령의 검토와 과제 63 1. 국가인적자원개발 관련 법령의 체계 64 2. 법령 검토 및 정비의 기본 원리 75 3. 국가인적자원개발 관련 법령의 검토와 과제 80 Ⅵ. 국가인적자원개발을 위한 투자와 재원 91 1. 인적자원개발을 위한 투자의 필요성 91 2. 인적자원개발을 위한 투자의 우선 순위 93 3. 인적자원개발을 위한 투자의 방법 106 Ⅶ. 요약 및 결론 111 참고문헌 115 ABSTRACT 12

O-GlcNAcylation of RIPK1 rescues red blood cells from necroptosis

Necroptosis is a type of cell death with excessive inflammation and organ damage in various human diseases. Although abnormal necroptosis is common in patients with neurodegenerative, cardiovascular, and infectious diseases, the mechanisms by which O-GlcNAcylation contributes to the regulation of necroptotic cell death are poorly understood. In this study, we reveal that O-GlcNAcylation of RIPK1 (receptor-interacting protein kinase1) was decreased in erythrocytes of the mouse injected with lipopolysaccharide, resulting in the acceleration of erythrocyte necroptosis through increased formation of RIPK1-RIPK3 complex. Mechanistically, we discovered that O-GlcNAcylation of RIPK1 at serine 331 in human (corresponding to serine 332 in mouse) inhibits phosphorylation of RIPK1 at serine 166, which is necessary for the necroptotic activity of RIPK1 and suppresses the formation of the RIPK1-RIPK3 complex in Ripk1 -/- MEFs. Thus, our study demonstrates that RIPK1 O-GlcNAcylation serves as a checkpoint to suppress necroptotic signaling in erythrocytes.ope

Neurorestoration induced by mesenchymal stem cells: potential therapeutic mechanisms for clinical trials

Stem cells are emerging as therapeutic candidates in a variety of diseases because of their multipotent capacities. Among these, mesenchymal stem cells (MSCs) derived from bone marrow, umbilical cord blood or adipose tissue, comprise a population of cells that exhibit extensive proliferative potential and retain the ability to differentiate into multiple tissue-specific lineage cells including osteoblasts, chondrocytes, and adipocytes. MSCs have also been shown to enhance neurological recovery, although the therapeutic effects seem to be derived from an indirect paracrine effect rather than direct cell replacement. MSCs secrete neurotrophic factors, promote endogenous neurogenesis and angiogenesis, encourage synaptic connection and remyelination of damaged axons, decrease apoptosis, and regulate inflammation primarily through paracrine actions. Accordingly, MSCs may prevail as a promising cell source for cell-based therapy in neurological diseases.ope

DNA double-strand break-free CRISPR interference delays Huntington's disease progression in mice

Huntington’s disease (HD) is caused by a CAG repeat expansion in the huntingtin (HTT) gene. CRISPR-Cas9 nuclease causes double-strand breaks (DSBs) in the targeted DNA that induces toxicity, whereas CRISPR interference (CRISPRi) using dead Cas9 (dCas9) suppresses the target gene expression without DSBs. Delivery of dCas9-sgRNA targeting CAG repeat region does not damage the targeted DNA in HEK293T cells containing CAG repeats. When this study investigates whether CRISPRi can suppress mutant HTT (mHTT), CRISPRi results in reduced expression of mHTT with relative preservation of the wild-type HTT in human HD fibroblasts. Although both dCas9 and Cas9 treatments reduce mHTT by sgRNA targeting the CAG repeat region, CRISPRi delays behavioral deterioration and protects striatal neurons against cell death in HD mice. Collectively, CRISPRi can delay disease progression by suppressing mHtt, suggesting DNA DSB-free CRISPRi is a potential therapy for HD that can compensate for the shortcoming of CRISPR-Cas9 nuclease.ope

Fibroblast Growth Factor-2 Induced by Enriched Environment Enhances Angiogenesis and Motor Function in Chronic Hypoxic-Ischemic Brain Injury

This study aimed to investigate the effects of enriched environment (EE) on promoting angiogenesis and neurobehavioral function in an animal model of chronic hypoxic-ischemic (HI) brain injury. HI brain damage was induced in seven day-old CD-1® mice by unilateral carotid artery ligation and exposure to hypoxia (8% O2 for 90 min). At six weeks of age, the mice were randomly assigned to either EE or standard cages (SC) for two months. Rotarod, forelimb-use asymmetry, and grip strength tests were performed to evaluate neurobehavioral function. In order to identify angiogenic growth factors regulated by EE, an array-based multiplex ELISA assay was used to measure the expression in frontal cortex, striatum, and cerebellum. Among the growth factors, the expression of fibroblast growth factor-2 (FGF-2) was confirmed using western blotting. Platelet endothelial cell adhesion molecule-1 (PECAM-1) and α-smooth muscle actin (α-SMA) were also evaluated using immunohistochemistry. As a result, mice exposed to EE showed significant improvements in rotarod and ladder walking performances compared to SC controls. The level of FGF-2 was significantly higher in the frontal cortex of EE mice at 8 weeks after treatment in multiplex ELISA and western blot. On the other hand, FGF-2 in the striatum significantly increased at 2 weeks after exposure to EE earlier than in the frontal cortex. Expression of activin A was similarly upregulated as FGF-2 expression pattern. Particularly, all animals treated with FGF-2 neutralizing antibody abolished the beneficial effect of EE on motor performance relative to mice not given anti-FGF-2. Immunohistochemistry showed that densities of α-SMA+ and PECAM-1+ cells in frontal cortex, striatum, and hippocampus were significantly increased following EE, suggesting the histological findings exhibit a similar pattern to the upregulation of FGF-2 in the brain. In conclusion, EE enhances endogenous angiogenesis and neurobehavioral functions mediated by upregulation of FGF-2 in chronic hypoxic-ischemic brain injury.ope

Induction of Striatal Regeneration Delays Motor Deterioration in a Mouse Model of Huntington’s Disease

Intraventricular administration of brain-derived neurotrophic factor (BDNF) can induce striatal neurogenesis. Epidermal growth factor (EGF), by expanding the mitotic pool of neural stem/progenitor cells in the subventricular zone (SVZ) responsive to neuronal instruction by BDNF, can potentiate this process. The objective of this study was to investigate the induction of striatal regeneration and consequent functional benefits after chronic infusion of BDNF and EGF in a R6/2 transgenic mouse model of Huntington’s disease (HD). At 6 weeks of age, the mice were randomly assigned to groups receiving a continuous 2-week infusion of one of the following treatments into the ventricle: combination of BDNF and EGF (B/E), BDNF, EGF, or phosphate buffered saline (PBS). Two weeks after treatment, the B/E-treated mice revealed a significant increase of new neurons co-stained with BrdU and βIII-tubulin in the ventricular side of neostriata (VZ~300 μm), compared with PBS controls. The newly generated cells were also expressed as migrating neuroblasts co-labeled with doublecortin or PSA-NCAM in the SVZ. The survival rates of the new neurons were in the range of 30~50% at 6 weeks after treatment. For behavioral assessments, the B/E combination therapy group showed a significant delay in motor deterioration relative to PBS controls in both constant and accelerating rotarod as well as locomotor activity test 6 weeks after treatment. However, administration of BDNF alone did not exhibit significant delays in motor deterioration in most of behavioral assessments. Neither did motor performance improve in R6/2 mice treated only with EGF. In conclusion, induction of striatal regeneration by the intraventricular administration of BDNF and EGF delayed disease progression in HD. Therefore, this treatment may offer a promising strategy for restoration of motor function in HDope

뇌허혈 마우스 모델에서 재프로그래밍 인자의 생체내 발현을 통한 성상교세포의 치료 가능성

의과학Cerebral ischemia and stroke can lead incurable brain damage or death. Astrocytes, one of the most abundant cells in the brain, are activated by injury such as ischemia. Reactive astrocytes, in particular, play a crucial role in recovery from brain injury. Four reprogramming factors (Pou5f1, Sox2, Myc, and Klf4) expression have been used to convert cell types, but it has rarely been studied promoting functional recovery by expression of reprogramming factors in ischemic injury. The aim of this study is therefore to determine whether in vivo transient expression of reprogramming factor can improve neurobehavioral function. Cerebral ischemia was induced by two methods—transient bilateral common carotid artery occlusion (BCCAO) and permanent unilateral common carotid artery ligation with hypoxia (8% O2)—after which brains were treated (in the lateral ventricle or striatum) with doxycycline (DOX) in transgenic mice in which the four reprogramming factors were expressed by doxycycline. Either doxycycline (DOX-1; 1 μg/ml, DOX-100; 100 μg/ml) or phosphate-buffered saline (PBS) was then infused into the brain via an osmotic pump for 7 days. In the BCCAO model, histologic evaluation showed that this transient expression of reprogramming factor induced the proliferation of astrocytes and neural progenitors, while neurons and glial scar formation was not observed. Furthermore, in vivo expression of reprogramming factor caused neuroprotective effects and angiogenesis in the striatum. Tumor formation was not observed in any group. Importantly, the rotarod and ladder walking tests showed to promote functional restoration from ischemic damage via the expression of the four reprogramming factors. To elucidate the therapeutic mechanisms associated with astrogliosis, RNA sequencing analysis was performed in order to identify a transcriptome that was significantly changed in the DOX-100 group compared to PBS group. Among downregulated genes (complement C3, C4a, C4b, C1qa, C1qb and C1qc) and astrocyte markers (GFAP, Vimentin and S100β) were validated using qRT-PCR. Because C3 is a detrimental astrocyte marker, C3 in particular was measured using histologic analysis. The results showed that C3 was significantly reduced in DOX-100 treated mice compared with the DOX-1 and PBS groups. A hypoxic-ischemic (HI) model, a stroke model used in another experimental group, was used to compare efficacy of reprogrammed expression in two areas of the brain, the ventricle and striatum. That results showed that the astrocytes and neural progenitors were significantly proliferated, but not neurons or glial scar, and the condition of blood vessels in the injured brain was improved following in vivo reprogramming factor expression. Furthermore, in vivo reprogramming factor expression was protective of neurons under hypoxic ischemic conditions. Notably, neurobehavioral evaluations such as the grip strength, cylinder, ladder walking and open field tests showed functional recovery was dramatically improved via the expression of the four reprogramming factors in the lateral ventricle. Interestingly, the expression of the reprogramming factors in the striatum did not lead to changes in neurological function in any group. In the rotarod test, there were no significant differences in both the lateral ventricular-targeted and striatum-targeted group. Tumor development was not observed in the lateral ventricle-targeted group, but the striatum-targeted group showed that abnormal cell proliferation in DOX-100 treated mice brain. Furthermore, treatment with DOX-1,000 (doxycycline; 1,000 μg/ml) lead to tumor formation in the striatum-targeted group. Taken together, newly generated astrocytes are essential for protecting neurons from damage following cerebral ischemia (BCCAO and HI mouse model) and for enhancing blood vessels. These results show that a therapeutic potential of methods that aim to improve functional recovery by reducing reactive astrocytes (harmful A1 astrocytes) in BCCAO mouse models. In the HI mouse model, we noted a recovery effect in the group in which the lateral ventricle was targeted with the expression of reprogramming factors, but not in the striatum-targeted group. Therefore, targeting the lateral ventricle for expression of reprogramming factors may offer better therapeutic results.open박