Comparative analyses of geological laboratory programs of middle school science curricular in Korea, U.S.A., and Japan

본 연구는 미국, 일본, 우리나라의 중학교 과학 교과 내용 중 지질학 분야의 실험 내용을 비교·연구함으로써, 우리나라 교과내용 중 실험 내용의 타당성을 검증하여 그 개선점을 알아보는데 목적이 있다. 연구자료로는 세 나라의 중학 과학 또는 지구과학 교과서를 사용하였으며, 그 중 지질학 분야에 관하여 학습 내용의 범위 및 실험 주제에 관련된 주요 기본 개념, 실험 과제수, 실험의 기구 및 재료, 실험의 체제 (전개과정 ) , 실험의 형태, 실험 과정 중의 유의점, 실험결과 해석의 기술 제시 , 실험 활동의 배경 등을 비교· 분석하였다. 그 결과, 다음과 같은 결론을 얻었다. 1. 세 나라의 중학 과학 교과 내용 중, 지질학 분야의 실험들은 각각 그 나라의 교육 환경 및 지질의 특성을 잘 반영하고 있다. 특히, 미국의 경우는 교사의 지시나 지도가 많이 필요치 않으며, 실험실에서 자유롭게 실험 활동을 할 수 있도록 실험 내용이 전개되어 있다 2. 한 면당 실험 과제수는 미국이 0.17 , 일본이 0 .40 , 우리나라가 0.23이다. 그리고 세 나라의 실험에서 사용되는 기구 및 재료는 주위에서 용이하게 구입할 수 있는 것들이 대부분이며, 동일한 개념을 습득하게 하는 실험일지라도 각 나라마다 준비물이나 절차에는 약간의 차이가 있다. 3. 실험의 형태는 세 나라의 실험이 모두 개별 실험, 구조화된 실험, 정성적 실험, 탐색 실험이 많으며, 미국의 경우 직접 활동 실험이 많은 데 비해 (73.7 % ) 일본과 우리나라의 경우는 관찰 실험이 많다 (각각 44.4%, 46.7 % ) . 4. 실험 과정 중의 유의 사항이 실험 내용 중에 언급된 수는 미국이 13번, 일본이 2번, 우리나라가 1번이며, 실험 곁과를 해석 ·처리함에 있어서 표, 그래프, 그림 등을 요구한 경우는 미국이 17, 일본이 10, 우리나라가 6번이다. 5. 실험에 소요되는 시간은 1차시 또는 1차시 이내로 배정되어 있으며, 실험 ·실습 및 관찰 등의 과제가 행해지는 장소는 주로 실험실이다.;A comparative study of geological part of science laboratory programs in the Korean, American and Japanese middle school science curricular was carried out to improve the laboratory subjects and to develop the standard science laboratory programs in our country. The curricular were analyzed in terms of the number of subjects , the fundamental concepts, the kinds of experimental tools, the type of laboratory procedures, the method of the result presentation and evaluation and the investigation of the theoretical background of the Laboratory works. The analytical results are as follows. (1) Laboratory works in geological part in the science curricular in the three countries are strongly depended on their educational environments and geology of each country. (2) The number of experimental subject per total pages of the textbook is 0.17 in U.S.A., 0.40 in Japan and 0.23 in Korea. For laboratory works, easily available materials were used in three countries. In spite of the same basis of experimental concept, some differences were found in prerequisites and procedures among three countries. (3) According to the classification of experimental types, it is clear that three countries choose individual, structural, qualitative, observatory and direct activity experiments. The laboratory programs were emphasized on observatory experiment in Japan(44.4%) and Korea(46.7%). Meanwhile, the U.S.A. stress on the direct activity experiment (73.7%). (4) In American laboratory programs, the directions are given in detail before the laboratory works. In experimental procedures in Korea and Japan, however, are the detail directions and cautions. For evaluating the data are used in all the countries table, graph and figures. (5) Time for each type of laboratory activity is assigned for one period or less than one period and a place of experiment is limited in laboratory room rather than field trips.목차 = ⅲ 논문개요 = ⅶ Ⅰ. 서론 = 1 Ⅱ. 선행연구 = 3 Ⅲ. 연구자료 및 방법 = 7 A. 연구자료 = 7 B. 연구방법 = 8 Ⅳ. 연구결과 및 고찰 = 15 Ⅴ. 결론 = 47 참고문헌 = 50 부록 = 53 ABSTRACT = 6

Suppression of ceramide-mediated apoptosis by Hsp70

학위논문(박사)--서울대학교 대학원 :의학과 생화학전공,1997.Docto

SMARCA3, a chromatin-remodeling factor, is required for p11-dependent antidepressant action

p11, through unknown mechanisms, is required for behavioral and cellular responses to selective serotonin reuptake inhibitors (SSRIs). We show that SMARCA3, a chromatin-remodeling factor, is a target for the p11/annexin A2 heterotetrameric complex. Determination of the crystal structure indicates that SMARCA3 peptide binds to a hydrophobic pocket in the heterotetramer. Formation of this complex increases the DNA-binding affinity of SMARCA3 and its localization to the nuclear matrix fraction. In the dentate gyrus, both p11 and SMARCA3 are highly enriched in hilar mossy cells and basket cells. The SSRI fluoxetine induces expression of p11 in both cell types and increases the amount of the ternary complex of p11/annexin A2/SMARCA3. SSRI-induced neurogenesis and behavioral responses are abolished by constitutive knockout of SMARCA3. Our studies indicate a central role for a chromatin-remodeling factor in the SSRI/p11 signaling pathway and suggest an approach to the development of improved antidepressant therapies. PaperClip: © 2013 Elsevier Inc

APP intracellular domain-WAVE1 pathway reduces amyloid-beta production

An increase in amyloid-beta (A beta) production is a major pathogenic mechanism associated with Alzheimer's disease (AD)(1,2), but little is known about possible homeostatic control of the amyloidogenic pathway. Here we report that the amyloid precursor protein (APP) intracellular domain (AICD) downregulates Wiskott-Aldrich syndrome protein (WASP)-family verprolin homologous protein 1 (WAVE1 or WASF1) as part of a negative feedback mechanism to limit A beta production. The AICD binds to the Wasf1 promoter, negatively regulates its transcription and downregulates Wasf1 mRNA and protein expression in Neuro 2a (N2a) cells. WAVE1 interacts and colocalizes with APP in the Golgi apparatus. Experimentally reducing WAVE1 in N2a cells decreased the budding of APP-containing vesicles and reduced cell-surface APP, thereby reducing the production of A beta. WAVE1 downregulation was observed in mouse models of AD. Reduction of Wasf1 gene expression dramatically reduced A beta levels and restored memory deficits in a mouse model of AD. A decrease in amounts of WASF1 mRNA was also observed in human AD brains, suggesting clinical relevance of the negative feedback circuit involved in homeostatic regulation of Ab production

Ahnak scaffolds p11/Anxa2 complex and L-type voltage-gated calcium channel and modulates depressive behavior

Genetic polymorphisms of the L-type voltage-gated calcium channel (VGCC) are associated with psychiatric disorders including major depressive disorder. Alterations of S100A10 (p11) level are also implicated in the etiology of major depressive disorder. However, the existence of an endogenous regulator in the brain regulating p11, L-type VGCC, and depressive behavior has not been known. Here we report that Ahnak, whose function in the brain has been obscure, stabilizes p11 and Anxa2 proteins in the hippocampus and prefrontal cortex in the rodent brain. Protein levels of Ahnak, p11, and Anxa2 are highly and positively correlated in the brain. Together these data suggest the existence of an Ahnak/p11/Anxa2 protein complex. Ahnak is expressed in p11-positive as well as p11-negative neurons. Ahnak, through its N-terminal region, scaffolds the L-type pore-forming alpha 1 subunit and, through its C-terminal region, scaffolds the beta subunit of VGCC and the p11/Anxa2 complex. Cell surface expression of the alpha 1 subunits and L-type calcium current are significantly reduced in primary cultures of Ahnak knockout (KO) neurons compared to wild-type controls. A decrease in the L-type calcium influx is observed in both glutamatergic neurons and parvalbumin (PV) GABAergic interneurons of Ahnak KO mice. Constitutive Ahnak KO mice or forebrain glutamatergic neuron-selective Ahnak KO mice display a depression-like behavioral phenotype similar to that of constitutive p11 KO mice. In contrast, PV interneuron-selective Ahnak KO mice display an antidepressant-like behavioral phenotype. Our results demonstrate L-type VGCC as an effector of the Ahnak/p11/Anxa2 complex, revealing a novel molecular connection involved in the control of depressive behavior

v-Fps 단백질의 leucine zipper와 SH2영역이 단백질 상호결합에 미치는 영향에 관한 연구

학위논문(석사)--서울대학교 대학원 :의학과 생화학전공,1995.Maste

Upregulation of neuronal nitric oxide synthase in the periphery promotes pain hypersensitivity after peripheral nerve injury

Peripheral nerve injury often results in neuropathic pain that is manifested as hyperalgesia, and allodynia. Several studies suggest a functional role for neuronal nitric oxide synthase (nNOS) in the development or maintenance of neuropathic pain, but such a contribution remains unclear. In our current study, we found that intraplantar injection of the NOS substrate l-arginine or NO donor 3-morpholino-synonimine (SIN-1) produced mechanical hypersensitivity that lasted more than 24 h. Following L5 spinal nerve ligation (L5 SNL), immunoreactivity for nNOS in the ipsilateral L5 but not L4 dorsal root ganglion (DRG) was dramatically increased in mainly small- and medium-sized neurons and non-neuronal cells. L5 SNL caused increased nNOS immunoreactivity in the ipsilateral sciatic nerve, mainly in Schwann cells and the ipsilateral glabrous hind paw skin, mainly on the basement membrane. Furthermore, total nNOS protein and mRNA in the ipsilateral sciatic nerve and hind paw skin were markedly upregulated following nerve injury. Intraplantar injection of the NOS inhibitor 7-nitroindazole (7-NI) or the non-specific NOS inhibitor l-N G-nitro-arginine methyl ester (l-NAME) effectively suppressed SNL-induced mechanical allodynia. Collectively, these data suggest that in the periphery nNOS upregulation induced by peripheral nerve injury contributes to mechanical hypersensitivity during the maintenance phase of neuropathic pain. Blocking nNOS signaling in the periphery may thus be a novel therapeutic strategy for the treatment of neuropathic pain. © 2011 IBRO

Regulatory B subunits of protein phosphatase 2A are involved in site-specific regulation of tau protein phosphorylation

Alzheimer's disease; Phosphorylation; Protein phosphatase 2A; Tau protei

Aberrant Hypomethylation of Solute Carrier Family 6 Member 12 Promoter Induces Metastasis of Ovarian Cancer

Purpose: Ovarian cancer (OC) is the most fatal of gynecological malignancies with a high rate of recurrence. We aimed to evaluate the expression of solute carrier family 6, member 12 (SLC6A12) and methylation of its promoter CpG sites in a xenograft mouse model of metastatic OC, and to investigate the regulatory mechanisms that promote aggressive properties during OC progression. Materials and Methods: Expression of SLC6A12 mRNA was determined by reverse-transcription quantitative polymerase chain reaction (RT-qPCR), and DNA methylation status of its promoter CpGs was detected by quantitative methylation-specific PCR. The metastatic potential of SLC6A12 was evaluated by in vitro migration/invasion transwell assays. Gene expression and DNA methylation of SLC6A12 and clinical outcomes were further investigated from publicly available databases from curatedOvarianData and The Cancer Genome Atlas. Results: SLC6A12 expression was 8.1-14.0-fold upregulated and its DNA methylation of promoter CpG sites was 41-62% decreased in tumor metastases. After treatment with DNA methyltransferase inhibitor and/ or histone deacetylase inhibitor, the expression of SLC6A12 was profoundly enhanced (similar to 8.0-fold), strongly supporting DNA methylation-dependent epigenetic regulation of SLC6A12. Overexpression of SLC6A12 led to increased migration and invasion of ovarian carcinoma cells in vitro, approximately 2.0-fold and 3.3-fold, respectively. The meta-analysis showed that high expression of SLC6A12 was significantly associated with poor overall survival [hazard ratio (HR)=1.07, p value=0.016] and that low DNA methylation levels of SLC6A12 at specific promoter CpG site negatively affected patient survival. Conclusion: Our findings provide novel evidence for the biological and clinical significance of SLC6A12 as a metastasis-promoting gene