보육과 현장중심 교육과정 개발 : DACUM법을 중심으로 Based on the DACUM Method

김정신,노은호,이행숙,정해은,조희진 한국영유아보육학회 2004 한국영유아보육학 Vol.0 No.36

The quality of childhood educare teacher is the most important element in evaluation of the quality of childhood educare. However, the current curricula for the childhood educare in colleges are operated individually without a standard curriculum and there are many problems in the certification system of childhood educare teacher. So, it is hard to discuss about the specialty of the childhood educare teachers. Hence, an immediate development of a standard curriculum which fully reflect the needs of the field is necessary to meet the demand of the times and to enhance the quality of childhood educare service by producing qualified teachers. To fulfill the aforementioned needs, the procedure of the DACUM Method which is useful in developing vocational training course is used in this study. And based on the results, a field centered curriculum of the Dept. Child Care and Education is developed by the job analysis of the childhood educare teachers and by collecting the needs of the field. Educare planning and activities, development and evaluation of the educare program, consultation and education of the family, utilization of the regional resources, and after-class guidance of the children were found to be the principal jobs of the childhood educare teachers.

중증 화상 환자에서 영양지원

박지영,목혜숙,신현선,노순예,김애심,백금선,김도헌,허준,전욱 대한화상학회 2003 대한화상학회지 Vol.6 No.2

흰쥐 중추신경계내 난소로 투사하는 미주신경로에 관한 연구

김명주,장명세,고미희,노해숙,조해영,오문유,이봉희 濟州大學校 基礎科學硏究所 2001 基礎科學硏究 Vol.14 No.1

본 실험은 부교감신경의 하나인 미주신경이 난소를 지배하는 신경으로 관여하고 있는지를 pseudorabies 바이러스를 이용하여 난소신경로와 난소주사후 미주신경절단을 통하여 조사한 연구 보고이다. 이를 위하여 Sprague Dawley계 암흰쥐를 대상으로 pseudorabies 바이러스를 난소에 주사한 무리와 난소 주사후 미주신경을 절단한 무리에서 뇌를 적출하여 pseudorabies 바이러스에 대한 면역조직화학 염색을 시행하여 비교하였다. 본 실험결과 미주신경 중추신경로내의 상위신경핵들이 pseudorabied 바이러스에 대하여 양성반응이 줄어들었거나 관찰되지 않는 차이를 보였다. 즉 적색핵, 종말판혈관기관, 줄무늬체, 침상핵과 이마엽겉질은 부분적으로 난소의 미주신경로에 관여하고 있으며 미주신경등쪽핵, 고립로핵, 최후영역, 청색반점, 팔옆핵, 코리케퓨즈핵, 흑색질 및 시각교차위핵은 양성반응이 관찰되지 않아 미주신경으로 투사하는 부교감신경핵으로 조사되었다. The mammalian ovary has been known as receiving its innervation by sympathetic and sensory neurons of the peripheral nervous system from the brain. Recently, there were several functional reports that the vagus nerves were also regulating the ovarian function, but the vagus nerve had not been identified by clear morphological evidence. A viral transneuronal tracing technique has been used to demonstrate the morphological evidence for the central vagal involvement in ovarian innervation in brain areas. Bartha strain of pseudorabies virus injection was made into the ovary of Sprague Dawley rats. In experimental group, the vagus nerve of the same injection side was removed right after ovarian injection. At five days after initial injection, all the rats were sacrificed and brains were processed for immunohistochemistry. Several central nuclei including hypothalamic paraventricular nucleus showed strong bilateral positive labelings after unilateral injection in control rats, but the positive labelings were disappeared or decreased in several hypothalamic nuclei and nuclei of the vagus nerve. I n conclusion, these results provide the morphological evidence that vagus nerve has neural connection to ovary and by which the central nervous system may maintains the state of ovulation and reproduction as a possible parasympathetic routes in mammals.

Acetoacetate protects neuronal cells from oxidative glutamate toxicity

Noh, Hae Sook,Hah, Young-Sool,Nilufar, Rashidova,Han, Jaehee,Bong, Jae-Hwan,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung Wiley Subscription Services, Inc., A Wiley Company 2006 JOURNAL OF NEUROSCIENCE RESEARCH - Vol.83 No.4

<P>Glutamate cytotoxicity contributes to neuronal degeneration in many central nervous system (CNS) diseases, such as epilepsy and ischemia. We previously reported that a high-fat and low-carbohydrate diet, the ketogenic diet (KD), protects against kainic acid-induced hippocampal cell death in mice. We hypothesized based on these findings that ketosis resulting from KD might inhibit glutamate cytotoxicity, resulting in inhibition of hippocampal neuronal cell death. Therefore, we investigated the role of ketone bodies [acetoacetate (AA) and β-hydroxybutyrate (β-OHB)] both in a mouse hippocampal cell line (HT22) and in rat primary hippocampal neurons. As a result, we found that pretreatment with 5 mM lithium AA and 4 mM Na β-OHB protected the HT22 hippocampal cell line and primary hippocampal neuronal culture against 5 mM glutamate toxicity and that up to 2 hr of pretreatment with 5 mM AA had a protective effect against 5 mM glutamate toxicity in the HT22 cell line. Pretreatment with 5 mM AA decreased ROS production of HT22 cell line at 2 and 8 hr exposure of glutamate, and it decreased the appearance of annexin V-positive HT22 cells, which are indicative of an early stage of apoptosis, and propidium iodide-positive HT22 cells, which are indicative of necrosis. © 2006 Wiley-Liss, Inc.</P>

PEBP1, a RAF kinase inhibitory protein, negatively regulates starvation-induced autophagy by direct interaction with LC3

Noh, Hae Sook,Hah, Young-Sool,Zada, Sahib,Ha, Ji Hye,Sim, Gyujin,Hwang, Jin Seok,Lai, Trang Huyen,Nguyen, Huynh Quoc,Park, Jae-Yong,Kim, Hyun Joon,Byun, June-Ho,Hahm, Jong Ryeal,Kang, Kee Ryeon,Kim, D Informa UK (TaylorFrancis) 2016 AUTOPHAGY Vol.12 No.11

<P>Autophagy plays a critical role in maintaining cell homeostasis in response to various stressors through protein conjugation and activation of lysosome-dependent degradation. MAP1LC3B/LC3B (microtubule- associated protein 1 light chain 3 ) is conjugated with phosphatidylethanolamine (PE) in the membranes and regulates initiation of autophagy through interaction with many autophagy-related proteins possessing an LC3-interacting region (LIR) motif, which is composed of 2 hydrophobic amino acids (tryptophan and leucine) separated by 2 non-conserved amino acids (WXXL). In this study, we identified a new putative LIR motif in PEBP1/RKIP (phosphatidylethanolamine binding protein 1) that was originally isolated as a PE-binding protein and also a cellular inhibitor of MAPK/ERK signaling. PEBP1 was specifically bound to PE-unconjugated LC3 in cells, and mutation (WXXL mutated to AXXA) of this LIR motif disrupted its interaction with LC3 proteins. Interestingly, overexpression of PEBP1 significantly inhibited starvation-induced autophagy by activating the AKT and MTORC1 (mechanistic target of rapamycin [serine/threonine kinase] complex 1) signaling pathway and consequently suppressing the ULK1 (unc-51 like autophagy activating kinase 1) activity. In contrast, ablation of PEBP1 expression dramatically promoted the autophagic process under starvation conditions. Furthermore, PEBP1 lacking the LIR motif highly stimulated starvation-induced autophagy through the AKT-MTORC1-dependent pathway. PEBP1 phosphorylation at Ser153 caused dissociation of LC3 from the PEBP1-LC3 complex for autophagy induction. PEBP1-dependent suppression of autophagy was not associated with the MAPK pathway. These findings suggest that PEBP1 can act as a negative mediator in autophagy through stimulation of the AKT-MTORC1 pathway and direct interaction with LC3.</P>

Ketogenic diet protects the hippocampus from kainic acid toxicity by inhibiting the dissociation of bad from 14-3-3

Noh, Hae Sook,Kim, Yoon Sook,Kim, Young Hee,Han, Jae Yoon,Park, Chang Hwan,Kang, Ahn Ki,Shin, Hee Suk,Kang, Sang Soo,Cho, Gyeong Jae,Choi, Wan Sung Wiley Subscription Services, Inc., A Wiley Company 2006 JOURNAL OF NEUROSCIENCE RESEARCH - Vol.84 No.8

<P>The ketogenic diet (KD) is often effective for intractable epilepsy, but its antiepileptic mechanisms remain largely unknown. Within the cell death/survival pathway, Akt and its downstream protein Bad play an important role in kainic acid (KA)-induced cell death. Therefore, we investigated the effects of a KD on KA-induced changes in the Akt/Bad/14-3-3 signaling pathway by evaluating Akt, Bad, 14-3-3, and cleaved caspase-3 expression levels as well as their relative interactions. Our results showed that a KD did not affect the expression levels of Akt, Bad, Bcl-xL, Bax, and 14-3-3 but increased phospho-Akt [serine 473; p-Akt (Ser473)] and phospho-Bad [serine 136; p-Bad (Ser136)] expression levels as well as decreased cleaved caspase-3 levels following a KA-induced seizure in the hippocampus. Furthermore, we found that a KD increased the protein–protein interaction between 14-3-3 and p-Bad (Ser136), which might be phosphorylated by p-Akt (Ser473), and decreased interaction of Bad and Bcl-xL. These results suggest that a KD might protect, at least partially, the hippocampus from KA-induced cell death via inhibiting the dissociation of Bad from 14-3-3. © 2006 Wiley-Liss, Inc.</P>

Neuroprotective effects of the ketogenic diet

Noh, Hae Sook,Kim, Yoon Sook,Choi, Wan Sung Blackwell Publishing Inc 2008 Epilepsia Vol.49 No.suppl8

<P><SMALL>SUMMARY</SMALL></P><P><B>The ketogenic diet (KD) is an alternative treatment for medically refractory epilepsy. Despite numerous mechanistic hypotheses advanced to explain the anticonvulsant action of the KD, few studies to date have addressed the molecular changes in brain following KD treatment. Here, we present recent experimental results based on systemic administration of kainic acid (KA) in rodents. KA typically induces acute limbic seizures and results in cellular and molecular alterations, accompanied by neuronal death mainly in limbic structures, similar to what has been observed in surgically resected temporal lobe tissue in epileptic patients. We have reported that neuronal degeneration induced by KA is ameliorated by KD treatment via diverse protective mechanisms, including inhibition of caspase-3-mediated apoptosis in hippocampal neurons. Neuroprotective strategies such as the KD, if implemented early, might exert an antiepileptogenic effect, and could prevent associated learning and memory deficits.</B></P>

Propofol Protects the Autophagic Cell Death Induced by the Ischemia/Reperfusion Injury in Rats

Noh, Hae-Sook,Shin, Il-Woo,Ha, Ji-Hye,Hah, Young-Sool,Baek, Seon-Mi,Kim, Deok-Ryong Korean Society for Molecular and Cellular Biology 2010 Molecules and cells Vol.30 No.5

Autophagy has been implicated in cardiac cell death during ischemia/reperfusion (I/R). In this study we investigated how propofol, an antioxidant widely used for anesthesia, affects the autophagic cell death induced by the myocardial I/R injury. The infarction size in the myocardium was dramatically reduced in rats treated with propofol during I/R compared with untreated rats. A large number of autophagic vacuoles were observed in the cardiomyocytes of I/R-injured rats but rarely in I/R-injured rats treated with propofol. While LC3-II formation, an autophagy marker, was up-regulated in the I/R-injured myocardium, it was significantly down-regulated in the myocardial tissues of I/R-injured and propofol-treated rats. Moreover, propofol inhibited the I/R-induced expression of Beclin-1, and it accelerated phosphorylation of mTOR during I/R and Beclin-1/Bcl-2 interaction in cells, which indicates that it facilitates the inhibitory pathway of autophagy. These data suggest that propofol protects the autophagic cell death induced by the myocardial I/R injury.

Mitotic Cell Cycle Checkpoints(Cell Cycle and Cell Death) : Calpain-mediated cleavage of Beclin 1 is specifically associated with the oxidative stress-induced autophagic cell death

( Hae Sook Noh ),( Young Sool Hah ),( Deok Ryong Kim ) 한국생화학분자생물학회 (구 한국생화학회) 2008 생화학분자생물학회 춘계학술발표논문집 Vol.2008 No.-

The Changes in the Expression of γ-Aminobutyric Acid Related Enzymes in the Mouse Hippocampus Following Ketogenic Diet

노해숙(Hae Sook Noh),권오영(Oh-Young Kwon),윤혜정(Hae Jeong Yun),강상수(Sang Soo Kang),조경제(Gyeong Jae Cho),최완성(Wan Sung Choi) 대한해부학회 2007 Anatomy & Cell Biology Vol.40 No.3

케톤생성 식이요법은 항경련 약물에 반응하지 않는 난치성 소아간질에 오래 전부터 사용되고 있는 효과적인 치료 방법 중에 하나이다. 그러나 항경련 기전에 관해서는 현재까지 거의 알려져 있지 않다. 본 연구에서는 케톤생성 식이요법이 억제성 신경전달 물질인 GABA의 발현에 미치는 영향을 면역 조직 화학법과 노던 블랏팅으로 관찰하였다. 그 결과, 케톤생성 식이요법이 해마 내 GABA의 발현을 증가시키고, GABA transporter1(GABA-Tp)과 GABA transaminase (GABA-T) mRNA의 레벨을 감소시키는 것을 관찰할 수 있었다. 이러한 결과들로부터, 케톤생성 식이요법은 GABA의 재흡수를 억제하거나, 분해를 억제하여 연접 공간에서 GABA 수준을 증가시킴으로써 항경련 효과를 유도해 냄을 유추할 수 있었다. The ketogenic diet (KD) has been used to treat intractable childhood epilepsy. However, its mechanism of action remains unknown. In the present study, we examined the effects of KD on the expression of multiple constituents of the GABAergic system in the hippocampus through immunohistochemistry and northern blot analysis. From the results, we have shown that KD increased expression of GABA and decreased GABA transporter1 (GABATp) and GABA transaminase (GABA-T) mRNA levels in the hippocampus. These results suggest that the neuroinhibitory effect of KD may be mediated, at least in part, by the increment of GABAergic activity in the hippocampus. KD may increase the GABA levels in the synaptic space by limiting GABA reuptake and in the presynaptic nerve terminal by inhibiting GABA degradation.