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웹(Web)을 이용한 간호사의 투약과오 예방 프로그램 개발
박인숙,박현애,최원자,조인숙,조문숙 서울대학교 간호대학 간호과학연구소 1999 간호학 논문집 Vol.13 No.2
The purpose of this study is to develop a web-based education program for medication errors through that nurses can improve and be reminded their knowledge of medication precautions. The method used for the program development was based on the Educational Software Design and Development Guideline which was published by Korea Educational Development Institute in 1996. Research team for the program development consisted of content experts, instruction designers, a system developer, a graphic expert and user coordinators. The program development steps were as follows; 1) Related educational materials such as principles, precautions, guidelines for medication, categories and cases of medication errors as well as policy for health institution to reduce such errors were reviewed. 2) System was analyzed and designed to detail the user requirements and to deliver the learning contents more effectively and instructively. 3) The learning contents were summarized and illustrated through the instructive strategy. 4) System was implemented on the Web. Contents covered by the program were principles of medication and medication errors, guidelines to prevent medication errors, nursing care when medication errors occur, preventive strategies for the medication errors, categories of possible medication errors, care study of the medication errors. The effectiveness of the education program with the clinical nurses needs to be tested in the future.
Jeong Gu Kang,Sang Yoon Park,Suena Ji,Insook Jang,Sujin Park,Hyun Sil Kim,Sung-Min Kim,Jong In Yook,Yong-Il Park,Jürgen Roth,Jin Won Cho 한국당과학회 2011 한국당과학회 학술대회 Vol.2011 No.1
In general the extent of protein O-GlcNAc modification (O-GlcNAcylation) decreases when cellular glucose concentrations fall below normal levels. However, recent reports demonstrated that O-GlcNAcylation was increased by glucose deprivation in HepG2 and Neuro-2a cells. Here, we report increased O-GlcNAcylation in non-small cell lung carcinoma A549 cells and various cells in response to glucose deprivation. Although the level of O-GlcNAc transferase was not changed, it contained less O-GlcNAc and the activity was increased. Also, the activity of O-GlcNAcase was reduced. The studied glycogen containing cells, and we show that its degradation by glucose deprivation provides a source for UDP-GlcNAc required for increased O-GlcNAcylation under this condition. This required active glycogen phosphorylase and resulted in increased glutamine:fructose-6-phosphate amidotransferase, the first and rate-limiting enzyme in the hexosamine biosynthetic pathway. Interestingly, glucose deprivation reduced the amount of phosphofructokinase 1, a regulatory glycolytic enzyme, and blocked ATP synthesis. These findings suggest that glycogen is the source for increased O-GlcNAcylation but not for generating ATP in response to glucose deprivation and it may be useful for cancer cells to survive.
Gu, Hyemin,An, Hyun-Jin,Kim, Jung-Yeon,Kim, Woon-Hae,Gwon, Mi-Gyeong,Kim, Hyun-Ju,Han, Sang Mi,Park, InSook,Park, Sok Cheon,Leem, Jaechan,Park, Kwan-Kyu Elsevier 2019 Food and chemical toxicology Vol.129 No.-
<P><B>Abstract</B></P> <P> <I>Porphyromonas gingivalis</I> (<I>P. gingivalis</I>) is one of the major periodontal pathogens leading to inflammation and alveolar bone resorption. Bone resorption is induced by osteoclasts, which are multinucleated giant cells. Osteoclastic bone resorption is mediated by enhanced receptor activator of nuclear factor-kappa B ligand (RANKL) signaling. Therefore, the down-regulation of RANKL downstream signals is regarded as an effective therapeutic target in the treatment of bone loss-associated disorders. The aim of this study was to evaluate whether purified bee venom (BV) could attenuate <I>P. gingivalis</I>-induced inflammatory periodontitis and RANKL-induced osteoclast differentiation. Inflammatory periodontitis induced by <I>P. gingivalis</I> increased alveolar bone resorption and increased expression of TNF-α and IL-1β, while BV treatment resulted in decreased bone loss and pro-inflammatory cytokines. Similarly, RANKL-induced multinucleated osteoclast differentiation and osteoclast-specific gene expression, such as nuclear factor of activated T cells 1 (NFATc1), cathepsin K, tartrate-resistant acid phosphatase (TRAP), and integrin αvβ3 were significantly suppressed by treatment with BV. We show that BV reduces <I>P. gingivalis</I>-induced inflammatory bone loss-related periodontitis <I>in vivo</I> and RANKL-induced osteoclast differentiation, activation, and function <I>in vitro</I>. These results suggest that BV exerts positive effects on inflammatory periodontitis associated osteoclastogenesis.</P> <P><B>Highlights</B></P> <P> <UL> <LI> BV diminished osteoclast differentiation and function. </LI> <LI> BV blocked the MAPKs signaling pathway. </LI> <LI> BV ameliorated bone resorption associated with periodontitis. </LI> </UL> </P>
낙상예방 활동의 지속적 질 관리 프로세스 확립을 위한 위험 사정도구 평가
박인숙,조인숙,김은만,김민경 한국간호과학회 간호행정학회 2011 간호행정학회지 Vol.17 No.4
Purpose: The aims of study were; (1) to evaluate the validity and sensitivity of a fall-risk assessment tool, and (2) to establish continuous quality improvement (CQI) methods to monitor the effective use of the risk assessment tool. Methods: A retrospective case-control cohort design was used. Analysis was conducted for 90 admissions as cases and 3,716 as controls during the 2006 and 2007 calendar years was conducted. Fallers were identified from the hospital’s Accident Reporting System, and non-fallers were selected by randomized selection. Accuracy estimates, sensitivity analysis and logistic regression were used. Results: At the lower cutoff score of one, sensitivity, specificity, and positive and negative predictive values were 82.2%, 19.3%, 0.03%, and 96.9%, respectively. The area under the ROC was 0.60 implying poor prediction. Logistic regression analysis showed that five out of nine constitutional items; age, history of falls, gait problems, and confusion were significantly associated with falls. Based on these results, we suggested a tailored falls CQI process with specific indexes. Conclusion: The fall-risk assessment tool was found to need considerable reviews for its validity and usage problems in practice. It is also necessary to develop protocols for use and identify strategies that reflect changes in patient conditions during hospital stay.
Selective Autophagy Receptors Interact with EDEM1 During itsDegradation
Insook Jang,Sujin Park,Bruno Guhl,Jin Won Cho,Jürgen Roth 한국당과학회 2012 한국당과학회 학술대회 Vol.2012 No.1
EDEM1 is an endoplasmic reticulum-associated protein degradation (ERAD) component. ERAD is a cellular pathway that targets misfolded and misassembled glycoproteins for degradation. EDEM1 is involved in the recognition of misfolded luminal glycoproteins and in routing them for dislocation to the cytosol, followed by their degradation. EDEM1 interacts with substrate glycoproteins after their exit from the calnexin/calreticulin cycle and after processing by ER-mannosidase I. Although EDEM1 was proposed to be lectin–like and to react with Man8GlcNAc2 oligosaccharides, itsmechanism of action and its fate are still largely unknown. In a previous report, we found that EDEM1 becomes rapidly degraded and that this occurs by basal autophagy. Here, we show that EDEM1 forms complexes with the selective autophagy receptor p62, NBR1 and Alfy. This was demonstrated in HepG2 cells by double immunogold electron microscopy. Furthermore, we show the interaction between p62 and EDEM1 by immunoprecipitation- Western blot experiments. By serial section analysis, the origin of the phagophore for selective autophagy of EDEM1 could be identified as modified parts of rough ER cisternae. Hence, we provide new insight into the details of EDEM1 degradation process.