Chung Hwa University of Medical Technology

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    永康榮民醫院網站改善計畫(一)架構與內容分析

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    [[note]]合作廠商:永康榮民醫院合約期間:98.1.1~98.12.3

    殯葬禮儀服務產學需求面之研究

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    [[note]]合作廠商:中華殯葬教育學會合約期間:98.3.1~99.8.3

    結合甘薯之傳統中式點心開發

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    [[note]]合作廠商:台南縣新化區農產品加通生產合作社合約期間:98.11.1~99.10.3

    台南縣幼稚園家長參與親子運動會動機之探討

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    [[note]]合作廠商:童恩創意活動工作室合約期間:98.5.1~98.8.3

    The effects of different selenium compounds supplementation on glutathione peroxidase and monoamine oxidase in cell models

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    目錄 i 圖目錄 iv 表目錄 v 致 謝 vi 縮寫對照表 vii 中文摘要 viii Abstract x 第一章 緒論 1 第一節 前言 1 第二節 文獻回顧 2 一、 硒在人體健康上所扮演的角色 2 二、 硒之化學形式與添加 2 三、 硒之抗氧化功能與機制 3 四、 硒對單胺氧化酶(monoamine oxidase, MAO)之影響 5 第三節 實驗目的與設計 7 實驗設計 8 第二章 不同硒形式的補充對RAW 264.7細胞抗氧化之影響 9 第一節 前言 9 第二節 材料與方法 9 1. 細胞株來源及培養條件 9 2. 硒來源 10 3. 細胞存活率分析 10 4. 蛋白質測定法 11 5. GPX 活性測定 12 6. GPX活性計算及表示 12 7. 免疫轉印法 13 8. 統計分析 22 第三節 結果 23 1. 不同硒形式補充對RAW 264.7細胞生長之影響 23 2. 不同硒形式補充對RAW264.7細胞GPX酵素活性之影響 23 3. 不同硒形式補充對RAW264.7細胞GPX1蛋白質表現量之影響 24 第三章 不同硒形式的補充對大腦神經膠細胞抗氧化之影響 30 第一節 前言 30 第二節 材料與方法 31 1. 細胞株來源及培養條件 31 2. 細胞存活率分析 31 3. 單胺氧化酶活性之分析 31 4. H2O2生成量測定 33 5. 單胺氧化酶活性計算及表示 33 6. 蛋白質測定法 33 7. GPX activity測定 34 8. 利用免疫轉印法測定蛋白質表現量 34 9. 統計分析 34 第三節 結果 35 1. 不同硒形式補充對C6細胞生長之影響 35 2. 不同硒形式補充對C6細胞GPX活性及蛋白質表現量之影響 35 3. 不同硒形式補充對C6細胞MAO活性之影響 36 第四章 含硒包裝水對RAW 264.7及C6細胞抗氧化能力之影響 44 第一節 前言 44 第二節 材料與方法 44 1. 細胞株來源及培養條件 44 2. 硒來源 44 3. 細胞存活率分析 48 4. 單胺氧化酶活性分析 48 5. 蛋白質測定法 48 6. GPX activity測定 48 7. 利用免疫轉印法測定蛋白質表現量 48 8. 統計分析 48 第三節 結果 49 1. MS補充對RAW 264.7及C6細胞之影響 49 2. MS補充對RAW 264.7及C6細胞GPX活性及GPX1蛋白質表現量之影響 49 3. MS補充對C6細胞MAO活性之影響 50 第五章 綜合討論 58 1. 硒補充對腹腔細胞與神經相關細胞存活率之比較 59 2. 硒補充對RAW 264.7及 C6兩種細胞內GPX的影響不同 61 3. 硒補充降低MAO活性的可能原因 63 4. 硒補充降低MAO活性的生理意義 64 5. 含硒包裝水的抗老化效應 65 第六章 結論 66 第七章 總結與未來展望 67 參考文獻 69 參考文獻 Alfred W. J. Bach, N. C. L., Deborah L. Johnson, Creed W. Abell, Michael E. Bembenek, Sau-Wah Kwan, Peter H. Seeburg, and Jean C. Shih (1988). cDNA cloning of human liver monoamine oxidase A and B: molecular basis of differences in enzymatic properties. Proc Natl Acad Sci U S A 4934-4938. Allan, C. B., Lacourciere, G. M., and Stadtman, T. C. (1999). Responsiveness of selenoproteins to dietary selenium. Annu Rev Nutr 19, 1-16. Alper, G., Girgin, F. K., Ozgonul, M., Mentes, G., and Ersoz, B. (1999). MAO inhibitors and oxidant stress in aging brain tissue. Eur Neuropsychopharmacol 9, 247-252. Alvarado, C., Alvarez, P., Puerto, M., Gausseres, N., Jimenez, L., and De la Fuente, M. (2006). Dietary supplementation with antioxidants improves functions and decreases oxidative stress of leukocytes from prematurely aging mice. Nutrition 22, 767-777. Ansari, M. A., Ahmad, A. S., Ahmad, M., Salim, S., Yousuf, S., Ishrat, T., and Islam, F. (2004). Selenium protects cerebral ischemia in rat brain mitochondria. Biol Trace Elem Res 101, 73-86. Bordoni, A., Biagi, P. L., Angeloni, C., Leoncini, E., Danesi, F., and Hrelia, S. (2005). Susceptibility to hypoxia/reoxygenation of aged rat cardiomyocytes and its modulation by selenium supplementation. J Agric Food Chem 53, 490-494. Brigelius-Flohe, R. (1999). Tissue-specific functions of individual glutathione peroxidases. Free Radical Biology and Medicine 27, 951-965. Butterfield, D. A., Howard, B., Yatin, S., Koppal, T., Drake, J., Hensley, K., Aksenov, M., Aksenova, M., Subramaniam, R., Varadarajan, S., et al. (1999). Elevated oxidative stress in models of normal brain aging and Alzheimer's disease. Life Sci 65, 1883-1892. Castano, A., Cano, J., and Machado, A. (1993). Low selenium diet affects monoamine turnover differentially in substantia nigra and striatum. J Neurochem 61, 1302-1307. Chen, J., and Berry, M. J. (2003). Selenium and selenoproteins in the brain and brain diseases. J Neurochem 86, 1-12. Chu, F. F., Doroshow, J. H., and Esworthy, R. S. (1993). Expression, characterization, and tissue distribution of a new cellular selenium-dependent glutathione peroxidase, GSHPx-GI. J Biol Chem 268, 2571-2576. Cutler, R. G. (1991). Antioxidants and aging. Am J Clin Nutr 53, 373S-379S. Ge, K., and Yang, G. (1993). The epidemiology of selenium deficiency in the etiological study of endemic diseases in China. Am J Clin Nutr 57, 259S-263S. Han, X. H., Hong, S. S., Lee, D., Lee, J. J., Lee, M. S., Moon, D. C., Han, K., Oh, K. W., Lee, M. K., Ro, J. S., and Hwang, B. Y. (2007). Quinolone alkaloids from evodiae fructus and their inhibitory effects on monoamine oxidase. Arch Pharm Res 30, 397-401. Holben, D. H., and Smith, A. M. (1999). The diverse role of selenium within selenoproteins: a review. J Am Diet Assoc 99, 836-843. Iadecola, C. (1997). Bright and dark sides of nitric oxide in ischemic brain injury. Trends in Neurosciences 20, 132-139. Ip, C. (1998). Lessons from basic research in selenium and cancer prevention. J Nutr 128, 1845-1854. Jaya Prasanthi, R. P., Hariprasad Reddy, G., Bhuvaneswari Devi, C., and Rajarami Reddy, G. (2005). Zinc and calcium reduce lead induced perturbations in the aminergic system of developing brain. Biometals 18, 615-626. Jenner, P. (1996). Oxidative stress in Parkinson's disease and other neurodegenerative disorders. Pathol Biol (Paris) 44, 57-64. Jocobs, M., and Frost, C. (1981). Toxicological effects of sodium selenite in Sprague-Dawley rats. J Toxicol Environ Health 575-585. Johnson, V. J., Tsunoda, M., and Sharma, R. P. (2000). Increased production of proinflammatory cytokines by murine macrophages following oral exposure to sodium selenite but not to seleno-L-methionine. Arch Environ Contam Toxicol 39, 243-250. Kahler, W., Kuklinski, B., Ruhlmann, C., and Plotz, C. (1993). [Diabetes mellitus--a free radical-associated disease. Results of adjuvant antioxidant supplementation]. Z Gesamte Inn Med 48, 223-232. Kajander, E. O., Harvima, R. J., Kauppinen, L., Akerman, K. K., Martikainen, H., Pajula, R. L., and Karenlampi, S. O. (1990). Effects of selenomethionine on cell growth and on S-adenosylmethionine metabolism in cultured malignant cells. Biochem J 267, 767-774. Kim, S. H., Johnson, V. J., Shin, T. Y., and Sharma, R. P. (2004). Selenium attenuates lipopolysaccharide-induced oxidative stress responses through modulation of p38 MAPK and NF-kappaB signaling pathways. Exp Biol Med (Maywood) 229, 203-213. Liu, J. (2003). This student paper was written as an assignment in the graduate course. Free Radicals in Biology and Medicine. Lowry, O. H., Rosebrough, N. J., Farr, A. L., and Randall, R. J. (1951). Protein measurement with the Folin phenol reagent. J Biol Chem 193, 265-275. Mazzio, E. A., Harris, N., and Soliman, K. F. (1998). Food constituents attenuate monoamine oxidase activity and peroxide levels in C6 astrocyte cells. Planta Med 64, 603-606. Morrison, D. G., and Medina, D. (1988). Distinguishing features of cytotoxic and pharmacological effects of selenite in murine mammary epithelial cells in vitro. Toxicol Lett 44, 307-314. Nagatsu, T., and Sawada, M. (2006). Molecular mechanism of the relation of monoamine oxidase B and its inhibitors to Parkinson's disease: possible implications of glial cells. J Neural Transm Suppl, 53-65. Naoi, M., and Maruyama, W. (1993). Type B monoamine oxidase and neurotoxins. Eur Neurol 33 Suppl 1, 31-37. Omar, R., and Pappolla, M. (1993). Oxygen free radicals as inducers of heat shock protein synthesis in cultured human neuroblastoma cells: relevance to neurodegenerative disease. Eur Arch Psychiatry Clin Neurosci 242, 262-267. Oreland, L., and Gottfries, C. G. (1986). Brain and brain monoamine oxidase in aging and in dementia of Alzheimer's type. Prog Neuropsychopharmacol Biol Psychiatry 10, 533-540. Paglia, D. E., and Valentine, W. N. (1967). Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J Lab Clin Med 70, 158-169. Perez-Campo, R., Lopez-Torres, M., Cadenas, S., Rojas, C., and Barja, G. (1998). The rate of free radical production as a determinant of the rate of aging: evidence from the comparative approach. J Comp Physiol [B] 168, 149-158. Pfeifer, H., Conrad, M., Roethlein, D., Kyriakopoulos, A., Brielmeier, M., Bornkamm, G. W., and Behne, D. (2001). Identification of a specific sperm nuclei selenoenzyme necessary for protamine thiol cross-linking during sperm maturation. Faseb J 15, 1236-1238. Prabhu, K. S., Zamamiri-Davis, F., Stewart, J. B., Thompson, J. T., Sordillo, L. M., and Reddy, C. C. (2002). Selenium deficiency increases the expression of inducible nitric oxide synthase in RAW 264.7 macrophages: role of nuclear factor-kappaB in up-regulation. Biochem J 366, 203-209. Richardson, D. R. (2005). More roles for selenoprotein P: local selenium storage and recycling protein in the brain. Biochem J 386, e5-7. Rosenblat, M., and Aviram, M. (1998). Macrophage Glutathione Content and Glutathione Peroxidase Activity Are Inversely Related to Cell-Mediated Oxidation of LDL: In Vitro and In Vivo Studies. Free Radical Biology and Medicine 24, 305-317. Saito, Y., Yoshida, Y., Akazawa, T., Takahashi, K., and Niki, E. (2003). Cell death caused by selenium deficiency and protective effect of antioxidants. J Biol Chem 278, 39428-39434. Savaskan, N. E., Brauer, A. U., Kuhbacher, M., Eyupoglu, I. Y., Kyriakopoulos, A., Ninnemann, O., Behne, D., and Nitsch, R. (2003). Selenium deficiency increases susceptibility to glutamate-induced excitotoxicity. Faseb J 17, 112-114. Savolainen, H. (1978). Superoxide dismutase and glutathione peroxidase activities in rat brain. Res Commun Chem Pathol Pharmacol 21, 173-176. Schweizer, U., Brauer, A. U., Kohrle, J., Nitsch, R., and Savaskan, N. E. (2004). Selenium and brain function: a poorly recognized liaison. Brain Research Reviews 45, 164-178. Schweizer, U., Streckfuss, F., Pelt, P., Carlson, B. A., Hatfield, D. L., Kohrle, J., and Schomburg, L. (2005). Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply. Biochem J 386, 221-226. Shilo, S., and Tirosh, O. (2003). Selenite activates caspase-independent necrotic cell death in Jurkat T cells and J774.2 macrophages by affecting mitochondrial oxidant generation. Antioxid Redox Signal 5, 273-279. Sian, J., Gerlach, M., Youdim, M. B., and Riederer, P. (1999). Parkinson's disease: a major hypokinetic basal ganglia disorder. J Neural Transm 106, 443-476. Sinha, R., and El-Bayoumy, K. (2004). Apoptosis is a critical cellular event in cancer chemoprevention and chemotherapy by selenium compounds. Curr Cancer Drug Targets 4, 13-28. Smith, M. A., Perry, G., Richey, P. L., Sayre, L. M., Anderson, V. E., Beal, M. F., and Kowall, N. (1996). Oxidative damage in Alzheimer's. Nature 382, 120-121. Takahashi, K., Avissar, N., Whitin, J., and Cohen, H. (1987). Purification and characterization of human plasma glutathione peroxidase: a selenoglycoprotein distinct from the known cellular enzyme. Arch Biochem Biophys 256, 677-686. Takizawa, S., Matsushima, K., Shinohara, Y., Ogawa, S., Komatsu, N., Utsunomiya, H., and Watanabe, K. (1994). Immunohistochemical localization of glutathione peroxidase in infarcted human brain. J Neurol Sci 122, 66-73. Tang, Y. L., Wang, S. W., and Lin, S. M. (2008). Both inorganic and organic selenium supplements can decrease brain monoamine oxidase B enzyme activity in adult rats. Br J Nutr, 1-6. Turnlund, J. R., Keyes, W. R., and Peiffer, G. L. (1995). Molybdenum absorption, excretion, and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Am J Clin Nutr 62, 790-796. Ursini, F., Heim, S., Kiess, M., Maiorino, M., Roveri, A., Wissing, J., and Flohe, L. (1999). Dual function of the selenoprotein PHGPX during sperm maturation. Science 285, 1393-1396. Venkateswaran, V., Klotz, L. H., and Fleshner, N. E. (2002). Selenium modulation of cell proliferation and cell cycle biomarkers in human prostate carcinoma cell lines. Cancer Res 62, 2540-2545. Yang G, Z. R., Yin S, Gu L, Yan B, Liu Y, Liu Y, Li X. (1989). Studies of safe maximal daily dietary selenium intake in a seleniferous area in China. I. Selenium intake and tissue selenium levels of the inhabitants. J Trace Elem Electrolytes Health Dis, 123-130. Yeh, J. Y., Ou, B. R., Liang, Y. C., Burchfiel, J., Butler, J. A., Forsberg, N. E., and Whanger, P. D. (2006). Mechanism for proliferation inhibition by various selenium compounds and selenium-enriched broccoli extract in rat glial cells. Biometals 19, 611-621. Youdim, M. B., and Bakhle, Y. S. (2006). Monoamine oxidase: isoforms and inhibitors in Parkinson's disease and depressive illness. Br J Pharmacol 147 Suppl 1, S287-296. Zhang, J., and Piantadosi, C. A. (1991). Prevention of H2O2 generation by monoamine oxidase protects against CNS O2 toxicity. J Appl Physiol 71, 1057-1061. Zhang, S., Zhou, Z., and Fu, J. (2003). Effect of manganese chloride exposure on liver and brain mitochondria function in rats. Environ Res 93, 149-157. Zhang, Z., Miyatake, S., Saiki, M., Asahi, M., Yukawa, H., Toda, H., Kikuchi, H., Yoshimura, S. I., and Hashimoto, N. (2000). Selenium and glutathione peroxidase mRNA in rat glioma. Biol Trace Elem Res 73, 67-76. 王詩維 (2005). 綠茶多酚化合物對大腦單胺氧化酶活性之影響中華醫事學院生物科技研究所碩士論文. 江美靜 (2006). 類黃酮抑制LPS 及TPA 所引發大鼠神經膠質瘤細胞(glioma C6)發炎反應. 國立屏東科技大學生物科技研究所碩士論文. 吳其真 (1998). 甘藷澱粉磷解酶之生化及免疫學研究. 國立台灣大學農業化學研究所碩士論文.[[abstract]]硒是人體內麩胱甘肽過氧化酶(GPX)的重要成份﹐被歸類為具抗氧化功能的營養素。單胺氧化酶 (Monoamine oxidase, MAO) 在人體老化、及其他神經相關疾病(如:帕金森氏症、憂鬱症)扮演重要角色。MAO活性的增加,與體內氧化壓力增加有關,且被認為是老化的指標。硒的生物利用率與毒性常取決於有機或無機的形式,因此本研究旨在探討不同硒形式的補充對GPX活性與蛋白質表現,以及對MAO活性之影響。本研究有三個部份,第一個部份是比較無機硒(sodium selenite)與有機硒(seleno-methionine)添加,對巨噬細胞(RAW 264.7) GPX活性及蛋白質表現的影響。結果發現,不同硒形式(有機硒、無機硒)補充會增加GPX活性及蛋白質的表現量。結果顯示,隨著無機硒添加的濃度(25ng/mL~500ng/mL)增加,GPX活性及蛋白質表現量均明顯較高;有機硒各濃度添加對細胞GPX活性之影響,與無機硒的結果相似。以MTT法測得本實驗所採用之添加濃度,並不影響細胞存活率。以上結果表示硒確實可以增加RAW264.7細胞GPX活性。第二部分在探討不同硒形式對大腦神經膠(C6)細胞GPX及MAO活性的影響。以不影響C6細胞生長之濃度(25ng/mL~ 500ng/mL),添加於培養液中,結果指出,兩種形式硒添加,均隨濃度增加,MAO活性明顯較低。而兩種形式硒補充對GPX蛋白質含量及活性,均沒有影響。第三部份是利用所建立的細胞模式探討市面上唯一含硒包裝水原料(MS),對細胞GPX及MAO活性的影響。含硒包裝水使用「健康元素水」原料200倍濃縮液,配製成相當成品濃度1, 5, 10, 20倍組(含硒濃度約為9, 45, 90, 180 ng/mL亞硒酸鈉當量)。結果顯示,MS添加可增加巨噬細胞GPX活性,並不影響蛋白質表現量;對大腦神經膠細胞GPX活性及蛋白質表現量並沒有影響,但具有抑制MAO活性之作用。综合以上結果,兩種硒形式補充,會增加巨噬細胞內GPX活性及蛋白質表現量,不影響大腦神經膠細胞株GPX,但可以降低C6細胞MAO活性,顯示硒具有抗氧化作用,並可減少大腦氧化損傷的作用。本實驗結果可作為預防老化、帕金森氏症、憂鬱症的保健食品之開發依據。 Selenium (Se) is the important composition of glutathione peroxidase (GPX). Therefore, selenium perform in the role of antioxidation function. The enzyme monoamine oxidase (MAO-B) plays an important role on aging-related diseases, such as Parkinson’s and Alzheimer’s diseases. Because of the observation that MAO-B activity is increased during ageing, it is regarded as the index of ageing. The purpose of this study was to understand the effects of organic / inorganic selenium supplements on GPX enzyme activity, GPX protein expression, and MAO enzyme activity. Firstly, the effects of selenite and seleno-methionine on RAW 264.7 cells were studied. It demonstrated that both organic / inorganic supplements are able to dose-dependent increase the activity and protein expression of GPX. However, the cell growth curves were analysed by MTT method, and it showed that the Se doses used in this study have no influence on RAW 264.7 cell growth. Therefore, our study indicated that the GPX enzyme activity is activated by inorganic / organic Se in RAW 264.7 cells. Secondary, the effects of selenite and seleno-methionine on C6 cells were studied. The concentration (25ng/mL~ 500ng/mL) was used in the medium of C6 cells. It demonstrated that a dose-dependent decrease on MAO enzyme activity was showed by inorganic / organic Se treatments. However, neither GPX enzyme activity nor GPX protein expression increase was observed by inorganic / organic Se treatments in C6 cells. In addition, we further analyzed the effects of Se-containing mineral water (MS) on GPX and MAO by the cell model methods constructed above. The Se-containing mineral water stock (200X) was diluted to 1X, 5X, 10X, and 20X (equal to 9, 45, 90, and 180 ng/mL selenite equivalent). It exhibited that GPX activity increase in RAW 264.7 cells and MAO activity decrease in C6 cells by MS treatments. However, there are no influences on GPX protein expression in RAW 264.7 cells and C6 cells, and no influence on GPX activity in C6 cells treated by MS. In conclusion, inorganic / organic Se treatments increase GPX enzyme activity and protein expression in RAW 264.7 cells, and decrease MAO enzyme activity in C6 cells. These results may propose the possible application of selenium supplements for the prevention of ageing, Parkinson’s disease, and depression

    Gene Therapy and Analysis of the Effect of Anti-Inflammatory Factors for Osteoarthritis

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    研究領域:臨床醫學類, 生物技術, 藥

    早期外傷病患疾病意象之質性探討

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    研究領域:護理學, 臨床醫學類, 公共衛生學 計畫編號:NSC98-2314-B273-004[[abstract]]隨著醫學與科技進步,外傷後病患存活率提高,導致後續照顧與復健的成本及失能後照護的成本日益增加。外傷後病患生活品質不佳甚至無法恢復到外傷前的狀態,是許多研究共同的發現。過去的外傷相關研究中,以外傷後第3、6、12個月進行追蹤之量性研究為主。國內有一研究使用認知心理學的理論- 疾病意象理論後發現,疾病意象” 可以有效預測外傷後病患的生活品質。由於疾病意象理論可以詮釋病患如何調適健康問題或疾病,並說明個體可自行解讀與調節疾病以利恢復健康。本計畫擬採用探索性的質性研究法,應用疾病意象理論,探討早期外傷病患之疾病意象。本計畫之先驅研究訪談二位外傷病患,發現國內外傷病患確實有獨特的疾病意象。正式研究採樣標準為18歲以上,受傷嚴重指數9分以上(排除認知功能有缺陷)的中度到重度外傷病患。擬採用半結構訪談指引於南部某教學醫院收案,資料分析預採用Colaizzi’s (1978)的步驟,預定訪談15-20 位個案。預期研究結果可提供國內外傷醫護人員,深入瞭解病患對外傷的“疾病意象”,以有效的協助外傷病患面對日後可能的身、心、社會等各方面的問題,並且能夠及早準備與適應。由於本研究是第一個同時使用理論與質性研究設計於外傷病患的研究,預期研究結果可以建構本土外傷相關研究的基礎。另一貢獻則在建構外傷護理新知識,補強之前國內外多數研究於外傷後數週開始,而缺乏提早介入外傷病患之機會。 Traumatic injury is the leading cause of death and disability for individuals during their productive working years. Advances in trauma management have improved survival, thus the need for acute and ongoing care has risen, and the associated growing health expenditures for traumatic injury have risen. Studies have repeatedly shown that the pre-injury level of quality of life cannot be regained. Previous studies more focus on tracking patients with traumatic injury form three to 12 months or beyond after hospital discharge using quantitative approaches including two domestic studies. One of the domestic studies has successfully used the Common Sense Model of Illness Representations (CSMIR) to predict quality of life in patients with traumatic injury. Basically, the model is used to understand how people develop and use their own interpretation of their illness conditions. In the model, individuals are self-regulating systems to coping and appraise their health threatening condition. This research plan will use exploratory phenomenology to explore illness representations in patients with traumatic injury. A pilot study has been done by interviewing two participants to modify the interview guide. In the formal study, the criteria for participants will be adult patients with Injury Severity Scores (ISS) over 9 or greater. Semi structured audio-taped interviews will be used to interview 15-20 participants in the formal study. Importantly, this is the first study to conduct in patients with tramtic injury using qualitative research as well as theorectical framework. The findings will built a new knowledge for nursing professonals in domestic trama care. Additionally, approching patients in their early recovery of truamtic injury will provide a new infomation to nursing professonals worldwide

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