跳到主要內容

臺灣博碩士論文加值系統

(35.153.100.128) 您好!臺灣時間:2022/01/22 06:55
字體大小: 字級放大   字級縮小   預設字形  
回查詢結果 :::

詳目顯示

我願授權國圖
: 
twitterline
研究生:吳明訓
研究生(外文):Ming-Hsun Wu
論文名稱:糖尿病性末期腎病變血液透析患者的氧化壓力指標
論文名稱(外文):Evaluation of oxidant stress in diabetic end stage renal disease patients with hemodialysis
指導教授:陳昇明陳昇明引用關係鄭劍廷
學位類別:碩士
校院名稱:國立中興大學
系所名稱:生命科學院碩士在職專班
學門:生命科學學門
學類:生物學類
論文種類:學術論文
論文出版年:2002
畢業學年度:90
語文別:中文
論文頁數:117
中文關鍵詞:氧化壓力氧化修飾的低密度脂蛋白血液透析
外文關鍵詞:oxidative stressoxidized Low density lipoproteinhemodialysis
相關次數:
  • 被引用被引用:0
  • 點閱點閱:1495
  • 評分評分:
  • 下載下載:0
  • 收藏至我的研究室書目清單書目收藏:12
氧化壓力(oxidative stress)與老化、細胞自然凋零(apoptosis)、癌症及多數疾病有關,而末期腎病變(end stage renal disease)患者在血液透析(hemodialysis)過程中體內會加速氧化壓力的產生。所以氧化壓力標幟在臨床醫學的診斷與監控應該是一個重要的指標。本研究以氧化修飾的低密度脂蛋白(oxidized low density lipoprotein;ox-LDL)作為氧化壓力的評估指標,探討ox-LDL在血液透析前後的變化,並評估造成血液透析患者氧化壓力上升的因子、心血管疾病監測指標之間的關係,以探究ox-LDL成為臨床氧化壓力評估指標的可能性。
本實驗分對照組(健康成人)與實驗組(糖尿病性末期腎病變血液透析患者),共74支檢體(對照組12支;血液透析前、後各31支),分別檢測ox-LDL、PCOOH、CBC、HbA1C、cholesterol、triglyceride、HDL-cholesterol、LDL- cholesterol、TIBC、serum iron、apolipoprotein A1、apolipoprotein B-100、lipoprotein(a)、hs-CRP、homocysteine等項目。利用student’s t test 來比較實驗組與對照組之間的差異,與利用配對(paired) t test 來比較血液透析前與後的差異,以p<0.05 表示有統計上的差異。
實驗結果顯示ox-LDL與PCOOH對照組均明顯低於血液透析患者(ox-LDL:15.96±3.21 vs 19.76±7.85 mU/L,p<0.05;PCOOH:388±1002 vs 5440±7313 pmol/mL,p<0.05),而血液透析後的結果明顯高於透析前(ox-LDL:27.22±9.62 vs 19.76±7.85 mU/L,p<0.05;PCOOH:6497.87±5042 vs 5440±7313 pmol/mL,p=ns),經白蛋白(albumin)校正後,統計結果未因校正而改變。綜合以上結果可知:高氧化壓力族群的ox-LDL與PCOOH濃度明顯高於正常人,而在血液透析後因透析系統與血液的不相容,使患者體內的氧化壓力增加,亦呈現在ox-LDL與PCOOH的濃度變化上,因此ox-LDL與PCOOH應可作為臨床監控氧化壓力的指標。
探討ox-LDL與造成氧化壓力升高的因子之間的關係,發現當接受透析的時間越長、糖尿病患者體內血糖控制不良、白血球活化比率越高,均會使ox-LDL的平均濃度明顯偏高。另外,因為ox-LDL是造成動脈粥瘤硬化(atherosclerosis)的危險因子,所以我們以心血管疾病(cardiovascular disease)發生危險率來分組,發現當危險率大於正常人的兩倍以上時,ox-LDL的濃度也明顯偏高(23.00±7.48 vs 13.85±4.39,p<0.05)。但與臨床常用的心血管疾病檢測指標lipoprotein (a)、Homocysteine比較,發現ox-LDL與兩者間並沒有相關,所以ox-LDL應可作為篩檢或監測心血管疾病的互補指標。
綜合以上結果,發現可使用簡易的酵素免疫分析法來偵測血清中ox-LDL濃度,作為臨床上因血液透析導致氧化壓力升高,而引起的心血管疾病的監測與篩檢指標。
Oxidative stress raised by various kinds of pathological conditions may lead to aging, apoptosis, cancer, and other diseases. Increased oxidative stress in end stage renal disease (ESRD) patients with chronic hemodialysis may contribute to cardiovascular diseases. Therefore, oxidative stress markers should be selected for diagnosis and monitoring in clinical medicine. In this study, oxidized low-density lipoprotein (ox-LDL) was used as an index for evaluating oxidative stress change in the ESRD patients before and after hemodialysis. We evaluated the possible relationship between ox-LDL and other risk factors causing oxidative stress during hemodialysis course and speculated the possible occurrence of cardiovascular events in clinical evaluation by ox-LDL.
The subjects in this study were divided into two groups: normal control and ESRD experimental groups. The parameters of ox-LDL, PCOOH, CBC, HbA1C, cholesterol, triglyceride, HDL-cholesterol, LDL- cholesterol, TIBC, serum iron, apolipoprotein A1, apolipoprotein B-100, lipoprotein(a), hs-CRP, and homocysteine in the serum of each test subject were assayed.
Our results showed that the levels of ox-LDL and PCOOH in the normal control group were significantly lower than those in hemodialysis patients (ox-LDL: 15.96±3.21 vs 19.76±7.85 mU/L, p<0.05; PCOOH: 388±1002 vs 5440±7313 pmol/mL, p<0.05). These oxidized parameters were further increased after hemodialysis when compared to those values before dialysis (ox-LDL: 27.22±9.62 vs 19.76±7.85 mU/L, p<0.05; PCOOH: 6497.87±5042 vs5440±7313 pmol/mL, p=ns).
We confirmed that higher oxidative stress such as ox-LDL and PCOOH was found in the ESRD patients when compared to the normal control subjects. Furthermore, the oxidative stress shown by the change in the concentration of ox-LDL and PCOOH was consistently enhanced after hemodialysis because of the incompatibility of dialysis systems and blood. It is speculated that serum ox-LDL and PCOOH can be used as an index for monitoring oxidative stress in clinical situations. Analysis of the relationships between ox-LDL and other risk factors such as time for hemodialysis, level of blood sugar, and degree of leukocyte activation revealed that long-term hemodialysis, increased blood sugar, and enhanced activation of leukocytes increases oxidative stress and the mean concentration of ox-LDL.
Additionally, ox-LDL is one of the risk factors for leading to atherosclerosis, we correlated the ox-LDL and the risk for cardiovascular event occurrence in the tested patients. We found that increased risk factor score above 2 is associated with higher concentration of ox-LDL in a positive correlation pattern (23.00±7.48 vs 13.85±4.39, p<0.05). However, there was no correlation between ox-LDL and commonly used index like lipoprotein(a) and homocysteine. Based on our evaluation, serum ox-LDL level can be used as a complementary index for cardiovascular disease screening and monitoring.
In summary, serum ox-LDL level by a simple ELISA method can be successfully used for monitoring and screening clinical situation of oxidative stress like hemodialysis induced cardiovascular diseases.
目 錄 頁次
中文摘要 -------------------------------------------- I
英文摘要 -------------------------------------------- III
致 謝 -------------------------------------------- V
目 錄 -------------------------------------------- VII
縮 寫 表 -------------------------------------------- IX
第 一 章 緒 論-------------------------------------- 1
1-1 氧化壓力------------------------------------ 2
1-2 糖尿病-------------------------------------- 8
1-3 血液透析------------------------------------ 15
1-4 研究目的------------------------------------ 20
第 二 章 材料與方法---------------------------------- 22
2-1 檢體---------------------------------------- 23
2-2 生化項目分析-------------------------------- 24
2-3 血液常規項目分析---------------------------- 28
2-4 特殊蛋白檢測-------------------------------- 30
2-5 醣化血色素檢測------------------------------ 31
2-6 同胱胺酸檢測-------------------------------- 32
2-7 磷脂膽鹼水合過氧化物檢測-------------------- 32
2-8 氧化修飾的低密度脂蛋白測定------------------ 33
2-9 統計分析------------------------------------ 34
第 三 章 結 果-------------------------------------- 40
3-1 基本資料分析-------------------------------- 41
3-2 血液常規檢查結果統計分析-------------------- 42
3-3 生化項目檢查結果統計分析-------------------- 43
3-4 臨床常用於檢測心血管疾病篩檢指標檢測結果分析- 44
3-5 氧化壓力指標的統計分析---------------------- 45
3-6 利用白蛋白校正檢驗數據---------------------- 46
3-7 以血液透析前後體重變化校正數據-------------- 47
第 四 章 討 論-------------------------------------- 77
4-1 臨床常用脂質類檢測標幟與ox-LDL之間的關係探討- 78
4-2 氧化壓力因子與ox-LDL之間的關係探討---------- 80
4-3 探討ox-LDL與臨床心血管疾病監控指標的關係---- 84
第 五 章 總 結--------------------------------------- 94
參考文獻 --------------------------------------------- 96
英文部分:
1.Anderson M. E., Naanuma A., Meister A. Protection anginst toxicity by administration of gluathione ester. FASEB J 1990; 4: 325-330.
2.Anthony S., W. David., R. James., E. Delia., N. Marcel., W. Fred., Y. Albert., and T. Tai-Lan., Human endothelial cells are defective in diabetic vascular disease. J. Surg. Res. 1994; 57: 647-653.
3.Bachmann J., and Tepel M. Hyperhomocysteinemia and the risk for vascular disease in hemodialysis patients. J. Am. Soc. Nephrol. 1995; 6: 121-125.
4.Barsacchi R., Pelosi G., Maffei S. Myocardial vitamin E is consumed during cardiopulmonary bypass: indirect evidence of free radical generation in human ischemic heat. Int. J. Cardiol. 1992; 37(3): 339-343.
5.Basaga H.S. Biochemical aspects of free radicals. Biochem. Cell. Biol. 1990; 68: 989-998.
6.Becker B.N., Himmelfarb J., Henrich W.L., Hakim R.M. Reassessing the cardiac risk profile in chronic haemo- dialysis patients: A hypothesis on the role of oxidant stress and other non-traditional cardiac risk factors. J. Am. Soc. Nephorl. 1997; 8: 475-486.
7.Cafe C., Torri C., Marzatico F. Cellular and molecular events of ischemic brain demage. Funct. Neurol. 1993; 8: 121-133.
8.Chen H.C., Tsai J.C., Tsai J.H., Lai Y.I.I. Recombinant human erythropoietin enhances superoxide production by FMLP-stimulated polymorphonnuclear leukocytes in hemodialysis patient. Kidney. Int. 1997; 52: 1390-1394.
9.Cross C.E., Halliwell B., Borish E.T. Oxygen radicals and human disease. Ann. Int. Med. 1987; 107: 526-545.
10.Curtis M.J., Pugsley M.K., Walker M.J. Endogenous chemical mediators of ventricular arrhythmias in ischemic heat disease. Cardiovasc. Res. 1993; 27: 703-719.
11.Cutler R.G., Taylor A.E., Matalon S., Ward P. Aging and oxygen radicals, In Physiology of Oxygen Radicals. Am. Physiological. Society. 1986; pp 251-285.
12.Diamond J.R. The role of reactive oxygen species in animal models of glomerular disease. Am. J. kid. Dis. 1992; 19: 292-300.
13.Diplock A.T., Chaleux J.L., Crozier-Willi G., Kok F.S., Rice Evans C., Roberforid M., Shahl W., Wina-Ribes J. Functional food sciences and defences against reactive oxygen species. Brit. J. Nutr. 1998; 80: S77- S112.
14.Ehlerding G., Schaeffer J., Drommer W., Miyata T., Koch K.M., Floege J. Alterations of synovial tissue and their potential role in the deposition of beta2-microglobulin assodated amyloid. Nephrol. Dial. Traneplant. 1998; 13: 1465-1475.
15.Foody J.M., Milberg J.A., Robinson K., Pearce G.L., Jacobsen D.W. Homocysteine and lipoprotein (a) interact to increase CAD risk in young men and women. Thrombosis & Vascular Biology. 2000; 20: 493-499.
16.Freeman B.A., and Crapo J.D. Biology of disease: free radicals and tissue injury. Lab. Invest. 1982; 47: 412-426.
17.Friedman E. A. Advanced glycosylated end products and hyperglycemia in the pathogenesis of diabetic complica- tions. Diabetes. Care. 1999; 22: B65-B71.
18.Fuller C. J., Chandalia M., Garg A., Grundy S.M., and Jialal I. RRR-alpha-tocopheryl acetate supplementation at phar- macologic doses decreases low- density- lipoprotein oxida- tive susceptibility but not protein glycation in patients with diabetes mellitus. Am. J. Clin. Nutr. 1996; 63: 753-759.
19.Gadek J.E. Adverase effects of neutrophils on the lung. Am. J. Med. 1992; 92(6A): 27S-31S.
20.Galli F., Canestrari F., Buoncristiani U. Biological effects of oxidant stress in haemodialysis: The possible roles of vitamin E. Blood. Purif. 1999; 17: 79-94.
21.Goncogul Haklar, Itir Yegenaga, A. Suha Yalcin Evalution of oxidant Stress in chronic hemodialysis patients: use of different parameters. Clinica. Chimica. Acta. 1995; 234: 109-114.
22.Goodnough L. T., Skikne B., Brugnara C. Erythropoie- tin, iron, and erythropoiesis. Blood. 2000; 96: 823-833.
23.Granger D.N. Role of xanthine oxidase and granulocytes in ischemia-reperfusion injury. Am. J. Physiol. 1988; 255: 1269-1275.
24.Hakim R.M. Clinical implications of hemodialysis membrane biocompatibility. Kidney. Int. 1993; 44: 484 -494.
25.Halliwell B., Guktteridge J.M.C. Free Radicals in Bioligy and medicine. 3rd., Oxford. University Perss. 1999.
26.Halliwell B., Gutteridge J.M.C. Role of free radicals and catalytic metal ions in human disease: an overview. Mehods. Enzymol. 1990; 186: 1-89.
27.Halliwell B. Current status review: Free radicals, reactive oxygen species and human disease: a critical evaluation with special reference to atheroslerosis. Br. J. Exp. Path. 1989; 70: 737-757.
28.Erman D. The free-radical theory of ageing. In: Pryor WA, ed. Free Radicals in Biology. Academic. Press. London. 1982; 5: 255-275.
29.Ikizler T.A., Hakim R.M. Nutrition in endstage renal disease. Kidney. Int. 1996; 50: 343-357.
30.Ismail N., Becker B.N., Strezlczy K.P. Renal disease and hypertension in non-insulin-dependent diabetes mellitus. Kidney. Int. 1999; 55: 1-18.
31.Knudsen P.J., Leon J., Ng A.K., Shaldon S., Floege J., Koch K.M. Hemodialysis-related induction of beta2- microglobulin and interleukin-1 synthesis and release by mononuclear phagocytes. Nephron. 1989; 53: 188-193.
32.Knudsen P.J., Shaldon S., Floege J., Koch K.M. Hemodialysis-related induction of beta2-microglobulin synthesis and release by mononuclear phagocytes. Int. Artif. Organs. 1990; 13: 73-76.
33.Knutson M.D., Lim A.K., Viteri F.E. A Practical and reliable method for measuring ethane and pentane in expired air from humans. Free. Radic. Biol. Med. 1999; 27: 560-571.
34.Knutson M.D., Walter P.B., Ames B.N. Both iron defici- ency and iron supplements increase lipid peroxidation in rats. J. Nutr. 2000; 130: 621-628.
35.Koenig J.S., Fischer M., Bulant E., Tiran B., Elmadfa I., Drumi W. Antioxidant status inpatients on chronic hemo- dialysis therapy: Impact of parenteral selenium supple- mentation. Wien. Klin. Wochenschr. 1997; 109: 13-19.
36.Kukreja R.C., Jesse R.L., Hess M.L. Singlet oxygen: a potential culprit in myocardial injury?Mole. Cell. Biochem. 1992; 111: 17-24.
37.Lähteenmäki T.A., Seppo L., Laakso J., Korpela R., Vanhanen H., Tikkanen M.J., Vapaatalo H. Oxidized LDL From Subjects With Different Dietary Habits Modifies Atherogenic Processes In Endothelial and Smooth Muscle Cells. Life. Sciences. 2000; 66: 455-465.
38.Lamiere N., Tetta C. Hemodialysis and Oxidant stress. Blood. Purif. 1999; 17: 55-72.
39.Le Meur Y., Fixe P., Aligier J.C., Leroux-Robert C., Praloran V. Macrophage colony stimulating factor involvement in uremic patients. Kidney. Int. 1996; 50: 1007-1012.
40.Lentz S.R. Impaired anticoagulant response to infusion of thrombin in atherosclerotic monkeys associated with acquired defects in the protein C system. Arterioscler. Thrombo. & Vasc. Biol. 1999; 19: 1744-1750.
41.Linas S.L., whittenburg D., Repine J.E. Role of xanthine oxidase in ischemia/repelfusion injury. Am. J. Physiol. 1990; 258: 711-716.
42.London G.M., Parfrey P.S. Cardiac disease in chronic uremia Pathogenesis. Adv. Ren. Replace. Ther. 1997; 4: 194-211.
43.Lyson T.J. Oxidated low density lipoprotein: a role in the pathogenesis of atherosclerosis in diabetes? Diabetic. Med. 1991; 8: 411-419.
44.Marzatico F., Cafe C. Oxygen radicals and other toxic oxygen metabolites as key mediators of the central nervous system tissue injury. Funct. Neurol. 1993; 8: 51-66.
45.Mendall M.A., Patel P., Ballam L. C reactive protein and its relation to cardiovascular risk factors: a population based cross sectional study. B.M.J. 1996; 312: 1061- 1065.
46.Miyazawa T., Yasuda K., Fujimoto K., Kaneda T. Presence of phosphatidylcholine hydroperoxide in human plasma. J. Biochem. 1988; 103: 744-746.
47.Monks T.J., Anders M.W., Dekant W., Stevens J.L., Lau S.S., Ven Bladeren P.J. Glutathione conjugate mediated toxicities. Toxicol. Appl. Pharnacol. 1990; 106: 1-19.
48.Morena M., Cristol J.P., Bosc J.Y., Tetta C., Forret G., Descomps B., Canaud B. Convective and diffusive losses of vutamin C during hemodiafiltration session: A contributive factor to oxidative stress in hemodialysis patient. Nephrol. Dial. Transplant. 1998; 13: 467-471.
49.Morrow D.A., Ridker P.M. High sensitivity C-Reactive Protein(hs-CRP): A novel risk marker in cardiovascular disease. Preventive Cardiology. 1999; 24: 13-16.
50.Nguyen T.T., Ellefson R.D. Predictive value of electroph- oretically detected Lipoprotein(a) for coronary heart disease and cerebrovascular disease in a community based cohort of 9936 men and women. Circulation. 1997; 96: 1390-1397.
51.Oberley, L.W. Free radical and diabetes. Free Radic. Biol. Med. 1998; 5: 113-124.
52.Ohls R.K., Ehrenkranz R.A., Wright L.L., Lemons J.A., Korones S.B., Stoll B.J., Stark A.R., Shankaran S., Donovan E.F., Close N.C., Das A. Effects of Early Erythropoietin Therapy on the Transfusion Requirements of Preterm Infants Below 1250 Grams Birth Weight: A Multicenter, Randomized, Controlled Trial. Pediatrics. 2001; 108: 934-942.
53.Paller M.S., Holdal J.R., Ferris T.F. Oxygen free radicals in ischemic acute renal failure in the rat. J. Clin. Invest. 1984; 74: 1156-1164.
54.Pang R.W.C., Janus E.D., Lam K.S.I., Kraft H.G. Lipoprotein (a): a new risk factor in coronary heart disease. J.A.M.A. 1997; 13: 5-6.
55.Peuchant E., Carbonneau M.A., Dubourg L., Thomas M.J., Penomat A., Vallot C., Clere M. Lipoperoxidation in plasma and red blood cells of patients undergoing hemodialysis: Vitamins A. E. and iron status. Ferr Radio. Biol. Med. 1994; 16: 339-346.
56.Pyorala K. Diabetes and coronary artery disease: what a coincidence? J. Cardiovasc. Pharmacol. 1990; 16: 8-14.
57.Reaven G.M., Chen Y.D.I., Jeppesen J., Maheux P. Krauss R.M. Insulin resistance and hyperinsulinemia in indivi- duals with small dense low density lipoprotein particles. J. Clin. Invest. 1993; 92: 141-146.
58.Reid T.M., Loeb L.A. Effect of DNA-repair enzymes on mutagenesis by oxygen free radicals. Mutat. Res. 1993; 289: 181-186.
59.Rice-Evans C.A., Diplock A.T. Current status of anti- oxidant therapy. Free Radio. Biol. Med. 1993; 15: 77-96.
60.Ridker P.M., Cushman M., Stampfer M.J., Tracy R.P., Hennekens C.H. Plasma concentration of C-Reactive Protein and risk of developing peripheral vascular disease. Circulation. 1998; 97: 425-428.
61.Ridker P.M., Glynn R.J., Hennekens C.H. C-Reactive Protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction. Circulation. 1998; 97: 2007-2011.
62.Schaeler R.M., Gilge U., Goehl H., Heidland A. Evaluation of a new polyamide membrane in high-flux dialysis. Blood. Purif. 1990; 8: 23-31.
63.Seybold Z.V., Abraham W.M., Gazeroglu H., Wanner A. Lmpairment of airway mucociliary transport by Pseudo- monas aeruginosa products. Role of oxygen radicals. Am. Rev. Respir. Dis. 1992; 146: 1173-1176.
64.Sowers J.R., Epstein M. Diabetes mellitus and associated hypertension, vascular disease, and nephropathy: An update. Hypertension. 1995; 26: 869-879.
65.Stein J.H., McBride P.E. Hyperhomocysteinemia and atherosclerotic vascular disease: pathophysiology, screening, and treatment. Arch. Intern. Med. 1998; 97: 138-141.
66.Sudha S., Alexa B., Jacob S., Paul F.J., Irwin H.R., Ralph B.D., Peter W.F., Philip A. Plasma Homocysteine as a Risk Factor for Dementia and Alzheimer's Disease. N. Engl. J. Med. 2002; 346: 476-483.
67.Sun A., Hedert S.C. Rapid hypertonic cell volume regulation in the perfused inner medullary-collecting duct. Kidney. Int. 1989; 36: 832-842.
68.Tetta C., Biasioli S., Schiaren R. An overview of hemodialysis and oxidant stress. Blood. Purif. 1999; 17: 118-126.
69.Tsao P.S., Niebanor J.R., Buitrago P.S., Lin B.Y., Wang J.P., Cooke Y.D., Chen I. Reaven G.M. Interaction of diabetes and hypertension on determinants of endothelial adhesiveness. Arterioscler. Thromb. Vasc. Biol. 1998; 18: 947-953.
70.Ungvari Z., Pacher P. Dysfunction of nitric oxide mediation in isolated rat arterioles with methionine diet-induced Hyperhomocysteinemia. Arterioscler, Thrombo. & Vasc Biol. 1999; 19: 1899-1904.
71.Vischer U.M. Hyperglycemia and the pathogenesis of atherosclerosis: lessons from murine models. Euro. J. Endocrinol. 1999; 140: 1-3.
72.Weinberg J.M. Schrier R.W., Gottschalk C.W. The cellular basis of nephrotoxicity. Diease of the kidney. 5th ed. 1993; 1036-1041.
73.Wilcken D.E., Wang X.L., Adachi T., Hara H., Duarte. Relationship between homocysteine and superoxide dismutase in homocystinuria: possible relevance to cardiovascular risk. Arteriosclerosis, Thrombosis. & Vascular Biology. 2000; 20: 1199-1202.
74.Wolff S.P., Jiang Z.Y., Hunt J.V. Protein glycation and oxidative stress in diabetes mellitus and aging. Free. Radio. Biol. Med. 1991; 10: 339-352.
75.Zenser T.V., Davis B.B. Enzyme systems involved in the formation of reactive metabolites in the renal metulla: Cooxidation via prostaglandin H synthetase. Fund. Am. Appl. Toxicol. 1984.
76.Zenset T.V., Mattammal M.B., Daves B.B. Demonstration of separate pathways for the metabolism of organic compounds in rabbit kidney. J. Pharmacol. Exp. Ther. 1979; 208: 418-21.
中文部分:
1.中華民國公共衛生概況 (2000),行政院衛生署,臺北,臺灣。
2.譚柱光, 黃東坡 : 人工腎臟,立大圖書,86年,12月修訂版.
3.詹爾昌: Risk assessment of cardiovascular disease Using Oxidized-LDL as indicator. 健康維護檢驗新知研討會. 2000; 8-9.
4.洪冠予, 陳萬裕 : 自由基與腎臟疾病,腎臟與透析,83年,6卷,2期,79-87.
QRCODE
 
 
 
 
 
                                                                                                                                                                                                                                                                                                                                                                                                               
第一頁 上一頁 下一頁 最後一頁 top