(3.235.191.87) 您好!臺灣時間:2021/05/13 04:46
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:::

: 
twitterline
研究生:邱雅婷
研究生(外文):Ya-Ting Chou
論文名稱:低氧運動在嗜中性白血球殺菌能力之影響
論文名稱(外文):Effects of hypoxic exercise on bactericidal capacity of neutrophil in men
指導教授:王鐘賢王鐘賢引用關係
指導教授(外文):J.S. Wang
學位類別:碩士
校院名稱:長庚大學
系所名稱:復健科學研究所
學門:醫藥衛生學門
學類:復健醫學學類
論文種類:學術論文
論文出版年:2008
畢業學年度:96
論文頁數:134
中文關鍵詞:低氧運動嗜中性白血球補體活化吞噬作用呼吸氧爆作用
外文關鍵詞:hypoxiaexerciseneutrophilcomplement activationphagocytosisrespiratory burst
相關次數:
  • 被引用被引用:0
  • 點閱點閱:409
  • 評分評分:系統版面圖檔系統版面圖檔系統版面圖檔系統版面圖檔系統版面圖檔
  • 下載下載:25
  • 收藏至我的研究室書目清單書目收藏:0
背景與目的:血液當中嗜中性白血球在免疫系統中佔有一個很重要的角色,主要利用噬菌作用和呼吸爆破的方式來防禦及消滅外來入侵的微生物,然而在運動或低氧環境的介入下所採用的強度,及其如何調節血液當中嗜中性白血球的活性,進而如何能來影響運動合併低氧加強排除外在病原體的入侵,目前仍不清楚。本篇研究主要目的檢測各種的運動合併低氧介入,嗜中性白血球對大腸桿菌的的吞噬作用和造成呼吸爆破的影響及相關分子的機制。
方法:健康靜態生活的年輕男性,其執行六個階段的實驗。首先,必須在常壓低氧艙一各小時分別為六階段的實驗:常氧21% O2劇烈運動(運動至最大攝氧量 ) 和中度運動 (50%最大攝氧量 ) 、兩個低氧運動 (中度運動12% and 15% O2)、兩個單純低氧( 12% and 15% O2 ) 於介入前和介入後與兩小時後抽取前壁靜脈血液,並以流氏細胞儀檢測嗜中性白血球的噬菌作用和呼吸氧爆作用、與其細胞膜之黏著分子(CD11a, CD11b, CD62L)、補體接受器(CD88 and CD35)和Fc III receptor (CD16b)之表現以及C1q結合至嗜中性白血球的能力為何,更進一步來探討嗜中性白血球在凋亡蛋白酵素3的活化程度和磷脂絲胺酸膜外翻來測量凋亡的情況,來加以了解噬菌細胞最後清除途徑;且利用NADPH oxidase的抑制劑,來偵測出氧爆作用所產生的自由基的途徑。
結果:在常氧狀態下,劇烈運動會引發較高的噬菌作用和呼吸氧爆作用,且在嗜中性白血球CD11a、CD11b的表現能力會高於中度運動;若運動合併低氧12% 或15% O2 的中度運動,則可以提升嗜中性白血球對呼吸氧爆的活性,同時強化 CD11a、CD11b和CD62L表現;此外,劇烈運動及中度運動皆可以增加嗜中性白血球在CD88表現和降低C1q 結合能力,此改變與在兩個低氧下執行中度運動相似,一樣有顯著的差異。最後在劇烈運動和12%氧濃度中度運動下會增加凋亡蛋白酶3的活性,且增加磷脂絲胺酸外翻讓巨噬細胞所清除。
結論:中度運動合併12% 或15% O2 低氧濃度介入,可以增強嗜中性白血球對外來入侵大腸桿菌吞噬及氧爆作用,並且能向上調節黏著分子的表現;由本結果可以得知菸醯胺腺嘌呤二核酸磷酸氧化酶驅使的氧化劑會導致細胞表面的改變,使噬菌細胞產生磷脂絲胺酸膜外翻,進而被巨噬細胞所辨識將它吞入清除,最後,可由本實驗了解嗜中性白血球在凋亡蛋白酶活化上的清除是凋亡蛋白非依賴過程。
臨床意義:此研究之預期成果可以協助我們瞭解對嗜中性白血球的影響,進而應用此設計出安全及有效的物理治療策略,提升了先天免疫的功能,增進個體對外來病菌的防禦能力。
Background and Purpose: Blood neutrophil plays an important role in the immune system, forming the first defense against invading microorganisms by phagocytosis and oxidative burst. Although exercise or hypoxia intervention was observed to modulate blood neutrophil activity in an intensity manner, effect of exercise combined with hypoxia on elimination of bacteria by neutrophil remains unclear. This study investigates how exercise combined with hypoxia affects phagocytosis and oxidative burst of neutrophil to E.coli and its underlying molecular mechanism.
Methods: fourteen healthy sedentary healthy young men engaged six conditions in a normobaric hypoxia chamber for 1 hour: two normoxic exercise [i.e., strenuous exercise (SE, up to VO2max) and moderate exercise (ME, 50%VO2max) in 21% O2], two hypoxic exercise (i.e., ME in 12% and 15% O2), and two hypoxic conditions (i.e., 12% and 15% O2). Before, immediately, and 2 hours following various interventions, niutrophil functions (phagocytic and oxidative burst activities), adhesion molecules (CD11a, CD11b, CD62L), complement receptors (CD88 and CD35), and FcIII receptor (CD16b), binding of C1q, caspase3 activity and Phosphatidylserine (PS) exposure to neutrophil were measured using flow cytometery.
Results: The combined with 12% or 15% O2 intervention, ME promoted the extent of oxidative burst activities of neutrophils, accompanied by augmenting the increases of neutrophil CD11a, CD11b and CD62L expressions by this exercise. Additionally, normoxic SE and ME increased neutrophil CD88 expression and decreased binding of C1q to neutrophil, which changes were similar to two hypoxic ME. Indeed, SE and 12%ME inhibit of the oxidative burst led to decrease caspase activation and clearance by macrophages. The inhibition
NADPH oxidase can increase Phosphatidylserine (PS) exposure and unchanged caspase3 activation to neutrophil.
Conclusions: ME combined with 12% or 15%O2 intervention enhanced E.coli.-induced oxidative burst of neutrophils, possibly by up-regulating expressions of adhesion molecules on neutrophils. NADPH oxidase- derived oxidants trigger cell surface changes that result in macrophage recognition and engulfment of phagocytic cells. This phagocytic neutrophil clearance is a caspase-independent process.
Clinical Relevance: this study will clarifie the relationships between exercises combined with hypoxia and neutrophil function to provide a safe and effective strategy of physical therapy to improve innate immune response and increase resistance to bacteria infection.
目錄
摘要 Ⅴ
第一章 緒論(Introduction)...............1
第一節 研究背景及目的.....................1
第二節 研究假設..........................4
第二章 文獻回顧(Literature Review).....5
第一節 低氧簡介..........................5
第二節 低氧環境下的生理適應反應............6
第三節 低氧與氧化壓力的相關性..............7
第四節 免疫系統和發炎的相關性..............9
第五節 噬菌細胞在發炎反應中的角色..........11
第六節 補體與噬菌細胞在發炎反應中的關聯.....14
第七節 運動和免疫的相關反應................17
第三章 實驗設計(Experimental Design)....18
第一節 實驗材料..........................18
第二節 實驗方法..........................24
受試者..................................24
實驗流程................................24
多形核性白血球萃取.......................25
細胞膜上補體受器與黏著分子的測定...........25
噬菌性白血球的吞噬作用測定................26
噬菌性白血球的氧爆作用測定................27
偵測細胞膜外翻試驗.......................29
活化凋亡蛋白試驗.........................30
統計分析................................31
第四章 實驗結果(Results)...............33
第一節 受試者基本資料、身體狀況和活動情形調查33
第二節 不同低氧濃度、運動強度、低氧合併中度運動對於心跳、血壓、血氧飽和度、心肺功能、乳酸之影響...............34
第三節 不同低氧濃度、運動強度、低氧合併中度運動對於血球數目之影響......................................35
第四節 不同低氧濃度、運動強度、低氧合併中度運動對於白血球黏著分子之影響....................................35
第五節 不同低氧濃度、運動強度、低氧合併中度運動對於補體活化以及白血球的抗原受器及補體受器之影響 ...............38
第六節 不同低氧濃度、運動強度、合併低氧運動對於噬菌細胞的行為影響.......................................43
第七節 不同低氧濃度、運動強度、合併低氧運動對於噬菌細胞的清除及死亡........................................46
第五章 討論(Discussion)...................49
第六章 結論(Conclusion)...................59

圖表附錄............................61
附錄一 受測者基本資料.................115
附錄二 身體狀況與活動情況調查表........117

參考文獻(References)...............105

圖表目錄
表一 受測者基本資料...................61
表二 不同低氧濃度和運動強度介入下肺部功能的表現........62
表三 不同低氧濃度和運動強度介入對粘著分子和補體抗體接受器的表現 64
表四 不同低氧濃度和運動強度介入對嗜中性白血球吞噬大腸桿菌的表現 65
表五 不同低氧濃度和運動強度介入對嗜中性白血球吞噬大腸桿菌產生活性氧的表現...............................66
表六 不同低氧濃度和運動強度介入偵測嗜中性白血球吞早期凋亡的基礎値和刺激值...............................68
表七 不同低氧濃度和運動強度介入對凋亡蛋白3的影響 69
圖一 白血球趨化作用(Chemotaxis).......70
圖二 嗜中性球外滲作用的四個步驟..........71
圖三 補體主要的四大功能.................72
圖四 補體活化的三大路徑.................73
圖五 抗原調理作用......................74
圖六 實驗流程 .........................75
圖七 在不同低氧濃度、運動強度、低氧合併中度運動介入下看血氧飽和度(SaO2)和心跳(HR)變化................76
圖八 在不同低氧濃度、運動強度、低氧合併中度運動介入下對SBP、DBP、MBP的改變..............................77
圖九 在不同低氧濃度、運動強度、低氧合併中度運動介入pH値、PaCO2 、HCO3-、乳酸的改變......................78
圖十 在不同低氧濃度、運動強度、低氧合併中度運動介入多型核性白血球的數量....................................79
圖十一 在不同低氧濃度、運動強度、低氧合併中度運動介入多型核性白血球分類的數量...............................80
圖十二 利用低氧、運動和低氧運動下分別不同刺激的方式,影響白血球CD62L的螢光表現..........................81
圖十三 利用低氧、運動和低氧運動下分別不同刺激的方式,影響白血球CD11a的螢光表現..........................82
圖十四 利用低氧、運動和低氧運動下分別不同刺激的方式,影響白血球CD11b的螢光表現..........................83
圖十五 利用低氧、運動和低氧運動下分別不同刺激的方式,影響白血球CD16b的螢光表現...........................84
圖十六 利用低氧、運動和低氧運動下分別不同刺激的方式,影響白血球CD35的螢光表現................................85
圖十七 利用低氧、運動和低氧運動下分別不同刺激的方式,影響白血球CD88的螢光表現................................86
圖十八 利用低氧、運動和低氧運動下分別不同刺激的方式,影響白血球C1q的螢光表現..................................87
圖十九 利用低氧、運動和低氧運動下分別不同刺激的方式,偵測補體所行走路俓......................................88
圖二十 噬菌細胞吞噬E.coil接螢光後吞噬作用的螢光表現...... 89
圖二十一 不同低氧濃度、運動強度、低氧合併中度運動影響噬菌細胞的噬菌能力......................................90
圖二十二 不同低氧濃度、運動強度、低氧合併中度運動影響噬菌細胞的噬菌能力,噬菌細胞吞噬E.coil的程度上.............91
圖二十三 噬菌細胞吞噬E.coil後的氧爆作用之螢光表現....93
圖二十四 不同低氧濃度、運動強度、低氧合併中度運動介入下立即影響噬菌細胞的呼吸氧爆及NADPH的抑制能力 ..............94
圖二十五 不同低氧濃度、運動強度、低氧合併中度運動介入下放置四小時影響噬菌細胞的呼吸氧爆及NADPH的抑制能力..........96
圖二十六 不同低氧濃度、運動強度、低氧合併中度運動介入放置四小時E.coli影響噬菌細胞的呼吸氧爆及NADPH的抑制能力...97
圖二十七 不同低氧濃度、運動強度、低氧合併中度運動介入下放置四小時後,偵測嗜中性白血球早期凋亡的基礎値和刺激値.....99
圖二十八 不同低氧濃度、運動強度、低氧合併中度運動介入下放置E.coli四小時,偵測嗜中性白血球早期凋亡的基礎値和刺激値...101
圖二十九 不同低氧濃度、運動強度、低氧合併中度運動介入放置四小時,對凋亡蛋白菌3的影響............................103
圖三十 不同低氧濃度、運動強度、低氧合併中度運動介入下加入E.coli放置四小時後,對凋亡蛋白3的影響...................104
參考文獻(References)
1. Abid MR, Kachra Z, Spokes KC, Aird WC. NADPH oxidase activity is required for endothelial cell proliferation and migration. FEBS Lett. 2000, 15; 486:252-6.
2. Abid MR, Spokes KC, Shih SC, Aird WC. NADPH oxidase activity selectively modulates vascular endothelial growth factor signaling pathways.J Biol Chem. 2007, 30; 282:35373-85.
3. Ali MH, Schlidt SA, Chandel NS, Hynes KL, Schumacker PT, Gewertz BL. Endothelial permeability and IL-6 production during hypoxia: role of ROS in signal transduction.Am J Physiol. 1999, 277:L1057-65.
4. Akgul C, Moulding DA, Edwards SW.Molecular control of neutrophil apoptosis. FEBS Lett. 2001, 5; 487:318-22.
5. Babior BM Lambeth JD, Nauseef W.The neutrophil NADPH oxidase.Arch Biochem Biophys. 2002, 15; 397:342-4.
6. Baudry N, Danialou G, Boczkowski J, Vicaut E. In vivo study of the effect of systemic hypoxia on leukocyte-endothelium interactions.Am J Respir Crit Care Med. 1998, 158:477-83.
7. Blannin AK. Chatwin LJ,Cave R et al. Effect of submaximal cycling and endurance training on neutrophil phagocytotic activity in middle-aged men. Br J Sports Med. 1996, 30:125-9.
8. Carroll MC.The complement system in regulation of adaptive immunity. Nat Immunol. 2004, 5:981-6.
9. Carroll MC. The role of complements and complement receptors in induction and regulation of immunity. Annu Rev Immunol. 1998, 16:545-68.
10. Choukèr A, Demetz F, Martignoni A, Smith L, Setzer F, Bauer A, Hölzl J, Peter K, Christ F, Thiel M. Strenuous physical exercise inhibits granulocyte activation induced by high altitude. J Appl Physiol. 2005 Feb; 98:640-7.
11. Collard CD, Väkevä A, Morrissey MA, Agah A, Rollins SA, Reenstra WR, Buras JA, Meri S, Stahl GL. Complement activation after oxidative stress: role of the lectin complement pathway. Am J Pathol. 2000, 156:1549-56.
12. Collard CD, Bukusoglu C, Agah A, Colgan SP, Reenstra WR, Morgan BP, Stahl GL.Hypoxia-induced expression of complement receptor type 1 (CR1, CD35) in human vascular endothelial cells.Am J Physiol. 1999, 276:C450-8.
13. Cook-Mills JM.Reactive oxygen species regulation of immune function. Mol Immunol. 2002, 39:497-8.
14. C zermak BJ. Lentsch AB. Bless NM. Schmal H. Friedl HP. Ward PA. Role of complement in in vitro and in vivo lung inflammatory reactions. J Leukoc Biol. 1998, 64:40-8.
15. DeLeo FR, Allen LA, Apicella M, Nauseef WM.NADPH oxidase activation and assembly during phagocytosis. J Immunol. 1999, 15; 163:6732-40.
16. Dufaux B, Order U. Complement activation after prolonged exercise. Clin Chim Acta. 1989, 13; 179:45-9.
17. Dahlgren C, Karlsson A. Respiratory burst in human neutrophils. J Immunol Methods. 1999, 17; 232:3-14.
18. Favoreel HW, Van de Walle GR, Nauwynck HJ, Pensaert MB. Virus complement evasion strategies.J Gen Virol. 2003, 84:1-15.
19. Fadeel B, Ahlin A, Henter JI, Orrenius S, Hampton MB. Involvement of caspases in neutrophil apoptosis: regulation by reactive oxygen species. Blood. 1998, 15; 92:4808-18.
20. Forman HJ, Torres M. Reactive oxygen species and cell signaling: respiratory burst in macrophage signaling. Am J Respir Crit Care Med. 2002, 15; 166:S4-8.
21. Fraser DA, Bohlson SS, Jasinskiene N, Rawal N, Palmarini G, Ruiz S, Rochford R, Tenner AJ.C1q and MBL components of the innate immune system, influence monocyte cytokine expression. J Leukoc Biol. 2006, 80:107-16.
22. Fujita T. Evolution of the lectin-complement pathway and its role in innate immunity. Nat Rev Immunol. 2002, 2:346-53.
23. Gasque P.Complement: a unique innate immune sensor for danger signals. Mol Immunol. 2004, 41:1089-98.
24. Gonzalez C, Sanz-Alfayate G, Agapito MT, Gomez-Niño A, Rocher A, Obeso A. Significance of ROS in oxygen sensing in cell systems with sensitivity to physiological hypoxia. Respir Physiol Neurobiol. 2002, 22; 132:17-41.
25. Gougerot-Pocidalo MA, el Benna J, Elbim C, Chollet-Martin S, Dang MC.[Regulation of human neutrophil oxidative burst by pro- and anti-inflammatory cytokines] J Soc Biol. 2002, 196:37-46.
26. Goldsby RA, Kindt TJ, Osborne BA. Kuby Immunology. Chapter15.W. H. Freeman and Company, New York, 2002.371-393.
27. Granfeldt D, Dahlgren C.An intact cytoskeleton is required for prolonged respiratory burst activity during neutrophil phagocytosis. Inflammation. 2001, 25:165-9.
28. John G. Wood, Leone F. Mattioli, and Norberto C. Gonzalez. Hypoxia causes leukocyte adherence to mesenteric venules in nonacclimatized, but not in acclimatized, rats. J Appl Physiol.1999, 7:873-881.
29. Kirk EA. Dinauer MC. Rosen H. Chait A. Heinecke JW. LeBoeuf RC. Impaired superoxide production due to a deficiency in phagocyte NADPH oxidase fails to inhibit atherosclerosis in mice. Arterioscler Thromb Vasc Biol. 2000, 20:1529-35.
30. Kirschfink M, Mollnes TE.Modern complement analysis. Clin Diagn Lab Immunol. 2003, 10:982-9.
31. Kong T, Eltzschig HK, Karhausen J, Colgan SP, Shelley CS.Leukocyte adhesion during hypoxia is mediated by HIF-1-dependent induction of beta2 integrin gene expression.Proc Natl Acad Sci U S A. 2004, 101:10440-5.
32. Lash GE. Fitzpatrick TE. Graham CH. Effect of hypoxia on cellular adhesion to vitronectin and fibronectin. Biochem Biophys Res Commun. 2001, 287:622-9.
33. Ley K, Laudanna C, Cybulsky MI, Nourshargh S. Getting to the site of inflammation: the leukocyte adhesion cascade updated. Nat Rev Immunol. 2007, 7:678-89.
34. Levada-Pires AC, Lambertucci RH, Mohamad M, Hirabara SM, Curi R, Pithon-Curi TC. Exercise training raises expression of the cytosolic components of NADPH oxidase in rat neutrophils. Eur J Appl Physiol. 2007 100:153-60.
35. Michiels C.Physiological and pathological responses to hypoxia. Am J Pathol. 2004, 164:1875-82.
36. Mastellos D, Morikis D, Isaacs SN, Holland MC, Strey CW, Lambris JD.Complement: structure, functions, evolution, and viral molecular mimicry. Immunol Res. 2003; 27:367-86.
37. Mackinnon LT. Chronic exercise training effects on immune function. Med Sci Sports Exerc. 2000, 32(7 Suppl):S369-76.
38. Mazzeo RS. Altitude, exercise and immune function. Exerc Immunol Rev. 2005, 11:6-16.
39. Medzhitov R, Janeway CA Jr. Decoding the patterns of self and nonself by the innate immune system. Science. 2002, 296:298-300.
40. Mold C, Morris CA. Complement activation by apoptotic endothelial cells following hypoxia/reoxygenation. Immunology. 2001,102:359-64.
41. Nakagiri A, Sunamoto M, Murakami M. NADPH oxidase is involved in ischaemia/reperfusion-induced damage in rat gastric mucosa via ROS production--role of NADPH oxidase in rat stomachs. Inflammopharmacology. 2007, 15:278-81.
42. Neubauer JA. Invited review: Physiological and pathophysiological responses to intermittent hypoxia. J Appl Physiol. 2001, 90:1593-9.
43. Nieman DC. Is infection risk linked to exercise workload? Med Sci Sports Exerc. 2000, 32:S406-11.
44. Nieman DC, Pedersen BK. Exercise and immune function. Recent developments.Sports Med. 1999, 27:73-80.
45. Orth TA. Allen JA. Wood JG. Gonzalez NC. Exercise training prevents the inflammatory response to hypoxia in cremaster venules. Am J Physiol. 2005, 98:2113-8
46. Peake JM. Exercise-induced alterations in neutrophil degranulation and respiratory burst activity: possible mechanisms of action. Exerc Immunol Rev. 2002, 8:49-100.
47. Pedersen BK, Steensberg A. Exercise and hypoxia: effects on leukocytes and interleukin-6-shared mechanisms? Med Sci Sports Exerc. 2002, 34:2004-13.
48. Pedersen BK, Hoffman-Goetz L. Exercise and the immune system: regulation, integration, and adaptation. Physiol Rev. 2000, 80:1055-81.
49. Pialoux V. Mounier R. Ponsot E. Rock E. Mazur A. Dufour S. Richard R. Richalet JP. Coudert J. Fellmann N. Effects of exercise and training in hypoxia on antioxidant/pro-oxidant balance.2006, 60:1345-54.
50. Rada B, Leto TL.Oxidative innate immune defenses by nox/duox family NADPH oxidases.Contrib Microbiol. 2008,15:164-87.
51. Roos D, van Bruggen R, Meischl C. Oxidative killing of microbes by neutrophils. Microbes Infect. 2003,:1307-15.
52. Roth MB. Nystul T. Buying time in suspended animation. Scientific American. 2005, 292:48-55.
53. Rowbottom DG, Green KJ.Acute exercise effects on the immune system. Med Sci Sports Exerc. 2000, 32:S396-405.
54. Sanders KA, Sundar KM, He L, Dinger B, Fidone S, Hoidal JR. Role of components of the phagocytic NADPH oxidase in oxygen sensing.J Appl Physiol. 2002, 93:1357-64.
55. Simon HU, Haj-Yehia A, Levi-Schaffer F. Role of reactive oxygen species (ROS) in apoptosis induction.Apoptosis. 2000, 5:415-8.
56. Shen YC, Sung YJ, Chen CF.Magnolol inhibits Mac-1 (CD11b/CD18)- dependent neutrophil adhesion: relationship with its antioxidant effect. Eur J Pharmacol. 1998, 5; 343:79-86.
57. Smith JK, Chi DS, Krish G, Reynolds S, Cambron G. Effect of exercise on complement activity.Ann Allergy. 1990, 65:304-10.
58. Stuart LM, Ezekowitz RA. Phagocytosis and comparative innate immunity: learning on the fly. Nat Rev Immunol. 2008, 8:131-41.
59. Steiner DR, Gonzalez NC, Wood JG.Interaction between reactive oxygen species and nitric oxide in the microvascular response to systemic hypoxia.J Appl Physiol. 2002, 93:1411-8.
60. Steiner DR. Gonzalez NC. Wood JG. Leukotriene B. Leukotriene B (4) Promotes reactive oxidant generation and leukocyte adherence during acute hypoxia. J Appl Physiol. 2001, 91:1160-7.
61. Underhill DM, Ozinsky A. Phagocytosis of microbes: complexity in action. Annu Rev Immunol. 2002, 20:825-52.
62. Wientjes FB, Segal AW.NADPH oxidase and the respiratory burst. Semin Cell Biol. 1995, 6:357-65.
63. Walport MJ, Davies KA.Complement and immune complexes. Res Immunol. 1996, 147:103-9.
64. Wilkie RP, Vissers MC, Dragunow M, Hampton MB. A functional NADPH oxidase prevents caspase involvement in the clearance of phagocytic neutrophils. Infect Immun. 2007, 75:3256-63.
65. White CW. Commentary on "Hypoxia, hypoxic signaling, tissue damage, and detection of reactive oxygen species (ROS)". Free Radic Biol Med. 2006, 15; 40:923-7.
66. Wood JG, Johnson JS, Mattioli LF, Gonzalez NC.Systemic hypoxia increases leukocyte emigration and vascular permeability in conscious rats. J Appl Physiol. 2000, 89:1561-8.
67. Wood JG. Johnson JS. Mattioli LF. Gonzalez NC. Systemic hypoxia promotes leukocyte-endothelial adherence via reactive oxidant generation. J Appl Physiol. 1999, 87:1734-40.
68. Woods JA, Davis JM, Smith JA, Nieman DC. Exercise and cellular innate immune function.Med Sci Sports Exerc. 1999, 31:57-66.
69. Woods J, Lu Q, Ceddia MA, Lowder T. Special feature for the Olympics: effects of exercise on the immune system: exercise-induced modulation of macrophage function. Immunol Cell Biol. 2000, 78:545-53.
70. 劉晃均。系統性低氧在男性之血栓發炎中所扮演的角色。長庚大學復健科學研究所。碩士論文;2007
QRCODE
 
 
 
 
 
                                                                                                                                                                                                                                                                                                                                                                                                               
第一頁 上一頁 下一頁 最後一頁 top
無相關期刊
 
系統版面圖檔 系統版面圖檔