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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 吳寬墩 | |
dc.contributor.author | Vin-Cent Wu | en |
dc.contributor.author | 吳允升 | zh_TW |
dc.date.accessioned | 2021-06-17T00:46:54Z | - |
dc.date.available | 2017-03-02 | |
dc.date.copyright | 2012-03-02 | |
dc.date.issued | 2012 | |
dc.date.submitted | 2011-12-27 | |
dc.identifier.citation | Ader, R., K. Chatterjee, T. Ports, B. Brundage, B. Hiramatsu and W. Parmley. Immediate and sustained hemodynamic and clinical improvement in chronic heart failure by an oral angiotensin-converting enzyme inhibitor. Circulation. 1980 May;61(5):931-7.
Aicher, A., M. Rentsch, K. Sasaki, J. W. Ellwart, F. Fandrich, R. Siebert, et al. Nonbone marrow-derived circulating progenitor cells contribute to postnatal neovascularization following tissue ischemia. Circ Res. 2007 Mar 2;100(4):581-9. Arima, S., K. Kohagura, H. L. Xu, A. Sugawara, A. Uruno, F. Satoh, et al. Endothelium-derived nitric oxide modulates vascular action of aldosterone in renal arteriole. Hypertension. 2004 Feb;43(2):352-7. Arriza, J. L., C. Weinberger, G. Cerelli, T. M. Glaser, B. L. Handelin, D. E. Housman, et al. Cloning of human mineralocorticoid receptor complementary DNA: structural and functional kinship with the glucocorticoid receptor. Science. 1987 Jul 17;237(4812):268-75. Asahara, T., H. Masuda, T. Takahashi, C. Kalka, C. Pastore, M. Silver, et al. Bone marrow origin of endothelial progenitor cells responsible for postnatal vasculogenesis in physiological and pathological neovascularization. Circ Res. 1999 Aug 6;85(3):221-8. Asahara, T., T. Murohara, A. Sullivan, M. Silver, R. van der Zee, T. Li, et al. Isolation of putative progenitor endothelial cells for angiogenesis. Science. 1997 Feb 14;275(5302):964-7. Assmus, B., V. Schachinger, C. Teupe, M. Britten, R. Lehmann, N. Dobert, et al. Transplantation of Progenitor Cells and Regeneration Enhancement in Acute Myocardial Infarction (TOPCARE-AMI). Circulation. 2002 Dec 10;106(24):3009-17. Assmus, B., C. Urbich, A. Aicher, W. K. Hofmann, J. Haendeler, L. Rossig, et al. HMG-CoA reductase inhibitors reduce senescence and increase proliferation of endothelial progenitor cells via regulation of cell cycle regulatory genes. Circ Res. 2003 May 16;92(9):1049-55. Banai, S., M. T. Jaklitsch, M. Shou, D. F. Lazarous, M. Scheinowitz, S. Biro, et al. Angiogenic-induced enhancement of collateral blood flow to ischemic myocardium by vascular endothelial growth factor in dogs. Circulation. 1994 May;89(5):2183-9. Bangham, A. D. and W. T. Mason. Anesthetics may act by collapsing pH gradients. Anesthesiology. 1980 Aug;53(2):135-41. Benjamin, L. E., D. Golijanin, A. Itin, D. Pode and E. Keshet. Selective ablation of immature blood vessels in established human tumors follows vascular endothelial growth factor withdrawal. J Clin Invest. 1999 Jan;103(2):159-65. Benndorf, R. A., U. M. Gehling, D. Appel, R. Maas, E. Schwedhelm, K. Schlagner, et al. Mobilization of putative high-proliferative-potential endothelial colony-forming cells during antihypertensive treatment in patients with essential hypertension. Stem Cells Dev. 2007 Apr;16(2):329-38. Bergmann, A., C. Eulenberg, M. Wellner, S. Rolle, F. Luft and R. Kettritz. Aldosterone abrogates nuclear factor kappaB-mediated tumor necrosis factor alpha production in human neutrophils via the mineralocorticoid receptor. Hypertension. 2010 Feb;55(2):370-9. Bernini, G., F. Galetta, F. Franzoni, M. Bardini, C. Taurino, M. Bernardini, et al. Arterial stiffness, intima-media thickness and carotid artery fibrosis in patients with primary aldosteronism. J Hypertens. 2008 Dec;26(12):2399-405. Blumenfeld, J. D., J. E. Sealey, Y. Schlussel, E. D. Vaughan, Jr., T. A. Sos, S. A. Atlas, et al. Diagnosis and treatment of primary hyperaldosteronism. Ann Intern Med. 1994 Dec 1;121(11):877-85. Briguori, C., U. Testa, R. Riccioni, A. Colombo, E. Petrucci, G. Condorelli, et al. Correlations between progression of coronary artery disease and circulating endothelial progenitor cells. Faseb J.Jun;24(6):1981-8. Cacciatore, F., G. Bruzzese, D. F. Vitale, A. Liguori, F. de Nigris, C. Fiorito, et al. Effects of ACE inhibition on circulating endothelial progenitor cells, vascular damage, and oxidative stress in hypertensive patients. Eur J Clin Pharmacol. 2011 Sep;67(9):877-83. Cai, H. and D. G. Harrison. Endothelial dysfunction in cardiovascular diseases: the role of oxidant stress. Circ Res. 2000 Nov 10;87(10):840-4. Callaghan, M. J., D. J. Ceradini and G. C. Gurtner. Hyperglycemia-induced reactive oxygen species and impaired endothelial progenitor cell function. Antioxid Redox Signal. 2005 Nov-Dec;7(11-12):1476-82. Caprio, M., B. G. Newfell, A. la Sala, W. Baur, A. Fabbri, G. Rosano, et al. Functional mineralocorticoid receptors in human vascular endothelial cells regulate intercellular adhesion molecule-1 expression and promote leukocyte adhesion. Circ Res. 2008 Jun 6;102(11):1359-67. Chang, H. W., T. S. Chu, H. Y. Huang, S. C. Chueh, V. C. Wu, Y. M. Chen, et al. Down-regulation of D2 dopamine receptor and increased protein kinase Cmu phosphorylation in aldosterone-producing adenoma play roles in aldosterone overproduction. J Clin Endocrinol Metab. 2007 May;92(5):1863-70. Chang, H. W., V. C. Wu, C. Y. Huang, H. Y. Huang, Y. M. Chen, T. S. Chu, et al. D4 dopamine receptor enhances angiotensin II-stimulated aldosterone secretion through PKC-{varepsilon} and calcium signaling. Am J Physiol Endocrinol Metab. 2008 Mar;294(3):E622-9. Chen, Y. H., S. J. Lin, F. Y. Lin, T. C. Wu, C. R. Tsao, P. H. Huang, et al. High glucose impairs early and late endothelial progenitor cells by modifying nitric oxide-related but not oxidative stress-mediated mechanisms. Diabetes. 2007 Jun;56(6):1559-68. Cheng, S., K. S. Cohen, S. Y. Shaw, M. G. Larson, S. J. Hwang, E. L. McCabe, et al. Association of Colony-Forming Units With Coronary Artery and Abdominal Aortic Calcification. Circulation. 2010 Sep 7;122(12):1176-1182. Choi, Y. H., K. Neef, M. Reher, O. J. Liakopoulos, M. Zeriouh, T. Wittwer, et al. The influence of pre-operative risk on the number of circulating endothelial progenitor cells during cardiopulmonary bypass. Cytotherapy.12(1):79-87. Chung, S. D., K. H. Huang, H. J. Yu, K. D. Wu and S. C. Chueh. Diagnosis of bilateral aldosterone-producing adenomas. Kidney Int. 2007 Jul;72(2):228. Corry, D. B. and M. L. Tuck. The effect of aldosterone on glucose metabolism. Curr Hypertens Rep. 2003 Apr;5(2):106-9. Deanfield, J. E., J. P. Halcox and T. J. Rabelink. Endothelial function and dysfunction: testing and clinical relevance. Circulation. 2007 Mar 13;115(10):1285-95. Doi, S. A., S. Abalkhail, M. M. Al-Qudhaiby, K. Al-Humood, M. F. Hafez and K. A. Al-Shoumer. Optimal use and interpretation of the aldosterone renin ratio to detect aldosterone excess in hypertension. J Hum Hypertens. 2006 Jul;20(7):482-9. Duprez, D. A. Is vascular stiffness a target for therapy? Cardiovasc Drugs Ther. 2010 Aug;24(4):305-10. Endtmann, C., T. Ebrahimian, T. Czech, O. Arfa, U. Laufs, M. Fritz, et al. Angiotensin II Impairs Endothelial Progenitor Cell Number and Function In Vitro and In Vivo: Implications for Vascular Regeneration. Hypertension. 2011 Aug 8. Ergun, S. and U. M. Gehling. Non-bone-marrow-derived endothelial progenitor cells: what is their exact location? Circ Res. 2007 Aug 3;101(3):e31. Fadini, G. P., A. Coracina, I. Baesso, C. Agostini, A. Tiengo, A. Avogaro, et al. Peripheral blood CD34+KDR+ endothelial progenitor cells are determinants of subclinical atherosclerosis in a middle-aged general population. Stroke. 2006 Sep;37(9):2277-82. Fadini, G. P., M. Miorin, M. Facco, S. Bonamico, I. Baesso, F. Grego, et al. Circulating endothelial progenitor cells are reduced in peripheral vascular complications of type 2 diabetes mellitus. J Am Coll Cardiol. 2005 May 3;45(9):1449-57. Fallo, F., F. Veglio, C. Bertello, N. Sonino, P. Della Mea, M. Ermani, et al. Prevalence and characteristics of the metabolic syndrome in primary aldosteronism. J Clin Endocrinol Metab. 2006 Feb;91(2):454-9. Farquharson, C. A. and A. D. Struthers. Spironolactone increases nitric oxide bioactivity, improves endothelial vasodilator dysfunction, and suppresses vascular angiotensin I/angiotensin II conversion in patients with chronic heart failure. Circulation. 2000 Feb 15;101(6):594-7. Farquharson, C. A. and A. D. Struthers. Aldosterone induces acute endothelial dysfunction in vivo in humans: evidence for an aldosterone-induced vasculopathy. Clin Sci (Lond). 2002 Oct;103(4):425-31. Fernandez Pujol, B., F. C. Lucibello, U. M. Gehling, K. Lindemann, N. Weidner, M. L. Zuzarte, et al. Endothelial-like cells derived from human CD14 positive monocytes. Differentiation. 2000 May;65(5):287-300. Fraccarollo, D., P. Galuppo, S. Schraut, S. Kneitz, N. van Rooijen, G. Ertl, et al. Immediate mineralocorticoid receptor blockade improves myocardial infarct healing by modulation of the inflammatory response. Hypertension. 2008 Apr;51(4):905-14. Friedrich, E. B., K. Walenta, J. Scharlau, G. Nickenig and N. Werner. CD34-/CD133+/VEGFR-2+ endothelial progenitor cell subpopulation with potent vasoregenerative capacities. Circ Res. 2006 Feb 17;98(3):e20-5. Funder, J. W., R. M. Carey, C. Fardella, C. E. Gomez-Sanchez, F. Mantero, M. Stowasser, et al. Case detection, diagnosis, and treatment of patients with primary aldosteronism: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2008 Sep;93(9):3266-81. Funder, J. W., P. T. Pearce, R. Smith and A. I. Smith. Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated. Science. 1988 Oct 28;242(4878):583-5. Giacchetti, G., V. Ronconi, G. Lucarelli, M. Boscaro and F. Mantero. Analysis of screening and confirmatory tests in the diagnosis of primary aldosteronism: need for a standardized protocol. J Hypertens. 2006 Apr;24(4):737-745. Gomez-Sanchez, C. E., A. F. de Rodriguez, D. G. Romero, J. Estess, M. P. Warden, M. T. Gomez-Sanchez, et al. Development of a panel of monoclonal antibodies against the mineralocorticoid receptor. Endocrinology. 2006 Mar;147(3):1343-8. Gonzalez, A., M. Rota, D. Nurzynska, Y. Misao, J. Tillmanns, C. Ojaimi, et al. Activation of cardiac progenitor cells reverses the failing heart senescent phenotype and prolongs lifespan. Circ Res. 2008 Mar 14;102(5):597-606. Granger, J. P., S. Kassab, J. Novak, J. F. Reckelhoff, B. Tucker and M. T. Miller. Role of nitric oxide in modulating renal function and arterial pressure during chronic aldosterone excess. Am J Physiol. 1999 Jan;276(1 Pt 2):R197-202. Guder, G., J. Bauersachs, S. Frantz, D. Weismann, B. Allolio, G. Ertl, et al. Complementary and incremental mortality risk prediction by cortisol and aldosterone in chronic heart failure. Circulation. 2007 Apr 3;115(13):1754-61. Gunaruwan, P., M. Schmitt, J. Taylor, L. Lee, A. Struthers and M. Frenneaux. Lack of rapid aldosterone effects on forearm resistance vasculature in health. J Renin Angiotensin Aldosterone Syst. 2002 Jun;3(2):123-5. Gunnells, J. C., Jr., C. E. Grim, R. R. Robinson and N. M. Wildermann. Plasma renin activity in healthy subjects and patients with hypertension. Preliminary experience with a rapid and quantitative bio-assay. Arch Intern Med. 1967 Mar;119(3):232-40. Hattori, K., B. Heissig, Y. Wu, S. Dias, R. Tejada, B. Ferris, et al. Placental growth factor reconstitutes hematopoiesis by recruiting VEGFR1(+) stem cells from bone-marrow microenvironment. Nat Med. 2002 Aug;8(8):841-9. Hill, J. M., G. Zalos, J. P. Halcox, W. H. Schenke, M. A. Waclawiw, A. A. Quyyumi, et al. Circulating endothelial progenitor cells, vascular function, and cardiovascular risk. N Engl J Med. 2003 Feb 13;348(7):593-600. Horita, Y., T. Inenaga, H. Nakahama, H. Ishibashi-Ueda, Y. Kawano, S. Nakamura, et al. Cause of residual hypertension after adrenalectomy in patients with primary aldosteronism. Am J Kidney Dis. 2001 May;37(5):884-9. Hristov, M., W. Erl and P. C. Weber. Endothelial progenitor cells: mobilization, differentiation, and homing. Arterioscler Thromb Vasc Biol. 2003 Jul 1;23(7):1185-9. Hsu, S. P., M. S. Wu, C. C. Yang, K. C. Huang, S. Y. Liou, S. M. Hsu, et al. Chronic green tea extract supplementation reduces hemodialysis-enhanced production of hydrogen peroxide and hypochlorous acid, atherosclerotic factors, and proinflammatory cytokines. Am J Clin Nutr. 2007 Nov;86(5):1539-47. Huang, P. H., Y. H. Chen, H. Y. Tsai, J. S. Chen, T. C. Wu, F. Y. Lin, et al. Intake of Red Wine Increases the Number and Functional Capacity of Circulating Endothelial Progenitor Cells by Enhancing Nitric Oxide Bioavailability. Arterioscler Thromb Vasc Biol. 2010 Jan 21;30(4):869-877. Huang, P. H., Y. H. Chen, C. H. Wang, J. S. Chen, H. Y. Tsai, F. Y. Lin, et al. Matrix metalloproteinase-9 is essential for ischemia-induced neovascularization by modulating bone marrow-derived endothelial progenitor cells. Arterioscler Thromb Vasc Biol. 2009 Aug;29(8):1179-84. Imanishi, T., C. Moriwaki, T. Hano and I. Nishio. Endothelial progenitor cell senescence is accelerated in both experimental hypertensive rats and patients with essential hypertension. J Hypertens. 2005 Oct;23(10):1831-7. Isner, J. M. and T. Asahara. Angiogenesis and vasculogenesis as therapeutic strategies for postnatal neovascularization. J Clin Invest. 1999 May;103(9):1231-6. Iwakura, A., C. Luedemann, S. Shastry, A. Hanley, M. Kearney, R. Aikawa, et al. Estrogen-mediated, endothelial nitric oxide synthase-dependent mobilization of bone marrow-derived endothelial progenitor cells contributes to reendothelialization after arterial injury. Circulation. 2003 Dec 23;108(25):3115-21. Joffe, H. V. and G. K. Adler. Effect of aldosterone and mineralocorticoid receptor blockade on vascular inflammation. Heart Fail Rev. 2005 Jan;10(1):31-7. Kayes-Wandover, K. M. and P. C. White. Steroidogenic enzyme gene expression in the human heart. J Clin Endocrinol Metab. 2000 Jul;85(7):2519-25. Kido, M., K. Ando, M. L. Onozato, A. Tojo, M. Yoshikawa, T. Ogita, et al. Protective effect of dietary potassium against vascular injury in salt-sensitive hypertension. Hypertension. 2008 Feb;51(2):225-31. Kissel, C. K., R. Lehmann, B. Assmus, A. Aicher, J. Honold, U. Fischer-Rasokat, et al. Selective functional exhaustion of hematopoietic progenitor cells in the bone marrow of patients with postinfarction heart failure. J Am Coll Cardiol. 2007 Jun 19;49(24):2341-9. Knox, F. G., J. C. Burnett, Jr., D. E. Kohan, W. S. Spielman and J. C. Strand. Escape from the sodium-retaining effects of mineralocorticoids. Kidney Int. 1980 Mar;17(3):263-76. Kobayashi, N., H. Fukushima, H. Takeshima, W. Koguchi, Y. Mamada, H. Hirata, et al. Effect of Eplerenone on Endothelial Progenitor Cells and Oxidative Stress in Ischemic Hindlimb. Am J Hypertens. 2010 Apr 29;23(9):1007-1013. Kocher, A. A., M. D. Schuster, M. J. Szabolcs, S. Takuma, D. Burkhoff, J. Wang, et al. Neovascularization of ischemic myocardium by human bone-marrow-derived angioblasts prevents cardiomyocyte apoptosis, reduces remodeling and improves cardiac function. Nat Med. 2001 Apr;7(4):430-6. Kolla, V., N. M. Robertson and G. Litwack. Identification of a mineralocorticoid/glucocorticoid response element in the human Na/K ATPase alpha1 gene promoter. Biochem Biophys Res Commun. 1999 Dec 9;266(1):5-14. Kuo, C. C., V. C. Wu, K. H. Huang, S. M. Wang, C. C. Chang, C. C. Lu, et al. Verification and evaluation of aldosteronism demographics in the Taiwan Primary Aldosteronism Investigation Group (TAIPAI Group). J Renin Angiotensin Aldosterone Syst. 2011 Mar 10. Kuo, C. C., V. C. Wu, C. W. Tsai and K. D. Wu. Relative kidney hyperfiltration in primary aldosteronism: a meta-analysis. J Renin Angiotensin Aldosterone Syst. 2011 Jun;12(2):113-22. Kuo, C. C., W. S. Yang, V. C. Wu, C. W. Tsai, W. J. Wang and K. D. Wu. Hypokalemic paralysis: the interplay between primary aldosteronism and hyperthyroidism. Eur J Clin Invest. 2009 Aug;39(8):738-9. Kuo, H. K., C. Y. Chen, H. M. Liu, C. J. Yen, K. J. Chang, C. C. Chang, et al. Metabolic risks, white matter hyperintensities, and arterial stiffness in high-functioning healthy adults. Int J Cardiol. 2009 Mar 3. Kusche-Vihrog, K., K. Urbanova, A. Blanque, M. Wilhelmi, H. Schillers, K. Kliche, et al. C-Reactive Protein Makes Human Endothelium Stiff and Tight. Hypertension. 2010 Dec 13;12(13 ( epublish). Lacolley, P., C. Labat, A. Pujol, C. Delcayre, A. Benetos and M. Safar. Increased carotid wall elastic modulus and fibronectin in aldosterone-salt-treated rats: effects of eplerenone. Circulation. 2002 Nov 26;106(22):2848-53. Ladage, D., K. Brixius, C. Steingen, U. Mehlhorn, R. H. Schwinger, W. Bloch, et al. Mesenchymal stem cells induce endothelial activation via paracine mechanisms. Endothelium. 2007 Mar-Apr;14(2):53-63. Ladage, D., N. Schutzeberg, T. Dartsch, B. Krausgrill, M. Halbach, C. Zobel, et al. Hyperaldosteronism is associated with a decrease in number and altered growth factor expression of endothelial progenitor cells in rats. Int J Cardiol. 2010 Jan 28;Jan(28 (epublish). Ladage, D., N. Schutzeberg, T. Dartsch, B. Krausgrill, M. Halbach, C. Zobel, et al. Hyperaldosteronism is associated with a decrease in number and altered growth factor expression of endothelial progenitor cells in rats. Int J Cardiol. 2011 Jun 2;149(2):152-6. Lee, C. W., P. H. Huang, S. S. Huang, H. B. Leu, C. C. Huang, T. C. Wu, et al. Decreased circulating endothelial progenitor cell levels and function in essential hypertensive patients with electrocardiographic left ventricular hypertrophy. Hypertens Res. 2011 Jun 9. Leite-Dellova, D. C., M. Oliveira-Souza, G. Malnic and M. Mello-Aires. Genomic and nongenomic dose-dependent biphasic effect of aldosterone on Na+/H+ exchanger in proximal S3 segment: role of cytosolic calcium. Am J Physiol Renal Physiol. 2008 Nov;295(5):F1342-52. Leone, A. M., M. Valgimigli, M. B. Giannico, V. Zaccone, M. Perfetti, D. D'Amario, et al. From bone marrow to the arterial wall: the ongoing tale of endothelial progenitor cells. Eur Heart J. 2009 Apr;30(8):890-9. Leopold, J. A., A. Dam, B. A. Maron, A. W. Scribner, R. Liao, D. E. Handy, et al. Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity. Nat Med. 2007 Feb;13(2):189-97. Liao, C. H., S. C. Chueh, K. D. Wu, M. H. Hsieh and J. Chen. Laparoscopic partial adrenalectomy for aldosterone-producing adenomas with needlescopic instruments. Urology. 2006 Sep;68(3):663-7. Lin, Y. H., H. H. Lee, K. L. Liu, J. K. Lee, S. R. Shih, S. C. Chueh, et al. Reversal of myocardial fibrosis in patients with unilateral hyperaldosteronism receiving adrenalectomy. Surgery. 2011 Apr 22. Lin, Y. H., S. M. Wang, V. C. Wu, J. K. Lee, C. C. Kuo, R. F. Yen, et al. The association of serum potassium level with left ventricular mass in patients with primary aldosteronism. Eur J Clin Invest. 2011 Jul;41(7):743-50. Lu, C. C., V. C. Wu, K. L. Liu, M. F. Cheng, Y. W. Wu, S. C. Chueh, et al. The Effectiveness of I-131 6-beta-iodomethyl-19-norcholesterol SPECT/CT for Primary Aldosteronism Patients with Inconclusive Adrenal Venous Sampling and Computed Tomographic Results. JOURNAL OF NUCLEAR MEDICINE. 2009:In press. Madero, M., C. L. Wassel, C. A. Peralta, S. S. Najjar, K. Sutton-Tyrrell, L. Fried, et al. Cystatin C associates with arterial stiffness in older adults. J Am Soc Nephrol. 2009 May;20(5):1086-93. Mahmud, A. and J. Feely. Aldosterone-to-renin ratio, arterial stiffness, and the response to aldosterone antagonism in essential hypertension. Am J Hypertens. 2005 Jan;18(1):50-5. Mancini, G. B., G. C. Henry, C. Macaya, B. J. O'Neill, A. L. Pucillo, R. G. Carere, et al. Angiotensin-converting enzyme inhibition with quinapril improves endothelial vasomotor dysfunction in patients with coronary artery disease. The TREND (Trial on Reversing ENdothelial Dysfunction) Study. Circulation. 1996 Aug 1;94(3):258-65. Marumo, T., H. Uchimura, M. Hayashi, K. Hishikawa and T. Fujita. Aldosterone impairs bone marrow-derived progenitor cell formation. Hypertension. 2006 Sep;48(3):490-6. Massaad, C., N. Houard, M. Lombes and R. Barouki. Modulation of human mineralocorticoid receptor function by protein kinase A. Mol Endocrinol. 1999 Jan;13(1):57-65. McCurley, A. and I. Z. Jaffe. Mineralocorticoid receptors in vascular function and disease. Mol Cell Endocrinol. 2011 Jun 24. Michel, F., M. L. Ambroisine, M. Duriez, C. Delcayre, B. I. Levy and J. S. Silvestre. Aldosterone enhances ischemia-induced neovascularization through angiotensin II-dependent pathway. Circulation. 2004 Apr 27;109(16):1933-7. Michowitz, Y., E. Goldstein, D. Wexler, D. Sheps, G. Keren and J. George. Circulating endothelial progenitor cells and clinical outcome in patients with congestive heart failure. Heart. 2007 Sep;93(9):1046-50. Milliez, P., X. Girerd, P. F. Plouin, J. Blacher, M. E. Safar and J. J. Mourad. Evidence for an increased rate of cardiovascular events in patients with primary aldosteronism. J Am Coll Cardiol. 2005 Apr 19;45(8):1243-8. Min, T. Q., C. J. Zhu, W. X. Xiang, Z. J. Hui and S. Y. Peng. Improvement in endothelial progenitor cells from peripheral blood by ramipril therapy in patients with stable coronary artery disease. Cardiovasc Drugs Ther. 2004 May;18(3):203-9. Mulatero, P., F. Rabbia, A. Milan, C. Paglieri, F. Morello, L. Chiandussi, et al. Drug effects on aldosterone/plasma renin activity ratio in primary aldosteronism. Hypertension. 2002 Muller-Ehmsen, J., D. Braun, T. Schneider, R. Pfister, N. Worm, K. Wielckens, et al. Decreased number of circulating progenitor cells in obesity: beneficial effects of weight reduction. Eur Heart J. 2008 Jun;29(12):1560-8. Nagasawa, T., S. Hirota, K. Tachibana, N. Takakura, S. Nishikawa, Y. Kitamura, et al. Defects of B-cell lymphopoiesis and bone-marrow myelopoiesis in mice lacking the CXC chemokine PBSF/SDF-1. Nature. 1996 Aug 15;382(6592):635-8. Nagata, D., M. Takahashi, K. Sawai, T. Tagami, T. Usui, A. Shimatsu, et al. Molecular mechanism of the inhibitory effect of aldosterone on endothelial NO synthase activity. Hypertension. 2006 Jul;48(1):165-71. Nehme, J. A., P. Lacolley, C. Labat, P. Challande, E. Robidel, C. Perret, et al. Spironolactone improves carotid artery fibrosis and distensibility in rat post-ischaemic heart failure. J Mol Cell Cardiol. 2005 Sep;39(3):511-9. Nietlispach, F., B. Julius, R. Schindler, A. Bernheim, C. Binkert, W. Kiowski, et al. Influence of acute and chronic mineralocorticoid excess on endothelial function in healthy men. Hypertension. 2007 Jul;50(1):82-8. Nishizaka, M. K., M. A. Zaman, S. A. Green, K. Y. Renfroe and D. A. Calhoun. Impaired endothelium-dependent flow-mediated vasodilation in hypertensive subjects with hyperaldosteronism. Circulation. 2004 Jun 15;109(23):2857-61. Nomura, K., S. Toraya, N. Horiba, M. Ujihara, M. Aiba and H. Demura. Plasma aldosterone response to upright posture and angiotensin II infusion in aldosterone-producing adenoma. J Clin Endocrinol Metab. 1992 Jul;75(1):323-7. Novitsky, Y. W., K. W. Kercher, M. J. Rosen, W. S. Cobb, S. Jyothinagaram and B. T. Heniford. Clinical outcomes of laparoscopic adrenalectomy for lateralizing nodular hyperplasia. Surgery. 2005 Dec;138(6):1009-16; discussion 1016-7. Oliver, J. J. and D. J. Webb. Noninvasive assessment of arterial stiffness and risk of atherosclerotic events. Arterioscler Thromb Vasc Biol. 2003 Apr 1;23(4):554-66. Omura, M., H. Sasano, T. Fujiwara, K. Yamaguchi and T. Nishikawa. Unique cases of unilateral hyperaldosteronemia due to multiple adrenocortical micronodules, which can only be detected by selective adrenal venous sampling. Metabolism. 2002 Mar;51(3):350-5. Ortiz, R. M., A. Mamalis and L. G. Navar. Aldosterone Receptor Antagonism Reduces Urinary C-Reactive Protein Excretion in Angiotensin II-Infused, Hypertensive Rats. J Am Soc Hypertens. 2009 May-Jun;3(3):184-91. Palmer, R. M., D. S. Ashton and S. Moncada. Vascular endothelial cells synthesize nitric oxide from L-arginine. Nature. 1988 Jun 16;333(6174):664-6. Park, S., J. B. Kim, C. Y. Shim, Y. G. Ko, D. Choi, Y. Jang, et al. The influence of serum aldosterone and the aldosterone-renin ratio on pulse wave velocity in hypertensive patients. J Hypertens. 2007 Jun;25(6):1279-83. Pierce, G. L., S. D. Beske, B. R. Lawson, K. L. Southall, F. J. Benay, A. J. Donato, et al. Weight loss alone improves conduit and resistance artery endothelial function in young and older overweight/obese adults. Hypertension. 2008 Jul;52(1):72-9. Pitt, B., W. Remme, F. Zannad, J. Neaton, F. Martinez, B. Roniker, et al. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 2003 Apr 3;348(14):1309-21. Qian, C., R. G. Schoemaker, W. H. van Gilst and A. J. Roks. The role of the renin-angiotensin-aldosterone system in cardiovascular progenitor cell function. Clin Sci (Lond). 2009 Feb;116(4):301-14. Rafii, S., S. Meeus, S. Dias, K. Hattori, B. Heissig, S. Shmelkov, et al. Contribution of marrow-derived progenitors to vascular and cardiac regeneration. Semin Cell Dev Biol. 2002 Feb;13(1):61-7. Ribstein, J., G. Du Cailar, P. Fesler and A. Mimran. Relative glomerular hyperfiltration in primary aldosteronism. J Am Soc Nephrol. 2005 May;16(5):1320-5. Ridker, P. M., N. Rifai, L. Rose, J. E. Buring and N. R. Cook. Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events. N Engl J Med. 2002 Nov 14;347(20):1557-65. Rocha, R. and J. W. Funder. The pathophysiology of aldosterone in the cardiovascular system. Ann N Y Acad Sci. 2002 Sep;970(89-100. Rocha, R., A. E. Rudolph, G. E. Frierdich, D. A. Nachowiak, B. K. Kekec, E. A. Blomme, et al. Aldosterone induces a vascular inflammatory phenotype in the rat heart. Am J Physiol Heart Circ Physiol. 2002 Nov;283(5):H1802-10. Romagni, P., F. Rossi, L. Guerrini, C. Quirini and V. Santiemma. Aldosterone induces contraction of the resistance arteries in man. Atherosclerosis. 2003 Feb;166(2):345-9. Rosenzweig, A. Circulating endothelial progenitors--cells as biomarkers. N Engl J Med. 2005 Sep 8;353(10):1055-7. Rossi, G. P., A. Belfiore, G. Bernini, G. Desideri, B. Fabris, C. Ferri, et al. Comparison of the captopril and the saline infusion test for excluding aldosterone-producing adenoma. Hypertension. 2007 Aug;50(2):424-31. Rossi, G. P., G. Bernini, C. Caliumi, G. Desideri, B. Fabris, C. Ferri, et al. A prospective study of the prevalence of primary aldosteronism in 1,125 hypertensive patients. J Am Coll Cardiol. 2006 Dec 5;48(11):2293-300. Rossi, G. P., M. Bolognesi, D. Rizzoni, T. M. Seccia, A. Piva, E. Porteri, et al. Vascular remodeling and duration of hypertension predict outcome of adrenalectomy in primary aldosteronism patients. Hypertension. 2008 May;51(5):1366-71. Rosso, A., A. Balsamo, R. Gambino, P. Dentelli, R. Falcioni, M. Cassader, et al. p53 Mediates the accelerated onset of senescence of endothelial progenitor cells in diabetes. J Biol Chem. 2006 Feb 17;281(7):4339-47. Salguero, G., E. Akin, C. Templin, D. Kotlarz, C. Doerries, U. Landmesser, et al. Renovascular hypertension by two-kidney one-clip enhances endothelial progenitor cell mobilization in a p47phox-dependent manner. J Hypertens. 2008 Feb;26(2):257-68. Schachinger, V., M. B. Britten and A. M. Zeiher. Prognostic impact of coronary vasodilator dysfunction on adverse long-term outcome of coronary heart disease. Circulation. 2000 Apr 25;101(16):1899-906. Schiffrin, E. L. Effects of aldosterone on the vasculature. Hypertension. 2006 Mar;47(3):312-8. Schmidt-Lucke, C., L. Rossig, S. Fichtlscherer, M. Vasa, M. Britten, U. Kamper, et al. Reduced number of circulating endothelial progenitor cells predicts future cardiovascular events: proof of concept for the clinical importance of endogenous vascular repair. Circulation. 2005 Jun 7;111(22):2981-7. Schmidt, B. M., A. Montealegre, C. P. Janson, N. Martin, C. Stein-Kemmesies, A. Scherhag, et al. Short term cardiovascular effects of aldosterone in healthy male volunteers. J Clin Endocrinol Metab. 1999 Oct;84(10):3528-33. Schmidt, B. M., S. Oehmer, C. Delles, R. Bratke, M. P. Schneider, A. Klingbeil, et al. Rapid nongenomic effects of aldosterone on human forearm vasculature. Hypertension. 2003 Aug;42(2):156-60. Schmidt, B. M., U. Sammer, I. Fleischmann, M. Schlaich, C. Delles and R. E. Schmieder. Rapid nongenomic effects of aldosterone on the renal vasculature in humans. Hypertension. 2006 Apr;47(4):650-5. Sealey, J. E., P. Trenkwalder, F. Gahnem, D. Catanzaro and J. H. Laragh. Plasma renin methodology: inadequate sensitivity and accuracy of direct renin assay for clinical applications compared with the traditional enzymatic plasma renin activity assay. J Hypertens. 1995 Jan;13(1):27-30; discussion 31. Sechi, L. A., M. Novello, R. Lapenna, S. Baroselli, E. Nadalini, G. L. Colussi, et al. Long-term renal outcomes in patients with primary aldosteronism. Jama. 2006 Jun 14;295(22):2638-45. Segal, M. S., R. Shah, A. Afzal, C. M. Perrault, K. Chang, A. Schuler, et al. Nitric oxide cytoskeletal-induced alterations reverse the endothelial progenitor cell migratory defect associated with diabetes. Diabetes. 2006 Jan;55(1):102-9. Shintani, S., T. Murohara, H. Ikeda, T. Ueno, T. Honma, A. Katoh, et al. Mobilization of endothelial progenitor cells in patients with acute myocardial infarction. Circulation. 2001 Jun 12;103(23):2776-9. Slight, S. H., J. Joseph, V. K. Ganjam and K. T. Weber. Extra-adrenal mineralocorticoids and cardiovascular tissue. J Mol Cell Cardiol. 1999 Jun;31(6):1175-84. Stary, H. C., A. B. Chandler, R. E. Dinsmore, V. Fuster, S. Glagov, W. Insull, Jr., et al. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation. 1995 Sep 1;92(5):1355-74. Stehr, C. B., R. Mellado, M. P. Ocaranza, C. A. Carvajal, L. Mosso, E. Becerra, et al. Increased levels of oxidative stress, subclinical inflammation, and myocardial fibrosis markers in primary aldosteronism patients. J Hypertens. 2010 Oct;28(10):2120-6. Steinmetz, M., G. Nickenig and N. Werner. Endothelial-regenerating cells: an expanding universe. Hypertension.Mar;55(3):593-9. Steinmetz, M., G. Nickenig and N. Werner. Endothelial-regenerating cells: an expanding universe. Hypertension. 2010 Mar;55(3):593-9. Sugiura, T., T. Kondo, Y. Kureishi-Bando, Y. Numaguchi, O. Yoshida, Y. Dohi, et al. Nifedipine improves endothelial function: role of endothelial progenitor cells. Hypertension. 2008 Sep;52(3):491-8. Sutton-Tyrrell, K., S. S. Najjar, R. M. Boudreau, L. Venkitachalam, V. Kupelian, E. M. Simonsick, et al. Elevated aortic pulse wave velocity, a marker of arterial stiffness, predicts cardiovascular events in well-functioning older adults. Circulation. 2005 Jun 28;111(25):3384-90. Takahashi, T., C. Kalka, H. Masuda, D. Chen, M. Silver, M. Kearney, et al. Ischemia- and cytokine-induced mobilization of bone marrow-derived endothelial progenitor cells for neovascularization. Nat Med. 1999 Apr;5(4):434-8. Takai, S., D. Jin, M. Muramatsu, K. Kirimura, H. Sakonjo and M. Miyazaki. Eplerenone inhibits atherosclerosis in nonhuman primates. Hypertension. 2005 Nov;46(5):1135-9. Takeda, Y., T. Yoneda, M. Demura, K. Furukawa, I. Miyamori and H. Mabuchi. Effects of high sodium intake on cardiovascular aldosterone synthesis in stroke-prone spontaneously hypertensive rats. J Hypertens. 2001 Mar;19(3 Pt 2):635-9. Tateishi-Yuyama, E., H. Matsubara, T. Murohara, U. Ikeda, S. Shintani, H. Masaki, et al. Therapeutic angiogenesis for patients with limb ischaemia by autologous transplantation of bone-marrow cells: a pilot study and a randomised controlled trial. Lancet. 2002 Aug 10;360(9331):427-35. Tepper, O. M., J. Carr, R. J. Allen, Jr., C. C. Chang, C. D. Lin, R. Tanaka, et al. Decreased circulating progenitor cell number and failed mechanisms of stromal cell-derived factor-1alpha mediated bone marrow mobiliza | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/66622 | - |
dc.description.abstract | 原發性皮質醛酮症(PA)是一個常見可以治癒的高血壓疾病。過去二十年來的研究發現,原發性皮質醛酮症的盛行率增加,有的研究報告發現在高血壓病人中盛行率達12%。原發性皮質醛酮症病人具有較一般高血壓的病人更高的心血管疾病。新進研究更發現受損的內皮細胞層可以藉由骨髓釋放至血液中的內皮前驅幹細胞(EPC)來修復,藉以維持血管內皮細胞層的功能性與完整性,而新生血管能提供缺氧組織所需要的血液循環,以減少因組織缺氧所造成的器官傷害,促進血管新生亦是近年來用來治療缺氧性心臟病或周邊血管疾病相當受重視的治療方式之一。但是皮質醛酮素對內皮前驅幹細胞的影響則尚屬未知,原發性皮質醛酮症較原發性高血壓(EH)可導致較高心血管事件發生率,很可能通過鹽皮質激素受體(MR)導致內皮細胞功能障礙的。在開刀前原發性皮質醛酮瘤病人有較高的血清皮質醛酮素,開完刀後血清皮質醛酮素明顯減少,因此原發性皮質醛酮瘤病人,提供了一個很好的機會,可以觀察皮質醛酮素影響內皮前驅幹細胞變化的機會。本計劃探討原發性皮質醛酮症病人術前術後,病人血管內皮幹細胞數目和功能是否隨著病人高血壓、皮質醛酮素和鉀離子的改善而改善;因而收集病人術前和術後內皮細胞功能、血管硬度和心血管指標等資料。並且在體外測試研究皮質醛酮素對血管內皮前驅幹細胞生長、增生及凋亡影響的方式。我們推測,原發性皮質醛酮症患者有缺陷的內皮前驅幹細胞,即可能造成動脈血管硬化和疾病的進展。因此整個研究計畫除了將臨床發現銜接到實驗室的研究之外,也包括從細胞株到病人實際的研究,探尋與疾病相關的生物指標與病理機制。希望藉由研究單一性的高血壓疾病,期待找出未明的心臟血管疾病調控機轉,進而尋找治療方式,減緩皮質醛酮素引起心臟血管疾病,未來能提供高血壓治療另一個方向。
我們進行了一項前瞻性研究,原發性皮質醛酮症患者,在接受單側腎上腺切除術或給予安達通(spironolactone)治療前及治療後6個月,給予完整評估。本研究是在多個轉介中心醫院進行,觀測治療後動脈血管硬度和內皮前驅幹細胞的改變,以及術後高血壓的恢復。共113例原發性皮質醛酮症患者(87例診斷皮質醛酮腺瘤,26例特異性皮質醛酮增生)和55例高血壓患者。 原發性皮質醛酮症患者比高血壓患者有較高的動脈血管硬度(P = 0.006)。然而,在接受單側腎上腺切除或給予安達通(spironolactone)治療後6個月,可以觀察到原發性皮質醛酮症患者比高血壓患者有較低的內皮前驅幹細胞和循環內皮細胞集落形成單位(CFU)(P<0.05)。內皮前驅幹細胞被證實表現鹽皮質激素受體(MR),用廣義加法模型(Generalized Additive Models, GAMs)分析。血漿皮質醛酮素濃度與循環的內皮前驅幹細胞數量呈負相關(p值= 0.021)。動脈血管硬度與循環的內皮前驅幹細胞數量呈負相關(P = 0.029)。體外高劑量皮質醛酮素(10-5和10 – 6M)抑制內皮前驅幹細胞的增殖和血管生成。血清高敏感C反應蛋白(hS-CRP)與循環的內皮前驅幹細胞數量呈負相關(p值= 0.03),並且在手術後降低。單側腎上腺切除六個月後,腎上腺切除術患者有顯著減少氧化活性(Log [RHOCL計數]%,1 ±0.112對比0.933±0.102,p值=0.047)。其中45例接受單側腎上腺切除術,32例(71%)高血壓獲得治癒。術前的循環內皮前驅幹細胞[Log CD34+ / KDR+(%)]可以預測腎上腺切除後,高血壓是否可治癒,(p值= 0.003)。皮質醛酮素對內皮前驅幹細胞的增殖有一個雙相(biphasic)作用。低劑量皮質醛酮素(10-9和10 -8M)加入早期和晚期內皮前驅幹細胞與的數量顯著增加內皮前驅幹細胞分化。與此相反,較高劑量皮質醛酮(10-5,10-6 M)則顯著減少內皮前驅幹細胞。這兩種效應被加入安達通(spironolactone)所減弱。在體外血管生成實驗以皮質醛酮素影響晚期的內皮前驅幹細胞新生血管效應。經過5天的培養,高皮質醛酮素較低皮質醛酮素導致管狀形成功能顯著降低。這種作用是劑量皮質醛酮依賴性(平均總長度和節點數,均p<0.001)。皮質醛酮素,無論是高或低劑量,並不會影響內皮前驅幹細胞凋亡。皮質醛酮素也不會改變衰老相關β-半乳糖苷酶陽性的內皮前驅幹細胞百分比。 原發性皮質醛酮症患者有相對不足的內皮前驅幹細胞,可以引起皮質醛酮症患者血管病變。可以以內皮前驅幹細胞的數量和能力缺損表示。這樣皮質醛酮素導致內皮前驅幹細胞的數量減少的機制在皮質醛酮素直接激活的鹽皮質激素受體會影響內皮前驅幹細胞的增殖和間接影響通過高皮質醛酮素引起的高C反應蛋白和氧化壓力。經過長期的後續追蹤,發現單側腎上腺切除或給予安達通(spironolactone) ,提供治療上改善內皮前驅幹細胞數量的策略。此外,長期高皮質醛酮素抑制內皮前驅幹細胞生成和增殖和減弱血管新生功能。循環的內皮前驅幹細胞可能是一個有價值的生物標誌物,其可用來評估原發性皮質醛酮症患者的發病率及較高的動脈硬度與心血管疾病風險,並預測術後高血壓恢復治癒率。這些發現可能將皮質醛酮素誘導血管病變提供新的見解,對新生血管增加新的意義,並確定新的治療目標,增加高血壓心血管疾病研究的進展。 | zh_TW |
dc.description.abstract | Growing evidence has shown that high plasma aldosterone level leads to a risk of cardiovascular diseases (CVD), including fatal stroke and sudden cardiac death. In addition, long-term exposure to increased aldosterone levels resulted in renal and metabolic sequelae independently of the blood pressure level. This phenomenon is best demonstrated in patients with primary aldosteronism (PA) who have excessive and inappropriate production of aldosterone. The excessive production of aldosterone in PA is associated with a high incidence of cardiovascular events, in comparison with essential hypertension (EH).
A total of 113 PA patients (87 patients with a diagnosis of aldosterone-producing adenoma, 26 with idiopathic hyperaldosteronism) and 55 patients with EH were enrolled. PA patients had higher arterial stiffness than EH patients (p = 0.006). However, lower numbers of circulating EPC and endothelial colony forming units (CFU) were observed in PA patients than in EH patients (p<0.05), which was ameliorated at six months after adrenalectomy or treatment with spironolactone. Expression of MR was identified in EPC. The plasma aldosterone concentration was inversely correlated with the number of circulating EPC (p =0.021) by the general additive model. The circulating number of EPC was inversely correlated with arterial stiffness (p=0.029) and the Framingham risk score (p=0.001). Serum high sensitively C-reactive protein was inversely correlated with the circulating EPC number (p=0.03) and decreased in patients after operation. Among the 45 patients who went through unilateral adrenalectomy, 32 (71%) were cured of hypertension. Preoperative number of circulation of EPC (Log[EPC number%] > -3.6) could predicted the curability of hypertension after adrenalectomy. (p=0.003). There was a biphasic effect of aldosterone on EPC proliferation. Incubation of early EPC with a low aldosterone level (10-9 and 10-8 M) for 5 days significantly increased the number of early EPC. However, higher dosage of aldosterone (10-6M) decreased the EPC number. EPC also showed a biphasic response to aldosterone, i.e., an increase of cell proliferation at low aldosterone level (10-9 and 10-8M), and a decrease at high aldosterone level (10-5 and 10-6M). Both effects were blunted by adding spironolactone. Aldosterone, in either a low or high dose, did not affect the percentage of senescence-associated β-galactosidase-positive EPC or apoptosis of EPC. After 5 days’ incubation with 10-6 M aldosterone, the functional capacity for tube formation of late EPC was significantly reduced (p<0.01). In contrast, a low dosages of aldosterone (10-8~10-9M) increased tube formation. This effect of aldosterone was dose-dependent (average total length and nodes number, all < 0.001). Our study clearly showed that human EPC express MR both at gene and protein levels. The expression of MR and 11β-HSD2 in EPC, therefore, indicates that EPC have the capacity to modulate gene expression in response to aldosterone specifically. In accordance with the animal experiments, our study reveals a long-term in vivo effect of high aldosterone level on the number of circulating EPC in PA patients, with an inverse association between PAC and EPC numbers. A correlation of PAC with oxidative stress and endothelial inflammation was observed in PA patients, and the oxidative stress was attenuated after adrenalectomy. Increased intracellular ROS may result in EPC mobilization and impaired neovascularization capacity. Accordingly, CRP augments the effect of aldosterone on endothelial cell stiffness. In our study, a significant correlation between CRP level and aldosterone was noted in PA patients. Moreover, there was an inverse correlation between CRP and EPC numbers, and a reduction of CRP level accompanied by an increase of EPC number was noted in APA patients after adrenalectomy. Chronic aldosterone excess leads to vascular morphological change (wall thickening and carotid artery fibrosis) and vascular dysfunction (central stiffness), independent of blood pressure (BP). In the present study, we further demonstrate that the lower the preoperative EPC number, the higher the risk of residual hypertension after adrenalectomy. The finding indicates that EPC play an important role in both normal endothelial function and vasculature. The inverse correlation between PAC and EPC number and the change of EPC numbers in response to the treatment of PA indicates that aldosterone contributes to the decreased EPC number in PA patients. The mechanisms accounting for low EPC numbers in PA patients are the direct activation of MR on EPC proliferation and an indirect effect through a high CRP level and oxidative stress caused by an excess of aldosterone. Low EPC numbers in PA plays a crucial role in the high incidence of arterial stiffness and in predicting residual hypertension in APA patients after adrenalectomy. | en |
dc.description.provenance | Made available in DSpace on 2021-06-17T00:46:54Z (GMT). No. of bitstreams: 1 ntu-101-Q91421028-1.pdf: 2474624 bytes, checksum: c0f333625fcf9339dcfb276f2c1d0909 (MD5) Previous issue date: 2012 | en |
dc.description.tableofcontents | 口試委員會審定書..I
致謝.. II 中文摘要…III 英文摘要…VI 博士論文內容 第一章 緒論1 第二章 研究方法與材料…23 第三章 結果…34 第四章 討論…39 第五章 展望…56 第六章 論文英文簡述…65 第七章 參考文獻76 第八章 圖表…89 第九章 附錄…112 | |
dc.language.iso | zh-TW | |
dc.title | 原發性皮質醛酮症:內皮前驅幹細胞是皮質醛酮血管病變和預後的指標 | zh_TW |
dc.title | Endothelial progenitor cells in primary aldosteronism:a biomarker of severity for aldosterone vasculopathy and prognosis | en |
dc.type | Thesis | |
dc.date.schoolyear | 100-1 | |
dc.description.degree | 博士 | |
dc.contributor.coadvisor | 陳玉怜 | |
dc.contributor.oralexamcommittee | 陳肇文,王兆弘,陳永祥,葉坤輝 | |
dc.subject.keyword | 原發性皮質醛酮症,皮質醛酮素,內皮幹細胞,群落單位,動脈血管硬度,C反應蛋白質,氧化壓力, | zh_TW |
dc.subject.keyword | Primary aldosteronism,endothelial progenitor cells,colony forming units,arterial stiffness,CRP,oxidative stress, | en |
dc.relation.page | 120 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2011-12-27 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 臨床醫學研究所 | zh_TW |
顯示於系所單位: | 臨床醫學研究所 |
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