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  5. <title>UTas ePrints - Polymorphisms in the tissue factor pathway inhibitor gene are not associated with ischaemic stroke</title>
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  13. <meta content="Sayer, M.S." name="eprints.creators_name" />
  14. <meta content="Cole, V.J." name="eprints.creators_name" />
  15. <meta content="Adams, M.J." name="eprints.creators_name" />
  16. <meta content="Baker, Ross I." name="eprints.creators_name" />
  17. <meta content="Staton, J.M." name="eprints.creators_name" />
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  24. <meta content="2007-10-31 02:09:02" name="eprints.datestamp" />
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  27. <meta content="Polymorphisms in the tissue factor pathway inhibitor gene
  28. are not associated with ischaemic stroke" name="eprints.title" />
  29. <meta content="pub" name="eprints.ispublished" />
  30. <meta content="321008" name="eprints.subjects" />
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  32. <meta content="The present study aimed to determine whether four
  33. previously described polymorphisms found within the
  34. tissue factor pathway inhibitor (TFPI) gene are associated
  35. with free plasma TFPI levels or with TFPI activity as well as
  36. the risk of ischaemic stroke in stroke patients and
  37. control individuals. We conducted a case–control study of
  38. 162 first-ever ischaemic stroke cases and 170 randomly
  39. selected community control individuals. The TFPI genotype
  40. was determined for the T-287C, C-399T, Intron 7 C-33T, and
  41. Val264Met (G874A) polymorphisms. Free plasma TFPI and
  42. TFPI activity were measured during the first 7 days and
  43. 3–6 months after the acute stroke event. Free plasma TFPI
  44. levels were significantly lowered 3–6 months after stroke
  45. compared with levels observed in the patient group
  46. during the acute phase of the stroke (mean, 16.3 versus
  47. 22.46 ng/ml; PU0.046) and among the control group
  48. (mean, 16.3 versus 22.79 ng/ml; P<0.0001). Conversely,
  49. TFPI activity was significantly up-regulated during the acute
  50. phase (mean, 1.30 versus 1.11 U/ml; PU0.0051) and
  51. remained elevated 3–6 months later (mean, 1.28 versus
  52. 1.11 U/ml; PU0.03). The TFPI gene polymorphisms studied
  53. were not significantly associated with TFPI levels or activity,
  54. nor with the risk of ischaemic stroke. In conclusion, the TFPI
  55. activity and concentration in plasma varied significantly
  56. after an ischaemic stroke; however, these variations
  57. were not found to be due to the presence of any of the
  58. genetic mutations analysed in this study. Our results are
  59. consistent with the emerging model suggesting the
  60. lipoprotein-bound portion of TFPI has a significant influence
  61. on coagulation and diseases of haemostasis." name="eprints.abstract" />
  62. <meta content="2007" name="eprints.date" />
  63. <meta content="published" name="eprints.date_type" />
  64. <meta content="Blood Coagulation and Fibrinolysis" name="eprints.publication" />
  65. <meta content="18" name="eprints.volume" />
  66. <meta content="7" name="eprints.number" />
  67. <meta content="703-708" name="eprints.pagerange" />
  68. <meta content="TRUE" name="eprints.refereed" />
  69. <meta content="0957-5235" name="eprints.issn" />
  70. <meta content="http://www.bloodcoagulation.com" name="eprints.official_url" />
  71. <meta content="References
  72. 1 McVey JH. Tissue factor pathway. Baillieres Best Pract Res Clin Haematol
  73. 1999; 12:361–372.
  74. 2 Dahm A, van HV, Bendz B, Rosendaal F, Bertina RM, Sandset PM. Low
  75. levels of tissue factor pathway inhibitor (TFPI) increase the risk of venous
  76. thrombosis. Blood 2003; 101:4387–4392.
  77. 3 Sandset PM, Abildgaard U, Larsen ML. Heparin induces release of
  78. extrinsic coagulation pathway inhibitor (EPI). Thromb Res 1988; 50:803–
  79. 813.
  80. 4 Lindahl AK, Abildgaard U, Stokke G. Release of extrinsic pathway inhibitor
  81. after heparin injection: increased response in cancer patients. Thromb Res
  82. 1990; 59:651–656.
  83. 5 Novotny WF, Brown SG, Miletich JP, Rader DJ, Broze GJ Jr. Plasma
  84. antigen levels of the lipoprotein-associated coagulation inhibitor in patient
  85. samples. Blood 1991; 78:387–393.
  86. 6 Lindahl AK, Jacobsen PB, Sandset PM, Abildgaard U. Tissue factor
  87. pathway inhibitor with high anticoagulant activity is increased in
  88. postheparin plasma and in plasma from cancer patients. Blood Coagul
  89. Fibrinolysis 1991; 2:713–721.
  90. 7 Nordfang O, Bjorn SE, Valentin S, Nielsen LS, Wildgoose P, Beck TC,
  91. Hedner U. The C-terminus of tissue factor pathway inhibitor is essential to
  92. its anticoagulant activity. Biochemistry 1991; 30:10371–10376.
  93. 8 Adams MJ, Thom J, Hankey GJ, Baker RI, Gilmore G, Staton J,
  94. Eikelboom JW. The tissue factor pathway in ischaemic stroke.
  95. Blood Coagul Fibrinolysis 2006; 17:527–532.
  96. 9 Girard TJ, Warren LA, Novotny WF, Likert KM, Brown SG,
  97. Miletich JP, Broze GJ Jr. Functional significance of the Kunitz-type
  98. inhibitory domains of lipoprotein-associated coagulation inhibitor.
  99. Nature 1989; 338:518–520.
  100. 10 Amini-Nekoo A, Futers TS, Moia M, Mannucci PM, Grant PJ, Ariens RA.
  101. Analysis of the tissue factor pathway inhibitor gene and antigen levels in
  102. relation to venous thrombosis. Br J Haematol 2001; 113:537–543.
  103. 11 Ameziane N, Seguin C, Borgel D, Fumeron F, Moatti D, Alhenc-Gelas M,
  104. et al. The –33T!C polymorphism in intron 7 of the TFPI gene influences
  105. the risk of venous thromboembolism, independently of the factor V Leiden
  106. and prothrombin mutations. Thromb Haemost 2002; 88:195–199.
  107. 12 Moatti D, Seknadji P, Galand C, Poirier O, Fumeron F, Desprez S, et al.
  108. Polymorphisms of the tissue factor pathway inhibitor (TFPI) gene in patients
  109. with acute coronary syndromes and in healthy subjects: impact of the
  110. V264M substitution on plasma levels of TFPI. Arterioscler Thromb Vasc
  111. Biol 1999; 19:862–869.
  112. 13 Kleesiek K, Schmidt M, Gotting C, Brinkmann T, Prohaska W. A first
  113. mutation in the human tissue factor pathway inhibitor gene encoding
  114. [P151L]TFPI. Blood 1998; 92:3976–3977.
  115. 14 Mues GI, Sarode R. Allele frequencies of tissue factor pathway inhibitor
  116. polymorphisms in African-American, Hispanic and Caucasian populations.
  117. Thromb Haemost 2002; 88:875–877.
  118. 15 Wang L, Hirayasu K, Ishizawa M, Kobayashi Y. Purification of genomic DNA
  119. from human whole blood by isopropanol-fractionation with concentrated
  120. Nal and SDS. Nucleic Acids Res 1994; 22:1774–1775.
  121. 16 Moatti D, Haidar B, Fumeron F, Gauci L, Boudvillain O, Seknadji P, et al.
  122. A new T-287C polymorphism in the 50 regulatory region of the tissue factor
  123. pathway inhibitor gene. Association study of the T-287C and C-399T
  124. polymorphisms with coronary artery disease and plasma TFPI levels.
  125. Thromb Haemost 2000; 84:244–249.
  126. 17 Miyata T, Sakata T, Kumeda K, Uchida K, Tsushima M, Fujimura H, et al.
  127. C-399T polymorphism in the promoter region of human tissue factor
  128. pathway inhibitor (TFPI) gene does not change the plasma TFPI antigen
  129. level and does not cause venous thrombosis. Thromb Haemost 1998;
  130. 80:345–346.
  131. 18 Moatti D, Meirhaeghe A, Ollivier V, Bauters C, Amouyel P, de Prost D.
  132. Polymorphisms of the tissue factor pathway inhibitor gene and the risk of
  133. restenosis after coronary angioplasty. Blood Coagul Fibrinolysis 2001;
  134. 12:317–323.
  135. 19 Arnaud E, Moatti D, Emmerich J, Aiach M, de Prost D. No link between the
  136. TFPI V264M mutation and venous thromboembolic disease. Thromb
  137. Haemost 1999; 82:159–160.
  138. 20 Novo G, Caplice N, Tantillo R, Bonura F, Simari R, Novo S. TFPI antigen and
  139. activity levels in patients with asymptomatic atherosclerosis and target
  140. organ acute and chronic complications. Int Angiol 2005; 24:366–371." name="eprints.referencetext" />
  141. <meta content="Sayer, M.S. and Cole, V.J. and Adams, M.J. and Baker, Ross I. and Staton, J.M. (2007) Polymorphisms in the tissue factor pathway inhibitor gene are not associated with ischaemic stroke. Blood Coagulation and Fibrinolysis, 18 (7). pp. 703-708. ISSN 0957-5235" name="eprints.citation" />
  142. <meta content="http://eprints.utas.edu.au/2341/1/Sayer_et_al_2007.pdf" name="eprints.document_url" />
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  144. <meta content="Polymorphisms in the tissue factor pathway inhibitor gene
  145. are not associated with ischaemic stroke" name="DC.title" />
  146. <meta content="Sayer, M.S." name="DC.creator" />
  147. <meta content="Cole, V.J." name="DC.creator" />
  148. <meta content="Adams, M.J." name="DC.creator" />
  149. <meta content="Baker, Ross I." name="DC.creator" />
  150. <meta content="Staton, J.M." name="DC.creator" />
  151. <meta content="321008 Haematology" name="DC.subject" />
  152. <meta content="The present study aimed to determine whether four
  153. previously described polymorphisms found within the
  154. tissue factor pathway inhibitor (TFPI) gene are associated
  155. with free plasma TFPI levels or with TFPI activity as well as
  156. the risk of ischaemic stroke in stroke patients and
  157. control individuals. We conducted a case–control study of
  158. 162 first-ever ischaemic stroke cases and 170 randomly
  159. selected community control individuals. The TFPI genotype
  160. was determined for the T-287C, C-399T, Intron 7 C-33T, and
  161. Val264Met (G874A) polymorphisms. Free plasma TFPI and
  162. TFPI activity were measured during the first 7 days and
  163. 3–6 months after the acute stroke event. Free plasma TFPI
  164. levels were significantly lowered 3–6 months after stroke
  165. compared with levels observed in the patient group
  166. during the acute phase of the stroke (mean, 16.3 versus
  167. 22.46 ng/ml; PU0.046) and among the control group
  168. (mean, 16.3 versus 22.79 ng/ml; P<0.0001). Conversely,
  169. TFPI activity was significantly up-regulated during the acute
  170. phase (mean, 1.30 versus 1.11 U/ml; PU0.0051) and
  171. remained elevated 3–6 months later (mean, 1.28 versus
  172. 1.11 U/ml; PU0.03). The TFPI gene polymorphisms studied
  173. were not significantly associated with TFPI levels or activity,
  174. nor with the risk of ischaemic stroke. In conclusion, the TFPI
  175. activity and concentration in plasma varied significantly
  176. after an ischaemic stroke; however, these variations
  177. were not found to be due to the presence of any of the
  178. genetic mutations analysed in this study. Our results are
  179. consistent with the emerging model suggesting the
  180. lipoprotein-bound portion of TFPI has a significant influence
  181. on coagulation and diseases of haemostasis." name="DC.description" />
  182. <meta content="2007" name="DC.date" />
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  293. <h1 class="ep_tm_pagetitle">Polymorphisms in the tissue factor pathway inhibitor gene are not associated with ischaemic stroke</h1>
  294. <p style="margin-bottom: 1em" class="not_ep_block"><span class="person_name">Sayer, M.S.</span> and <span class="person_name">Cole, V.J.</span> and <span class="person_name">Adams, M.J.</span> and <span class="person_name">Baker, Ross I.</span> and <span class="person_name">Staton, J.M.</span> (2007) <xhtml:em>Polymorphisms in the tissue factor pathway inhibitor gene are not associated with ischaemic stroke.</xhtml:em> Blood Coagulation and Fibrinolysis, 18 (7). pp. 703-708. ISSN 0957-5235</p><p style="margin-bottom: 1em" class="not_ep_block"></p><table style="margin-bottom: 1em" class="not_ep_block"><tr><td valign="top" style="text-align:center"><a href="http://eprints.utas.edu.au/2341/1/Sayer_et_al_2007.pdf"><img alt="[img]" src="http://eprints.utas.edu.au/style/images/fileicons/application_pdf.png" class="ep_doc_icon" border="0" /></a></td><td valign="top"><a href="http://eprints.utas.edu.au/2341/1/Sayer_et_al_2007.pdf"><span class="ep_document_citation">PDF</span></a> - Full text restricted - Requires a PDF viewer<br />106Kb</td><td><form method="get" accept-charset="utf-8" action="http://eprints.utas.edu.au/cgi/request_doc"><input accept-charset="utf-8" value="2998" name="docid" type="hidden" /><div class=""><input value="Request a copy" name="_action_null" class="ep_form_action_button" onclick="return EPJS_button_pushed( '_action_null' )" type="submit" /> </div></form></td></tr></table><p style="margin-bottom: 1em" class="not_ep_block">Official URL: <a href="http://www.bloodcoagulation.com">http://www.bloodcoagulation.com</a></p><div class="not_ep_block"><h2>Abstract</h2><p style="padding-bottom: 16px; text-align: left; margin: 1em auto 0em auto">The present study aimed to determine whether four&#13;
  295. previously described polymorphisms found within the&#13;
  296. tissue factor pathway inhibitor (TFPI) gene are associated&#13;
  297. with free plasma TFPI levels or with TFPI activity as well as&#13;
  298. the risk of ischaemic stroke in stroke patients and&#13;
  299. control individuals. We conducted a case–control study of&#13;
  300. 162 first-ever ischaemic stroke cases and 170 randomly&#13;
  301. selected community control individuals. The TFPI genotype&#13;
  302. was determined for the T-287C, C-399T, Intron 7 C-33T, and&#13;
  303. Val264Met (G874A) polymorphisms. Free plasma TFPI and&#13;
  304. TFPI activity were measured during the first 7 days and&#13;
  305. 3–6 months after the acute stroke event. Free plasma TFPI&#13;
  306. levels were significantly lowered 3–6 months after stroke&#13;
  307. compared with levels observed in the patient group&#13;
  308. during the acute phase of the stroke (mean, 16.3 versus&#13;
  309. 22.46 ng/ml; PU0.046) and among the control group&#13;
  310. (mean, 16.3 versus 22.79 ng/ml; P&lt;0.0001). Conversely,&#13;
  311. TFPI activity was significantly up-regulated during the acute&#13;
  312. phase (mean, 1.30 versus 1.11 U/ml; PU0.0051) and&#13;
  313. remained elevated 3–6 months later (mean, 1.28 versus&#13;
  314. 1.11 U/ml; PU0.03). The TFPI gene polymorphisms studied&#13;
  315. were not significantly associated with TFPI levels or activity,&#13;
  316. nor with the risk of ischaemic stroke. In conclusion, the TFPI&#13;
  317. activity and concentration in plasma varied significantly&#13;
  318. after an ischaemic stroke; however, these variations&#13;
  319. were not found to be due to the presence of any of the&#13;
  320. genetic mutations analysed in this study. Our results are&#13;
  321. consistent with the emerging model suggesting the&#13;
  322. lipoprotein-bound portion of TFPI has a significant influence&#13;
  323. on coagulation and diseases of haemostasis.</p></div><table style="margin-bottom: 1em" cellpadding="3" class="not_ep_block" border="0"><tr><th valign="top" class="ep_row">Item Type:</th><td valign="top" class="ep_row">Article</td></tr><tr><th valign="top" class="ep_row">Subjects:</th><td valign="top" class="ep_row"><a href="http://eprints.utas.edu.au/view/subjects/321008.html">320000 Medical and Health Sciences &gt; 321000 Clinical Sciences &gt; 321008 Haematology</a></td></tr><tr><th valign="top" class="ep_row">ID Code:</th><td valign="top" class="ep_row">2341</td></tr><tr><th valign="top" class="ep_row">Deposited By:</th><td valign="top" class="ep_row"><span class="ep_name_citation"><span class="person_name">Dr Murray J Adams</span></span></td></tr><tr><th valign="top" class="ep_row">Deposited On:</th><td valign="top" class="ep_row">31 Oct 2007 13:09</td></tr><tr><th valign="top" class="ep_row">Last Modified:</th><td valign="top" class="ep_row">09 Jan 2008 02:30</td></tr><tr><th valign="top" class="ep_row">ePrint Statistics:</th><td valign="top" class="ep_row"><a target="ePrintStats" href="/es/index.php?action=show_detail_eprint;id=2341;">View statistics for this ePrint</a></td></tr></table><p align="right">Repository Staff Only: <a href="http://eprints.utas.edu.au/cgi/users/home?screen=EPrint::View&amp;eprintid=2341">item control page</a></p>
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