9. Kamitani, A., et al., Enhanced predictability of myocardial infarction in Japanese by combined genotype analysis. Hypertension, 1995. 25(5): p. 950-3.
10. Vasku, A., et al., Angiotensin I-converting enzyme and angiotensinogen gene interaction and prediction of essential hypertension. Kidney Int, 1998. 53(6): p. 1479-82.
11. Anderson, T. J., Assessment and treatment of endothelial dysfunction in humans. J Am Coll Cardiol, 1999. 34(3): p. 631-8.
12. Harrison, D. G., Cellular and molecular mechanisms of endothelial cell dysfunction. J Clin Invest, 1997. 100(9): p. 2153-7.
13. Jeerooburkhan, N., et al., Genetic and environmental determinants of plasma nitrogen oxides and risk of ischemic heart disease. Hypertension, 2001. 38(5): p. 1054-61.
14. Pereira, T. V., et al., Three endothelial nitric oxide (NOS3) gene polymorphisms in hypertensive and normotensive individuals: meta-analysis of 53 studies reveals evidence of publication bias. J Hypertens, 2007. 25(9): p. 1763-74.
15. Trochu, J. N., [Should statins be part of the treatment of heart failure?]. Ann Cardiol Angeiol (Paris), 2004. 53(4): p. 209-16.
16. Yu, C. K., et al., Endothelial nitric oxide synthase gene polymorphism (Glu298Asp) and development of pre-eclampsia: a case-control study and a meta-analysis. BMC Pregnancy Childbirth, 2006. 6: p. 7.
17. Sandrim, V. C., et al., eNOS haplotypes associated with gestational hypertension or preeclampsia. Pharmacogenomics, 2008. 9(10): p. 1467-73.
18. Ameno, K., et al., Autopsy and postmortem examination case study on genetic risk factors for cardiac death: polymorphisms of endothelial nitric oxide synthase gene Glu298Asp variant and T-786C mutation, human paraoxonase 1 (PON1) gene and alpha2beta-adrenergic receptor gene. Vojnosanit Pregl, 2006. 63(4): p. 357-61; discussion 362-3.
19. van der Put, N. M., et al., Mutated methylenetetrahydrofolate reductase as a risk factor for spina bifida. Lancet, 1995. 346(8982): p. 1070-1.
20. James, S. J., et al., Abnormal folate metabolism and mutation in the methylenetetrahydrofolate reductase gene may be maternal risk factors for Down syndrome. Am J Clin Nutr, 1999. 70(4): p. 495-501.
21. Mills, J. L., et al., Methylenetetrahydrofolate reductase thermolabile variant and oral clefts. Am J Med Genet, 1999. 86(1): p. 71-4.
22. Skibola, C. F., et al., Polymorphisms in the methylenetetrahydrofolate reductase gene are associated with susceptibility to acute leukemia in adults. Proc Natl Acad Sci U S A, 1999. 96(22): p. 12810-5.
23. Lucock, M., Is folic acid the ultimate functional food component for disease prevention? BMJ, 2004. 328(7433): p. 211-4.
24. Catania, J. and D. S. Fairweather, DNA methylation and cellular ageing. Mutat Res, 1991. 256(2-6): p. 283-93.
25. Vanyushin, B. F., et al., The 5-methylcytosine in DNA of rats. Tissue and age specificity and the changes induced by hydrocortisone and other agents. Gerontologia, 1973. 19(3): p. 138-52.
26. Costello, J. F. and C. Plass, Methylation matters. J Med Genet, 2001. 38(5): p. 285-303.
27. Goodman, C. S., et al., Which thrombophilic gene mutations are risk factors for recurrent pregnancy loss? Am J Reprod Immunol, 2006. 56(4): p. 230-6.
28. Yenicesu, G. I., et al., A prospective case-control study analyzes 12 thrombophilic gene mutations in Turkish couples with recurrent pregnancy loss. Am J Reprod Immunol, 2009. 63(2): p. 126-36.
29. Matok, I., et al., Exposure To Folic Acid Antagonists During The First Trimester of Pregnancy and the Risk of Major Malformations. British Journal of Clinical Pharmacology, 2009. Early View, Date: September 2009.
30. Boccia, S., et al., Meta-analyses of the methylenetetrahydrofolate reductase C677T and A1298C polymorphisms and risk of head and neck and lung cancer. Cancer Lett, 2008.
31. Stidley, C. A., et al., Multivitamins, folate, and green vegetables protect against gene promoter methylation in the aerodigestive tract of smokers. Cancer Res, 2010. 70(2): p. 568-74.
32. Barbosa, P. R., et al., Association between decreased vitamin levels and MTHFR, MTR and MTRR gene polymorphisms as determinants for elevated total homocysteine concentrations in pregnant women. Eur J Clin Nutr, 2008. 62(8): p. 1010-21.
33. Laraqui, A., et al., Influence of methionine synthase (A2756G) and methionine synthase reductase (A66G) polymorphisms on plasma homocysteine levels and relation to risk of coronary artery disease. Acta Cardiol, 2006. 61(1): p. 51-61.
34. Wilson, A., et al., A common variant in methionine synthase reductase combined with low cobalamin (vitamin B12) increases risk for spina bifida. Mol Genet Metab, 1999. 67(4): p. 317-23.
35. Zhu, H., et al., Homocysteine remethylation enzyme polymorphisms and increased risks for neural tube defects. Mol Genet Metab, 2003. 78(3): p. 216-21.
36. Varga, E. A., B. A. Kerlin, and M. W. Wurster, Social and ethical controversies in thrombophilia testing and update on genetic risk factors for venous thromboembolism. Semin Thromb Hemost, 2008. 34(6): p. 549-61.
37. Haverkate, F. and M. Samama, Familial dysfibrinogenemia and thrombophilia. Report on a study of the SSC Subcommittee on Fibrinogen. Thromb Haemost, 1995. 73(1): p. 151-61.
38. van 't Hooft, F. M., et al., Two common, functional polymorphisms in the promoter region of the beta-fibrinogen gene contribute to regulation of plasma fibrinogen concentration. Arterioscler Thromb Vasc Biol, 1999. 19(12): p. 3063-70.
39. Humphries, S. E., J. A. Henry, and H. E. Montgomery, Gene-environment interaction in the determination of levels of haemostatic variables involved in thrombosis and fibrinolysis. Blood Coagul Fibrinolysis, 1999. 10 Suppl 1: p. S17-21.
40. Bots, M. L., et al., Level of fibrinogen and risk of fatal and non-fatal stroke. EUROSTROKE: a collaborative study among research centres in Europe. J Epidemiol Community Health, 2002. 56 Suppl 1: p. i14-8.
41. Sampaio, M. F., et al., AMI is associated with polymorphisms in the NOS3 and FGB but not in PAI-1 genes in young adults. Clin Chim Acta, 2007. 377(1-2): p. 154-62.
42. Scarabin, P. Y., et al., Genetic variation at the beta-fibrinogen locus in relation to plasma fibrinogen concentrations and risk of myocardial infarction. The ECTIM Study. Arterioscler Thromb, 1993. 13(6): p. 886-91.
43. Martiskainen, M., et al., Fibrinogen gene promoter -455 A allele as a risk factor for lacunar stroke. Stroke, 2003. 34(4): p. 886-91.
44. Martinelli, N., et al., Combined effect of hemostatic gene polymorphisms and the risk of myocardial infarction in patients with advanced coronary atherosclerosis. PLoS ONE, 2008. 3(2): p. e1523.
45. Panahloo, A., et al., Determinants of plasminogen activator inhibitor 1 activity in treated NIDDM and its relation to a polymorphism in the plasminogen activator inhibitor 1 gene. Diabetes, 1995. 44(1): p. 37-42.
46. Simpson, A. J., et al., The effects of chronic smoking on the fibrinolytic potential of plasma and platelets. Br J Haematol, 1997. 97(1): p. 208-13.
47. Kruithof, E. K., Regulation of plasminogen activator inhibitor type 1 gene expression by inflammatory mediators and statins. Thromb Haemost, 2008. 100(6): p. 969-75.
48. Ma, Z., D. Paek, and C. K. Oh, Plasminogen activator inhibitor-1 and asthma: role in the pathogenesis and molecular regulation. Clin Exp Allergy, 2009. 39(8): p. 1136-44.
49. Kohler, H. P. and P. J. Grant, Plasminogen-activator inhibitor type 1 and coronary artery disease. N Engl J Med, 2000. 342(24): p. 1792-801.
50. Carmeliet, P., et al., Inhibitory role of plasminogen activator inhibitor-1 in arterial wound healing and neointima formation: a gene targeting and gene transfer study in mice. Circulation, 1997. 96(9): p. 3180-91.
51. Wiklund, P. G., et al., Plasminogen activator inhibitor-1 4G/5G polymorphism and risk of stroke: replicated findings in two nested case-control studies based on independent cohorts. Stroke, 2005. 36(8): p. 1661-5.
52. Naran, N. H., N. Chetty, and N. J. Crowther, The influence of metabolic syndrome components on plasma PAI-1 concentrations is modified by the PAI-1 4G/5G genotype and ethnicity. Atherosclerosis, 2008. 196(1): p. 155-63.
53. Jeng, J. R., Association of PAI-1 gene promoter 4g/5g polymorphism with plasma PAI-1 activity in Chinese patients with and without hypertension. Am J Hypertens, 2003. 16(4): p. 290-6.
54. Balta, G., C. Altay, and A. Gurgey, PAI-1 gene 4G/5G genotype: A risk factor for thrombosis in vessels of internal organs. Am J Hematol, 2002. 71(2): p. 89-93.
55. Pastinen, T., et al., Array-based multiplex analysis of candidate genes reveals two independent and additive genetic risk factors for myocardial infarction in the Finnish population. Hum Mol Genet, 1998. 7(9): p. 1453-62.
56. Vergouwen, M. D., et al., Plasminogen activator inhibitor-1 4G allele in the 4G/5G promoter polymorphism increases the occurrence of cerebral ischemia after aneurysmal subarachnoid hemorrhage. Stroke, 2004. 35(6): p. 1280-3.
|
Из за большого объема этот материал размещен на нескольких страницах:
1 2 3 4 5 6 |


