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Association of T3111C polymorphism in 3′-untranslated region of the Clock gene with the risk of essential arterial hypertension and coronary artery disease in the Russian population (Residents of Karelia)

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Abstract

Allele and genotype distributions of the T3111C polymorphism in 3′-untranslated region of the Clock gene were examined in the groups of Russian patients with essential arterial hypertension (EAH) and coronary artery disease (CAD), and in control group of Russia residents of the Republic of Karelia. The genotype frequency distributions of the polymorphism examined in the EAH and CAD patients were statistically significantly different from that in the individuals without clinical signs of these diseases. The CC genotype frequency in EAH and CAD males was higher, and in the corresponding females it was lower than in males and females from the control group. Male CC carriers were characterized by a possible increased risk of EAH: OR (95% CI) = 1.42 (0.56; 3.58). Moreover, the presence of the CC genotype in males could increase the risk of CAD: OR (95% CI) = 1.58 (0.63; 3.93).

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Authors and Affiliations

  1. Institute of Biology, Karelian Research Center, Russian Academy of Sciences, Petrozavodsk, 185910, Republic of Karelia, Russia

    S. N. Kolomeichuk, I. V. Makeeva, L. V. Topchieva & N. N. Nemova

  2. Department of Faculty Therapy, Petrozavodsk State University, Petrozavodsk, 185000, Republic of Karelia, Russia

    V. A. Korneva

Authors
  1. S. N. Kolomeichuk
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  2. I. V. Makeeva
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  3. L. V. Topchieva
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  4. V. A. Korneva
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  5. N. N. Nemova
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Correspondence to S. N. Kolomeichuk.

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Original Russian Text © S.N. Kolomeichuk, I.V. Makeeva, L.V. Topchieva, V.A. Korneva, N.N. Nemova, 2011, published in Genetika, 2011, Vol. 47, No.10, pp. 1411–1415.

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Kolomeichuk, S.N., Makeeva, I.V., Topchieva, L.V. et al. Association of T3111C polymorphism in 3′-untranslated region of the Clock gene with the risk of essential arterial hypertension and coronary artery disease in the Russian population (Residents of Karelia). Russ J Genet 47, 1256–1259 (2011). https://doi.org/10.1134/S1022795411100097

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  • DOI: https://doi.org/10.1134/S1022795411100097

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