OBJECTIVE: To identify quantitative trait loci (QTL) contributing to the variation in blood pressure in a west African population. METHODS: We conducted a multi-stage genome scan in a population sample from rural Nigeria. A 10 centimorgan genome-wide screen for log-transformed systolic blood pressure (SBP) and diastolic blood pressure (DBP) was first performed based on 1054 individuals from 188 families. In the second phase we performed a similar analysis in an independent sample of 621 individuals from 101 families. In a third follow-up fine mapping phase we genotyped 25 additional markers in the three regions identified in the first two phases. RESULTS: Genome-wide significant linkage evidence was found for SBP on chromosome 7p (lod = 4.73, genome wide P < or = 0.01, point-wise P = 1.53 x 10) in the combined sample. Suggestive linkage evidence was also detected on 6q (lod = 2.9, point-wise P = 0.00013) and 7q (lod = 2.6, point-wise P = 0.00027) for SBP, and 7q (lod = 1.6, point-wise P = 0.003) for DBP. CONCLUSIONS: This study has identified several regions that may harbor genetic variants affecting the variation in blood pressure. Further association mapping under the linkage peaks will be required to refine the linkage evidence that has emerged from our analysis.
OBJECTIVE: To identify quantitative trait loci (QTL) contributing to the variation in blood pressure in a west African population. METHODS: We conducted a multi-stage genome scan in a population sample from rural Nigeria. A 10 centimorgan genome-wide screen for log-transformed systolic blood pressure (SBP) and diastolic blood pressure (DBP) was first performed based on 1054 individuals from 188 families. In the second phase we performed a similar analysis in an independent sample of 621 individuals from 101 families. In a third follow-up fine mapping phase we genotyped 25 additional markers in the three regions identified in the first two phases. RESULTS: Genome-wide significant linkage evidence was found for SBP on chromosome 7p (lod = 4.73, genome wide P < or = 0.01, point-wise P = 1.53 x 10) in the combined sample. Suggestive linkage evidence was also detected on 6q (lod = 2.9, point-wise P = 0.00013) and 7q (lod = 2.6, point-wise P = 0.00027) for SBP, and 7q (lod = 1.6, point-wise P = 0.003) for DBP. CONCLUSIONS: This study has identified several regions that may harbor genetic variants affecting the variation in blood pressure. Further association mapping under the linkage peaks will be required to refine the linkage evidence that has emerged from our analysis.
Authors: Sobha Puppala; Dawn K Coletta; Jennifer Schneider; Shirley L Hu; Vidya S Farook; Thomas D Dyer; Rector Arya; John Blangero; Ravindranath Duggirala; Ralph A DeFronzo; Christopher P Jenkinson Journal: Hum Hered Date: 2011-02-05 Impact factor: 0.444
Authors: Jeannette Simino; Gang Shi; Rezart Kume; Karen Schwander; Michael A Province; C Charles Gu; Sharon Kardia; Aravinda Chakravarti; Georg Ehret; Richard A Olshen; Stephen T Turner; Low-Tone Ho; Xiaofeng Zhu; Cashell Jaquish; Dina Paltoo; Richard S Cooper; Alan Weder; J David Curb; Eric Boerwinkle; Steven C Hunt; Dabeeru C Rao Journal: Am J Hypertens Date: 2010-12-09 Impact factor: 2.689
Authors: Sasha Z Prisco; Jessica R C Priestley; Brian D Weinberg; Anthony R Prisco; Matthew J Hoffman; Howard J Jacob; Michael J Flister; Julian H Lombard; Jozef Lazar Journal: Am J Physiol Heart Circ Physiol Date: 2014-08-22 Impact factor: 4.733
Authors: Sasha Z Prisco; Jeremy W Prokop; Allison B Sarkis; Nan Cher Yeo; Matthew J Hoffman; Colin C Hansen; Howard J Jacob; Michael J Flister; Jozef Lazar Journal: Hypertension Date: 2014-07-07 Impact factor: 10.190