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排序方式: 共有84条查询结果,搜索用时 15 毫秒
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Todd Woodard Sigurdur Sigurdsson John D. Gotal Alyssa A. Torjesen Lesley A. Inker Thor Aspelund Gudny Eiriksdottir Vilmundur Gudnason Tamara B. Harris Lenore J. Launer Andrew S. Levey Gary F. Mitchell 《Journal of the American Society of Nephrology : JASN》2015,26(5):1181-1187
Aortic stiffening, assessed by carotid-femoral pulse wave velocity, is associated with CKD. Transmission of excessive flow pulsatility into the low-impedance renal microvasculature may mediate this association. However, direct analyses of macrovascular–microvascular relations in the kidney are limited. Using arterial tonometry, iohexol clearance, and magnetic resonance imaging, we related arterial stiffness, GFR, urinary albumin excretion, and potential mediators, including renal artery pulsatility index, renal vascular resistance, and arterial volume in the cortex, in 367 older adults (ages 72–92 years) participating in the Age, Gene/Environment Susceptibility-Reykjavik Study. In a model adjusted for age, sex, heart rate, and body size, aortic stiffness was related to GFR (Slope of regression B=−2.28±0.85 ml/min per SD, P=0.008) but not urine albumin (P=0.09). After accounting for pulsatility index, the relation between aortic stiffness and GFR was no longer significant (P=0.10). Mediation analysis showed that 34% of the relation between aortic stiffness and GFR was mediated by pulsatility index (95% confidence interval of indirect effect, −1.35 to −0.29). An additional 20% or 36% of the relation was mediated by lower arterial volume in the cortex or higher renal vascular resistance, respectively, when offered as mediators downstream from higher pulsatility index (95% confidence interval of indirect effect including arterial volume in the cortex, −2.22 to −0.40; 95% confidence interval of indirect effect including renal vascular resistance, −2.51 to −0.76). These analyses provide the first evidence that aortic stiffness may contribute to lower GFR by transferring excessive flow pulsatility into the susceptible renal microvasculature, leading to dynamic constriction or vessel loss. 相似文献
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Eiriksdottir G Aspelund T Bjarnadottir K Olafsdottir E Gudnason V Launer LJ Harris TB 《Atherosclerosis》2006,186(1):222-224
OBJECTIVE: C-reactive protein (CRP), an inflammatory marker, was linked to coronary heart disease (CHD) in the Reykjavik study cohort. Recent genetic studies have shown that the apolipoprotein E (APOE) epsilon4 allele is associated with lower CRP levels. Statin treatment has also been shown to lower CRP levels. In the Age Gene/Environment Susceptibility (AGES)-Reykjavik Study, we examined the association of APOE genotypes with CRP accounting for the effect of statin treatment, previous CHD and a mid-life measurement of erythrocyte sedimentation rate (ESR), an inflammatory marker associated with risk in this cohort. METHODS AND RESULTS: The first 2296 participants (mean age 76+/-6 years, 42% men) in the AGES-Reykjavik Study were genotyped for APOE CRP concentration was measured with a high sensitivity method. A general linear model was used to evaluate the association of APOE genotype to CRP levels. The frequencies of the APOE alleles are epsilon2=0.06, epsilon3=0.78 and epsilon4=0.16. CRP levels ranged from 0.2 to 56.6 mg/L, median 1.9 mg/L. Participants carrying one or two epsilon4 alleles have significantly lower CRP levels than non-carriers and this effect was observed in a dose-dependent manner. This trend is the same in users and non-users of statin treatment. CONCLUSIONS: This study suggests that the contribution of the epsilon4 allele towards lowering CRP levels is independent and may be by a different mechanism than how statins affect inflammation. 相似文献
4.
Comparison of Handgrip and Leg Extension Strength in Predicting Slow Gait Speed in Older Adults 下载免费PDF全文
Maren S. Fragala PhD Dawn E. Alley PhD Michelle D. Shardell PhD Tamara B. Harris MD Robert R. McLean DSc Douglas P. Kiel MD Peggy M. Cawthon PhD Thuy‐Tien L. Dam MD Luigi Ferrucci MD PhD Jack M. Guralnik MD PhD Stephen B. Kritchevsky PhD Maria T. Vassileva PhD Vilmunder Gudnason MD PhD Gudny Eiriksdottir MS Annemarie Koster PhD Anne Newman MD MPH Kristin Siggeirsdottir MS Suzanne Satterfield MD Stephanie A. Studenski MD Anne M. Kenny MD 《Journal of the American Geriatrics Society》2016,64(1):144-150
5.
Chengxuan Qiu MD PhD Mary Frances Cotch PhD Sigurdur Sigurdsson MSc Ronald Klein MD MPH Fridbert Jonasson MD Barbara E. K. Klein MD MPH Melissa Garcia MPH Palmi V. Jonsson MD Tamara B. Harris PhD Gudny Eiriksdottir MSc Olafur Kjartansson MD Mark A. van Buchem MD PhD Vilmundur Gudnason MD PhD Lenore J. Launer PhD 《Annals of neurology》2009,65(5):569-576
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Rachel A. Murphy Ilse Reinders Melissa E. Garcia Gudny Eiriksdottir Lenore J. Launer Rafn Benediktsson Vilmundur Gudnason Palmi V. Jonsson Tamara B. Harris 《Diabetes care》2014,37(12):3213-3219
OBJECTIVEStudies in type 2 diabetes report both increased mortality for normal weight and no evidence of an obesity paradox. We aimed to examine whether adipose tissue, muscle size, and physical function, which are known to vary by weight, mediate associations between BMI and mortality.RESULTSThe median follow-up was 6.66 years, and there were 85, 59, and 44 deaths among normal weight, overweight, and obese participants, respectively. There was no mortality risk for obese participants and an increased risk among normal weight compared with overweight participants (HR 1.72 [95% CI 1.12–2.64]). Associations remained with adjustment for adipose tissues and knee extensor strength; however, mortality risk for normal weight was attenuated following adjustment for thigh muscle (HR 1.36 [95% CI 0.87–2.11]) and gait speed (HR 1.44 [95% CI 0.91–2.27]). Linear regression confirmed with bootstrapping indicated that thigh muscle size mediated 46% of the relationship between normal weight and mortality.CONCLUSIONSNormal weight participants had elevated mortality risk compared with overweight participants. This paradoxical association was mediated in part by muscle size. 相似文献
7.
O'Donnell CJ Kavousi M Smith AV Kardia SL Feitosa MF Hwang SJ Sun YV Province MA Aspelund T Dehghan A Hoffmann U Bielak LF Zhang Q Eiriksdottir G van Duijn CM Fox CS de Andrade M Kraja AT Sigurdsson S Elias-Smale SE Murabito JM Launer LJ van der Lugt A Kathiresan S;CARDIoGRAM Consortium Krestin GP Herrington DM Howard TD Liu Y Post W Mitchell BD O'Connell JR Shen H Shuldiner AR Altshuler D Elosua R Salomaa V Schwartz SM Siscovick DS Voight BF Bis JC Glazer NL Psaty BM Boerwinkle E Heiss G 《Circulation》2011,124(25):2855-2864
8.
G Eiriksdottir M K Bolla B Thorsson G Sigurdsson S E Humphries V Gudnason 《Atherosclerosis》2001,159(1):187-192
The aim of this study was to examine whether the well-established effect of the common TaqIB polymorphism in intron 1 of the gene for cholesterol ester transfer protein (CETP) on high density lipoprotein cholesterol (HDL-C) concentration and increased risk of myocardial infarction (MI), could be explained by the recently identified -629C>A functional polymorphism in the promoter. Non-fatal MI cases (388 male) and a control group of 794 healthy men were recruited from the 30 year long prospective Reykjavik Study. In the healthy men the frequency of the TaqIB B2 allele was 0.47 (95% CI: 0.44-0.50) and there was a strong allelic association with the -629A allele (D=-0.21, P<0.0001), which had a frequency of 0.52 (95% CI: 0.49-0.56). B2B2 homozygotes displayed 15% higher HDL-C levels than subjects homozygous for the B1 allele (P<0.0001). Homozygotes for the -629A allele displayed 14% higher HDL-C concentrations than subjects homozygous for the -629C allele (P<0.0001). The frequencies of the alleles associated with lower HDL-C were significantly higher in cases compared with controls, 0.59 versus 0.53 (TaqIB B1) and 0.52 versus 0.48 (-629 C) respectively (P<0.05 for both). There was a significantly higher risk for MI in B1B1 homozygotes (OR=1.44, 95% CI: 1.10-1.87, P<0.01), compared to the other genotypes combined. This was not observed for the CC homozygotes (OR=1.16, 95% CI: 0.87-1.54). In addition, homozygotes for the TaqI B2 allele experienced a first MI 2 years later than men with other genotypes, 59 versus 61 years (P<0.05). This effect was not seen for the promoter polymorphism. These results strongly confirm the role of the CETP gene and the TaqIB variant as a risk factor for MI and suggest that another functional polymorphism is yet to be discovered in the CETP gene, that will explain the effect on MI associated with TaqIB observed in this study. 相似文献
9.
Ma Yuan Sajeev Gautam VanderWeele Tyler J. Viswanathan Anand Sigurdsson Sigurdur Eiriksdottir Gudny Aspelund Thor Betensky Rebecca A. Grodstein Francine Hofman Albert Gudnason Vilmundur Launer Lenore Blacker Deborah 《European journal of epidemiology》2022,37(6):591-601
European Journal of Epidemiology - The apolipoprotein E allele 4 (APOE-ε4) is established as a major genetic risk factor for cognitive decline and late-onset Alzheimer’s disease.... 相似文献