SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Gansevoort Ron T) "

Sökning: WFRF:(Gansevoort Ron T)

  • Resultat 31-40 av 53
  • Föregående 123[4]56Nästa
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
31.
  • Lu, Yingchang, et al. (författare)
  • New loci for body fat percentage reveal link between adiposity and cardiometabolic disease risk
  • 2016
  • Ingår i: Nature Communications. - 2041-1723 .- 2041-1723. ; 7
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>To increase our understanding of the genetic basis of adiposity and its links to cardiometabolic disease risk, we conducted a genome-wide association meta-analysis of body fat percentage (BF%) in up to 100,716 individuals. Twelve loci reached genome-wide significance (P &lt; 5 x 10(-8)), of which eight were previously associated with increased overall adiposity (BMI, BF%) and four (in or near COBLL1/GRB14, IGF2BP1, PLA2G6, CRTC1) were novel associations with BF%. Seven loci showed a larger effect on BF% than on BMI, suggestive of a primary association with adiposity, while five loci showed larger effects on BMI than on BF%, suggesting association with both fat and lean mass. In particular, the loci more strongly associated with BF% showed distinct cross-phenotype association signatures with a range of cardiometabolic traits revealing new insights in the link between adiposity and disease risk.</p>
  •  
32.
  • Matsushita, K, et al. (författare)
  • Measures of chronic kidney disease and risk of incident peripheral artery disease : a collaborative meta-analysis of individual participant data
  • 2017
  • Ingår i: The Lancet Diabetes and Endocrinology. - Elsevier. - 2213-8587. ; 5:9, s. 718-728
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Some evidence suggests that chronic kidney disease is a risk factor for lower-extremity peripheral artery disease. We aimed to quantify the independent and joint associations of two measures of chronic kidney disease (estimated glomerular filtration rate [eGFR] and albuminuria) with the incidence of peripheral artery disease. Methods In this collaborative meta-analysis of international cohorts included in the Chronic Kidney Disease Prognosis Consortium (baseline measurements obtained between 1972 and 2014) with baseline measurements of eGFR and albuminuria, at least 1000 participants (this criterion not applied to cohorts exclusively enrolling patients with chronic kidney disease), and at least 50 peripheral artery disease events, we analysed adult participants without peripheral artery disease at baseline at the individual patient level with Cox proportional hazards models to quantify associations of creatinine-based eGFR, urine albumin-to-creatinine ratio (ACR), and dipstick proteinuria with the incidence of peripheral artery disease (including hospitalisation with a diagnosis of peripheral artery disease, intermittent claudication, leg revascularisation, and leg amputation). We assessed discrimination improvement through c-statistics. Findings We analysed 817 084 individuals without a history of peripheral artery disease at baseline from 21 cohorts. 18 261 cases of peripheral artery disease were recorded during follow-up across cohorts (median follow-up was 7·4 years [IQR 5·7–8·9], range 2·0–15·8 years across cohorts). Both chronic kidney disease measures were independently associated with the incidence of peripheral artery disease. Compared with an eGFR of 95 mL/min per 1·73 m2, adjusted hazard ratios (HRs) for incident study-specific peripheral artery disease was 1·22 (95% CI 1·14–1·30) at an eGFR of 45 mL/min per 1·73 m2 and 2·06 (1·70–2·48) at an eGFR of 15 mL/min per 1·73 m2. Compared with an ACR of 5 mg/g, the adjusted HR for incident study-specific peripheral artery disease was 1·50 (1·41–1·59) at an ACR of 30 mg/g and 2·28 (2·12–2·44) at an ACR of 300 mg/g. The adjusted HR at an ACR of 300 mg/g versus 5 mg/g was 3·68 (95% CI 3·00–4·52) for leg amputation. eGFR and albuminuria contributed multiplicatively (eg, adjusted HR 5·76 [4·90–6·77] for incident peripheral artery disease and 10·61 [5·70–19·77] for amputation in eGFR <30 mL/min per 1·73 m2 plus ACR ≥300 mg/g or dipstick proteinuria 2+ or higher vs eGFR ≥90 mL/min per 1·73 m2 plus ACR <10 mg/g or dipstick proteinuria negative). Both eGFR and ACR significantly improved peripheral artery disease risk discrimination beyond traditional predictors, with a substantial improvement prediction of amputation with ACR (difference in c-statistic 0·058, 95% CI 0·045–0·070). Patterns were consistent across clinical subgroups. Interpretation Even mild-to-moderate chronic kidney disease conferred increased risk of incident peripheral artery disease, with a strong association between albuminuria and amputation. Clinical attention should be paid to the development of peripheral artery disease symptoms and signs in people with any stage of chronic kidney disease. Funding American Heart Association, US National Kidney Foundation, and US National Institute of Diabetes and Digestive and Kidney Diseases.
  •  
33.
  • Pennells, Lisa, et al. (författare)
  • Equalization of four cardiovascular risk algorithms after systematic recalibration: individual-participant meta-analysis of 86 prospective studies.
  • 2019
  • Ingår i: European heart journal. - 1522-9645. ; 40:7, s. 621-631
  • Tidskriftsartikel (refereegranskat)abstract
    • AIMS: There is debate about the optimum algorithm for cardiovascular disease (CVD) risk estimation. We conducted head-to-head comparisons of four algorithms recommended by primary prevention guidelines, before and after 'recalibration', a method that adapts risk algorithms to take account of differences in the risk characteristics of the populations being studied. METHODS AND RESULTS: Using individual-participant data on 360 737 participants without CVD at baseline in 86 prospective studies from 22 countries, we compared the Framingham risk score (FRS), Systematic COronary Risk Evaluation (SCORE), pooled cohort equations (PCE), and Reynolds risk score (RRS). We calculated measures of risk discrimination and calibration, and modelled clinical implications of initiating statin therapy in people judged to be at 'high' 10 year CVD risk. Original risk algorithms were recalibrated using the risk factor profile and CVD incidence of target populations. The four algorithms had similar risk discrimination. Before recalibration, FRS, SCORE, and PCE over-predicted CVD risk on average by 10%, 52%, and 41%, respectively, whereas RRS under-predicted by 10%. Original versions of algorithms classified 29-39% of individuals aged ≥40 years as high risk. By contrast, recalibration reduced this proportion to 22-24% for every algorithm. We estimated that to prevent one CVD event, it would be necessary to initiate statin therapy in 44-51 such individuals using original algorithms, in contrast to 37-39 individuals with recalibrated algorithms. CONCLUSION: Before recalibration, the clinical performance of four widely used CVD risk algorithms varied substantially. By contrast, simple recalibration nearly equalized their performance and improved modelled targeting of preventive action to clinical need. © The Author(s) 2018. Published by Oxford University Press on behalf of the European Society of Cardiology.
34.
  • Tin, Adrienne, et al. (författare)
  • Target genes, variants, tissues and transcriptional pathways influencing human serum urate levels
  • 2019
  • Ingår i: Nature Genetics. - 1061-4036 .- 1546-1718. ; 51:10, s. 1459-1474
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Elevated serum urate levels cause gout and correlate with cardiometabolic diseases via poorly understood mechanisms. We performed a trans-ancestry genome-wide association study of serum urate in 457,690 individuals, identifying 183 loci (147 previously unknown) that improve the prediction of gout in an independent cohort of 334,880 individuals. Serum urate showed significant genetic correlations with many cardiometabolic traits, with genetic causality analyses supporting a substantial role for pleiotropy. Enrichment analysis, fine-mapping of urate-associated loci and colocalization with gene expression in 47 tissues implicated the kidney and liver as the main target organs and prioritized potentially causal genes and variants, including the transcriptional master regulators in the liver and kidney, HNF1A and HNF4A. Experimental validation showed that HNF4A transactivated the promoter of ABCG2, encoding a major urate transporter, in kidney cells, and that HNF4A p.Thr139Ile is a functional variant. Transcriptional coregulation within and across organs may be a general mechanism underlying the observed pleiotropy between urate and cardiometabolic traits.</p>
  •  
35.
  • Wormser, David, et al. (författare)
  • Adult height and the risk of cause-specific death and vascular morbidity in 1 million people : individual participant meta-analysis
  • 2012
  • Ingår i: International Journal of Epidemiology. - 0300-5771 .- 1464-3685. ; 41:5, s. 1419-1433
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Background The extent to which adult height, a biomarker of the interplay of genetic endowment and early-life experiences, is related to risk of chronic diseases in adulthood is uncertain. Methods We calculated hazard ratios (HRs) for height, assessed in increments of 6.5 cm, using individual-participant data on 174 374 deaths or major non-fatal vascular outcomes recorded among 1 085 949 people in 121 prospective studies. Results For people born between 1900 and 1960, mean adult height increased 0.5-1 cm with each successive decade of birth. After adjustment for age, sex, smoking and year of birth, HRs per 6.5 cm greater height were 0.97 (95% confidence interval: 0.96-0.99) for death from any cause, 0.94 (0.93-0.96) for death from vascular causes, 1.04 (1.03-1.06) for death from cancer and 0.92 (0.90-0.94) for death from other causes. Height was negatively associated with death from coronary disease, stroke subtypes, heart failure, stomach and oral cancers, chronic obstructive pulmonary disease, mental disorders, liver disease and external causes. In contrast, height was positively associated with death from ruptured aortic aneurysm, pulmonary embolism, melanoma and cancers of the pancreas, endocrine and nervous systems, ovary, breast, prostate, colorectum, blood and lung. HRs per 6.5 cm greater height ranged from 1.26 (1.12-1.42) for risk of melanoma death to 0.84 (0.80-0.89) for risk of death from chronic obstructive pulmonary disease. HRs were not appreciably altered after further adjustment for adiposity, blood pressure, lipids, inflammation biomarkers, diabetes mellitus, alcohol consumption or socio-economic indicators. Conclusion Adult height has directionally opposing relationships with risk of death from several different major causes of chronic diseases.</p>
  •  
36.
  • Carrero, Juan Jesus, et al. (författare)
  • Albuminuria changes are associated with subsequent risk of end-stage renal disease and mortality
  • 2017
  • Ingår i: Kidney International. - 0085-2538 .- 1523-1755. ; 91:1, s. 244-251
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Current guidelines for chronic kidney disease (CKD) recommend using albuminuria as well as estimated glomerular filtration rate (eGFR) to stage CKD. However, CKD progression is solely defined by change in eGFR with little regard to the risk implications of change in albuminuria. This is an observational study from the Stockholm CREAtinine Measurements (SCREAM) project, a health care utilization cohort from Stockholm, Sweden, with laboratory measures from 2006-2011 and follow-up through December 2012. Included were 31,732 individuals with two or more ambulatory urine albumin to creatinine ratio (ACR) tests. We assessed the association between change in ACR during a baseline period of 1, 2, or 3 years and end-stage renal disease (ESRD) or death. Using a 2-year baseline period, there were 378 ESRD events and 1712 deaths during a median of 3 years of follow-up. Compared to stable ACR, a 4-fold increase in ACR was associated with a 3.08-times (95% confidence interval 2.59 to 3.67) higher risk of ESRD while a 4-fold decrease in ACR was associated with a 0.34-times (0.26 to 0.45) lower risk of ESRD. Similar associations were found in people with and without diabetes mellitus, with and without hypertension, and also when adjusted for the change in eGFR during the same period. The association between change in ACR and mortality was weaker: ACR increase was associated with mortality, but the relationship was largely flat for ACR decline. Results were consistent for 1-, 2-, and 3-year ACR changes. Thus, changes in albuminuria are strongly and consistently associated with the risk of ESRD and death.</p>
  •  
37.
  • Chang, Alex R, et al. (författare)
  • Adiposity and risk of decline in glomerular filtration rate meta-analysis of individual participant data in a global consortium
  • 2019
  • Ingår i: BMJ. British Medical Journal. - 1756-1833. ; 364
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>OBJECTIVE:</strong> To evaluate the associations between adiposity measures (body mass index, waist circumference, and waist-to-height ratio) with decline in glomerular filtration rate (GFR) and with all cause mortality.</p><p><strong>DESIGN:</strong> Individual participant data meta-analysis.</p><p><strong>SETTING:</strong> Cohorts from 40 countries with data collected between 1970 and 2017.</p><p><strong>PARTICIPANTS:</strong> Adults in 39 general population cohorts (n=5 459 014), of which 21 (n=594 496) had data on waist circumference; six cohorts with high cardiovascular risk (n=84 417); and 18 cohorts with chronic kidney disease (n=91 607).</p><p><strong>MAIN OUTCOME MEASURES:</strong> GFR decline (estimated GFR decline ≥40%, initiation of kidney replacement therapy or estimated GFR &lt;10 mL/min/1.73 m<sup>2</sup>) and all cause mortality.</p><p><strong>RESULTS:</strong> Over a mean follow-up of eight years, 246 607 (5.6%) individuals in the general population cohorts had GFR decline (18 118 (0.4%) end stage kidney disease events) and 782 329 (14.7%) died. Adjusting for age, sex, race, and current smoking, the hazard ratios for GFR decline comparing body mass indices 30, 35, and 40 with body mass index 25 were 1.18 (95% confidence interval 1.09 to 1.27), 1.69 (1.51 to 1.89), and 2.02 (1.80 to 2.27), respectively. Results were similar in all subgroups of estimated GFR. Associations weakened after adjustment for additional comorbidities, with respective hazard ratios of 1.03 (0.95 to 1.11), 1.28 (1.14 to 1.44), and 1.46 (1.28 to 1.67). The association between body mass index and death was J shaped, with the lowest risk at body mass index of 25. In the cohorts with high cardiovascular risk and chronic kidney disease (mean follow-up of six and four years, respectively), risk associations between higher body mass index and GFR decline were weaker than in the general population, and the association between body mass index and death was also J shaped, with the lowest risk between body mass index 25 and 30. In all cohort types, associations between higher waist circumference and higher waist-to-height ratio with GFR decline were similar to that of body mass index; however, increased risk of death was not associated with lower waist circumference or waist-to-height ratio, as was seen with body mass index.</p><p><strong>CONCLUSIONS:</strong> Elevated body mass index, waist circumference, and waist-to-height ratio are independent risk factors for GFR decline and death in individuals who have normal or reduced levels of estimated GFR.</p>
  •  
38.
  • Coresh, Josef, et al. (författare)
  • Change in albuminuria and subsequent risk of end-stage kidney disease : an individual participant-level consortium meta-analysis of observational studies.
  • 2019
  • Ingår i: The Lancet Diabetes and Endocrinology. - 2213-8587 .- 2213-8595. ; 7:2, s. 115-127
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>BACKGROUND:</strong> Change in albuminuria as a surrogate endpoint for progression of chronic kidney disease is strongly supported by biological plausibility, but empirical evidence to support its validity in epidemiological studies is lacking. We aimed to assess the consistency of the association between change in albuminuria and risk of end-stage kidney disease in a large individual participant-level meta-analysis of observational studies.</p><p><strong>METHODS:</strong> In this meta-analysis, we collected individual-level data from eligible cohorts in the Chronic Kidney Disease Prognosis Consortium (CKD-PC) with data on serum creatinine and change in albuminuria and more than 50 events on outcomes of interest. Cohort data were eligible if participants were aged 18 years or older, they had a repeated measure of albuminuria during an elapsed period of 8 months to 4 years, subsequent end-stage kidney disease or mortality follow-up data, and the cohort was active during this consortium phase. We extracted participant-level data and quantified percentage change in albuminuria, measured as change in urine albumin-to-creatinine ratio (ACR) or urine protein-to-creatinine ratio (PCR), during baseline periods of 1, 2, and 3 years. Our primary outcome of interest was development of end-stage kidney disease after a baseline period of 2 years. We defined an end-stage kidney disease event as initiation of kidney replacement therapy. We quantified associations of percentage change in albuminuria with subsequent end-stage kidney disease using Cox regression in each cohort, followed by random-effects meta-analysis. We further adjusted for regression dilution to account for imprecision in the estimation of albuminuria at the participant level. We did multiple subgroup analyses, and also repeated our analyses using participant-level data from 14 clinical trials, including nine clinical trials not in CKD-PC.</p><p><strong>FINDINGS:</strong> Between July, 2015, and June, 2018, we transferred and analysed data from 28 cohorts in the CKD-PC, which included 693 816 individuals (557 583 [80%] with diabetes). Data for 675 904 individuals and 7461 end-stage kidney disease events were available for our primary outcome analysis. Change in ACR was consistently associated with subsequent risk of end-stage kidney disease. The adjusted hazard ratio (HR) for end-stage kidney disease after a 30% decrease in ACR during a baseline period of 2 years was 0·83 (95% CI 0·74-0·94), decreasing to 0·78 (0·66-0·92) after further adjustment for regression dilution. Adjusted HRs were fairly consistent across cohorts and subgroups (ie, estimated glomerular filtration rate, diabetes, and sex), but the association was somewhat stronger among participants with higher baseline ACR than among those with lower baseline ACR (p<sub>interaction</sub>&lt;0·0001). In individuals with baseline ACR of 300 mg/g or higher, a 30% decrease in ACR over 2 years was estimated to confer a more than 1% absolute reduction in 10-year risk of end-stage kidney disease, even at early stages of chronic kidney disease. Results were generally similar when we used change in PCR and when study populations from clinical trials were assessed.</p><p><strong>INTERPRETATION:</strong> Change in albuminuria was consistently associated with subsequent risk of end-stage kidney disease across a range of cohorts, lending support to the use of change in albuminuria as a surrogate endpoint for end-stage kidney disease in clinical trials of progression of chronic kidney disease in the setting of increased albuminuria.</p><p><strong>FUNDING:</strong> US National Kidney Foundation and US National Institute of Diabetes and Digestive and Kidney Diseases.</p>
  •  
39.
  • Coresh, Josef, et al. (författare)
  • Decline in estimated glomerular filtration rate and subsequent risk of end-stage renal disease and mortality
  • 2014
  • Ingår i: Journal of the American Medical Association (JAMA). - 0098-7484 .- 1538-3598. ; 311:24, s. 2518-2531
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>IMPORTANCE:</strong> The established chronic kidney disease (CKD) progression end point of end-stage renal disease (ESRD) or a doubling of serum creatinine concentration (corresponding to a change in estimated glomerular filtration rate [GFR] of −57% or greater) is a late event.</p><p><strong>OBJECTIVE:</strong> To characterize the association of decline in estimated GFR with subsequent progression to ESRD with implications for using lesser declines in estimated GFR as potential alternative end points for CKD progression. Because most people with CKD die before reaching ESRD, mortality risk also was investigated.</p><p><strong>DATA SOURCES AND STUDY SELECTION:</strong> Individual meta-analysis of 1.7 million participants with 12,344 ESRD events and 223,944 deaths from 35 cohorts in the CKD Prognosis Consortium with a repeated measure of serum creatinine concentration over 1 to 3 years and outcome data.</p><p><strong>DATA EXTRACTION AND SYNTHESIS:</strong> Transfer of individual participant data or standardized analysis of outputs for random-effects meta-analysis conducted between July 2012 and September 2013, with baseline estimated GFR values collected from 1975 through 2012.</p><p><strong>MAIN OUTCOMES AND MEASURES:</strong> End-stage renal disease (initiation of dialysis or transplantation) or all-cause mortality risk related to percentage change in estimated GFR over 2 years, adjusted for potential confounders and first estimated GFR.</p><p><strong>RESULTS:</strong> The adjusted hazard ratios (HRs) of ESRD and mortality were higher with larger estimated GFR decline. Among participants with baseline estimated GFR of less than 60 mL/min/1.73 m2, the adjusted HRs for ESRD were 32.1 (95% CI, 22.3-46.3) for changes of −57% in estimated GFR and 5.4 (95% CI, 4.5-6.4) for changes of −30%. However, changes of −30% or greater (6.9% [95% CI, 6.4%-7.4%] of the entire consortium) were more common than changes of −57% (0.79% [95% CI, 0.52%-1.06%]). This association was strong and consistent across the length of the baseline period (1 to 3 years), baseline estimated GFR, age, diabetes status, or albuminuria. Average adjusted 10-year risk of ESRD (in patients with a baseline estimated GFR of 35 mL/min/1.73 m2) was 99% (95% CI, 95%-100%) for estimated GFR change of −57%, was 83% (95% CI, 71%-93%) for estimated GFR change of −40%, and was 64% (95% CI, 52%-77%) for estimated GFR change of −30% vs 18% (95% CI, 15%-22%) for estimated GFR change of 0%. Corresponding mortality risks were 77% (95% CI, 71%-82%), 60% (95% CI, 56%-63%), and 50% (95% CI, 47%-52%) vs 32% (95% CI, 31%-33%), showing a similar but weaker pattern.</p><p><strong>CONCLUSIONS AND RELEVANCE:</strong> Declines in estimated GFR smaller than a doubling of serum creatinine concentration occurred more commonly and were strongly and consistently associated with the risk of ESRD and mortality, supporting consideration of lesser declines in estimated GFR (such as a 30% reduction over 2 years) as an alternative end point for CKD progression.</p>
  •  
40.
  • Grams, Morgan E, et al. (författare)
  • A Meta-analysis of the Association of Estimated GFR, Albuminuria, Age, Race, and Sex With Acute Kidney Injury
  • 2015
  • Ingår i: American Journal of Kidney Diseases. - 0272-6386 .- 1523-6838. ; 66:4, s. 591-601
  • Tidskriftsartikel (refereegranskat)abstract
    • <p><strong>BACKGROUND:</strong> Acute kidney injury (AKI) is a serious global public health problem. We aimed to quantify the risk of AKI associated with estimated glomerular filtration rate (eGFR), albuminuria (albumin-creatinine ratio [ACR]), age, sex, and race (African American and white).</p><p><strong>STUDY DESIGN:</strong> Collaborative meta-analysis.</p><p><strong>SETTING &amp; POPULATION:</strong> 8 general-population cohorts (1,285,049 participants) and 5 chronic kidney disease (CKD) cohorts (79,519 participants).</p><p><strong>SELECTION CRITERIA FOR STUDIES:</strong> Available eGFR, ACR, and 50 or more AKI events.</p><p><strong>PREDICTORS:</strong> Age, sex, race, eGFR, urine ACR, and interactions.</p><p><strong>OUTCOME:</strong> Hospitalized with or for AKI, using Cox proportional hazards models to estimate HRs of AKI and random-effects meta-analysis to pool results.</p><p><strong>RESULTS:</strong> 16,480 (1.3%) general-population cohort participants had AKI over a mean follow-up of 4 years; 2,087 (2.6%) CKD participants had AKI over a mean follow-up of 1 year. Lower eGFR and higher ACR were strongly associated with AKI. Compared with eGFR of 80mL/min/1.73m(2), the adjusted HR of AKI at eGFR of 45mL/min/1.73m(2) was 3.35 (95% CI, 2.75-4.07). Compared with ACR of 5mg/g, the risk of AKI at ACR of 300mg/g was 2.73 (95% CI, 2.18-3.43). Older age was associated with higher risk of AKI, but this effect was attenuated with lower eGFR or higher ACR. Male sex was associated with higher risk of AKI, with a slight attenuation in lower eGFR but not in higher ACR. African Americans had higher AKI risk at higher levels of eGFR and most levels of ACR.</p><p><strong>LIMITATIONS:</strong> Only 2 general-population cohorts could contribute to analyses by race; AKI identified by diagnostic code.</p><p><strong>CONCLUSIONS:</strong> Reduced eGFR and increased ACR are consistent strong risk factors for AKI, whereas associations of AKI with age, sex, and race may be weaker in more advanced stages of CKD.</p>
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 31-40 av 53
  • Föregående 123[4]56Nästa
Åtkomst
fritt online (11)
Typ av publikation
tidskriftsartikel (53)
Typ av innehåll
refereegranskat (52)
övrigt vetenskapligt (1)
Författare/redaktör
Gudnason, Vilmundur (23)
Hofman, Albert (22)
Gieger, Christian (22)
Coresh, Josef (22)
Verweij, Niek (22)
Zhang, Weihua (21)
visa fler...
Kooner, Jaspal S. (21)
Teumer, Alexander (20)
Mahajan, Anubha (20)
Luan, Jian'an (19)
Kovacs, Peter (19)
Harris, Tamara B. (19)
Lind, Lars, (18)
Scott, Robert A (18)
Feitosa, Mary F. (18)
Esko, Tonu (18)
Hayward, Caroline (18)
Campbell, Harry (18)
Hicks, Andrew A. (18)
Farrall, Martin (18)
Nolte, Ilja M (18)
Kumari, Meena (18)
Kleber, Marcus E. (18)
van der Harst, Pim (17)
Koenig, Wolfgang (17)
Kuusisto, Johanna, (16)
Demirkan, Ayse, (16)
Rose, Lynda M (16)
Langenberg, Claudia (16)
Mangino, Massimo (16)
Jackson, Anne U. (16)
Ferreira, Teresa (16)
Prokopenko, Inga (16)
Morris, Andrew P. (16)
Goel, Anuj (16)
Forouhi, Nita G. (16)
Blangero, John (15)
Hartman, Catharina A ... (15)
Stancáková, Alena, (15)
Salomaa, Veikko (15)
Peters, Annette (15)
McKnight, Barbara (15)
Eriksson, Johan G. (15)
Ärnlöv, Johan, (15)
Franco, Oscar H (15)
Vonk, Judith M (15)
Kanoni, Stavroula (15)
Justice, Anne E. (15)
Milani, Lili (15)
Chambers, John C. (15)
visa färre...
Lärosäte
Uppsala universitet (23)
Lunds universitet (15)
Karolinska Institutet (11)
Göteborgs universitet (8)
Umeå universitet (7)
Högskolan Dalarna (6)
visa fler...
Linköpings universitet (1)
Mittuniversitetet (1)
visa färre...
Språk
Engelska (53)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (52)
Naturvetenskap (1)
Teknik (1)

År

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy