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Dive into the research topics where Peter Nilsson is active.

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Featured researches published by Peter Nilsson.


Journal of Hypertension | 2007

2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC)

Giuseppe Mancia; Robert Fagard; Krzysztof Narkiewicz; Josep Redon; Alberto Zanchetti; Michael Boehm; Thierry Christiaens; Renata Cifkova; Guy De Backer; Anna F. Dominiczak; Maurizio Galderisi; Diederick E. Grobbee; Tiny Jaarsma; Paulus Kirchhof; Sverre E. Kjeldsen; Stéphane Laurent; Athanasios J. Manolis; Peter Nilsson; Luis M. Ruilope; Roland E. Schmieder; Per Anton Sirnes; Peter Sleight; Margus Viigimaa; Bernard Waeber; Faiez Zannad

2007 Guidelines for the Management of Arterial Hypertension : The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).


Nature Genetics | 2008

Meta-analysis of genome-wide association data and large-scale replication identifies additional susceptibility loci for type 2 diabetes

Eleftheria Zeggini; Laura J. Scott; Richa Saxena; Benjamin F. Voight; Jonathan Marchini; Tianle Hu; Paul I. W. de Bakker; Gonçalo R. Abecasis; Peter Almgren; Gitte Andersen; Kristin Ardlie; Kristina Bengtsson Boström; Richard N. Bergman; Lori L. Bonnycastle; Knut Borch-Johnsen; Noël P. Burtt; Hong Chen; Peter S. Chines; Mark J. Daly; Parimal Deodhar; Chia-Jen Ding; Alex S. F. Doney; William L. Duren; Katherine S. Elliott; Michael R. Erdos; Timothy M. Frayling; Rachel M. Freathy; Lauren Gianniny; Harald Grallert; Niels Grarup

Genome-wide association (GWA) studies have identified multiple loci at which common variants modestly but reproducibly influence risk of type 2 diabetes (T2D). Established associations to common and rare variants explain only a small proportion of the heritability of T2D. As previously published analyses had limited power to identify variants with modest effects, we carried out meta-analysis of three T2D GWA scans comprising 10,128 individuals of European descent and ∼2.2 million SNPs (directly genotyped and imputed), followed by replication testing in an independent sample with an effective sample size of up to 53,975. We detected at least six previously unknown loci with robust evidence for association, including the JAZF1 (P = 5.0 × 10−14), CDC123-CAMK1D (P = 1.2 × 10−10), TSPAN8-LGR5 (P = 1.1 × 10−9), THADA (P = 1.1 × 10−9), ADAMTS9 (P = 1.2 × 10−8) and NOTCH2 (P = 4.1 × 10−8) gene regions. Our results illustrate the value of large discovery and follow-up samples for gaining further insights into the inherited basis of T2D.


Blood Pressure | 2014

2013 ESH/ESC Practice Guidelines for the Management of Arterial Hypertension

Giuseppe Mancia; Robert Fagard; Krzysztof Narkiewicz; Josep Redon; Alberto Zanchetti; Michael Böhm; Thierry Christiaens; Renata Cifkova; Guy De Backer; Anna F. Dominiczak; Maurizio Galderisi; Diederick E. Grobbee; Tiny Jaarsma; Paulus Kirchhof; Sverre E. Kjeldsen; Stéphane Laurent; Athanasios J. Manolis; Peter Nilsson; Luis M. Ruilope; Roland E. Schmieder; Per Anton Sirnes; Peter Sleight; Margus Viigimaa; Bernard Waeber; Faiez Zannad

Correspondence to: Professor Giuseppe Mancia, Centro di Fisiologia Clinica e, Ipertensione, Via F. Sforza, 35, 20122, Milano, Italy. Tel: 39 039 233 3357; Fax: 39 039 322 274; E-mail: [email protected], Professor Robert Fagard, Hypertension & Cardiovascular Rehab. Unit, KU Leuven, University, Herestraat 49, 3000 Leuven, Belgium. Tel: 32 16 348 707; Fax: 32 16, 343 766; E-mail: [email protected]


IEEE Journal on Selected Areas in Communications | 2006

Algorithm and implementation of the K-best sphere decoding for MIMO detection

Zhan Guo; Peter Nilsson

K-best Schnorr-Euchner (KSE) decoding algorithm is proposed in this paper to approach near-maximum-likelihood (ML) performance for multiple-input-multiple-output (MIMO) detection. As a low complexity MIMO decoding algorithm, the KSE is shown to be suitable for very large scale integration (VLSI) implementations and be capable of supporting soft outputs. Modified KSE (MKSE) decoding algorithm is further proposed to improve the performance of the soft-output KSE with minor modifications. Moreover, a VLSI architecture is proposed for both algorithms. There are several low complexity and low-power features incorporated in the proposed algorithms and the VLSI architecture. The proposed hard-output KSE decoder and the soft-output MKSE decoder is implemented for 4/spl times/4 16-quadrature amplitude modulation (QAM) MIMO detection in a 0.35-/spl mu/m and a 0.13-/spl mu/m CMOS technology, respectively. The implemented hard-output KSE chip core is 5.76 mm/sup 2/ with 91 K gates. The KSE decoding throughput is up to 53.3 Mb/s with a core power consumption of 626 mW at 100 MHz clock frequency and 2.8 V supply. The implemented soft-output MKSE chip can achieve a decoding throughput of more than 100 Mb/s with a 0.56 mm/sup 2/ core area and 97 K gates. The implementation results show that it is feasible to achieve near-ML performance and high detection throughput for a 4/spl times/4 16-QAM MIMO system using the proposed algorithms and the VLSI architecture with reasonable complexity.


Journal of Hypertension | 2013

2013 Practice guidelines for the management of arterial hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology (ESC): ESH/ESC Task Force for the Management of Arterial Hypertension.

Giuseppe Mancia; Robert Fagard; Krzysztof Narkiewicz; Josep Redán; Alberto Zanchetti; Michael Böhm; Thierry Christiaens; Renata Cifkova; Guy De Backer; Anna F. Dominiczak; Maurizio Galderisi; Diederick E. Grobbee; Tiny Jaarsma; Paulus Kirchof; Sverre E. Kjeldsen; Stéphane Laurent; Athanasios J. Manolis; Peter Nilsson; Luis M. Ruilope; Roland E. Schmieder; Per Anton Sirnes; Peter Sleight; Margus Viigimaa; Bernard Waeber; Faiez Zannad

1. INTRODUCTION1.1 PrinciplesThe 2013 European Society of Hypertension/European Society of Cardiology (ESH/ESC) guidelines continue to adhere to some fundamental principles that inspired the 2003 and 2007 guidelines, namely to base recommendations on properly conducted studies identified from an ext


Nature Genetics | 2009

Association of common variants in NPPA and NPPB with circulating natriuretic peptides and blood pressure

Christopher Newton-Cheh; Martin G. Larson; Daniel Levy; Kenneth D. Bloch; Aarti Surti; Candace Guiducci; Sekar Kathiresan; Emelia J. Benjamin; Joachim Struck; Nils G. Morgenthaler; Andreas Bergmann; Stefan Blankenberg; Frank Kee; Peter Nilsson; Xiaoyan Yin; Leena Peltonen; Erkki Vartiainen; Veikko Salomaa; Joel N. Hirschhorn; Olle Melander; Thomas J. Wang

We examined the association of common variants at the NPPA-NPPB locus with circulating concentrations of the natriuretic peptides, which have blood pressure–lowering properties. We genotyped SNPs at the NPPA-NPPB locus in 14,743 individuals of European ancestry, and identified associations of plasma atrial natriuretic peptide with rs5068 (P = 8 × 10−70), rs198358 (P = 8 × 10−30) and rs632793 (P = 2 × 10−10), and of plasma B-type natriuretic peptide with rs5068 (P = 3 × 10−12), rs198358 (P = 1 × 10−25) and rs632793 (P = 2 × 10−68). In 29,717 individuals, the alleles of rs5068 and rs198358 that showed association with increased circulating natriuretic peptide concentrations were also found to be associated with lower systolic (P = 2 × 10−6 and 6 × 10−5, respectively) and diastolic blood pressure (P = 1 × 10−6 and 5 × 10−5), as well as reduced odds of hypertension (OR = 0.85, 95% CI = 0.79–0.92, P = 4 × 10−5; OR = 0.90, 95% CI = 0.85–0.95, P = 2 × 10−4, respectively). Common genetic variants at the NPPA-NPPB locus found to be associated with circulating natriuretic peptide concentrations contribute to interindividual variation in blood pressure and hypertension.


Annals of the Rheumatic Diseases | 2009

Incidence of severe knee and hip osteoarthritis in relation to different measures of body mass. A population-based prospective cohort study.

L.S. Lohmander; M Gerhardsson de Verdier; J. Rollof; Peter Nilsson; Gunnar Engström

OBJECTIVE To determine in a prospective population-based cohort study relationships between different measures of body mass and the incidence of severe knee and hip osteoarthritis defined as arthroplasty of knee or hip due to osteoarthritis. MATERIALS AND METHODS Body mass index (BMI), waist circumference, waist-hip ratio (WHR), weight and percentage of body fat (BF%) were measured at baseline in 11,026 men and 16,934 women from the general population. The incidence of osteoarthritis over 11 years was monitored by linkage with the Swedish hospital discharge register. RESULTS 471 individuals had knee osteoarthritis and 551 had hip osteoarthritis. After adjustment for age, sex, smoking and physical activity, the relative risks (RR) of knee osteoarthritis (fourth vs first quartile) were 8.1 (95% CI 5.3 to 12.4) for BMI, 6.7 (4.5 to 9.9) for waist circumference, 6.5 (4.6 to 9.43) for weight, 3.6 (2.6 to 5.0) for BF% and 2.2 (1.7 to 3.0) for WHR. Corresponding RR for hip osteoarthritis were 2.6 (2.0 to 3.4) for BMI, 3.0 (2.3 to 4.0) for weight, 2.5 (1.9 to 3.3) for waist, 1.3 (0.99 to 1.6) for WHR and 1.5 (1.2 to 2.0) for BF%. CONCLUSION All measures of overweight were associated with the incidence of knee osteoarthritis, with the strongest relative risk gradient observed for BMI. The incidence of hip osteoarthritis showed smaller but significant differences between normal weight and obesity. Our results support a major link between overweight and biomechanics in increasing the risk of knee and hip osteoarthritis in men and women.


Diabetes | 2008

Common Missense Variant in the Glucokinase Regulatory Protein Gene Is Associated With Increased Plasma Triglyceride and C-Reactive Protein but Lower Fasting Glucose Concentrations

Marju Orho-Melander; Olle Melander; Candace Guiducci; Pablo Perez-Martinez; Dolores Corella; Charlotta Roos; Ryan Tewhey; Mark J. Rieder; Jennifer L. Hall; Gonçalo R. Abecasis; E. Shyong Tai; Cullan Welch; Donna K. Arnett; Valeriya Lyssenko; Eero Lindholm; Richa Saxena; Paul I. W. de Bakker; Noël P. Burtt; Benjamin F. Voight; Joel N. Hirschhorn; Katherine L. Tucker; Thomas Hedner; Tiinamaija Tuomi; Bo Isomaa; Karl-Fredrik Eriksson; Marja-Riitta Taskinen; Björn Wahlstrand; Thomas Edward Hughes; Laurence D. Parnell; Chao Qiang Lai

OBJECTIVE—Using the genome-wide association approach, we recently identified the glucokinase regulatory protein gene (GCKR, rs780094) region as a novel quantitative trait locus for plasma triglyceride concentration in Europeans. Here, we sought to study the association of GCKR variants with metabolic phenotypes, including measures of glucose homeostasis, to evaluate the GCKR locus in samples of non-European ancestry and to fine- map across the associated genomic interval. RESEARCH DESIGN AND METHODS—We performed association studies in 12 independent cohorts comprising >45,000 individuals representing several ancestral groups (whites from Northern and Southern Europe, whites from the U.S., African Americans from the U.S., Hispanics of Caribbean origin, and Chinese, Malays, and Asian Indians from Singapore). We conducted genetic fine-mapping across the ∼417-kb region of linkage disequilibrium spanning GCKR and 16 other genes on chromosome 2p23 by imputing untyped HapMap single nucleotide polymorphisms (SNPs) and genotyping 104 SNPs across the associated genomic interval. RESULTS—We provide comprehensive evidence that GCKR rs780094 is associated with opposite effects on fasting plasma triglyceride (Pmeta = 3 × 10−56) and glucose (Pmeta = 1 × 10−13) concentrations. In addition, we confirmed recent reports that the same SNP is associated with C-reactive protein (CRP) level (P = 5 × 10−5). Both fine-mapping approaches revealed a common missense GCKR variant (rs1260326, Pro446Leu, 34% frequency, r2 = 0.93 with rs780094) as the strongest association signal in the region. CONCLUSIONS—These findings point to a molecular mechanism in humans by which higher triglycerides and CRP can be coupled with lower plasma glucose concentrations and position GCKR in central pathways regulating both hepatic triglyceride and glucose metabolism.


Diabetic Medicine | 2000

Relation between insulin resistance and carotid intima‐media thickness and stenosis in non‐diabetic subjects. Results from a cross‐sectional study in Malmö, Sweden

Bo Hedblad; Peter Nilsson; Lars Janzon; Göran Berglund

Aims To assess whether there is an association between insulin resistance and carotid intima‐media thickness and stenosis in non‐diabetic subjects free from symptomatic cardiovascular disease.


European Heart Journal | 2010

Orthostatic hypotension predicts all-cause mortality and coronary events in middle-aged individuals (The Malmö Preventive Project)

Artur Fedorowski; Lars Stavenow; Bo Hedblad; Göran Berglund; Peter Nilsson; Olle Melander

Aims Orthostatic hypotension (OH) has been linked to increased mortality and incidence of cardiovascular disease in various risk groups, but determinants and consequences of OH in the general population are poorly studied. Methods and results Prospective data of the Swedish ‘Malmö Preventive Project’ (n = 33 346, 67.3% men, mean age 45.7 ± 7.4 years, mean follow-up 22.7 ± 6.0 years) were analysed. Orthostatic hypotension was found in 6.2% of study participants and was associated with age, female gender, hypertension, antihypertensive treatment, increased heart rate, diabetes, low BMI, and current smoking. In Cox regression analysis, individuals with OH had significantly increased all-cause mortality (in particular those aged less than 42 years) and coronary event (CE) risk. Mortality and CE risk were distinctly higher in those with systolic blood pressure (BP) fall ≥30 mmHg [hazard ratio (HR): 1.6, 95% CI 1.3–1.9, P < 0.0001 and 1.6, 95% CI 1.2–2.1, P = 0.001] and diastolic BP fall ≥15 mmHg (HR: 1.4, 95% CI 1.1–1.9, P = 0.024 and 1.7, 95% CI 1.1–2.5, P = 0.01). In addition, impaired diastolic BP response had relatively greater impact (per mmHg) on CE incidence than systolic reaction. Conclusion Orthostatic hypotension can be detected in ∼6% of middle-aged individuals and is often associated with such comorbidities as hypertension or diabetes. Presence of OH increases mortality and CE risk, independently of traditional risk factors. Although both impaired systolic and diastolic responses predict adverse events, the diastolic impairment shows stronger association with coronary disease.

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Heiner Boeing

Cambridge University Hospitals NHS Foundation Trust

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Kay-Tee Khaw

University of Cambridge

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Rudolf Kaaks

German Cancer Research Center

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