sj-docx-1-sjp-10.1177_14034948221119611 – Supplemental material for Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study

Supplemental material, sj-docx-1-sjp-10.1177_14034948221119611 for Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study by Jukka Pihlman, Joel Nuotio, Suvi Rovio, Katja Pahkala, Saku Ruohonen, Eero Jokinen, Tomi P. Laitinen, David P. Burgner, Nina Hutri-Kähönen, Päivi Tossavainen, Leena Taittonen, Mika Kähönen, Jorma S.A. Viikari, Olli T. Raitakari, Costan G. Magnussen and Markus Juonala in Scandinavian Journal of Public Health</p

sj-docx-2-sjp-10.1177_14034948221119611 – Supplemental material for Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study

Supplemental material, sj-docx-2-sjp-10.1177_14034948221119611 for Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study by Jukka Pihlman, Joel Nuotio, Suvi Rovio, Katja Pahkala, Saku Ruohonen, Eero Jokinen, Tomi P. Laitinen, David P. Burgner, Nina Hutri-Kähönen, Päivi Tossavainen, Leena Taittonen, Mika Kähönen, Jorma S.A. Viikari, Olli T. Raitakari, Costan G. Magnussen and Markus Juonala in Scandinavian Journal of Public Health</p

sj-docx-3-sjp-10.1177_14034948221119611 – Supplemental material for Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study

Supplemental material, sj-docx-3-sjp-10.1177_14034948221119611 for Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study by Jukka Pihlman, Joel Nuotio, Suvi Rovio, Katja Pahkala, Saku Ruohonen, Eero Jokinen, Tomi P. Laitinen, David P. Burgner, Nina Hutri-Kähönen, Päivi Tossavainen, Leena Taittonen, Mika Kähönen, Jorma S.A. Viikari, Olli T. Raitakari, Costan G. Magnussen and Markus Juonala in Scandinavian Journal of Public Health</p

sj-docx-4-sjp-10.1177_14034948221119611 – Supplemental material for Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study

Supplemental material, sj-docx-4-sjp-10.1177_14034948221119611 for Exposure to parental smoking and cardiac structure and function in adulthood: the Cardiovascular Risk in Young Finns Study by Jukka Pihlman, Joel Nuotio, Suvi Rovio, Katja Pahkala, Saku Ruohonen, Eero Jokinen, Tomi P. Laitinen, David P. Burgner, Nina Hutri-Kähönen, Päivi Tossavainen, Leena Taittonen, Mika Kähönen, Jorma S.A. Viikari, Olli T. Raitakari, Costan G. Magnussen and Markus Juonala in Scandinavian Journal of Public Health</p

Slamming the door on trade policy discretion? : the WTO Appellate Body’s ruling on market distortions and production costs in EU-Biodiesel (Argentina)

This paper presents a legal-economic analysis of the Appellate Body’s decision that the WTO’s Anti-Dumping Agreement (ADA) precludes countries from taking into account government-created price distortions of major inputs when calculating anti-dumping duties, made in EU-Biodiesel (Argentina). In this case, the EU made adjustments to the price of biodiesel’s principal input – soybeans – in determining the cost of production of biodiesel in Argentina. The adjustment was made based on the uncontested finding that the price of soybeans in Argentina was distorted by the existence of an export tax scheme that resulted in artificially low soybean prices. The Appellate Body found that the EU was not permitted to take tax policy-induced price distortions into account in calculating dumping margins. We analyze the economic rationale for Argentina’s export tax system, distortions in biodiesel markets in Argentina and the EU, and the remaining trade policy options for addressing distorted international prices. We also assess whether existing subsidies disciplines would be more effective in addressing this problem and conclude that they would not

Coronary Artery Disease–Associated Locus on Chromosome 9p21 and Early Markers of Atherosclerosis

Background— Genome-wide association studies have recently identified a locus on chromosome 9p21 that influences risk of coronary artery disease (CAD). The effect of the locus on early markers of atherosclerosis is unknown. We examined its association with carotid intima-media thickness (CIMT) and brachial flow-mediated dilatation (FMD). Methods and Results— We genotyped 2277 individuals, age 24 to 39 years, from the Cardiovascular Risk in Young Finns Study with CIMT and FMD measurements and 1295 individuals, age 46 to 76 years, from the Health 2000 Survey with CIMT for rs1333049, the chromosome 9p21 variant showing the strongest association with CAD. Both mean and maximum CIMT were significantly higher (P<0.001) in the older subjects of the Health 2000 Survey compared with the Young Finns Study. However, there was no association of the rs1333049 genotype with either mean or maximum CIMT at either age (P=0.959 and 0.977 for the 2 phenotypes in the Young Finns Study and P=0.714 and 0.725 in the Health 2000 Survey). Similarly, there was no association of the locus with variation in FMD in the Young Finns cohort (P=0.521). Conclusions— The chromosome 9p21 locus does not influence CAD risk through a mechanism that also affects CIMT or induces early changes in FMD. We examined the association with carotid intima-media thickness and brachial flow mediated dilatation of the recently identified susceptibility locus for coronary artery disease on chromosome 9p21. We found no evidence that the risk variant affects either of these early markers of atherosclerosis, suggesting an alternate mechanism for its effect on risk of CAD

Sixteen new lung function signals identified through 1000 Genomes Project reference panel imputation

Lung function measures are used in the diagnosis of chronic obstructive pulmonary disease. In 38,199 European ancestry individuals, we studied genome-wide association of forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and FEV1/FVC with 1000 Genomes Project (Phase 1) imputed genotypes and followed up top associations in 54,550 Europeans. We identify 14 novel loci (P<5x10-8) in or near ENSA, RNU5F-1, KCNS3, AK097794, ASTN2, LHX3, CCDC91, TBX3, TRIP11, RIN3, TEKT5, LTBP4, MN1, AP1S2, and two novel signals at known loci NPNT and GPR126, providing a basis for new understanding of the genetic determinants of these traits and pulmonary diseases in which they are altered