Procuring infrastructure for international sporting events: mapping the field for IPACS and beyond

This article presents the results of a study of infrastructure procurement for international sporting events. The objective was to map both the institutional frameworks and the procedures and governance mechanisms. We were concerned only with the acquisition process and not with prior decisions on whether to host events, what to procure (such as the number and siting of stadiums) or subsequent maintenance. The aim was to provide information relevant to studying the implementation of procurement objectives and the risks to attaining those objectives and to lay the foundations for further work. The study originated in work by the authors in collaboration with the OECD to assist the International Partnership Against Corruption in Sport (IPACS) in managing integrity risks, but also provides a map that can facilitate future study of other issues, such as sustainability. The study sought to map procurement for key sport-specific infrastructure (such as stadiums and swimming pools) and a sample of other infrastructure (sport-specific, sport-related – such as athlete accommodation – and/or other infrastructure procured for the event (such as transport facilities) for 14 international events. It covered events of various sizes and types in the ten-year period to 2018, using public sources. Study data from the first ten projects above was used as the basis for the 2019 IPACS report on procurement standards and risk management in procuring infrastructure for sporting events (IPACS report). That report analysed the aggregate data to identify and analyse integrity risks and make concrete proposals for mitigating them. This article supplements the IPACS report by giving more information on the methodology; providing data from four additional projects, which offer further evidence and insights; and presenting the key information through a project-based, as well as aggregate, approach, to place it in context

CYP7A1 Gene Polymorphism Located in the 5′ Upstream Region Modifies the Risk of Coronary Artery Disease

Background. 7-Alpha cholesterol hydroxylase (CYP7A1), the first enzyme of classic conversion pathway leading from cholesterol to bile acids synthesis, is encoded by CYP7A1 gene. Its single nucleotide polymorphisms (SNPs) influence serum lipid levels and may be related to impaired lipid profile leading to coronary artery disease (CAD). The aim of the present study was to analyze the possible association between the rs7833904 CYP7A1 polymorphism and premature CAD. Material and Methods. Serum lipid levels and rs7833904 SNP were determined in 419 subjects: 200 patients with premature CAD and 219 age and sex matched controls. Results. The A allele carrier state was associated with CAD (OR = 1.76, 95% CI; 1.14–2.71, P=0.014). The effect was even stronger in the male subgroups (OR = 2.16, 95% CI; 1.28–3.65, P=0.003). There was no effect in the females. Risk factors of CAD and clinical phenotype of atherosclerosis were not associated with genotype variants of the rs7833904 SNP. Lipid profiles also did not differ significantly between individual genotypes. Conclusion. The CYP7A1 rs7833904 polymorphism may modify the risk of CAD. This effect is especially strong in male subjects. The studied polymorphism does not significantly influence serum lipid levels, in the present study

The rs2516839 Polymorphism of the USF1 Gene May Modulate Serum Triglyceride Levels in Response to Cigarette Smoking

Single nucleotide polymorphisms (SNPs) of the USF1 gene (upstream stimulatory factor 1) influence plasma lipid levels. This study aims to determine whether USF1 SNPs interact with traditional risk factors of atherosclerosis to increase coronary artery disease (CAD) risk. In the present study serum lipid levels and USF1 gene polymorphisms (rs2516839 and rs3737787) were determined in 470 subjects: 235 patients with premature CAD and 235 controls. A trend of increasing triglycerides (TG) levels in relation to the C allele dose of rs2516839 SNP was observed. The synergistic effect of cigarette smoking and C allele carrier state on CAD risk was also found (SIM = 2.69, p = 0.015). TG levels differentiated significantly particular genotypes in smokers (1.53 mmol/L for TT, 1.80 mmol/L for CT and 2.27 mmol/L for CC subjects). In contrast, these differences were not observed in the non-smokers subgroup (1.57 mmol/L for TT, 1.46 mmol/L for CT and 1.49 mmol/L for CC subjects). In conclusion, the rs2516839 polymorphism may modulate serum triglyceride levels in response to cigarette smoking. Carriers of the C allele seem to be particularly at risk of CAD, when exposed to cigarette smoking

Evaluation of Apolipoprotein M Serum Concentration as a Biomarker of HNF-1alpha MODY

Apolipoprotein M (apoM) is a 26-kDa protein expressed mainly in the liver and kidneys. It is present predominantly in high-density lipoproteins (HDL). ApoM expression is influenced by the hepatocyte nuclear factor-1α (HNF-1α), which is a transcription factor associated with the pathogenesis of MODY. Some earlier data suggested that apoM levels were lower in the serum of HNF-1α MODY subjects, than in that of other diabetics and healthy controls. The aim of this study was to evaluate apoM as a biomarker for HNF-1α MODY. We included in this study 48 HNF-1α mutation carriers (40 diabetic patients and 8 subjects with normal glucose levels in the fasted state) from the Polish Nationwide Registry of MODY. In addition, we examined 55 T2DM patients and 55 apparently healthy volunteers who had normal fasting glucose levels. ApoM was measured by the sandwich dot-blot technique with recombinant apoM (Abnova) as a protein standard, mouse anti-human apoM monoclonal primary antibody and rat anti-mouse HRP-conjugated secondary antibody (BD Biosciences). Mean apoM level in the MODY group was 13.6 μg/ml, SD 1.9 (13.5 μg/ml, SD 1.7 in diabetic subjects and 13.9 μg/ml, SD 2.0 in non-diabetic mutation carriers respectively). In the T2DM group, mean apoM level was 13.7 μg/ml, SD 2.1, while it reached 13.8 μg/ml, SD 2.0 in healthy controls. There was no difference between apoM serum concentrations in all the study groups. In summary, our study showed no association between HNF-1α mutations resulting in MODY phenotype and apoM levels. Thus, we cannot confirm the clinical usefulness of apoM as a biomarker of HNF-1α MODY