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      Coronary Artery Disease: A Study on the Joint Role of Birth Weight, Adenosine Deaminase, and Gender

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          An inverse relationship between birth weight and coronary artery diseases is well documented but it remains unclear which exposure in early life might underlie such association. Recently it has been reported an association between adenosine deaminase genetic polymorphism and coronary artery diseases. Gender differences in the degree of this association have been also observed. These observations prompted us to study the possible joint effects of BW, ADA, and gender on the susceptibility to coronary artery diseases. 222 subjects admitted to hospital for nonfatal coronary artery diseases, and 762 healthy consecutive newborns were studied. ADA genotypes were determined by DNA analysis. A highly significant complex relationship has emerged among ADA, birth weight, and gender concerning their role on susceptibility to coronary artery diseases in adult life. Odds ratio analysis suggests that low birth weight is more important in females than in males. ADA 2 allele appears protective in males, while in females such effect is obscured by birth weight.

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          Most cited references 32

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          Is birth weight a risk factor for ischemic heart disease in later life?

          An inverse association between birth weight and ischemic heart disease (IHD) has been seen in observational studies. We wanted to determine the strength and consistency of the association between birth weight and subsequent IHD. We conducted a systematic review of observational studies. Seventeen published studies of birth weight and subsequent IHD were identified that included a total of 144,794 singletons. Relative risk estimates for the association between birth weight and IHD were available from 16 of these studies. Additional data from 2 unpublished studies of 3801 persons were also included. In total, the analyses included data from 18 studies on 4210 nonfatal and 3308 fatal IHD events in 147,009 persons. The mean weighted estimate for the association between birth weight and the combined outcome of nonfatal and fatal IHD was 0.84 (95% CI: 0.81, 0.88) per kilogram of birth weight (P<0.0001). No significant heterogeneity was observed between estimates in different studies (P=0.09), nor was there evidence of publication bias (P=0.3, Begg test). Neither restricting the analysis to fatal IHD events nor adjusting for socioeconomic status had any appreciable effect on the findings. These findings are consistent with a 1 kg higher birth weight being associated with a 10-20% lower risk of subsequent IHD. However, even if causal, interventions to increase birth weight are unlikely to reduce the incidence of IHD materially. Further studies are needed to determine whether the observed association reflects a stronger underlying association with a related exposure or is due (at least in part) to residual confounding.
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            No increased mortality in later life for cohorts born during famine.

            Nutrition early in life may influence adult mortality. The fetal-origins hypothesis suggests that nourishment before birth and during the individual's infancy programs the development of risk factors for several important diseases of middle and old age. The present study was designed to evaluate the impact of extreme nutritional deprivation in utero and during infancy and early childhood on mortality in later life. The authors analyzed the survival of the cohorts born in Finland during the severe 1866-1868 famine and during the 5 years immediately preceding and 5 years immediately following the famine. The study included 331,932 individuals born prior to the famine, 161,744 born during the famine, and 323,321 born after the famine. The authors assessed survival by cohorts from birth to age 17 years and from age 17 to 40, 60, and 80 years, as well as average length of life after age 80 years. Survival from birth to age 17 years was significantly lower in cohorts born before and during the famine than in the cohorts born after the famine (males, 0.566 vs. 0.671, a difference of 0.105 (95% confidence interval (CI) 0.102-0.108); females, 0.593 vs. 0.692, a difference of 0.099 (95% CI 0.096-0.102)). At subsequent ages, including old age, mortality was practically identical in the famine-born cohorts and in the five cohorts born before and after the crisis. For both males and females, survival from 17 to 80 years and mean remaining lifetime at age 80 years were very similar across the 13 cohorts studied. These findings suggest that, although cohorts subjected to prolonged and extreme nutritional deprivation in utero and during infancy and early childhood suffer an immediate rise in mortality, after the crisis has passed, they carry no aftereffects that influence their survival in later life.
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              Bilirubin is an effective antioxidant of peroxynitrite-mediated protein oxidation in human blood plasma.

              Bilirubin is a bile pigment that may have an important role as an antioxidant. Its antioxidant potential is attributed mainly to the scavenging of peroxyl radicals. We investigated the reaction of bilirubin with peroxynitrite in phosphate buffer and in blood plasma. In phosphate buffer bilirubin was rapidly oxidized by micromolar concentrations of peroxynitrite, and its oxidation yield was higher at alkaline pH with an apparent pKa = 6.9. In contrast, the major oxidation product of bilirubin in plasma was biliverdin, and the pH profile of its oxidation yield showed a slightly increased oxidation at acidic pH without a clear inflection point. The addition of NaHCO3 to bilirubin decreased the peroxynitrite-dependent oxidation, suggesting that the reactive intermediates formed in the reaction between CO2 and peroxynitrite are less efficient oxidants of bilirubin. The antioxidant role of bilirubin was investigated in some peroxynitrite-mediated plasma protein modifications that are enhanced by CO2 (tryptophan oxidation and protein tyrosine nitration) or slightly decreased by CO2 (protein carbonyl groups). Bilirubin in the micromolar concentration range afforded a significant protection against all these oxidative modifications and, notably, protected plasma proteins even when the pigment was added 5 s after peroxynitrite (i.e., when peroxynitrite is completely decomposed). The loss of tryptophan fluorescence triggered by peroxynitrite was a relatively slow process fulfilled only after a few minutes. After this time, bilirubin was unable to reduce the tryptophan loss, and it was unable to reduce previously formed nitrated albumin or previously formed carbonyls. We deduce that bilirubin in plasma cannot react to a significant extent with peroxynitrite, and we suggest that bilirubin, through a hydrogen donation mechanism, participates as a scavenger of secondary oxidants formed in the oxidative process.

                Author and article information

                Cardiol Res Pract
                Cardiology Research and Practice
                SAGE-Hindawi Access to Research
                13 April 2010
                : 2009
                1Department of Biopathology and Imaging Diagnostics, University of Tor Vergata, 00133 Rome, Italy
                2Department of Cardiology, Valmontone Hospital, Rome, Italy
                3Department of Biology, MCA University of Camerino, Camerino, Italy
                4Unit of Gynecology, Valmontone Hospital, Rome, Italy
                5Department of Obstetrics and Gynaecology, Holy Hearth Catholic University, Rome, Italy
                Author notes
                *F. Gloria-Bottini: gloria@

                Recommended by Gerasimoss Filippatos

                Copyright © 2009 F. Gloria-Bottini et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Research Article

                Cardiovascular Medicine


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